Nyu Nursing: Ae Ii Test 1, Book Material

Front 1

reduced vision & blindness

Back 1

Different forms of reduced vision may affect any or all aspects of vision, including color, light, image, movement, and acuity. Reduced vision may be temporary, such as when cataracts obscure vision but surgery has not yet been planned or performed. Patients are legally blind if their best visual acuity with corrective lenses is 20/200 or less in the better eye or if the widest diameter of the visual field in that eye is no greater than 20 degrees.

Blindness can occur in one or both eyes. When one eye is affected, the field of vision is narrowed and depth perception is impaired. Central vision can be impaired by diseases involving the macula, such as macular edema or macular degeneration. Loss of peripheral vision occurs with glaucoma. The loss of side vision affects the patient's ability to drive and awareness of hazards in the periphery. (Ignatavicius 2013, p. 1073)

Front 2

reduced vision care

Back 2

Nursing interventions for the patient with reduced sight focus on communication, safety, ambulation, self-care, and support.

Communication is important in helping the patient remain independent and connected to the world. Reduced vision is a common occurrence, and many adaptive devices are available to help the person maintain independence. Many towns and cities have auditory traffic signals so that persons with reduced vision can know when it is safe to cross a street. Curbs in these areas may have high-contrast color paint to let the person know when to step up or down. Libraries have large-print books and books on tape. “Talking” clocks, watches, and timers are available. Playing cards, games, restaurant menus, calendars, and instruction booklets are available in large print sizes. Computer keyboards with high contrast and larger letters in the keys are available, as are large screens. Direct the patient with reduced vision to the local resources to obtain adaptive items and to learn how to use them (Watkinson, 2009).

Safety is a major issue for the person with reduced vision. For patients at home with reduced vision, the home is the place where they feel most safe. They are familiar with room and item location. For example, they may have counted the number of footsteps needed to move from one area to another within the home. It is important to stress to family and friends that changes in item location should not be made without input from the person with reduced vision.

Even people who have experienced gradually reduced vision over time and who have had time to adjust may benefit from having a person with vision assist in making adaptations in the home. Adaptations may include the following:

• Using tape and a heavy black marker, mark the 350-degree temperature setting on the oven and mark the 70-degree temperature setting on the heating or cooling thermostat.

• Paint or mark light switches in a deep color that contrasts with the surrounding wall.

• Label canned goods with large, bold, black letters on white tape.

• Teach the patient to feel for the crease in paper milk cartons that indicates the place to open the spout.

• Help the patient differentiate different drugs by altering the shape or contours of a bottle. Rubber bands can be wound around a bottle to change its texture. Raised symbols can be glued to caps to make identification easier.

The patient is most at risk for safety problems in an unfamiliar or changing environment. When a person with reduced vision must be hospitalized, promote safety and independence by orienting him or her to the new environment.

Most people with reduced vision had sight at some time and have background knowledge regarding size and shape that can be used when providing information. Many blind people have some degree of sight. When talking with a person who has limited sight or is blind, always use a normal tone of voice unless he or she is has a hearing problem.

First orient the patient to the immediate environment, including the size of the room. Use one object in the room, such as a chair or hospital bed, as the focal point during your description. Guide the person to the focal point, and orient him or her to the environment from that point. For example, you might say, “To the left of the bed is a chair.” Then describe all other objects in relation to the focal point. Go with the patient to other important areas, such as the bathroom, so that he or she can learn their locations. Highlight the location of the toilet, sink, and toilet paper holder. Never leave the patient with reduced vision in the center of an unfamiliar room.

Patients with reduced vision prefer to establish the location of important objects, such as the call light, water pitcher, and clock. Once their location has been fixed, do not move these items without the patient's consent. Do not move the location of chairs, stools, and wastebaskets without consulting the patient.

At mealtime, set up food on the tray using clock placement. For example, “There is sliced ham at the 6 o'clock position; peas are located at the 3 o'clock position; to the right of the plate is coffee; salt and pepper are next to the coffee.”

Ambulation with a patient who has reduced vision involves allowing him or her to grasp your arm at the elbow. Keep the arm close to your body so that he or she can detect your direction of movement. Alert the patient when obstacles are in the path ahead.

Patients may use a cane to detect obstacles, such as furniture, walls, or curbs. The cane is held in the dominant hand several inches off the floor and sweeps the ground where his or her foot will be placed next. The laser cane sends out signals to help detect obstacles.

Self-care and the ability to control the environment are important. Knock on the door before entering the hospital room or any other environment of a patient with reduced vision. State your name and the reason for visiting when entering the room. Coordinate with other members of the health care team to ensure this etiquette is used consistently. Mark the door to the room to indicate it is occupied by a person with reduced vision.

Support is needed, especially when the reduced vision is of sudden onset and may be permanent. Patients’ reactions to the loss of sight are similar to the reaction to loss of a body part. Allow the newly blind person a period of grieving for the “dead” (nonseeing) eye. He or she may feel hopeless and angry. With time, anger usually gives way to acceptance. The ability to cope may begin within days, but some patients mourn for months or years.

Patients benefit from the honest support that you can provide. They need to hear that it is normal to mourn, to cry, and to feel the loss. Help them move toward acceptance by encouraging the mastery of one task at a time and by providing positive reinforcement for each success. (Ignatavicius 2013, pp. 1074-1075)

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reduced vision care
(quick look)

Back 3

Always knock or announce your entrance into the patient's room or area and introduce yourself.

Ensure that all members of the health care team also use this courtesy of announcement and introduction.

Ensure that the patient's reduced vision is noted in the medical record, is communicated to all staff, is marked on the call board, and is identified on the door of the patient's room.

Determine to what degree the patient can see anything.

Orient the patient to the environment, counting steps with him or her to the bathroom.

Assist the patient in placing objects on the bedside table or in the bed and around the bed and room, and do not move them without the patient's permission.

Remove all objects and clutter between the patient's bed and the bathroom.

Ask the patient what type of assistance he or she prefers for grooming, toileting, eating, and ambulating, and communicate these preferences with the staff.

Describe food placement on a plate in terms of a clock face.

Open milk cartons; open salt, pepper, and condiment packages; and remove lids from cups and bowls.

Unless the patient also has a hearing problem, use a normal tone of voice when speaking.

When walking with the patient, offer him or her your arm and walk a step ahead. (Ignatavicius 2013, p. 1074)

Front 4

nursing diagnoses for patients with visual problems

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Disturbed sensory perception: Visual
Risk for injury
Social isolation
Self care deficit
Fear
Anxiety

Front 5

conjunctivitis

Back 5

Conjunctivitis is an inflammation or infection of the conjunctiva. Inflammation occurs from exposure to allergens or irritants. Infectious conjunctivitis occurs with bacterial or viral infection and is readily transmitted from person to person (Saligan & Yeh, 2008).

Allergic conjunctivitis manifestations are edema, a sensation of burning, a “bloodshot” eye appearance, excessive tears, and itching. Management includes vasoconstrictor and corticosteroid eyedrops (see Chart 49-2). Teach women to avoid using makeup near the eye until all symptoms have subsided.

Bacterial conjunctivitis, or “pink eye,” is usually caused by Staphylococcus aureus or Haemophilus influenzae. Manifestations are blood vessel dilation, mild edema, tears, and discharge. The discharge is watery at first and then becomes thicker, with shreds of mucus.

Cultures of the drainage are obtained to identify the organism. Drug therapy with topical antibiotics is prescribed to eliminate the infection. Nursing interventions focus on preventing infection spread to the other eye or to other people. Document the amount, color, and type of drainage. Remind the patient to wash his or her hands after touching the eye and before using eyedrops. Warn him or her not to touch the unaffected eye without first washing the hands and to avoid sharing washcloths and towels with others. Instruct women to discard eye makeup and applicators used at the time the infection developed to avoid the possibility of recontamination. (Ignatavicius 2013, p. 1056)

Front 6

glaucoma

Back 6

Glaucoma is a group of eye disorders resulting in increased IOP. Intraocular pressure (IOP) is the fluid pressure within the eye. As described in Chapter 48, the eye is a hollow organ. For proper eye function, the gel in the posterior segment (vitreous humor) and the fluid in the anterior segment (aqueous humor) must be present in set amounts that apply pressure inside the eye to keep it ball-shaped.

The gel-like vitreous humor is made as the eyes form and grow. Once eye growth is complete, this volume does not change. The aqueous humor, however, is continuously made from blood plasma. The ciliary bodies located behind the iris and just in front of the lens make and secrete this fluid (see Fig. 48-2 in Chapter 48). The fluid flows through the pupil into the bulging area in front of the iris. At the outer edges of the iris beneath the cornea, blood vessels collect fluid and return it to the blood. Usually about 1 mL of aqueous humor is present at all times, but it is continuously made and reabsorbed at a rate of about 5 mL daily. A normal IOP requires a balance between production and outflow of aqueous humor. If the IOP becomes too high, the extra pressure compresses retinal blood vessels and photoreceptors and their synapsing nerve fibers. This compression results in poorly oxygenated photoreceptors and nerve fibers. These sensitive nerve tissues become ischemic and die. When too many have died, sight is lost and the person is permanently blind. Tissue damage usually starts in the periphery and moves inward toward the fovea centralis. Left untreated, glaucoma can result in blindness. Glaucoma is usually painless, and the patient may be unaware of a gradual reduction in vision.

There are several causes and types of glaucoma (Table 49-3). It is classified as primary, secondary, or associated. In primary glaucoma, the most common form, the structures involved in circulation and reabsorption of the aqueous humor undergo direct pathologic change.

Primary Glaucoma
--Aging, Heredity, Central retinal vein occlusion

Associated Glaucoma
--Diabetes mellitus, Hypertension, Severe myopia, Retinal detachment

Secondary Glaucoma
--Uveitis, Iritis, Neovascular disorders, Trauma, Ocular tumors, Degenerative disease, Eye surgery

Glaucoma is a common cause of blindness in affluent countries. It is age-related, occurring in about 10% of people older than 80 years.

(Ignatavicius 2013, pp. 1062-1064)

Front 7

glaucoma
assessment and diagnosis

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Physical Assessment/Clinical Manifestations

Ophthalmoscopic examination of the patient with glaucoma shows cupping and atrophy of the optic disc. It becomes wider and deeper and turns white or gray. Visual fields are measured to determine the extent of peripheral vision loss. In POAG, the visual fields first show a small defect that gradually progresses to a larger field defect.

Manifestations of acute angle-closure glaucoma differ from those of POAG. The onset is acute, and the patient has sudden, severe pain around the eyes that radiates over the face. Headache or brow pain, nausea, and vomiting may occur. Other manifestations include seeing colored halos around lights and sudden blurred vision with decreased light perception. The sclera may appear reddened and the cornea foggy. Ophthalmoscopic examination reveals a shallow anterior chamber, cloudy aqueous humor, and a moderately dilated, nonreactive pupil.

Diagnostic Assessment

An elevated intraocular pressure (IOP) is measured by tonometry. In open-angle glaucoma, the tonometry reading is between 22 and 32 mm Hg (normal is 10 to 21 mm Hg). In angle-closure glaucoma, the tonometry reading may be 30 mm Hg or higher. Visual field testing by perimetry is performed, as is visualization by gonioscopy to determine whether the angle is open or closed (Sharts-Hopko & Glynn-Milley, 2009). Usually, the optic nerve is imaged to determine to what degree nerve damage is present. (Ignatavicius 2013, p. 1064)

Front 8

glaucoma
drug therapy

Back 8

Drug therapy for glaucoma focuses on reducing IOP through these mechanisms:

• Constricting the pupil so that the ciliary muscle is contracted, allowing better circulation of the aqueous humor to the site of absorption

• Reducing the production or increasing the absorption of aqueous humor

Eyedrop drugs are the mainstay of control for glaucoma. They do not improve lost vision but prevent more damage by decreasing IOP. The classes of drugs to manage glaucoma are the prostaglandins agonists, adrenergic agonists, beta-adrenergic blockers, cholinergic agonists, and carbonic anhydrase inhibitors. Most eyedrops cause tearing, mild burning, and blurred vision for a few minutes after instilling the drug. The sclera may also become red and itchy. Specific drug actions and nursing interventions are listed in Chart 49-7.

The priority nursing intervention for the patient on drug therapy for glaucoma is teaching. Provide written instructions similar to those in Chart 48-2 in Chapter 48. The benefit of drug therapy is achieved only when the drugs are used on the prescribed schedule, usually every 12 hours. Teach patients the importance of instilling the drops on time and not skipping doses. When more than one drug is prescribed, teach him or her to wait 10 to 15 minutes between drug instillations to prevent one drug from “washing out” or diluting another drug. Stress the need for good handwashing, keeping the eyedrop container tip clean, and avoiding touching the tip to any part of the eye. Also teach the technique of punctal occlusion (placing pressure on the corner of the eye near the nose) immediately after eyedrop instillation to prevent systemic absorption of the drug.

Systemic osmotic drugs may be given for angle-closure glaucoma as part of emergency management to rapidly reduce IOP. These agents include oral glycerin and IV mannitol (Osmitrol).

***Most eyedrops used for glaucoma therapy can be absorbed systemically and cause serious systemic problems. Although punctal occlusion should be used after instilling any type of eyedrop, it is critical to teach patients to use the technique with eyedrops for glaucoma.

(Ignatavicius 2013, p. 1066-1067)

Front 9

glaucoma
surgical management

Back 9

urgical Management

Surgery is used when drugs for the patient with open-angle glaucoma are not effective at controlling IOP. Two common procedures are laser trabeculoplasty and filtering microsurgery. A laser trabeculoplasty burns the trabecular meshwork, scarring it and causing the meshwork fibers to tighten. Tight fibers increase the size of the spaces between the fibers, improving outflow of aqueous humor and reducing IOP. Filtering microsurgery creates a drainage hole in the iris between the posterior and anterior chambers. Both are ambulatory surgery procedures.

If glaucoma fails to respond to common approaches or if the drainage hole does not remain open, other more invasive procedures may be used. These include deep sclerectomy, viscocanalostomy, or an implanted shunt (Sharts-Hopko & Glynn-Milley, 2009).

A sclerectomy for glaucoma involves removing a section of sclera and trabecular meshwork along with a section of the canal of Schlemm to allow more direct drainage of aqueous humor. A viscocanalostomy requires removal of a section of sclera but the main focus is artificially widening the canal of Schlemm to improve drainage. The implanted shunt has a small tube or filament connected to a flat plate positioned on the outside of the eye in the eye orbit. (The plate is not visible on the front part of the eye.) The open part of the fine tube is placed into the front chamber of the eye, just in front of the iris. The (Ignatavicius 2013, p. 1067)

Front 10

glaucoma
nursing care

Back 10

Nursing Focus On The Older Adult:
Promote Independent Living in Patients with Impaired Vision

Drugs
--Having a neighbor, relative, friend, or visiting nurse visit once a week to measure the proper drugs for each day may be helpful.
--If the patient is to take drugs more than once each day, it is helpful to use a container of a different shape (with a lid) each time. For example, if the patient is to take drugs at 9 AM, 1 PM, and 9 PM, the 9 AM drugs would be placed in a round container, the 1 PM drugs in a square container, and the 9 PM drugs in a triangular container.
--It is helpful to place each day's drug containers in a separate box with raised letters on the side of the box spelling out the day.
--“Talking clocks” are available for the patient with low vision.
--Some drug boxes have alarms that can be set for different times.

Communication
--Telephones with large, raised block numbers may be helpful. The best models are those with black numbers on a white phone or white numbers on a black phone.
--Telephones that have a programmable, automatic dialing feature are very helpful. Programmed numbers should include those for the fire department, police, relatives, friends, neighbors, and 911.

Safety
--It is best to leave furniture the way the patient wants it and not move it.
--Throw rugs are best eliminated.
--Appliance cords should be short and kept out of walkways.
--Lounge-style chairs with built-in footrests are preferable to footstools.
--Nonbreakable dishes, cups, and glasses are preferable to breakable ones.
--Cleansers and other toxic agents should be labeled with large, raised letters.
--Hook-and-loop (Velcro) strips at hand level may help mark the locations of switches and electrical outlets.

Food Preparation
--Meals on Wheels is a service that many older adults find helpful. This service brings meals at mealtime, cooked and ready to eat. The cost of this service varies, depending on the patient's ability to pay.
--Many grocery stores offer a “shop by telephone” service. The patient can either complete a computer booklet indicating types, amounts, and brands of items desired, or the store will complete this booklet over the telephone by asking the patient specific information. The store then delivers groceries to the patient's door (many stores also offer a “put away” service) and charges the patient's bank card.
--A microwave oven is a safer means of cooking than a standard stove, although many older patients are afraid of microwave ovens. If the patient has and will use a microwave oven, others can prepare meals ahead of time, label them, and freeze them for later use. Also, many microwavable complete frozen dinners that comply with a variety of dietary restrictions are available.
--Friends or relatives may be able to help with food preparation. Often relatives do not know what to give an older person for birthdays or other gift-giving occasions. One suggestion is a homemade prepackaged frozen dinner that the patient enjoys.

Personal Care
--Handgrips should be installed in bathrooms.
--The tub floor should have a nonskid surface.
--Male patients should use an electric shaver rather than a razor.
--Choosing a hairstyle that is becoming but easy to care for (avoiding parts) helps in independent living.
--Home hair care services may be available.

Diversional Activity
--Some patients can read large-print books, newspapers, and magazines (available through local libraries and vision services).
--Books, magazines, and some newspapers are available on audiotapes or discs.
--Patients experienced in knitting or crocheting may be able to create items fashioned from straight pieces, such as afghans.
--Card games, dominoes, and some board games that are available in large, high-contrast print may be helpful for patients with low vision.
(Ignatavicius 2013, p. 1066)

Front 11

primary open-angle glaucoma

Back 11

Primary open-angle glaucoma (POAG), the most common form of primary glaucoma, usually affects both eyes and has no symptoms in the early stages. Outflow of aqueous humor through the chamber angle is reduced. Because the fluid cannot leave the eye at the same rate it is produced, IOP gradually increases. (Ignatavicius 2013, p. 1064)

Front 12

POAG care

Back 12

Primary open-angle glaucoma (POAG) develops slowly, with gradual loss of visual fields that may go unnoticed because central vision is unaffected. At times, the patient may have foggy vision, reduced accommodation, mild aching in the eyes, or headaches and may require frequent changes in eyeglass prescriptions. Late manifestations occur after irreversible damage to optic nerve function and include seeing halos around lights, losing peripheral vision, and having decreased vision that does not improve with eyeglasses. (Ignatavicius 2013, p. 1064)

Front 13

primary angle-closure glaucoma

Back 13

Primary angle-closure glaucoma (also called PACG or acute glaucoma) is less common, has a sudden onset, and is an emergency. The basic problems are a narrowed angle and forward displacement of the iris. The iris pressing against the cornea closes the chamber angle, obstructing the outflow of aqueous humor. This can happen suddenly and without warning. It is more common in women and Asian patients (Ignatavicius 2013, p. 1064)

Front 14

refractive errors

Back 14

The ability of the eye to focus images on the retina depends on the length of the eye from front to back and the refractive power of the lens system. Refraction is the bending of light rays. Problems in either eye length or refraction can result in refractive errors.

Myopia is nearsightedness, in which the eye over-refracts the light and the bent images fall in front of, not on, the retina. Hyperopia, also called hypermetropia, is farsightedness, in which refraction is too weak, causing images to be focused behind the retina. Presbyopia is the age-related problem in which the lens loses its elasticity and is less able to change shape to focus the eye for close work. As a result, images fall behind the retina. This problem usually begins in people in their 30s and 40s. Astigmatism occurs when the curve of the cornea is uneven. Because light rays are not refracted equally in all directions, the image does not focus on the retina.

Refractive errors are diagnosed through a process known as refraction. The patient is asked to view an eye chart while lenses of different strengths are systematically placed in front of the eye. With each lens strength, he or she is asked whether the lenses sharpen or worsen vision. The strength of the lens needed to focus the image on the retina is expressed in measurements called diopters.

(Ignatavicius 2013, p. 1070)

Front 15

nonsurgical management
refractive errors

Back 15

Refractive errors are corrected with a lens that focuses light rays on the retina (see Fig. 48-5 in Chapter 48). Hyperopic vision is corrected with a convex lens that moves the image forward. Myopic vision is corrected with a biconcave lens to move the focused image back to the retina.

Eyeglasses are used to correct refractive errors. They are easy to use, durable, and relatively low cost. Disadvantages are a change in appearance, the weight of the frame on the nose, and reduced peripheral vision (only central vision is corrected with eyeglasses).

Contact lenses also correct refractive errors. Round plastic disks rest against the cornea and fit under the eyelid. Hard contact lenses correct errors in two ways—by changing the shape of the cornea and by providing direct refraction. Changing corneal shape increases its refracting ability. Direct refraction from the contact lens places the specific refractive power and shape needed in front of the eye so that light rays are correctly focused onto the retina.

Complications of hard contact lens wear include corneal edema, which occurs when the lenses are worn for an extended period. Corneal abrasion can result from overwear, which dries the cornea and causes small breaks, or from the irritation of the contact lens against the cornea.

Soft contact lenses are better tolerated than hard contact lenses. They are about the thickness of plastic wrap and can be worn for longer periods because they allow greater corneal access to moisture and oxygen. Problems with soft lenses are related to lens deterioration, deposits in the lens, and failure to follow correct lens care practices.

There are two types of soft contact lenses: daily-wear lenses (worn only during waking hours) and extended-wear lenses. Extended-wear contact lenses are worn continuously for days to several weeks, depending on the patient's environment, activities, and tolerance of the lenses. (Ignatavicius 2013, p. 1070)

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surgical management
refractive errors

Back 16

Surgery is a popular alternative for the treatment of refractive errors. The most common vision-enhancing surgery is laser in-situ keratomileusis (LASIK). This procedure is much more expensive than eyeglasses or any type of contact lens, and it is rarely covered by insurance.

LASIK can correct nearsightedness, farsightedness, and astigmatism using the excimer laser. The superficial layers of the cornea are lifted temporarily as a flap, and brief but powerful laser pulses reshape the deeper corneal layers. After reshaping is complete, the corneal flap is placed back into its original position.

Usually both eyes are treated at the same time, which is most convenient for the patient, although this practice has some risks. If the laser malfunctions or if instruments are contaminated, the vision in both eyes could be adversely affected (Ayers, 2010). Many patients have improved vision within an hour after surgery, although complete healing to best vision may take up to 4 weeks. The outer corneal layer is not damaged, and pain is minimal.

After LASIK correction of refractive errors, many patients no longer require eyeglasses or contact lenses. Overcorrection or undercorrection is possible, however, and some patients may need a mild prescription for a continued refractive error.

Complications include corneal clouding, chronic dry eyes, and refractive errors. Some patients have developed blurred vision and other refractive errors months to years after this surgery as a result of keratectasia. This problem is related to the formation of the corneal flap during surgery and laser-thinning of the cornea. The cornea then becomes unstable and does not refract appropriately.

Although it is a relatively safe procedure, not everyone should have LASIK. People for whom risks may outweigh benefits of LASIK surgery include anyone who has a disorder or is taking drugs that delay wound healing (e.g., human immune deficiency virus [HIV] disease, rheumatoid arthritis, other autoimmune diseases, diabetes), those whose refractive errors are unstable and require yearly changes in prescriptive correction, those who routinely engage in contact sports, those who have thin corneas, and those who have any type of dry eye syndrome (Ayers, 2010).

Another procedure, Intacs corneal ring placement, can enhance vision for nearsightedness. However, this procedure is most often performed for keratoconus. (Ignatavicius 2013, pp. 1070-1071)

Front 17

hearing loss

Back 17

Hearing loss is a common handicap worldwide. It may be conductive, sensorineural, or a combination of the two (Fig. 51-7). Conductive hearing loss occurs when sound waves are blocked from contact with inner ear nerve fibers because of external ear or middle ear disorders. If the inner ear sensory nerve fibers that lead to the cerebral cortex are damaged, the hearing loss is sensorineural. Combined hearing loss is mixed conductive-sensorineural.

The differences in conductive and sensorineural hearing loss are listed in Table 51-2. Disorders that cause conductive hearing loss are often corrected with minimal or no permanent damage. Sensorineural hearing loss is often permanent, and measures must be taken to prevent further damage or to amplify sounds as a means to improve hearing. (Ignatavicius 2013, pp. 1097-1098)

Front 18

conductive hearing loss

Back 18

Conductive hearing loss can be caused by any inflammation or obstruction of the external or middle ear by cerumen or foreign objects. Changes in the eardrum such as bulging, retraction, and perforations may indicate damage to middle ear structures, which leads to conductive hearing loss. Tumors, scar tissue, and overgrowth of soft bony tissue (otosclerosis) on the ossicles from previous middle ear surgery also lead to conductive hearing loss. (Ignatavicius 2013, p. 1098)

Front 19

sensorineural hearing loss

Back 19

Sensorineural hearing loss occurs when the inner ear or auditory nerve (cranial nerve VIII) is damaged. Prolonged exposure to loud noise can damage the hair cells of the cochlea. Many drugs are toxic to the inner ear structures, and their effects on hearing can be transient or permanent, dose related or non–dose related, and affect one or both ears. When ototoxic drugs (e.g., those listed in Table 50-1 in Chapter 50) are given to patients with reduced kidney function, increased ototoxicity can result because drug elimination is slower. Older patients are especially at risk for ototoxicity because of reduced kidney function. (Ignatavicius 2013, p. 1098)

Front 20

presbycusis

Back 20

Presbycusis is a sensorineural hearing loss that occurs as a result of aging (Ko, 2010). It is caused by breakdown or atrophy of cochlear nerve cells, loss of elasticity of the basilar membrane, or a decreased blood supply to the inner ear. Deficiencies of vitamin B12 and folic acid may play a role in presbycusis. Other causes include atherosclerosis, hypertension, infections, fever, Ménière's disease, diabetes, and ear surgery. Each disorder accelerates degenerative changes of the cochlea (Touhy & Jett, 2010). Trauma to the ear also contributes to sensorineural hearing loss (Ignatavicius 2013, p. 1098)

Front 21

genetics
hearing loss

Back 21

Some types of hearing loss in adults can have a genetic origin. Some syndromes in which a single gene mutation results in many abnormal manifestations also increase the risk for progressive hearing loss in adults. Two such syndromes are Usher's syndrome and Alport's syndrome (Nussbaum et al., 2007). Usher's syndrome, in addition to hearing loss, occurs with blindness as a result of retinitis pigmentosa. This syndrome has an autosomal recessive pattern of inheritance. Alport's syndrome, which causes abnormal kidney function in addition to hearing loss, has many forms and many patterns of inheritance. One type of adult-onset hearing loss that does not have any other physical problems is associated with a mutation in the GJB2 gene on chromosome 1 (Online Mendelian Inheritance in Man [OMIM], 2010). This problem has an autosomal dominant pattern of inheritance. (Ignatavicius 2013, p. 1098)

Front 22

older adults
hearing loss

Back 22

Because hearing loss may be gradual and affect only some aspects of hearing, many adults are unaware that their hearing is impaired. The actual incidence of hearing loss is not known, but hearing loss dramatically increases among people in their 70s and 80s (Ignatavicius 2013, p. 1098)

Front 23

communicating with older adults
hearing loss

Back 23

The results of this study indicated that more than 50% of adults older than 80 years experienced significant hearing loss, especially men. Nurses must consider this when communicating with older adults, especially during assessment and teaching sessions when miscommunication could result in serious problems. Although nurses should not assume that all older adults have a hearing loss, it is important to use communication techniques that improve information transfer in all situations. These include:
--Facing the patient during any communication
--Ensuring that your mouth is visible to the patient when you speak
--Making the environment as quiet as possible (turning radios and televisions off or down, closing the door to the hall, moving to a treatment room or conference room if the noise in the room is too loud and cannot be managed)
--Speaking clearly and at a pace that is slightly slower (such as that you would use for public speaking)
--Asking the patient to repeat the main points of what has been said in his or her own words
--Observing the patient's face and body language for cues that communication is effective or ineffective
(Ignatavicius 2013, p. 1098)

Front 24

health promotion
hearing loss

Back 24

For most people, hearing is an important factor in social interactions and to gain knowledge. With special care to the ears, hearing can be preserved at maximum levels. Address barriers to the use of hearing protection, exposure to loud music, and other modifiable risk factors that lead to hearing loss (Stephenson, 2009). Encourage everyone to have simple hearing testing performed as part of their annual health assessment.

Teach everyone the danger in using foreign objects (e.g., bobby-pins, Q-tips, toothpicks, keys) to clean the ear canal. These objects can scrape the skin of the canal, push cerumen up against the eardrum, and even puncture the eardrum. Explain that nothing smaller than a person's own fingertip should be inserted into the canal. If cerumen buildup is a problem, teach the person to use an ear irrigation syringe and proper solutions to remove it. (Chart 50-3 in Chapter 50 describes techniques to remove cerumen safely.)

Teach all people about protecting their ears from loud noises by wearing protective ear devices, such as over-the-ear headsets or foam ear inserts, when exposed to persistent loud noises. Suggest the use of earplugs when engaging in water sports to prevent ear infections, as well as using an over-the-counter product such as Swim-Ear to assist with drying the ear after swimming. (Ignatavicius 2013, p. 1098)

Front 25

assessment and clinical manifestations
hearing loss

Back 25

Hearing loss may be sudden or gradual and often affects both ears. The ability to hear high-frequency soft consonants—especially s, sh, f, th, and ch sounds—is lost first. Patients often state that they have no problem with hearing but cannot understand specific words. They might think that the speaker is mumbling. They often have continuous tinnitus in both ears. Vertigo may be present, depending on the extent of inner ear involvement.

Tuning fork tests help diagnose hearing loss (see Chapter 50). With the Weber test, the patient can usually hear sounds well in the ear with a conductive hearing loss because of bone conduction. With the Rinne test, the patient reports that sound transmitted by bone conduction is louder and more sustained than that transmitted by air conduction.

Otoscopic examination is performed to assess the external ear canal, the eardrum, and structures of the middle ear that can be seen through the eardrum (see Chapter 50). Findings from examination vary, depending on the cause of the hearing loss.

External ear canal obstruction can result in hearing loss. Inspect the canal, looking for:

• Whether the canal is open

• The amount and character of cerumen present

• The integrity of the skin lining the canal

• The presence of redness, exudates, lesions, or foreign objects

Middle ear infections can also reduce hearing. In infection or inflammation, the eardrum appears red, thickened, and bulging, with a loss of landmarks. Loss of eardrum mobility is seen with inspection through a pneumatic otoscope. Document the presence of scars or perforations on the eardrum.

Psychosocial Assessment

For people with a hearing loss, communication can become a struggle and they may isolate themselves because of the difficulty in talking and listening. Social isolation can lead to depression, fear, and despair. Be sensitive to emotional changes that may be related to reduced hearing and a decline in conversational skills. Encourage the patient and family to express their feelings and concerns about an actual or potential hearing loss.

Laboratory Assessment

No laboratory test diagnoses hearing loss. However, some laboratory findings can indicate problems that affect hearing.

White blood cell counts are elevated in the patient with acute or chronic otitis media. Microbial culture and antibiotic sensitivity tests can determine the causative organism and appropriate drug therapy when infection causes hearing loss.

The patient with hearing loss from peripheral neuropathy may have other systemic diseases, including human immune deficiency virus (HIV) disease or diabetes. Patients undergoing cancer chemotherapy or interferon therapy are at risk for neuropathic hearing loss.

Imaging Assessment

Imaging assessment can determine non-auditory problems affecting hearing ability. Skull x-rays are used to determine bony involvement in otitis media and the location of otosclerotic lesions, and CT and MRI are used to determine soft-tissue involvement and the presence and location of tumors.

Other Diagnostic Assessment

Audiometry can help determine the extent and type of hearing loss. An audiogram shows whether hearing loss is only conductive or whether it has a sensorineural component. This is important in determining possible causes of the hearing loss and in planning interventions. (Ignatavicius 2013, pp. 1099-1100)

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planning and implementation
hearing loss

Back 26

Increasing Hearing

Planning: Expected Outcomes

The patient with hearing impairment is expected to either have an increase in functional hearing or maintain existing hearing levels. Indicators include:

• No or minimal loss of high pitch tones

• No or minimal loss of ability to distinguish conversation from background environmental noise

• Turning toward sound

• Identifying discrete sounds

Interventions

Interventions are expected to identify the problem, halt the pathologic processes, and increase usable hearing. Nursing care priorities focus on teaching the patient about the use and care of an appropriate assistive device, providing support to the patient and family who are working to maintain or increase communication, and assisting patients to find local and Internet-based support services. (Ignatavicius 2013, p. 1100)

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nonsurgical management
hearing loss

Back 27

Interventions include early detection of hearing impairment, use of drug therapy and comfort measures, and use of assistive devices to amplify or augment the patient's usable hearing.

Early detection helps correct the problem causing the hearing loss. Assess for indications of hearing loss, as listed in Chart 51-5.

Drug therapy is focused on either correcting the underlying pathologic change or reducing the side effects of problems occurring with hearing loss. Topical antibiotics are given to patients with external otitis. Systemic antibiotics are needed when patients have other ear infections. Teach the patient receiving antibiotic therapy the importance of taking the drug or drugs exactly as prescribed and completing the entire course. Caution him or her to not stop the drug just because manifestations have improved. By treating the infection, antibiotics reduce local edema and improve hearing. When pain occurs with hearing disorders, analgesics are used, depending on the location and type of pain. Many ear disorders disturb equilibrium, causing vertigo and dizziness with nausea and vomiting. Antiemetic, antihistamine, antivertiginous, and benzodiazepine drugs can help correct nausea, vertigo, and dizziness.

Assistive devices are useful for patients with permanent, progressive hearing loss. Portable amplifiers can be used while watching television to avoid increasing the volume and disturbing others. Telephone amplifiers increase telephone volume, allowing the caller to speak in a normal voice. Flashing lights activated by the ringing telephone or a doorbell alert patients visually. In some cases, patients may have a specially trained dog to help them be aware of sounds (ringing telephones or doorbells, cries of other people, and potential dangers), in much the same way that a seeing-eye dog assists a blind person. Provide information about agencies that can assist the hearing-impaired person.

Small, portable audio amplifiers can assist in communicating with patients with hearing loss but who have chosen not to use a hearing aid. The use of audio amplifiers or allowing patients to use a stethoscope for listening helps you communicate with anyone who requires additional volume to hear speech.

A hearing aid is a miniature electronic amplifier that is usually used for patients with conductive hearing loss. Hearing aids are less effective for sensorineural hearing loss and may make hearing worse by amplifying background noise. The amplifier can be worn in one or both ears. Some hearing-impaired patients refuse to use hearing aids, believing that other people will think they are old. Most common hearing aids are small. Some are attached to a person's glasses and are visible to other people. Another type fits into the ear and is less noticeable. Newer devices fit completely in the canal with only a fine, clear filament visible. The cost of smaller hearing aids is greater than the cost of larger ones. Local agencies offer special classes for the hearing impaired that help the users benefit from this device.

Offer some special tips to help the patient adjust to the hearing aid. Hearing with a hearing aid is different from natural hearing. Teach the patient to start using the hearing aid slowly, at first wearing it only at home and only during part of the day. Listening to television and the radio and reading aloud can help the patient get used to new sounds. The tone or volume of the hearing aid can be adjusted. A difficult aspect of a hearing aid is the amplification of background noise. The patient must learn to concentrate and filter out background noises.

Teach the patient how to care for the hearing aid (Chart 51-6). Hearing aids are delicate devices that should be handled only by people who know how to care for them properly. The cost of the aids varies greatly but is a significant investment. (Ignatavicius 2013, pp. 100-1101)

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surgical management
hearing loss

Back 28

Many surgical interventions are available for patients with specific disorders leading to hearing loss.

Tympanoplasty

Tympanoplasty reconstructs the middle ear to improve conductive hearing loss. The procedures vary from simple reconstruction of the eardrum (myringoplasty) to replacement of the ossicles within the middle ear (ossiculoplasty). A type I tympanoplasty is used for a myringoplasty; a type II tympanoplasty is used in cases of greater damage, and it provides more extensive reconstruction.

Stapedectomy

A partial or complete stapedectomy with a prosthesis corrects some types of hearing loss. This procedure is most effective for patients with hearing loss related to otosclerosis. The average age for patients undergoing primary stapes surgery is increasing. Regardless of age, hearing usually improves after primary stapes surgery; however, some patients redevelop conductive hearing loss after surgery and revision surgery is needed.

Totally Implanted Devices

A newly approved device to treat bilateral moderate to severe sensorineural hearing loss is the Esteem system. It is designed to improve hearing to the same or better level as a high quality hearing aid but without any visible part. The device has three components that are totally implanted: a sound processor, a sensor, and a computer driver. Vibrations of the eardrum and ossicles are picked up by the sensor and converted to electric signals that are processed by the sound processor. Each processor is specifically programmed to the patient's specific hearing pathology. The processor filters out some background noise and amplifies the desired sound signal, which is then transferred to the driver. The driver then converts the processed signal into vibrations that are transmitted to the inner ear for sound perception (U.S. Food and Drug Administration, 2010).

Patient criteria for this new device include:
--Bilateral stable sensorineural hearing loss determined by pure-tone audiometry
--Speech discrimination score of 40% or higher (see Chapter 50)
--Healthy tympanic membrane, eustachian tube, and ossicles of the middle ear
Large enough space in the ear cavity to accommodate the parts of the device
--Minimum of 30 days of experience with an appropriately fitted hearing aid
--Absence of acute or chronic middle ear, inner ear, or mastoid infection
--Absence of Ménière's disease or recurring vertigo that requires treatment
--Absence of excessive sensitivity to silicone rubber, polyurethane, stainless steel, titanium, or gold

Possible complications of the device and the surgery required to implant it include:
--Temporary facial paralysis
--Changes in taste sensation
--Ongoing or new-onset tinnitus

Unlike more standard cochlear implants, the middle ear is entered and it is considered a surgical procedure. Care before and after surgery is similar to that required with stapedectomy. A distinct disadvantage is the cost of the implant and procedure, which exceeds $30,000 and is not currently covered by insurance. (Ignatavicius 2013, pp. 1101-1103)

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nursing intervenions: communication
hearing loss

Back 29

Nursing priorities focus on facilitating communication and reducing anxiety.

Use best practices that are listed in Chart 51-8 for communicating with a hearing-impaired patient. Do not shout at the patient because the sound may be projected at a higher frequency, making him or her less able to understand. The most obvious means of communicating is by the written word (if he or she is able to see, read, and write) or with pictures of familiar phrases and objects. Many television programs are now closed captioned (subtitled).

Assistive devices, described on p. 1100, can greatly increase communication for the patient with a hearing impairment.

Lip-reading and sign language can also increase communication. In lip-reading classes, patients are taught the special cues to look for when lip-reading and how to understand body language. However, the best lip-reader still misses more than half of what is being said. Because hearing is assisted by even minimal lip-reading, urge patients to wear their eyeglasses when talking with someone to see lip movement.

Sign languages, such as American Sign Language (ASL), combine speech with hand movements that signify letters, words, and phrases. These languages take time and effort to learn, and many people cannot learn them, just as many people cannot learn foreign languages.

Managing anxiety can increase the effectiveness of communication efforts. One source of anxiety is the possibility of permanent hearing loss. Provide accurate information about the likelihood of hearing returning. When the hearing impairment is likely to be permanent or become more profound, reassure patients that communication and social interaction can be maintained.

To reduce anxiety and prevent social isolation, assist patients to use resources and communication to make social contact satisfying. Ask about past or present diversional activities to identify the patient's most satisfying activities and social interactions, and determine the effort necessary to continue them. Activities can be altered to improve patient satisfaction. Someone accustomed to large gatherings might choose smaller groups instead. A quiet evening meal at home with friends might substitute for dinner in a noisy restaurant. (Ignatavicius 2013, pp. 1103-1104)

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Meniere's disease

Back 30

Ménière's disease has three features: tinnitus, one-sided sensorineural hearing loss, and vertigo, occurring in attacks that can last for several days. (Some patients have continuous manifestations of varying intensity rather than intermittent attacks.) Patients are almost totally incapacitated during an attack, and full recovery often takes several days. The pathology of Ménière's disease is an excess of endolymphatic fluid that distorts the entire inner-canal system. This distortion decreases hearing by dilating the cochlear duct, causes vertigo because of damage to the vestibular system, and stimulates tinnitus (Peate, 2009). At first, hearing loss is reversible, but repeated damage to the cochlea from increased fluid pressure leads to permanent hearing loss.

The exact cause of Ménière's disease is unknown, but it often occurs with infections, allergic reactions, and fluid imbalances. Long-term stress may also have a role in the disease.

Ménière's disease usually first occurs in people between the ages of 20 and 50 years. The disease is more common in men and in white people. Severe, debilitating attacks alternate with symptom-free periods. Patients often have certain manifestations before an attack of vertigo, such as headaches, increasing tinnitus, and a feeling of fullness in the affected ear.

Patients describe the tinnitus as a continuous, low-pitched roar or a humming sound, which worsens just before and during an attack. Hearing loss occurs first with the low-frequency tones but worsens to include all levels after repeated episodes. In the early stages of Ménière's disease, hearing is normal or nearly normal between episodes, but permanent hearing loss develops as the attacks increase.

Patients describe the vertigo as periods of whirling, which might even cause them to fall. The vertigo is so intense that even while lying down, the patient often holds the bed or ground to keep from falling. Severe vertigo usually lasts 3 to 4 hours, but he or she may feel dizzy long after the attack. Nausea and vomiting are common. Other manifestations include rapid eye movements (nystagmus) and severe headaches. (Ignatavicius 2013, p. 1096)

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nonsurgical management
Meniere's disease

Back 31

Nonsurgical Management

Teach patients to move the head slowly to prevent worsening of the vertigo. Nutrition and lifestyle changes can reduce the amount of endolymphatic fluid. Encourage patients to stop smoking because of the blood vessel–constricting effects.

Nutrition therapy with a hydrops diet may stabilize body fluid levels to prevent excess endolymph accumulation. The basic structure of this diet involves:

• Distributing food and fluid intake evenly throughout the day and from day to day

• Avoiding foods or fluids that have a high salt content

• Drinking adequate amounts of fluids (low in sugar) daily

• Avoiding caffeine-containing fluids and foods

• Limiting alcohol intake to one glass of beer or wine each day

• Avoiding foods containing monosodium glutamate (MSG)

Coordinate with a dietitian for more detailed information about hydrops diet therapy for reduction of Ménière's manifestations.

Drug therapy may reduce the vertigo and vomiting and restore normal balance. Mild diuretics are prescribed to decrease endolymph volume, which reduces vertigo, hearing loss, tinnitus, and aural fullness. Nicotinic acid has been found to be useful because of its vasodilatory effect. Antihistamines such as diphenhydramine hydrochloride (Benadryl, Allerdryl ) and dimenhydrinate (Dramamine, Gravol ), and antivertiginous drugs such as meclizine (Antivert, Bonamine ), help reduce the severity of or stop an acute attack. Antiemetics such as chlorpromazine hydrochloride (Thorazine, Novo-Chlorpromazine ), droperidol (Inapsine), promethazine (Phenergan), and ondansetron (Zofran) help reduce the nausea and vomiting. Diazepam (Valium, Apo-Diazepam ) calms the patient; reduces vertigo, nausea, and vomiting; and allows the patient to rest quietly during an attack. Intratympanic therapy with gentamicin and steroids is another method for preventing manifestations; however, some or all hearing is lost in the ear receiving this drug combination.

Another nonsurgical treatment is the Meniett device, which applies low-pressure micropulses to the inner ear for 5 minutes three times daily. This action displaces inner ear fluid and relieves manifestations. Placement of a tympanostomy tube in the eardrum of the affected ear is needed to use this therapy. Long-term success in control of vertigo is over 80%. Although hearing loss is not improved, Meniett device usage does not adversely affect balance, as do most forms of surgical therapy for Ménière's disease. (Ignatavicius 2013, p. 1096)

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surgical management
Meniere's disease

Back 32

For years, surgical treatment of Ménière's disease was a last resort because the hearing in the affected ear was often lost with the more radical procedures. When medical therapy is ineffective and the patient's general function is decreased significantly, surgery may be performed. The choice of the surgical procedure depends on the degree of usable hearing, the severity of the spells, and the condition of the opposite ear. The most radical procedure involves resection of the vestibular nerve or total removal of the labyrinth (labyrinthectomy), performed through the ear canal. The footplate of the stapes is moved aside, and the labyrinth is removed through the oval window.

Another procedure performed early in the course of the disease is endolymphatic decompression with drainage and a shunt (Lee & Pensak, 2008). The effectiveness of this procedure varies. The endolymphatic sac is drained, and a small tube is inserted to improve fluid drainage. Some patients report relief of vertigo with retention of their hearing. If an endolymphatic decompression has been performed, movement of the vestibular structures of the inner ear causes vertigo early after surgery. Reassure the patient that the vertigo is a temporary result of the surgical procedure, not the disease. (Ignatavicius 2013, pp. 1096-1097)

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bacterial skin infections

Back 33

Bacterial skin lesions usually start at the hair follicle, where bacteria easily collect and grow in the warm, moist environment. Folliculitis is a superficial infection involving only the upper portion of the follicle and is usually caused by Staphylococcus. The rash is raised and red and usually shows small pustules. Furuncles (boils) are also caused by Staphylococcus, but the infection is much deeper in the follicle (Fig. 27-7). This larger, sore-looking, raised bump may or may not have a pustular “head” at its point. Cellulitis is a generalized infection with either Staphylococcus or Streptococcus and involves the deeper connective tissue.

Minor skin trauma usually occurs before the appearance of folliculitis and furuncles and may or may not contribute to the development of cellulitis. Patients may spread the infection to other parts of their bodies by scratching or rubbing the skin with fingernails that have organisms under them. Furuncles are more likely to occur in areas of heat and moisture, such as in the hair-bearing skinfold areas. Cellulitis can occur as a result of secondary bacterial infection of an open wound, or it may be unrelated to skin trauma.

An increasingly common skin problem is infection with methicillin-resistant Staphylococcus aureus (MRSA) (Leung-Chen, 2008). This infection can range from mild folliculitis to extensive furuncles. It is easily spread to other body areas and to other people by direct contact with infected skin and by contact with articles of clothing, bed linens, athletic equipment, towels, and other objects used by a person with MRSA. The infection does not respond to cleansing with antibacterial soaps or most types of topical and many oral antibiotic therapies (Mendyk, 2008). If MRSA infects a wound or gains access into the blood, deep wound infection, sepsis, organ damage, and death can occur (Holcomb, 2008). The incidence of the problem is highest among adults living in communal environments, such as dormitories or prisons, and among patients in hospitals or other health care residential settings.

(Ignatavicius 2013, pp. 490-492)

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viral skin infections
(HSV)

Back 34

Herpes simplex virus (HSV) infection is the most common viral infection of adult skin. HSV infections are of two types. Type 1 (HSV-1) infections cause the classic recurring cold sore. The severity of the disease increases with age and is worse when the patient is immunosuppressed. Genital herpes, caused by type 2 infection (HSV-2), is also recurrent (see Chapter 76).

After the first infection, the virus remains in the body in a dormant state in the nerve ganglia and the patient has no symptoms. Reactivation stimulates the virus to travel the pathway of sensory nerves to the skin, where lesions reappear. In healthy people, recurrence of HSV infection is triggered by physical or psychological stressors, such as dry lips, sunburn, trauma, fever, menses, and fatigue. The virus can also be spread by direct contact between an actively infected person and a susceptible host. Autoinoculation, or transfer of either viral type from one part of the body to another, is also possible.

The time span between episodes and the severity of each attack vary. Outbreaks of oral herpes simplex usually last 3 to 10 days. The patient sheds virus and is contagious for the first 3 to 5 days. The patient may have tingling or burning of the lip before any lesion is evident.

The most common clinical picture of HSV-1 infection is isolated or grouped vesicles on a red base. The infection can occur anywhere on the skin and may be spread by respiratory droplets or by direct contact with an active lesion or virus-containing fluid (e.g., saliva). The lesions are painful and unsightly.

Herpetic whitlow is a form of herpes simplex infection occurring on the fingertips of medical personnel who have come in contact with viral secretions. This form of herpes can easily be spread to patients. Immunosuppressed patients are at increased risk for severe and persistent eruptions that can lead to life-threatening complications.
(Ignatavicius 2013, p. 492)

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herpes zoster
(viral skin infections)

Back 35

Herpes zoster (shingles), also known as varicella zoster, is caused by reactivation of the dormant varicella-zoster virus (VZV) in patients who have previously had chickenpox. The dormant virus resides in the dorsal root ganglia of the sensory nerves. The lesions of herpes zoster infections are similar to those of herpes simplex, but they have a different distribution pattern (Fig. 27-8). Multiple lesions occur in a segmental distribution on the skin area innervated by the infected nerve. Herpes zoster eruptions usually occur after several days of discomfort, which may vary from minor irritation and itching to severe, deep pain. The eruption usually lasts several weeks. Postherpetic neuralgia, severe pain persisting after the lesions have resolved, is a common complication in older patients. Early diagnosis of herpes zoster and prompt treatment with anti-viral drugs help decrease the duration and severity of postherpetic neuralgia.

Herpes zoster is a disease of immunosuppression, occurring most often and with greater severity in older people or in anyone who is immunosuppressed for any reason. The disorder can be accompanied by fever and malaise, often progressing to visceral involvement. It is contagious to people who have not previously had chickenpox and have not been vaccinated against the disease. Contagion is most likely when the lesions are present as fluid-filled blisters. Keeping patients with these lesions separated from other patients in the environment until the lesions have crusted reduces the risk for transmitting the virus to others. Complications include full-thickness skin necrosis, Bell's palsy, or eye infection, and scarring if the virus is introduced into the eye.

The vaccine Zostavax is available to prevent VZV reactivation and shingles. The Centers for Disease Control and Prevention (CDC) recommends the vaccine for anyone older than 60 years who has a healthy immune system. In 2011 the FDA approved this drug for use starting at age 50 years (FDA, 2011). This one-time subcutaneous injection is reported to reduce the incidence of shingles by as much as 64% (Wielowski, 2009). Cost remains a factor in widespread adoption (about $100 per dose), and few insurance carriers currently include this coverage. (Ignatavicius 2013, p. 492)

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health promotion & maintenance
(skin infections)

Back 36

Prevention of skin infections, especially bacterial and fungal infections, involves avoiding the offending organism and practicing good personal hygiene to remove the organism before infection can occur. Handwashing and not sharing personal items with others are the best ways to avoid contact with some of the most easily transmitted organisms, including MRSA. Chart 27-8 highlights strategies to teach patients and family members to prevent spread of the infection to other body areas and to other people (Mendyk, 2008).

For older adults who have had chickenpox and are, therefore, at risk for shingles (herpes zoster), a new vaccine has been approved, Zostavax. Its use is recommended for any adult older than 50 years who does not currently have shingles (FDA, 2011). It is given as a one-time subcutaneous injection. The drug should not be given as an IM or IV injection and should not be given to anyone who is immunosuppressed. The most common side effect is an injection site reaction of erythema, pain, tenderness, swelling, warmth, or pruritus. (Ignatavicius 2013, p. 493)

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skin cancer

Back 37

Pathophysiology

Overexposure to sunlight is the major cause of skin cancer, although other factors are associated. Because sun damage is an age-related skin finding, screening for suspicious lesions is an important part of physical assessment of the older adult. The most common skin cancers are actinic or solar keratosis, squamous cell carcinoma, basal cell carcinoma, and melanoma. Table 27-6 describes common skin cancers.

Etiology and Genetic Risk

Actinic keratoses are premalignant lesions of the cells of the epidermis. These lesions are common in people with chronically sun-damaged skin. Progression to squamous cell carcinoma may occur if lesions are untreated.

Squamous cell carcinomas are cancers of the epidermis. They can invade locally and are potentially metastatic. Lesions on the ear, lip, and external genitalia are more likely to invade and spread than those found elsewhere on the body. Chronic skin damage from repeated injury or irritation also predisposes to this malignancy.

Basal cell carcinomas arise from the basal cell layer of the epidermis (Fig. 27-15). Early malignant lesions often go unnoticed, and although metastasis is rare, underlying tissue destruction can progress to include vital structures. Genetic predisposition and chronic irritation are risk factors; however, UV exposure is the most common cause.

Melanomas are pigmented cancers arising in the melanin-producing epidermal cells (Fig. 27-16). Risk factors include genetic predisposition, excessive exposure to UV light, and the presence of one or more precursor lesions that resemble unusual moles. This skin cancer is highly metastatic, and a person's survival depends on early diagnosis and treatment.

Lighter skin and less pigmentation are genetically inherited traits. Also, a genetic mutation that is inherited in an autosomal-dominant pattern has been found for some cases of familial melanoma. The mutation occurs in a suppressor gene resulting in loss of control of cell growth. Two such mutated genes are CDKN2A, CDK4, and BRAF.

Incidence/Prevalence

The incidence of skin cancer is highest among light-skinned races and people older than 60 years (American Cancer Society, 2011). The incidence is higher among those who work outdoors, live at higher altitudes or lower latitudes, or spend significant amount of time sunbathing. Occupational exposure to arsenic or other chemical carcinogens also increases risk. The incidence of melanoma has increased during the past 30 years, accounting for 2% of all cancers and 1% of all cancer deaths (Ignatavicius 2013, pp. 502-503)

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health promotion & maintenance
(skin cancer)

Back 38

The single most effective prevention strategy for skin cancer is avoiding or reducing skin exposure to sunlight. However, even when people understand the cause of skin cancer and the seriousness of the disease, preventive behaviors are not always practiced. Common prevention practices include avoiding direct sunlight, using sunscreen, and wearing protective clothing (including hats) whenever a person is in the sun to prevent severe sunburn. Teach all people to avoid tanning beds and salons. Chart 27-12 lists methods of prevention to reduce the risk for skin cancer (McEnroe-Petitte, 2011).

Secondary prevention, early detection, is critical to survival with melanoma. Teach all people to be aware of their skin markings. Keeping a total body spot and lesion map can provide baseline information about suspicious lesions and help identify changes in a lesion or lesions earlier. Once a map is made, the person should systematically inspect his or her body monthly for new lesions and for changes in any existing lesions by performing thorough skin self-examination (TSSE). Often a partner is needed to help evaluate skin spots or lesions on the back. Some people find taking pictures of their skin on a regular basis makes identifying changes easier. Teach everyone to evaluate all skin lesions using the ABCDE guide for melanoma (see Chapter 26) and to consult his or her health care provider to examine any lesion having unusual characteristics. When lesions, such as moles, are present, they should be monitored yearly by a dermatologist or other health care professional.

Monthly TSSE is critically important for patients who have already had a melanoma lesion. A major positive influence for TSSE practice is working with a partner in this examination. (Ignatavicius 2013, pp. 503-504)

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assessment
(skin cancer)

Back 39

In addition to age and race, ask the patient about any family history of skin cancer and any past surgery for removal of skin growths. Recent changes in the size, color, or sensation of any mole, birthmark, wart, or scar are also significant. Ask about which geographic regions he or she has lived in and where he or she currently resides. Obtain information about occupational and recreational activities in relation to sun exposure, as well as any occupational history of exposure to chemical carcinogens (e.g., arsenic, coal tar, pitch, radioactive waste, radium). Ask whether any skin lesions are repeatedly irritated by the rubbing of clothing.

Skin that has been injured previously is at greater risk for cancer development, an effect known as Koebner's phenomenon. Ask the patient if he or she has ever experienced a severe skin injury that resulted in a scar. Examine all scarred skin areas for the presence of potentially cancerous lesions.

Skin cancers vary in their appearance and distribution. Although most skin cancers appear in sun-exposed areas of the body, inspect the entire skin surface. Systematically examine the skin for any unusual lesions, particularly moles, warts, birthmarks, and scars. Also examine hair-bearing areas of the body, such as the scalp and genitalia. Palpate lesions to determine surface texture. Document the location, size, color, and surface features of all lesions and any subjective reports of tenderness or itching. Use the ABCDE method of evaluating all lesions for possible melanoma (Ignatavicius 2013, p. 504)

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surgical management
(skin cancer)

Back 40

Surgical intervention is the most common means of managing any type of skin cancer. It can range from local removal of small lesions, with minimal discomfort and positive cosmetic results, to massive excision of large areas of the skin and underlying tissue for treatment of melanoma.

Cryosurgery involves the local application of liquid nitrogen (−200° C) to isolated lesions, causing cell death and tissue destruction. Local anesthesia is seldom needed because most patients have only minor discomfort during the procedure. Prepare patients for swelling and increased tenderness of the treated area when the skin thaws. Tissue freezing is followed in 1 to 2 days by hemorrhagic blister formation. Instruct patients to clean the sites with hydrogen peroxide to prevent infection. A topical antibiotic may also be prescribed.

Curettage and electrodesiccation may be used for small lesions that are not melanoma. This method can destroy the cancerous cells while minimizing damage to the surrounding uninvolved tissue. After a local anesthetic is given, the surgeon uses a dermal curette to scrape away the cancerous tissue. After curettage is complete, the surgeon places an electric probe on the wound and remnants of the tumor are destroyed by thermal energy.

Wounds created by this treatment heal by second intention, and scarring is usually minimal. Instruct patients in caring for the wound, including cleaning the wound, using prescribed antibacterial drugs, and applying dressings.

Excision is used for biopsy of small lesions. When the diagnosis is melanoma, a sentinel node may be biopsied to determine whether tumor spread has started. If the size and location of the lesion permit, surgical excision with primary closure is the preferred method. If the tumor has already been removed several times or if radiation therapy has damaged the surrounding skin, healing by second intention is indicated. This procedure allows the wound to be monitored for cancer recurrence. Skin grafts and flaps are used to repair large defects if tissue destruction is deep.

Mohs’ surgery, a specialized form of excision, is used to treat basal and squamous cell carcinomas. The cancerous tissue is sectioned horizontally in layers, and each layer is examined histologically to determine the presence of residual tumor cells. Although the procedure is long and tedious, cure rates are high and there is less removal of healthy tissue compared with other surgical methods.

Wide excision for deeper melanoma or other skin cancers that are large or invasive often involves removing full-thickness skin in the area of the lesion. Depending on tumor depth, subcutaneous tissues and lymph nodes may also be removed. If the remaining skin is easily moved without creating extensive tension, the wound may be just sutured closed. If the remaining skin is tight or the wound is large, skin grafts may be needed to close the surgical wound
(Ignatavicius 2013, p. 504)

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nonsurgical management
(skin cancer)

Back 41

Drug therapy may involve topical or systemic chemotherapy, biotherapy, or targeted therapy. Topical chemotherapy with 5-fluorouracil cream is used for treatment of multiple actinic keratoses or for widespread superficial basal cell carcinoma that would require several surgical procedures to eradicate. Therapy is continued for several weeks, and the treated areas become increasingly tender and inflamed as the lesions crust, ooze, and erode. Prepare the patient for an unsightly appearance during therapy, and reassure him or her that the cosmetic result will be positive.

After treatment is discontinued, cool compresses and topical corticosteroid preparations help decrease inflammation and promote comfort.

Systemic chemotherapeutic agents are used in the treatment of skin cancer except when the prognosis is poor, as in advanced melanoma.

Biotherapy with interferon is now an accepted treatment after surgery for melanomas that are at stage III or higher. The patient is first started on high-dose (20,000,000 units/m2) IV interferon infusions daily for 5 days per week for 4 weeks after the surgical wound is well healed. Maintenance doses of 10,000,000 units/m2 are continued three times per week for 1 year. The maintenance doses are given subcutaneously, and the patient must learn to self-inject the drug.

Agents that target lymphocyte control of tumor cell growth may be used for treatment of metastatic melanoma. The approved drug ipilimumab (Yervoy) and the experimental drug tremelimumab target the CTLA4 (cytotoxic T-lymphocyte–associated antigen 4) receptor and block it, resulting in greater activity of the lymphocyte. This allows the lymphocyte to attack melanoma cells. Because the receptor is present on certain lymphocytes, the side effects of these drugs include significant inflammation in many tissues (Rubin, 2009; Aschenbrenner, 2011).

Radiation therapy for skin cancer is limited to older patients with large, deeply invasive basal cell tumors and to those who are poor risks for surgery. Melanoma is resistant to radiation therapy; however, radiation therapy may be helpful for patients with metastatic disease when used in combination with systemic corticosteroids. (Ignatavicius 2013, pp. 504-505)

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seasonal influenza

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Pathophysiology

Seasonal influenza, or “flu,” is a highly contagious acute viral respiratory infection that can occur in adults of all ages. Epidemics are common and lead to complications of pneumonia or death, especially in older adults or debilitated or immunocompromised patients. Between 5% and 20% of the U.S. population develop influenza each year, and more than 36,000 deaths per year are caused by it (Kapustin, 2008). Hospitalization may be required. Influenza may be caused by one of several virus families, referred to as A, B, and C.

The patient with influenza often has a severe headache, muscle aches, fever, chills, fatigue, and weakness. Adults are contagious from 24 hours before symptoms occur and up to 5 days after they begin. Patients who are immunosuppressed may be contagious for several weeks. Sore throat, cough, and watery nasal discharge generally follow the initial symptoms for a week or longer. Most patients feel fatigued for 1 to 2 weeks after the acute episode has resolved. (Ignatavicius 2013, p. 645)

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health promotion & maintenance
(seasonal influenza)

Back 43

Vaccinations for the prevention of influenza are widely available. The vaccine is changed every year on the basis of which specific viral strains are most likely to pose a problem during the influenza season (i.e., late fall and winter). Usually, the vaccines contain three antigens for the three expected viral strains (trivalent influenza vaccine [TIV]). Influenza vaccinations can be taken as an IM injection (Fluviron, Fluzone) or as a live attenuated influenza vaccine (LAIV) by intranasal spray (FluMist). An attenuated virus is a live virus that has been altered to reduce its ability to cause an infection. The intranasal vaccine is live, and some people develop influenza symptoms after its use. It is recommended only for healthy people up to 49 years of age. People recommended to be vaccinated yearly include those older than 50 years, people with chronic illness or immune compromise, those living in institutions, people living with or caring for adults with health problems that put them at risk for severe complications of influenza, and health care personnel providing direct care to patients (Centers for Disease Control and Prevention [CDC], 2010c).

Teach the patient who is sick to reduce the risk for spreading the flu by thoroughly washing hands, especially after nose blowing, sneezing, coughing, rubbing the eyes, or touching the face. Other precautions include staying home from work, school, or places where people gather; covering the mouth and nose with a tissue when sneezing or coughing; disposing properly of used tissues immediately; and avoiding close contact with other people (e.g., kissing, hugging, handshaking). Although handwashing is a good method to prevent transmitting the virus in droplets from sneezing or coughing, many people cannot wash their hands as soon as they have coughed or sneezed. The technique recommended by the CDC for controlling flu spread is to sneeze or cough into the upper sleeve rather than into the hand (CDC, 2010a). (Respiratory droplets on the hands can contaminate surfaces and be transmitted to other people.) (Ignatavicius 2013, p. 645)

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collaborative-care
(seasonal influenza)

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Viral infections do not respond to traditional antibiotic therapy. Antiviral agents may be effective for prevention and treatment of some types of influenza. Amantadine (Symmetrel) and rimantadine (Flumadine) have been effective in the prevention and treatment of influenza A, although strains of resistant organisms are increasing. Ribavirin (Virazole) has been used for severe influenza B. Two drugs that may shorten the duration of influenza A and influenza B are zanamivir (Relenza), which is used as an oral inhalant, and oseltamivir (Tamiflu), which is an oral tablet. These drugs prevent viral spread in the respiratory tract by inhibiting a viral enzyme (neuraminidase) that allows the virus to penetrate respiratory cells. To be effective, they must be taken within 24 to 48 hours after the onset of manifestations.

Advise the patient to stay in bed for several days and increase fluid intake unless another problem requires fluid restriction. Saline gargles may ease sore throat pain. Antihistamines may reduce the rhinorrhea. Other supportive measures are the same as those for acute rhinitis. (Ignatavicius 2013, p. 645)

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pandemic influenza

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Pathophysiology

Many viral infections among animals and birds are not usually transmitted to humans. A few notable exceptions have occurred when these animal and bird viruses mutated and became highly infectious to humans. These infections are termed pandemic because they have the potential to spread globally. Such pandemics include the 1918 “Spanish” influenza that resulted in at least 40 million deaths worldwide and perhaps as many as 100 million deaths. This virus, the H1N1 strain, also known as “swine flu,” mutated and became highly infectious to humans. Most recently, the 2009 H1N1 influenza A resulted in a pandemic infection that spread to 215 countries. In the United States, the number of people infected with this virus during the pandemic is estimated at 61 million, resulting in more than 12,000 deaths (CDC, 2010b). A vaccine was developed in 2009 as a single antigen (monovalent) and was administered separately from the seasonal influenza vaccine. For the 2010-2011 influenza season, the trivalent seasonal vaccine contained the H1N1 antigen.

A new avian virus is the H5N1 strain, known as “avian influenza” or “bird flu,” that has infected millions of birds, especially in Asia, and now has started to spread by human-to-human contact. World health officials are concerned that this strain could become a pandemic because humans have essentially no naturally occurring immunity to this virus. Thus the infection could lead to a worldwide pandemic with very high mortality rates. (Ignatavicius 2013, pp. 645-646)

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health promotion & maintenance
(pandemic influenza)

Back 46

The prevention of a worldwide influenza pandemic of any virus is the responsibility of everyone. Health officials have been monitoring the situation with human outbreaks and with testing of both wild and domestic bird species throughout the world. Vaccines currently are available for both H1N1 and H5N1; however, the H5N1 vaccine is stockpiled and not part of general influenza vaccination. The recommended early approach to disease prevention with H5N1 is early recognition of new cases and the implementation of community and personal quarantine and social-distancing behaviors to reduce exposure to the virus.

Plans for prevention and containment in North America have been developed with the cooperation of most levels of government. When a cluster of cases is discovered in an area, the stockpiled vaccine is to be made available for immunizations. Because vaccination with this vaccine is a two-step process with the first IM injection followed 28 days later by a second IM injection, additional prevention measures are needed.

The antiviral drugs oseltamivir (Tamiflu) and zanamivir (Relenza) should be widely distributed. These drugs are not likely to prevent the disease but may reduce the severity of the infection and reduce the mortality rate. The infected patients should be cared for in strict isolation. All nonessential public activities in the area should be stopped. These include public gatherings of any type, attendance at schools, religious services, shopping, and many types of employment. People should stay home and use their emergency preparedness supplies (food, water, and drugs) they have stockpiled for at least 2 weeks (see Chapter 12). Travel to and from the affected area should be stopped.

Urge all people to pay attention to public health announcements and early warning systems for disease outbreaks. Teach them the importance of starting prevention behaviors immediately upon notification of an outbreak. Teach all people to have a minimum of a 2-week supply of all their prescribed drugs and at least a 2-week supply of nonperishable food and water for each member of the household. They should also have a battery-powered radio (and batteries) to keep informed of updates in an active prevention situation. See Chapter 12 for more information on items to have ready in the home for disaster preparedness. An influenza pandemic is a disaster, and containing it requires the cooperation of all people. (Ignatavicius 2013, p. 646)

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collaborative care
(pandemic influenza)

Back 47

Care of the patient with avian influenza focuses on supporting the patient and preventing spread of the disease. Both are equally important. The initial manifestations of avian influenza are similar to other respiratory infections—cough, fever, and sore throat. These progress rapidly to shortness of breath and pneumonia. In addition, diarrhea, vomiting, abdominal pain, and bleeding from the nose and gums occur. Ask any patient with these symptoms if he or she has recently (within the past 10 days) traveled to areas of the world affected by H5N1. If such travel has occurred, coordinate with the health care team to place the patient in an airborne isolation room with negative air pressure. These precautions remain until the diagnosis of H5N1 is ruled out or the threat of contagion is over. Diagnosis is made based on clinical manifestations and positive testing. The most rapid test currently approved for testing of H5N1 is the AVantage A/H5N1 Flu Test. It can detect a specific protein (NS1), which indicates the presence of H5N1, from nasal or throat swabs in less than 40 minutes.

When providing care to the patient with avian influenza, personal protective equipment is essential. Coordinate the protection activity by ensuring that anyone entering the patient's room for any reason wears a fit-tested respirator or a standard surgical mask (“Lessons Learned,” 2010). Use other Airborne Precautions and Contact Precautions as described in Chapter 25. Teach others to self-monitor for disease symptoms, especially of respiratory infection, for at least a week after the last contact with the patient. Use the antiviral drug oseltamivir (Tamiflu) or zanamivir (Relenza) within 48 hours of contact with the infected patient. All health care personnel working with patients suspected of having avian influenza are recommended to receive the vaccine in the recommended two-step process.

No effective treatment for this infection currently exists. Antibiotics and antiviral drugs cannot kill the virus or prevent its replication. Interventions are supportive to allow the patient's own immune system to fight the infection. Oxygen is given when hypoxia or breathlessness is present. Respiratory treatments to dilate the bronchioles and move respiratory secretions are used. If hypoxemia is not improved with oxygen therapy, intubation and mechanical ventilation may be needed. Antibiotics are used to treat a bacterial pneumonia that may occur with H5N1.

In addition to the need for respiratory support, the patient with H5N1 may have severe diarrhea and need fluid therapy. The Transmission Precautions may prevent the use of a scale to determine fluid needs by weight changes. Monitor the patient's hydration status, and carefully measure intake and output. The type of fluid therapy varies with the patient's cardiovascular status and the osmolarity of the blood. The two most important areas to monitor during rehydration are pulse rate and quality and urine output. (Ignatavicius 2013, pp. 646-647)

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head & neck cancer

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Pathophysiology

Head and neck cancer can disrupt breathing, eating, facial appearance, self-image, speech, and communication. This form of cancer can be devastating, even when treated successfully. The care needs for patients with these problems are complex, requiring a coordinated and comprehensive team approach. The patient can receive appropriate care only after the location and size of the tumor are accurately identified.

Head and neck cancers are usually squamous cell carcinomas and are slow growing. They are curable when treated early. The prognosis for those who have more advanced disease at diagnosis depends on the extent and location of the tumor. Untreated cancer of the head and neck is a fatal disease within 2 years of diagnosis (ACS, 2011).

The cancer begins when the mucosa is chronically irritated and becomes tougher and thicker (squamous metaplasia), often with a keratin layer (keratosis). At the same time, genes controlling cell growth are damaged, allowing excessive growth of these abnormal cells, which eventually become malignant. These lesions may then be seen as white, patchy lesions (leukoplakia) or red, velvety patches (erythroplakia).

Head and neck cancer first spreads (metastasizes) into nearby structures, such as lymph nodes, muscle, and bone. Later spread is systemic to distant sites, usually to the lungs or liver.

The cancer type and stage are determined by cellular analysis. Earlier stage cancers are described as carcinoma in situ and well differentiated. Without treatment, cancers progress to be moderately differentiated and, finally, poorly differentiated. Most head and neck cancers arise from mucous membrane and skin, but they also can start from salivary glands, the thyroid, or other structures. Treatment is based on tumor cell type and degree of spread at diagnosis.

Etiology

The two most important risk factors for head and neck cancer are tobacco and alcohol use, especially in combination. Other risk factors include voice abuse, chronic laryngitis, exposure to chemicals, dusts, and poor oral hygiene. Other possible risk factors are long-erm or severe gastroesophageal reflux disease (GERD) and infection with the human papilloma virus (Calloway, 2011).

Incidence/Prevalence

The frequency of head and neck carcinoma is increasing in North America. About 53,810 new cases of oral, pharyngeal, and laryngeal cancers are diagnosed each year and account for more than 13,000 deaths per year (ACS, 2011; Canadian Cancer Society, 2010). They affect men more often than women and are most common in people older than 60 years.
(Ignatavicius 2013, pp. 588-589)

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assessment
(head & neck cancer)

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History

The patient may have difficulty speaking because of hoarseness, shortness of breath, tumor bulk, and pain. Be sensitive to these difficulties during the interview, and pace the interview to avoid tiring the patient.

Ask about tobacco and alcohol use, history of acute or chronic laryngitis or pharyngitis, oral sores, and lumps in the neck. Calculate the patient's pack-years of smoking history (see Chapter 29). Ask about alcohol intake (how many drinks per day and for how many years). Showing concern and using a “matter-of-fact” approach during the interview may help make the patient more comfortable with these questions. Also ask about exposure to pollutants.

Assess problems related to risk factors. For example, nutrition may be poor because of alcohol intake and impaired liver function. Assess dietary habits and any weight loss. Ask about any chronic lung disease, which may have an impact on the patient's breathing pattern.

Physical Assessment/Clinical Manifestations

Table 31-1 lists the warning signs of head and neck cancer. With laryngeal cancer, painless hoarseness may occur because of tumor size and an inability for the vocal cords to come together for normal speech (phonation). Vocal cord lesions are the earliest form of laryngeal cancer. Any person who has a history of hoarseness, mouth sores, or a lump in the neck for 3 to 4 weeks should be evaluated for laryngeal cancer.

Inspection and palpation of the head and neck are important parts of the physical examination. An advanced practice nurse or physician may perform a laryngeal examination using a laryngeal mirror or fiberoptic laryngoscope. Lesions may be seen on inspection. The neck is palpated to assess for enlarged lymph nodes.

Psychosocial Assessment

Often the patient with head and neck cancer has a long-standing history of cigarette or alcohol use or both. Assess the adequacy of support systems and coping mechanisms. Document social and family support because the patient often needs extensive assistance at home after treatment. Collaborate with a social worker as needed. Assess the level of education or literacy of the patient and family to plan teaching before and after surgery.

Document any family history of cancer, as well as the patient's age, gender, occupation, and ability to perform ADLs. Ask the patient whether his or her occupation requires continual oral communication. Job retraining may be needed if treatment affects speech.

Laboratory Assessment

Diagnostic tests include a complete blood cell count, bleeding times, urinalysis, and blood chemistries. The patient with chronic alcoholism may have low protein and albumin levels from poor nutrition. Liver and kidney function tests are performed to rule out cancer spread and to evaluate the patient's ability to metabolize drugs and chemotherapy agents.

Imaging Assessment

Many types of imaging studies, including x-rays of the skull, sinuses, neck, and chest, are useful in diagnosing cancer spread, other tumors, and the extent of tumor invasion. Computed tomography (CT), with or without contrast media, helps evaluate the tumor's exact location. Magnetic resonance imaging (MRI) can help differentiate normal from diseased tissue.

The brain, bone, and liver are evaluated with nuclear imaging, bone scans, single-photon emission computerized tomography (SPECT) scans, and positron emission tomography (PET) scans. These tests help locate additional tumor sites.

Other Diagnostic Assessment

Other helpful tests include direct and indirect laryngoscopy, tumor mapping, and biopsy. Panendoscopy (laryngoscopy, nasopharyngoscopy, esophagoscopy, and bronchoscopy) is performed with general anesthesia to define the extent of the tumor. Tumor-mapping biopsies are performed to identify tumor location. Biopsy tissues taken at the time of the panendoscopy confirm the diagnosis and determine the tumor type, cell features, and location. Tumor staging by the TNM (tumor, nodes, metastasis) method (see Chapter 23) is also performed. (Ignatavicius 2013, pp. 589-590)

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warning signs
(head & neck cancer)

Back 50

--Pain
--Lump in the mouth, throat, or neck
--Difficulty swallowing
--Color changes in the mouth or tongue to red, white, gray, dark brown, or black
--Oral lesion or sore that does not heal in 2 weeks
--Persistent or unexplained oral bleeding
--Numbness of the mouth, lips, or face
--Change in the fit of dentures
--Burning sensation when drinking citrus juices or hot liquids
--Persistent, unilateral ear pain
--Hoarseness or change in voice quality
--Persistent or recurrent sore throat
--Shortness of breath
--Anorexia and weight loss (Ignatavicius 2013, p. 589)

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planning
(head & neck cancers)

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Analysis

The priority problems for the patient with head and neck cancer are:
--Potential for respiratory obstruction
--Risk for Aspiration related to edema, anatomic changes, or altered protective reflexes
--Anxiety related to threat of death, change in role status, or change in economic status
--Reduced self-concept related to tumor and treatment modalities

Planning and Implementation

Preventing Respiratory Obstruction

Without treatment, head and neck cancers grow to the point of airway obstruction. In addition, airway obstruction can occur as a complication of treatment modalities.

Planning: Expected Outcomes

The patient with head and neck cancer is expected to attain and maintain adequate tissue oxygenation.

Indicators include:
--Arterial blood gas values within the normal range
--Rate and depth of respiration within the normal range
--Pulse oximetry within the normal range (Ignatavicius 2013, p. 590)

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interventions
(head & neck cancers)

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Interventions

The focus of treatment is to remove or eradicate the cancer while preserving as much normal function as possible. The physician presents the available treatment options. Surgery, radiation, chemotherapy, or biotherapy may be used alone or in combination. In planning treatment options, the patient's physical condition, nutritional status, and age; the effects of the tumor on body function; and the patient's personal choice are all considered.

Treatment for laryngeal cancer may range from radiation therapy (for a small specific area or tumor) to total laryngopharyngectomy with bilateral neck dissections followed by radiation therapy. The specific treatment depends on the extent and location of the lesion. Voice-conservation procedures are used only if they do not risk incomplete removal of the tumor. Nursing care focuses on the patient's total needs, including preoperative preparation, competent in-hospital care, discharge planning and teaching, and extensive outpatient rehabilitation. (Ignatavicius 2013, p. 590)

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nonsurgical management
(head & neck cancers)

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Monitor the respiratory system by assessing respiratory rate, breath sounds, pulse oximetry, arterial blood gas values, and the results of pulmonary function tests. Airway obstruction can occur from tumor growth, edema, or both. Teach the patient to use the Fowler's and semi-Fowler's positions for best air exchange. Sitting upright in a reclining chair may promote more comfortable breathing. Chapters 5 and 9 provide additional information on palliation and pain control for patients who elect not to have therapy and for those whose therapy has not been effective.

Radiation therapy for treatment of small cancers in specific locations has a cure rate of at least 80%. Standard therapy uses 5000 to 7500 rad (radiation absorbed dose), usually over 6 weeks and in daily or twice-daily doses. Radiation may be used alone or in combination with surgery and chemotherapy (see Chapter 24). Because radiation therapy slows tissue healing, it might not be performed before surgery. Most patients have hoarseness, dysphagia, skin problems, and dry mouth for a few weeks after radiation therapy.

Hoarseness may become worse during therapy. Reassure the patient that voice improves within 4 to 6 weeks after completion of radiation therapy. Urge the patient to use voice rest and alternative means of communication until the effects of radiation therapy have passed.

Most patients have a sore throat and difficulty swallowing during radiation therapy to the neck. Gargling with saline or sucking ice may decrease discomfort. Mouthwashes and throat sprays containing a local anesthetic agent such as lidocaine or diphenhydramine can provide temporary relief. Analgesic drugs may be prescribed.

The skin at the site of irradiation becomes red and tender and may peel during therapy. Instruct the patient to avoid exposing this area to sun, heat, cold, and abrasive treatments such as shaving. Teach the patient to wear protective clothing made of soft cotton and to wash this area gently with a mild soap, such as Dove. At one time, patients were told to avoid using lotions or other skin care products within 4 hours of the radiation therapy; however, this practice is not evidence-based and is now controversial (Bieck, Phillips, & Steele-Moses, 2010). Teach patients to follow the radiation-oncology department's policy regarding the use and timing of skin care products.

If the salivary glands are in the irradiation path, the mouth becomes dry (xerostomia). This side effect is long-term and may be permanent. Some of the problems from reduced saliva include increased risk for dental caries, increased risk for oral infections, halitosis (bad breath), and taste changes. Fluoride gel trays and nightly fluoride treatments can reduce the incidence of tooth deterioration. The trays can be worn during radiation therapy to prevent radiation scatter from the beam deflecting off existing metal inside the mouth (Lambertz et al., 2010). Although there is no cure for xerostomia, interventions can help reduce the discomfort. Heavy fluid intake, particularly water, and humidification can help ease the discomfort. Some patients benefit from the use of artificial saliva, such as Salivart; moisturizing sprays or gels, such as Mouth Kote; or saliva stimulants, such as Salagen and cevimeline (cholinergic drugs).

Chemotherapy can be used alone or in addition to surgery or radiation for head and neck cancer. Often, chemotherapy and radiation therapy, chemoradiation, are used at the same time. Although the exact drugs used may vary, depending on cell origin, most chemotherapy regimens for head and neck cancers include cisplatin (National Comprehensive Cancer Network, 2010). The oral cavity effects of radiation are intensified with concurrent chemotherapy. These can be uncomfortable, and patients often request breaks in the treatment regimen. However, these breaks in treatment do affect the outcome of treatment and should be avoided (a process called NO SToPS). Intense patient education before treatment and support during treatment can improve patient adherence to the treatment plan (Lambertz et al., 2010). Chapter 24 discusses the general care needs of patients receiving chemotherapy.

Biotherapy in the form of epidermal growth factor receptor (EGFR) blockers may be effective for patients whose cancers overexpress the receptor. Currently, the drug approved for this purpose is cetuximab (Erbitux). Although it is a targeted therapy, this drug blocks EGFRs in normal tissues as well as those in the tumor. As a result, severe skin reactions are common. (Ignatavicius 2013, pp. 590-591)

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surgical management
(head & neck cancers)

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Tumor size and location (TNM classification) determines the type of surgery needed for the specific head and neck cancer. Very small, early-stage tumors may be removed by laser therapy or photodynamic therapy; however, few head and neck tumors are found at this stage and most require extensive traditional surgery. Reconstruction is also determined by the tumor size and amount of tissue to be resected and reconstructed. Surgical procedures for head and neck cancers include laryngectomy (total and partial), tracheotomy, and oropharyngeal cancer resections. The major types of surgery for laryngeal cancer include cord stripping, removal of a vocal cord (cordectomy), partial laryngectomy, and total laryngectomy. If cancer is in the lymph nodes in the neck or if the tumor has a high rate of nodal spread, the surgeon performs a nodal neck dissection along with removal of the primary tumor (“radical neck”). A pathologist evaluates the resected lymph nodes for possible tumor invasion. (Ignatavicius 2013, p. 591)

***Extensive pre/post-operative care descriptions on p.591

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preventing aspiration
(head & neck cancers)

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Planning: Expected Outcomes

The patient with head and neck cancer is expected to not aspirate food, gastric contents, or oral secretions into the lungs. Indicators include that the patient often or consistently demonstrates these behaviors:

• Positions self upright for eating or drinking

• Selects foods according to swallowing ability

• Chooses liquids and foods of proper consistency

Interventions

The surgical changes in the upper respiratory tract and altered swallowing mechanisms increase the patient's risk for aspiration. Aspiration can result in pneumonia, weight loss, and prolonged hospitalization. Chart 31-3 lists actions for aspiration prevention.

The presence of a nasogastric (NG) feeding tube may further increase the potential for aspiration because it keeps the lower esophageal sphincter partially open. The one exception is the patient who has undergone a total laryngectomy. In these cases, the airway is separated from the esophagus, making aspiration impossible; such a patient is not at risk.

A dynamic swallow study, such as a barium swallow under fluoroscopy, evaluates a patient's ability to protect the airway from aspiration and helps determine the appropriate method of swallow rehabilitation. In many cases, enteral feedings are used either because of the patient's inability to swallow or because of continued aspiration risk.

When an NG tube is in place, help prevent aspiration with the use of routine reflux precautions, including elevating the head of the bed and strictly adhering to tube feeding regimens (especially no bolus feedings at night). Check residual volume before each bolus feeding (or every 4 to 6 hours with continuous feeding), and evaluate the patient's tolerance of the tube feeding. If the residual volume is high (above 100 mL for bolus feeding or 2 hour's worth of continuous tube feeding, or as otherwise prescribed by the physician), withhold the feeding and notify the physician. Check the pH of pulmonary secretions. Because residual volume cannot be checked with narrow feeding tubes, use other techniques to assess tube placement. (See Chapter 63 for interventions related to NG tubes and tube feedings.)

Swallowing can be a major problem for the patient who has a tracheostomy tube. Swallowing can be normal if the cranial nerves and anatomic structures are intact. In a normal swallow, the larynx rises and moves forward to protect itself from the passing stream of food and saliva. Laryngeal rising also helps open the upper esophageal sphincter. The tracheostomy tube sometimes fixes the larynx in place, resulting in difficulty swallowing.

An inflated tracheostomy tube cuff can balloon backward into the esophagus and interfere with the passage of food. The wall between the posterior trachea and the esophagus is very thin, which allows this pushing action. The patient who is cognitively intact may adapt to eating normal food when the tracheostomy tube is small and the cuff is not inflated.

The patient who has had a partial vertical or supraglottic laryngectomy must be observed for aspiration. It is critical to teach the patient to use alternate methods of swallowing without aspirating. The “supraglottic” method of swallowing is especially effective after a partial laryngectomy or base-of-tongue resection (Chart 31-4). To reinforce teaching and learning, place a chart in the patient's room detailing the steps. A dynamic swallow study is performed to guide rehabilitation for swallowing and to evaluate the patient's ability to protect the airway.
(Ignatavicius 2013, pp. 594-595)

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best practices for preventing aspiration
(head & neck cancers)

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Best Practice For Patient Safety & Quality Care

Prevention of Aspiration During Swallowing:
--Avoid serving meals when the patient is fatigued.
--Provide smaller and more frequent meals.
--Provide adequate time; do not “hurry” the patient.
--Provide close supervision if the patient is self-feeding.
--Keep emergency suctioning equipment close at hand.
--Avoid water and other “thin” liquids.
--Thicken liquids.
--Avoid foods that generate thin liquids during the chewing process, such as fruit.
--Position the patient in the most upright position possible.
--When possible, completely (or at least partially) deflate the tube cuff during meals.
--Suction after initial cuff deflation to clear the airway and allow maximum comfort during the meal.
--Feed each bite or encourage the patient to take each bite slowly.
--Encourage the patient to “dry swallow” after each bite to clear residue from the throat.
--Avoid consecutive swallows by cup or straw.
--Provide controlled small volumes of liquids, using a spoon.
--Encourage the patient to “tuck” his or her chin down and move the forehead forward while swallowing.
--Allow the patient to indicate when he or she is ready for the next bite.
--If the patient coughs, stop the feeding until the patient indicates the airway has been cleared.
--Continuously monitor tolerance to oral food intake by assessing respiratory rate, ease, pulse oximetry, and heart rate. (Ignatavicius 2013, p. 596)

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atelectasis

Back 57

Collapse of alveoli.

(Ignatavicius 2013, p. 1730)

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pneumonia

Back 58

Pathophysiology

Pneumonia is an excess of fluid in the lungs resulting from an inflammatory process. The inflammation is triggered by many infectious organisms and by inhalation of irritating agents. Infectious pneumonias are categorized as community-acquired pneumonia (CAP) or health care–associated pneumonia (known as HAP or HAI), depending on where the patient was exposed to the infectious agent (Dobbins & Howard, 2011). HAPs are more likely to be resistant to some antibiotics than are CAPs.

The inflammation occurs in the interstitial spaces, the alveoli, and often the bronchioles. The process begins when organisms penetrate the airway mucosa and multiply in the alveoli. White blood cells (WBCs) migrate to the area of infection, causing local capillary leak, edema, and exudate. These fluids collect in and around the alveoli, and the alveolar walls thicken. Both events seriously reduce gas exchange and lead to hypoxemia, interfering with oxygenation and possibly leading to death. Red blood cells (RBCs) and fibrin also move into the alveoli. The capillary leak spreads the infection to other areas of the lung. If the organisms move into the bloodstream, sepsis results; if the infection extends into the pleural cavity, empyema (a collection of pus in the pleural cavity) results.

The fibrin and edema of inflammation stiffen the lung, reducing compliance and decreasing the vital capacity. Alveolar collapse (atelectasis) further reduces the ability of the lung to oxygenate the blood moving through it. As a result, arterial oxygen levels fall, causing hypoxemia.

Pneumonia may occur as lobar pneumonia with consolidation (solidification, lack of air spaces) in a segment or an entire lobe of the lung or as bronchopneumonia with diffusely scattered patches around the bronchi. The extent of lung involvement after the organism invades depends on the host defenses. Bacteria multiply quickly in a person whose immune system is compromised. Tissue necrosis results when an abscess forms and perforates the bronchial wall.

Etiology

Pneumonia develops when the immune system cannot combat the virulence of the invading organisms. Organisms from the environment, invasive devices, equipment and supplies, staff, or other people can invade the body. Risk factors are listed in Table 33-2. Pneumonia can be caused by bacteria, viruses, mycoplasmas, fungi, rickettsiae, protozoa, and helminths (worms). Noninfectious causes of pneumonia include inhalation of toxic gases, chemical fumes, and smoke and aspiration of water, food, fluid, and vomitus.

Incidence/Prevalence

In the United States, 2 to 5 million cases of pneumonia occur each year and it is the seventh leading cause of death (Schappert et al., 2008). The incidence is higher among older adults, nursing home residents, hospitalized patients, and those being mechanically ventilated. CAP is more common than HAP and occurs in late fall and winter as a complication of influenza. HAP is commonly acquired as a result of transmission during a hospital stay. A specific type of HAP is ventilator-associated pneumonia (VAP). HAP has a 20% to 50% mortality rate; the highest incidence is in those patients infected with Pseudomonas aeruginosa, Acinetobacter, Klebsiella, other “high-risk” organisms, or secondary bacteremia. (Ignatavicius 2013, p. 647)

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risk factors
(pneumonia)

Back 59

Community-Acquired Pneumonia
--Is an older adult
--Has never received the pneumococcal vaccination or received it more than 6 years ago
--Did not receive the influenza vaccine in the previous year
--Has a chronic health problem or other coexisting condition
--Has recently been exposed to respiratory viral or influenza infections
--Uses tobacco or alcohol or is exposed to high amounts of secondhand smoke

Health Care–Acquired Pneumonia
--Is an older adult
--Has a chronic lung disease
--Has presence of gram-negative colonization of the mouth, throat, and stomach
--Has an altered level of consciousness
--Has had a recent aspiration event
--Has presence of endotracheal, tracheostomy, or nasogastric tube
--Has poor nutritional status
--Has immunocompromised status (from disease or drug therapy)
--Uses drugs that increase gastric pH (histamine [H2] blockers, antacids) or alkaline tube feedings
--Is currently receiving mechanical ventilation (ventilator-associated pneumonia [VAP]) (Ignatavicius 2013, p. 647)

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health promotion & maintenance
(pneumonia)

Back 60

Antigens from 23 different types of pneumonia organisms are included in the pneumococcal polysaccharide vaccine (PPV23). Patient education is important in the prevention of pneumonia (Chart 33-4). Especially encourage people older than 65 years and those with a chronic health problem to receive the PPV23. This vaccine is usually given once; however, some experts believe that older adults and those with chronic health problems could benefit from a second vaccination if more than 5 years have passed since the first vaccination (American Lung Association [ALA], 2010a). Because pneumonia often follows influenza, especially among older adults, urge all people to receive the seasonal influenza vaccination yearly (Schweon, 2010).

Other prevention techniques include strict handwashing to avoid the spread of organisms and avoiding large gatherings of people during cold and flu season. Teach the patient who has a cold or the flu to see his or her health care provider if fever lasts more than 24 hours, if the problem lasts longer than 1 week, or if symptoms worsen.

Hospital respiratory therapy equipment must be well maintained and decontaminated or changed as recommended. Use sterile water rather than tap water in GI tubes, and institute Aspiration Precautions as indicated (see Chapter 31).

VAP is on the rise, especially among patients with endotracheal tubes in place for mechanical ventilation (American Association of Critical-Care Nurses [AACN], 2008; Luttenberger, 2010). Although just having the tube providing a direct connection between the environment and the patient's lower respiratory passageways increases the risk for VAP, the risk can be reduced with conscientious assessment and meticulous nursing care (Garcia et al., 2009). Three care actions, known as a “ventilator bundle,” have been shown to reduce the incidence of VAP—hand hygiene, oral care, and head-of-bed elevation. Oral care is critical in reducing the risk because many common organisms causing VAP are translocated from the patient's mouth into the respiratory tract. A variety of commercial products are available as oral care kits and suction kits specifically designed for patients who have an endotracheal tube. In addition, some types of endotracheal tubes have a separate lumen to allow for continuous suction of subglottic secretions to prevent their aspiration. However, the key to successful prevention of VAP remains nursing vigilance in assessment and oral care (Ames, 2011). Chart 33-5 lists best practices for preventing VAP.

(Ignatavicius 2013, pp. 647-649)

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prevention and education
(pneumonia)

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Patient And Family Education: Preparing For Self-Management

Preventing Pneumonia
--Know whether you are at risk for pneumonia (older than 65 years, have a chronic health problem [especially a respiratory problem], or have limited mobility and are confined to a bed or chair during your waking hours).
--Have the annual influenza vaccine after discussing appropriate timing of the vaccination with your primary health care provider.
--Discuss the pneumococcal vaccine with your primary health care provider, and have the vaccination as recommended.
--Avoid crowded public areas during flu and holiday seasons.
--If you have a mobility problem, cough, turn, move about as much as possible, and perform deep-breathing exercises.
--If you are using respiration equipment at home, clean the equipment as you have been taught.
--Avoid indoor pollutants, such as dust, secondhand (passive) smoke, and aerosols.
--If you do not smoke, do not start.
--If you smoke, seek professional help on how to stop (or at least decrease) your habit.
--Be sure to get enough rest and sleep on a daily basis.
--Eat a healthy, balanced diet.
--Drink at least 3 liters of nonalcoholic fluids each day (unless fluid restrictions are needed because of another health problem). (Ignatavicius 2013, p. 649)

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preventing VAP
(pneumonia)

Back 62

Best Practice for Patient Safety & Quality Care

Preventing Ventilator-Associated Pneumonia (VAP)
--If possible, perform oral care with a disinfecting oral rinse right before the intubation.
--Do not wear hand jewelry, especially rings, when providing care to ventilator patients.
--Wash hands before and after contact with the patient.
--Provide complete oral care at least every 12 hours.
--Remove subglottic secretions frequently (at least every 2 hours) or continuously (when the endotracheal tube has a separate lumen that opens directly above the tube cuff).
--Keep the head of the bed elevated to at least 30 degrees unless another health problem is a contraindication for this position.
--Verify that an initial x-ray has been obtained to confirm the placement of any nasogastric tube before instilling drugs, fluids, or feedings into the tube.
--Avoid turning the patient or placing him or her in the supine position (even briefly) within an hour after a bolus tube feeding.
--Work with the patient and health care team to assist in the weaning process as soon as possible

***Nursing Safety Priority Action Alert***

Assess the oral cavity every 6 hours for patients who are mechanically ventilated and have an endotracheal tube. After assessment, suction the oral cavity, and clean the tissues and gums using agents that reduce organisms and provide moisture every 6 hours. Place the ventilated patient on his or her side during oral care to help reduce the risk for aspiration. If teeth are present, brush them every 12 hours (Garcia et al., 2009). (Ignatavicius 2013, p. 649)

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assessment & diagnostics
(pneumonia)

Back 63

History

Assess for the risk factors for infection (see Table 33-2). Obtain the information from a family member if the patient is confused or too dyspneic. Document age; living, work, or school environment; diet, exercise, and sleep routines; swallowing problems; presence of a nasogastrointestinal tube; tobacco and alcohol use; past and current use of “street” drugs; and history of drug addiction and injection drug use. Ask about past respiratory illnesses and whether the patient has been exposed to influenza or pneumonia or has had a recent viral infection. Ask about recent skin rashes, insect bites, and exposure to animals.

If the patient has chronic respiratory problems, ask whether respiratory equipment is used in the home. Assess whether the patient's home cleaning level is adequate to prevent infection. Ask when he or she received the last influenza or pneumococcal vaccine.

Physical Assessment/Clinical Manifestations

Observe the general appearance. Many patients with pneumonia have flushed cheeks, bright eyes, and an anxious expression. The patient may have chest or pleuritic pain or discomfort, myalgia, headache, chills, fever, cough, tachycardia, dyspnea, tachypnea, hemoptysis, and sputum production. Severe chest muscle weakness also may be present from sustained coughing.

Observe the patient's breathing pattern, position, and use of accessory muscles. The hypoxic patient may be uncomfortable in a lying position and will sit upright, balancing with the hands. Assess the cough and the amount, color, consistency, and odor of sputum produced.

Crackles are heard with auscultation when fluid is in interstitial and alveolar areas. Wheezing may be heard if inflammation or exudate is in the airways. Bronchial breath sounds are heard over areas of density or consolidation. Fremitus is increased over areas of pneumonia, and percussion is dulled. Chest expansion may be diminished or unequal on inspiration.

In evaluating vital signs, compare the results with baseline values. The patient with pneumonia is likely to be hypotensive with orthostatic changes as a result of vasodilation and dehydration, especially the older adult. A rapid, weak pulse may indicate hypoxemia, dehydration, or impending shock. Dysrhythmias may be present as a result of cardiac tissue hypoxia. Common pneumonia manifestations and their causes are listed in Table 33-3.

Considerations for Older Adults

The older adult with pneumonia has weakness, fatigue, lethargy, confusion, and poor appetite. Fever and cough may be absent, but hypoxemia is often present. The most common manifestation of pneumonia in the older adult patient is acute confusion from hypoxia. The WBC count may not be elevated until the infection is severe. Waiting to treat the disease until more typical manifestations appear greatly increases the risk for sepsis and death (Touhy & Jett, 2010).

Psychosocial Assessment

The patient with pneumonia often has pain, fatigue, and dyspnea, all of which promote anxiety. Assess anxiety by looking at his or her facial expression and general tenseness of facial and shoulder muscles. Listen to him or her carefully, and use a calm, slow approach. Because of airway obstruction and muscle fatigue, the patient with dyspnea speaks in broken sentences. Keep the interview short if severe dyspnea or breathing discomfort is present.

Laboratory Assessment

Sputum is obtained and examined by Gram stain, culture, and sensitivity testing; however, the responsible organism often is not identified. A sputum sample is easily obtained from the patient who can cough into a specimen container. Extremely ill patients may need suctioning to obtain a sputum specimen. In these situations, a specimen is obtained by sputum trap (Fig. 33-1) during suctioning. A CBC is obtained to assess an elevated WBC count, which is a common finding except in older adults. Blood cultures may be performed to determine whether the organism has invaded the blood.

In severely ill patients, arterial blood gases (ABGs) may be performed to determine baseline arterial oxygen and carbon dioxide levels and help identify a need for supplemental oxygen. Serum electrolyte, blood urea nitrogen (BUN), and creatinine levels also are assessed. A high BUN level may occur as a result of dehydration. Hypernatremia (high blood sodium levels) occurs with dehydration as a result of fever and decreased fluid intake.

Imaging Assessment

Chest x-ray continues to be the most common diagnostic test for pneumonia but may not show changes until 2 or more days after manifestations are present. It usually appears on chest x-ray as an area of increased density. It may involve a lung segment, a lobe, one lung, or both lungs. In the older adult, the chest x-ray is essential for early diagnosis because pneumonia symptoms are often vague (Fowler, 2008; Touhy & Jett, 2010).

Other Diagnostic Assessment

Pulse oximetry is used to assess for hypoxemia. Invasive tests such as transtracheal aspiration, bronchoscopy, or direct needle aspiration of the lung may be needed. Thoracentesis is most often used in patients who have an accompanying pleural effusion.
(Ignatavicius 2013, pp. 649-651)

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clinical manifestations
(pneumonia)

Back 64

Front 65

interventions
(pneumonia)

Back 65

Priority problems for the patient with pneumonia are:
--Hypoxemia related to decreased diffusion at the alveolar-capillary membrane
--Potential for airway obstruction related to excessive tracheobronchial secretions, fatigue, chest discomfort, muscle weakness
--Potential for sepsis related to the presence of microorganisms in a very vascular area

*Managing Hypoxemia*

The patient with pneumonia is expected to have adequate oxygenation. Indicators of adequate oxygenation are:
--Maintenance of SaO2 of at least 95% or in the patient's normal range
--Absence of cyanosis
--Maintenance of cognitive orientation

Interventions to improve oxygenation are similar to those for the patient with chronic airflow limitation (CAL) (see Chapter 32). Nursing priorities include delivery of oxygen therapy and assisting the patient with bronchial hygiene.

Oxygen therapy is usually delivered by nasal cannula or mask unless the hypoxemia does not improve with these devices. The patient who is confused may not tolerate a facemask. Check the skin under the device and under the elastic band, especially around the ears, for areas of redness or skin breakdown. Actions for oxygen therapy are listed in Chart 30-1 in Chapter 30.

Incentive spirometry is a type of bronchial hygiene used in pneumonia. The objective is to improve inspiratory muscle action and to prevent or reverse atelectasis (alveolar collapse). Instruct the patient to exhale fully, then place the mouthpiece in his or her mouth, and then take a long, slow, deep breath for 3 to 5 seconds. Evaluate technique, and record the volume of air inspired. Teach the patient to perform 5 to 10 breaths per session every hour while awake.

*Preventing Airway Obstruction*

The patient with pneumonia is expected to maintain a patent airway. Indicators are:
--Effective cough
--Absence of pallor or cyanosis
--Absence of crackles and wheezes on auscultation
--Pulse oximetry at or above 95%

Interventions to avoid airway obstruction in pneumonia are similar to those for chronic obstructive pulmonary disease (COPD) or asthma. Because of fatigue, muscle weakness, chest discomfort, and excessive secretions, the patient often has difficulty clearing secretions. Help him or her cough and deep breathe at least every 2 hours. The alert patient may use an incentive spirometer to facilitate deep breathing and stimulate coughing. Encourage the alert patient to drink at least 2 liters of fluid daily to prevent dehydration unless another health problem requires fluid restriction. Adequate hydration may help thin secretions and make them easier to remove. Monitor intake and output, oral mucous membranes, and skin turgor to assess for and ensure adequate hydration, especially when fever and tachypnea are present.

Bronchodilators, especially beta2 agonists (see Chart 32-7 in Chapter 32), are prescribed when bronchospasm is present. They are initially given by nebulizer and then by metered-dose inhaler. Inhaled or IV steroids are used with acute pneumonia when airway swelling is present.

*Preventing Sepsis*

The patient with pneumonia is expected to be free of the invading organism and to return to a pre-pneumonia health status. Indicators are:
--Absence of fever
--Absence of pathogens in blood and sputum cultures
--WBC count and differential within normal limits

The key to effective treatment of pneumonia is eradication of the organism causing the infection. When sepsis accompanies pneumonia, the risk for death is high (Todd, 2010). Anti-infectives are given for all types of pneumonias except those caused by viruses. Which anti-infective therapy is prescribed is based on how the pneumonia was acquired (i.e., CAP or HAP). The exact drug or drugs and their routes of delivery are determined by the severity of the infection, the organism suspected or identified, and whether the patient has other conditions or factors that increase the risk for complications. Drug therapy choices must reflect the degree of drug resistance in the specific geographic area and in that hospital setting.

If IV drugs are used, the patient may be able to be switched to oral therapy in 2 or 3 days, depending on the response (e.g., stable clinical condition, afebrile). The course of anti-infective therapy varies with the drug used and the organism(s) involved. Usually anti-infectives are used for 5 to 7 days for a patient with uncomplicated CAP and up to 21 days for an immunocompromised patient or one with HAP.

Drug resistance is becoming increasingly common, especially for infections with Streptococcus pneumoniae. This problem is known as drug-resistant Streptococcus pneumoniae, or DRSP. DRSP is most common among people older than 65 years and among those who became infected as a result of exposure to young children from a day-care environment.

For pneumonia resulting from aspiration of food or stomach contents, interventions focus on preventing lung damage and treating the infection. Aspiration of acidic stomach contents can cause widespread inflammation, leading to acute respiratory distress syndrome (ARDS) and permanent lung damage (Eisenstadt, 2010). In these conditions, steroids and NSAIDs are used with antibiotics to reduce the inflammatory response. (Ignatavicius 2013, pp. 651-652)

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home care & self-management
(pneumonia)

Back 66

ome Care Management

No special changes are needed in the home. If the home has a second story, the patient may prefer to stay on one floor for a few weeks, because stair climbing increases fatigue and dyspnea. Toileting needs may be met by using a bedside commode if a bathroom is not located on the level the patient is using. Home care needs depend on the patient's level of fatigue, dyspnea, and family and social support.

The long recovery phase, especially in the older adult, can be frustrating. Fatigue, weakness, and a residual cough can last for weeks. Some patients fear they will never return to a “normal” level of functioning. Prepare them for the disease course, and offer reassurance that complete recovery will occur. After discharge, a home nursing assessment may be helpful (Chart 33-6).

Teaching for Self-Management

Review all drugs with the patient and family, and emphasize completing anti-infective therapy. Teach the patient to notify the health care provider if chills, fever, persistent cough, dyspnea, wheezing, hemoptysis, increased sputum production, chest discomfort, or increasing fatigue recurs or if symptoms fail to resolve. Instruct him or her to get plenty of rest and increase activity gradually.

An important aspect of education for the patient and family is the avoidance of upper respiratory tract infections and viruses. Teach him or her to avoid crowds (especially in the fall and winter when viruses are prevalent), people who have a cold or flu, and exposure to irritants such as smoke. Stress the importance of following his or her health care provider's recommendations for vaccination against influenza and pneumonia. A balanced diet and adequate fluid intake are essential.

Health Care Resources

Inform patients who smoke that smoking is a risk factor for pneumonia. Provide them with information on local smoking-cessation classes. The health care provider may prescribe nicotine patches. Urge patients to enroll in a smoking-cessation program for increased support. Provide information booklets on pneumonia, and urge the patient who has not already been vaccinated against influenza or pneumonia to take this preventive measure after the pneumonia has resolved. (Ignatavicius 2013, p. 652)

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tuberculosis (TB)

Back 67

Tuberculosis (TB) is a highly communicable disease caused by Mycobacterium tuberculosis. It is the most common bacterial infection worldwide (World Health Organization [WHO], 2010). The organism is transmitted via aerosolization (i.e., an airborne route) (Fig. 33-2). When a person with active TB coughs, laughs, sneezes, whistles, or sings, droplets become airborne and may be inhaled by others. Far more people are infected with the bacillus than actually develop active TB (Knechel, 2009).

The bacillus multiplies freely when it reaches a susceptible site (bronchi or alveoli). An exudative response occurs, causing pneumonitis. With the development of acquired immunity, further growth of bacilli is controlled in most initial lesions. These lesions usually resolve and leave little or no residual bacilli. Only a small percentage of people initially infected with the bacillus ever develop active TB.

Cell-mediated immunity develops 2 to 10 weeks after infection and is manifested by a positive reaction to a tuberculin test. The primary infection may be so small that it does not appear on a chest x-ray. The process of infection occurs in this order:

1 The granulomatous inflammation created by the tubercle bacillus in the lung becomes surrounded by collagen, fibroblasts, and lymphocytes.

2 Caseation necrosis, which is necrotic tissue being turned into a granular mass, occurs in the center of the lesion. If this area shows on x-ray, it is called Ghon's tubercle, or the primary lesion.

Areas of caseation then undergo resorption, degeneration, and fibrosis. These necrotic areas may calcify (calcification) or liquefy (liquefaction). If liquefaction occurs, the liquid material then empties into a bronchus and the evacuated area becomes a cavity (cavitation). Bacilli continue to grow in the necrotic cavity wall and spread via lymph channels into new areas of the lung.

A lesion also may progress by direct extension if bacilli multiply rapidly during inflammation. The lesions may extend through the pleura, resulting in pleural or pericardial effusion. Miliary or hematogenous TB is the spread of TB throughout the body when a large number of organisms enter the blood. Many tiny nodules scattered throughout the lung are seen on chest x-ray. The brain, liver, kidney, or bone marrow can become infected as a result of this spread.

Initial infection is seen more often in the middle or lower lobes of the lung. The local lymph nodes are infected and enlarged. An asymptomatic period usually follows the primary infection and can last for years or decades before clinical symptoms develop. An infected person is not infectious to others until manifestations of disease occur.

Secondary TB is a reactivation of the disease in a previously infected person. It is more likely when defenses are lowered, such as with older adults and people with HIV disease. The upper lobes are the most common site of reactivation and are referred to as Simon's foci.

Etiology

M. tuberculosis is a nonmoving, slow-growing, acid-fast rod transmitted via the airborne route. People who are usually infected are those having repeated close contact with an infectious person who has not yet been diagnosed with TB. The risk for transmission is reduced after the infectious person has received proper drug therapy for 2 to 3 weeks, clinical improvement occurs, and acid-fast bacilli (AFB) in the sputum are reduced. (Ignatavicius 2013, pp. 653-654)

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incidence & prevalence
(TB)

Back 68

Worldwide, 5.8 million people are diagnosed annually and an additional 8 million people are estimated to have undiagnosed disease (WHO, 2010). The incidence of TB has been steadily decreasing in the United States, although increases in incidence are seen in many other countries (ALA, 2010b). In the United States, the people who are at greatest risk for development of TB are:
--Those in constant, frequent contact with an untreated person
--Those who have decreased immune function or HIV
--People who live in crowded areas such as long-term care facilities, prisons, and mental health facilities
--Older homeless people
--Abusers of injection drugs or alcohol
--Lower socioeconomic groups
--Foreign immigrants (especially from Mexico, the Philippines, and Vietnam)

The incidence of TB among recent immigrants is nearly 10 times that of native-born Americans (ALA, 2010b). (Ignatavicius 2013, p. 654)

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assessment & clinical manifestations
(TB)

Back 69

Assessment

Early detection of TB depends on subjective findings rather than on observable symptoms. TB has a slow onset, and patients are not aware of symptoms until the disease is advanced. TB should be considered for any patient with a persistent cough or other symptoms compatible with TB, such as weight loss, anorexia, night sweats, hemoptysis, shortness of breath, fever, or chills.

History

Assess the patient's past exposure to TB. Ask about his or her country of origin and travel to foreign countries where incidence of TB is high. It is important to ask about the results of any previous tests for TB. Also ask whether the patient has had bacille Calmette-Guérin (BCG) vaccine. The BCG vaccine contains attenuated tubercle bacilli and is used in many countries to produce increased resistance to TB. Anyone who has received BCG vaccine within the previous 10 years will have a positive skin test that can complicate interpretation. Usually the size of the skin response decreases each year after BCG vaccination. These patients should be evaluated for TB with a chest x-ray or the QuantiFERON-TB Gold test.

The effectiveness of BCG vaccine in preventing TB is controversial, and it is not used widely for this purpose in the United States or Canada.

Physical Assessment/Clinical Manifestations

The patient with TB has progressive fatigue, lethargy, nausea, anorexia, weight loss, irregular menses, and a low-grade fever. Manifestations may have been present for weeks or months. Night sweats may occur with the fever. The patient has a cough and mucopurulent sputum, which may be streaked with blood. Chest tightness and a dull, aching chest pain occur with the cough. Ask about, assess for, and document the presence of any of these manifestations to help with diagnosis, to establish a baseline, and to plan nursing interventions.

Physical examination of the chest does not provide conclusive evidence of TB. Dullness with percussion may be heard over the involved lung fields, as may bronchial breath sounds, crackles, and increased transmission of spoken or whispered sounds. Partial obstruction of a bronchus from endobronchial disease or compression by lymph nodes may produce localized wheezing. (Ignatavicius 2013, pp. 654-656)

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diagnostics
(TB)

Back 70

Diagnostic Assessment

A new rapid test for tuberculosis has been developed and approved by the World Health Organization (2010). This test is the fully automated nucleic acid amplification test (NAAT) for tuberculosis. Results are available in less than 2 hours. Widespread use of this test is endorsed and should soon replace other diagnostic methods. Currently, diagnosis of TB is suggested by the manifestations and a positive smear for acid-fast bacillus. Sputum is obtained, smeared on a slide, and stained with a red dye. After the slide has dried, it is reated with an acid alcohol to remove the stain. TB does not de-stain with this procedure and remains red. The acid-fast bacillus test is not specific for TB (other organisms are also acid-fast), but it is used as a quick method to determine whether TB precautions should be started until more definitive testing can be completed with either the purified protein derivative two-step procedure or the QuantiFERON-TB Gold.

Blood analysis by an enzyme-linked immunosorbent assay using the QuantiFERON-TB Gold (QFT-G) is a relatively rapid test for the presence of M. tuberculosis. Results are ready in 24 hours and are most useful in the acute care setting to determine whether a symptomatic patient has TB.

Sputum culture confirms the diagnosis. Enhanced TB cultures and automated mycobacterial cultures require 1 to 4 weeks to determine a positive or negative result. After drugs are started, sputum samples are obtained again to determine therapy effectiveness. Cultures are usually negative after 3 months of treatment.

The tuberculin test (Mantoux test) is the most commonly used reliable test of TB infection. A small amount (0.1 mL) of purified protein derivative (PPD) is placed intradermally in the forearm. An area of induration (localized swelling with hardness of soft tissue), not just redness, measuring 10 mm or greater in diameter 48 to 72 hours after injection indicates exposure to and possible infection with TB (Fig. 33-3). If possible, the site is re-evaluated after 72 hours because the incidence of false-negative readings is greater at 48 hours. A positive reaction does not mean that active disease is present but indicates exposure to TB or the presence of inactive (dormant) disease. A reaction of 5 mm or greater is considered positive in people with HIV infection. A reduced skin reaction or a negative skin test does not rule out TB disease or infection of the very old or anyone who is severely immunocompromised. Failure to have a skin response because of reduced immune function when infection is present is called anergy.

Yearly screening is needed for anyone who comes into contact with people infected with TB. Screening is very important for foreign-born people and migrant workers. Participation in screening programs is enhanced when programs are delivered in a culturally sensitive and nonthreatening manner. Urge anyone who is considered high risk to have an annual TB screening test.

Once a person's skin test is positive for TB, a chest x-ray is used to detect active TB or old, healed lesions. Caseation and inflammation may be seen on the x-ray if the disease is active. Instruct anyone who has manifestations of TB to seek medical attention. The chest x-rays of HIV-infected patients may be normal or may show infiltrates in any lung zone and lymph node enlargement. (Ignatavicius 2013, p. 656)

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interventions
(TB)

Back 71

Combination drug therapy is the most effective method of treating TB and preventing transmission. Active TB is treated with a combination of drugs to which the organism is sensitive. Therapy continues until the disease is under control. The use of multiple-drug regimens destroys organisms as quickly as possible and reduces the emergence of drug-resistant organisms (Gribble & Williams, 2010). First-line therapy uses isoniazid (INH) and rifampin throughout the therapy; pyrazinamide is added for the first 2 months (Chart 33-7). This protocol shortens the therapy from 6 to 12 months to 6 months. Ethambutol is the recommended fourth drug in first-line therapy. These drugs are now available in two or three drug combinations. Variations of the first-line drugs along with other drug types are used when the patient does not tolerate the standard first-line therapy. Nursing interventions focus on patient teaching for drug therapy adherence and infection control.

Strict adherence to the prescribed drug regimen is crucial for suppressing the disease. Thus your major role is teaching the patient about drug therapy and stressing the importance of taking each drug regularly, exactly as prescribed, for as long as it is prescribed. Provide accurate information in multiple formats, such as pamphlets, videos, and drug-schedule worksheets. An anxious patient may not absorb information well. You may need to repeat the information and obtain the help of family members. To determine whether the patient understands how to take the drugs, ask him or her to describe the treatment regimen, side effects, and when to call the health care agency and physician.

The TB drugs may cause the patient to have nausea. Teach him or her to prevent nausea by taking the daily dose at bedtime. Antiemetics may also prevent this problem. Instruct him or her to eat a well-balanced diet that includes foods that are rich in iron, protein, and vitamins C and B. Collaborate with the dietitian for specialized needs.

The patient with TB has reduced physical stamina and also has concerns about the disease prognosis. Offer a positive outlook for the patient who adheres to the drug regimen. Tell him or her that fatigue will diminish as the treatment progresses. With current resistant strains of TB, however, emphasize that not taking the drugs as prescribed could lead to an infection that is drug resistant.

Multidrug-resistant TB (MDR TB) strains are emerging as are strains that are considered extensively drug-resistant (XDR TB), especially among patients who have HIV disease (Ferguson & Rhoads, 2009; Trossman, 2008). MDR TB is an infection that resists INH and rifampin. XDR TB is resistant not only to the first-line anti-tuberculosis drugs but also to the second-line antibiotics, including the fluoroquinolones and at least one of the aminoglycosides. Drug therapy for MDR TB and XDR TB is more limited than standard first-line therapy and requires higher doses for longer periods.

An area to stress when teaching the patient and family with either MDR TB or XDR TB is that the patient is not resistant to the drugs—the organism is. So, a person who acquires the infection and develops TB from a person who is infected with a resistant strain of bacillus will also have drug-resistant disease (Nelson, 2010). Thus teaching infection control strategies is a priority and should be constantly reinforced.

Other care issues for the patient with TB include teaching about infection prevention and what to expect about disease monitoring and participating in activities. TB is often treated outside the acute care setting, with the patient convalescing in the home setting. Airborne Precautions are not necessary in this setting because family members have already been exposed; however, all members of the household need to undergo TB testing. Teach the patient to cover the mouth and nose with a tissue when coughing or sneezing, to place used tissues in plastic bags, and to wear a mask when in contact with crowds until the drugs suppress infection.

Tell the patient that sputum specimens are needed usually every 2 to 4 weeks once drug therapy is initiated. When the results of three consecutive sputum cultures are negative, the patient is no longer infectious and may return to former employment. Remind him or her to avoid exposure to any inhalation irritants because these can cause further lung damage.

The hospitalized patient with active TB is placed on Airborne Precautions (see Chapter 25) in a well-ventilated room that has at least six exchanges of fresh air per minute. Allhealth care workers must wear an N95 or high-efficiency particulate air (HEPA) respirator when caring for the patient (Fig. 33-4). When hand and clothing contamination is a risk, use Standard Precautions with appropriate contact protection (i.e., gowns and gloves). Perform handwashing before and after patient care. Precautions are discontinued when the patient is no longer infectious.

***Nursing Safety Priority Drug Alert***

The first-line drugs used as therapy for tuberculosis all can damage the liver. Warn the patient to not drink any alcoholic beverages for the entire duration of TB therapy. (Duration of therapy is usually 6 months but can be as long as 2 years for MDR TB.)

***Nursing Safety Priority Action Alert***

Warn patients with extensively drug-resistant TB that absolute adherence to therapy is critical for survival and cure of the disease.
(Ignatavicius 2013, pp. 656-657)

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community-based care
(TB)

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Home Care Management

Most patients with TB are managed outside the hospital; however, patients may be diagnosed with TB while in the hospital for another problem. Discharge may be delayed if the living situation is high risk or if nonadherence is likely. Collaborate with the case manager or social service worker in the hospital or the community health nursing agency to ensure that the patient is discharged to the appropriate environment with continued supervision.

Teaching for Self-Management

Teach the patient to follow the drug regimen exactly as prescribed and always to have a supply on hand. Teach about side effects and ways of reducing them to ensure adherence. Remind him or her that the disease is usually no longer contagious after drugs have been taken for 2 to 3 consecutive weeks and clinical improvement is seen; however, he or she must continue with the prescribed drugs for 6 months or longer as prescribed. Directly observed therapy (DOT), in which a health care professional watches the patient swallow the drugs, may be indicated in some situations. This practice leads to more treatment successes, fewer relapses, and less drug resistance. A variation of this practice, DOTS (directly observed therapy–short course), is attributed to having saved many lives worldwide (The War on Tuberculosis, 2010; WHO, 2010).

The patient who has weight loss and severe lethargy should gradually resume usual activities as these problems decrease during treatment. Proper nutrition is needed to prevent infection recurrence.

To help with concerns about the contagious aspect of the infection, provide the patient with information about TB. A key to preventing transmission is identifying those in close contact with the infected person so that they can be tested and treated if needed. Identified contacts are assessed with a TB test and possibly a chest x-ray to determine infection status. Multidrug therapy may be indicated as a preventive strategy for heavily exposed individuals or for those who have other health problems that reduce the immune response.

Health Care Resources

Teach the patient to receive follow-up care by a health care provider for at least 1 year during active treatment. The American Lung Association (ALA) can provide free information to the patient about the disease and its treatment. In addition, Alcoholics Anonymous (AA) and other health care resources for patients with alcoholism are available if needed. Assist the patient who uses illicit drugs to locate a drug treatment program. Urge smokers to quit, and assist them in finding an appropriate smoking-cessation program. (Ignatavicius 2013, pp. 657-658)

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pneumothorax

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Any chest injury that allows air to enter the pleural space results in a rise in chest pressure and a reduction in vital capacity. Severity depends on the amount of lung collapse produced. Pneumothorax is often caused by blunt chest trauma and may occur with some degree of hemothorax. It can also occur as a complication of medical procedures (Day, 2011; Ruiz, 2011). The pneumothorax can be open (pleural cavity is exposed to outside air, as through an open wound in the chest wall) or closed (such as when a patient with chronic obstructive pulmonary disease [COPD] has a spontaneous pneumothorax). Assessment findings commonly include:
--Reduced breath sounds on auscultation
--Hyperresonance on percussion
--Prominence of the involved side of the chest, which moves poorly with respirations
--Deviation of the trachea away from (closed) or toward (open) the affected side

In addition, the patient may have pleuritic pain, tachypnea, and subcutaneous emphysema (air under the skin in the subcutaneous tissues) (Roman, 2010).

An ultrasound examination or a chest x-ray is used for diagnosis. Chest tubes may be needed to allow the air to escape and the lung to re-inflate. (Ignatavicius 2013, p. 683)

Front 74

tension pneumothorax

Back 74

Tension pneumothorax, a rapidly developing and life-threatening complication of blunt chest trauma, results from an air leak in the lung or chest wall. Air forced into the chest cavity causes complete collapse of the affected lung. Air that enters the pleural space during inspiration does not exit during expiration. As a result, air collects under pressure, compressing blood vessels and limiting blood return. This process leads to decreased filling of the heart and reduced cardiac output. If not promptly detected and treated, tension pneumothorax is quickly fatal. Causes include blunt chest trauma, mechanical ventilation with positive end-expiratory pressure (PEEP), closed–chest drainage (chest tubes), and insertion of central venous access catheters.

Assessment findings with tension pneumothorax include:
--Asymmetry of the thorax
--Tracheal movement away from midline toward the unaffected side
--Respiratory distress
--Absence of breath sounds on one side
--Distended neck veins
--Cyanosis
--Hypertympanic sound on percussion over the affected side

Pneumothorax is detectable on a chest x-ray. ABG assays show hypoxia and respiratory alkalosis.

A large-bore needle is inserted by the health care provider into the second intercostal space in the midclavicular line of the affected side as initial treatment for tension pneumothorax. Then, a chest tube is placed into the fourth intercostal space and the other end is attached to a water seal drainage system until the lung re-inflates.
(Ignatavicius 2013, pp. 683-684)

Front 75

hemothorax

Back 75

Hemothorax is a common problem occurring after blunt chest trauma or penetrating injuries. A simple hemothorax is a blood loss of less than 1500 mL into the chest cavity; a massive hemothorax is a blood loss of more than 1500 mL.

Bleeding is caused by injury to the lung tissue, such as lung contusions or lacerations, that can occur with rib and sternal fractures. Massive internal bleeding in blunt chest trauma may stem from the heart, great vessels, or the intercostal arteries.

Assessment findings vary with the size of the hemothorax. If it is small, the patient may not have symptoms. With a large hemothorax, the patient may have respiratory distress. In addition, breath sounds are reduced on auscultation. Percussion on the involved side produces a dull sound. Blood in the pleural space is visible on a chest x-ray and confirmed by thoracentesis.

Interventions focus on removing the blood in the pleural space to normalize breathing and to prevent infection. Anterior and posterior chest tubes are inserted to empty the pleural space. Closely monitor the chest tube drainage. Serial chest x-rays are used to determine treatment effectiveness.

An open thoracotomy is needed when there is initial blood loss of 1500 to 2000 mL from the chest or persistent bleeding at the rate of 200 mL/hr over 3 hours. Monitor the vital signs, blood loss, and intake and output. Assess the patient's response to the chest tubes, and infuse IV fluids and blood as prescribed. The blood lost through chest drainage can be infused back into the patient if needed. (Ignatavicius 2013, p. 684)

Front 76

placement & care
(chest tubes)

Back 76

The tip of the tube used to drain air is placed near the front lung apex (see Fig. 32-16). The tube that drains liquid is placed on the side near the base of the lung. After lung surgery, two tubes, anterior and posterior, are used. The puncture wounds are covered with airtight dressings.

The chest tube is connected to about 6 feet of tubing that leads to a collection device placed several feet below the chest. The tubing allows the patient to turn and move without pulling on the chest tube. Keeping the collection device below the chest allows gravity to drain the pleural space. When two chest tubes are inserted, they are joined by a Y-connector near the patient's body; the 6 feet of tubing is attached to the Y-connector.

Stationary chest tube drainage systems usually use a water seal mechanism that acts as a one-way valve to prevent air or liquid from moving back into the chest cavity. The Pleur-evac system is a common device using a one-piece disposable plastic unit with three chambers. The three chambers are connected to one another. The tube(s) from the patient is(are) connected to the first chamber in the series of three. This chamber is the drainage collection container. The second chamber in the series is the water seal to prevent air from moving back up the tubing system and into the chest. The third chamber, when suction is applied, is the suction regulator.

Chart 32-14 summarizes best safety practices when caring for a patient with a water seal chest tube drainage system. Check hourly to ensure the sterility and patency of any chest drainage system. Tape tubing junctions to prevent accidental disconnections, and keep an occlusive dressing at the chest tube insertion site. Keep sterile gauze at the bedside to cover the insertion site immediately if the chest tube becomes dislodged. Also keep padded clamps at the bedside for use if the drainage system is interrupted. Position the drainage tubing to prevent kinks and large loops of tubing, which can block drainage and prevent lung re-expansion.

Manipulation of the chest tube should be kept to a minimum. Do not vigorously “strip” the chest tube because this can create up to −400 cm of water negative pressure and damage lung tissue. If any tube manipulation is needed, gentle hand-over-hand “milking” of the tube, with stopping between each hand hold, is used to move blood clots and prevent obstruction (Halm, 2007). Follow physician prescriptions, as well as agency policies and guidelines on this action.

Assess the respiratory status and document the amount and type of drainage hourly. Usually the drainage in chamber one is not emptied unless the container is so full that the fluid is in danger of coming into contact with the chest drainage tube. The self-contained systems have calibrations on the collection chamber. Record the amount of hourly drainage. Notify the physician of drainage if more than 100 mL/hr occurs. After the first 24 hours, assess drainage at least every 8 hours.

Check the water seal chamber for unexpected bubbling created by an air leak in the system. Bubbling is normal during forceful expiration or coughing because air in the chest is being expelled. Continuous bubbling indicates an air leak that must be identified. Notify the physician if bubbling occurs continuously in the water seal chamber. On the physician's prescription, gently apply a padded clamp briefly on the drainage tubing close to the occlusive dressing. If the bubbling stops, the air leak may be at the chest tube insertion site or within the chest, requiring physician intervention. Air bubbling that does not cease when a padded clamp is applied indicates that the air leak is between the clamp and the drainage system. Release the clamp as soon as this assessment is made.

Mobile or portable chest tube drainage systems are “dry” chest drainage systems that do not use water to form a seal to prevent air from re-entering the patient's lung through the chest tube. Instead, these lightweight devices use a dynamic control “flutter” valve that prevents backflow of air. The flutter valve is a soft rubber tube surrounded by a harder plastic tube. When the patient exhales, air is forced from the chest cavity into the chest tube, under pressure. This pressure forces the soft flutter valve open and air moves into the harder surrounding tube shell (which has a vent for air). When the patient inhales, creating negative pressure in the chest tube, the soft sides of the flutter valve collapse on themselves (like the sides of a deflated balloon when a person sucks on the mouthpiece instead of blowing into the mouthpiece), closing the one-way valve. Portable units allow the patient to ambulate more freely and go home with chest tubes still in place. (Ignatavicius 2013, pp. 635-637)

Front 77

chest tube chambers

Back 77

In setting up the system, chamber one (nearest to the patient) does not at first have fluid in it. The tubing from the patient penetrates shallowly into this chamber, as does the tube connecting chamber one with chamber two.

Chamber one collects the fluid draining from the patient. This fluid is measured hourly during the first 24 hours. The fluid in chamber one must never fill to the point that it comes into direct contact with either the tube draining from the patient or the tube connecting this chamber to chamber two. If the tubing from the patient enters the fluid, drainage stops and can lead to a tension pneumothorax.

Chamber two is the water seal that prevents air from re-entering the patient's pleural space. As the trapped air leaves the pleural space, it will pass through chamber one (drainage collection chamber) before entering chamber two (the water seal chamber), which should always contain at least 2 cm of water to prevent air from returning to the patient. As trapped air from the patient's pleural space passes through the water seal, which serves as a one-way valve, the water will bubble. Once all the air has been evacuated from the pleural space, bubbling of the water seal stops.

The bubbling of the water in the water seal chamber indicates air drainage from the patient. Bubbling is usually seen when intrathoracic pressure is greater than atmospheric pressure, such as when the patient exhales, coughs, or sneezes. When the air in the pleural space has been removed, bubbling stops. A blocked or kinked chest tube also can cause bubbling to stop. Excessive bubbling in the water seal chamber (chamber two) may indicate an air leak. The water in the narrow column of the water seal chamber normally rises 2 to 4 inches during inhalation and falls during exhalation, a process called tidaling. An absence of fluctuation may mean that the lung has fully re-expanded or can mean that there is an obstruction in the chest tube (Bauman & Handley, 2011).

Chamber three is the suction control of the system. There are different types of suction, most commonly wet or dry. With wet suction, the fluid level in chamber three is prescribed by the health care provider (usually −20 cm water). The chamber is connected to wall suction, which is turned up until there is gentle bubbling in the chamber. With dry suction, the health care provider prescribes the suction level to be dialed in on the device. When connected to wall suction, the regulator is set to the amount indicated by the device's manufacturer. For either type of suction, the amount of suction in the system is determined not by the wall suction unit but by the chest tube drainage device. (Ignatavicius 2013, p. 635)

**Nursing Safety Priority Action Alert**

For a water seal chest tube drainage system, 2 cm of water is the minimum needed in the water seal to prevent air from flowing backward into the patient. Check the water level every shift and add sterile water to this chamber to the level marked on the indicator (specified by the manufacturer of the drainage system) (Durai et al., 2010). (Ignatavicius 2013, p. 635)

Front 78

best practice guidelines
(chest tubes)

Back 78

Management of Chest Tube Drainage Systems

Patient
--Ensure that the dressing on the chest around the tube is tight and intact. Depending on agency policy and the surgeon's preference, reinforce or change loose dressings.
--Assess for difficulty breathing.
--Assess breathing effectiveness by pulse oximetry.
--Listen to breath sounds for each lung.
--Check alignment of trachea.
--Check tube insertion site for condition of the skin. Palpate area for puffiness or crackling that may indicate subcutaneous emphysema.
--Observe site for signs of infection (redness, purulent drainage) or excessive bleeding.
--Check to see if tube “eyelets” are visible.
--Assess for pain and its location and intensity, and administer drugs for pain as prescribed.
--Assist patient to deep breathe, cough, perform maximal sustained inhalations, and use incentive spirometry.
--Reposition the patient who reports a “burning” pain in the chest.

Drainage System
--Do not “strip” the chest tube.
--Keep drainage system lower than the level of the patient's chest.
--Keep the chest tube as straight as possible, avoiding kinks and dependent loops.
--Ensure the chest tube is securely taped to the connector and that the connector is taped to the tubing going into the collection chamber.
--Assess bubbling in the water seal chamber; should be gentle bubbling on patient's exhalation, forceful cough, position changes.
--Assess for “tidaling.”
--Check water level in the water seal chamber, and keep at the level recommended by the manufacturer.
--Check water level in suction control chamber, and keep at the level prescribed by the surgeon (unless dry suction system is used).
--Clamp the chest tube only for brief periods to change the drainage system or when checking for air leaks.
--Check and document amount, color, and characteristics of fluid in the collection chamber, as often as needed according to the patient's condition and agency policy.
--Empty collection chamber or change the system before the drainage makes contact with the bottom of the tube.
--When sample of drainage is needed for culture or other laboratory test, obtain it from the chest tube; after cleansing chest tube, use a 20-gauge (or smaller) needle and draw up specimen into a syringe.

Immediately Notify Physician or Rapid Response Team for:
--Tracheal deviation
--Sudden onset or increased intensity of dyspnea
--Oxygen saturation less than 90%
--Drainage greater than 70 mL/hr
--Visible eyelets on chest tube
--Chest tube falls out of the patient's chest (first, cover the area with dry, sterile gauze)
--Chest tube disconnects from the drainage system (first, put end of tube in a container of sterile water and keep below the level of the patient's chest)
--Drainage in tube stops (in the first 24 hours) (Ignatavicius 2013, p. 637)

Front 79

coronary artery disease (CAD)
or
coronary heart disease (CHD)

Back 79

Coronary artery disease (CAD), also called coronary heart disease (CHD) or simply heart disease, is the single largest killer of American men and women in all ethnic groups. When the arteries that supply the myocardium (heart muscle) are diseased, the heart cannot pump blood effectively to adequately perfuse vital organs and peripheral tissues. The organs and tissues need oxygen in arterial blood for survival. When oxygenation and perfusion are impaired, the patient can have life-threatening clinical manifestations and possibly death.

The incidence of CAD has declined over the past decade. This decline is due to many factors, including increasingly effective treatment and an increased awareness and emphasis on reducing major cardiovascular risk factors (e.g., hypertension, smoking, high cholesterol). Some coronary events occur in patients without traditional risk factors.

Pathophysiology

Coronary artery disease (CAD) is a broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood, oxygen, and nutrients to the myocardium. When blood flow through the coronary arteries is partially or completely blocked, ischemia and infarction of the myocardium may result. Ischemia occurs when insufficient oxygen is supplied to meet the requirements of the myocardium. Infarction (necrosis, or cell death) occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to tissue. (Ignatavicius 2013, pp. 828-829)

tiology and Genetic Risk

Atherosclerosis is the primary factor in the development of CAD. Numerous risk factors contribute to atherosclerosis and subsequently to CAD (also see Chapter 38).

Nonmodifiable risk factors are personal characteristics that cannot be altered or controlled. These risk factors, which interact with each other, include age, gender, family history, and ethnic background. People with a family history of CAD are at high risk for developing the disease.

Modifiable risk factors are lifestyle choices that can be controlled by the patient, such as smoking and obesity. These factors are described later in the Health Promotion and Maintenance section of this chapter.

Incidence/Prevalence

According to the American Heart Association (AHA) (2010), 64% of women and 50% of men who had a myocardial infarction (MI) (“heart attack”) were not aware that they had CAD. The average age of a person having a first MI is 64.5 years for men and 70.3 years for women (AHA, 2010). Almost 30% of patients who have an MI die within 5 years after the event (AHA, 2010).

Every 25 seconds, a person in the United States has a major coronary event and 452,000 people die each year from an MI. Many people die from coronary heart disease without being hospitalized. Most of these are sudden deaths caused by cardiac arrest (AHA, 2010).

Many patients who survive MIs are not able to return to work. CAD is the leading cause of premature, permanent disability in the United States, accounting for about 20% of disability allowances by the Social Security Administration. (Ignatavicius 2013, p. 831)

Front 80

chronic stable angina pectoris

Back 80

Angina pectoris is chest pain caused by a temporary imbalance between the coronary arteries’ ability to supply oxygen and the cardiac muscle's demand for oxygen. Ischemia (lack of oxygen) that occurs with angina is limited in duration and does not cause permanent damage of myocardial tissue.

Angina may be of two main types: stable angina and unstable angina. Chronic stable angina (CSA) is chest discomfort that occurs with moderate to prolonged exertion in a pattern that is familiar to the patient. The frequency, duration, and intensity of symptoms remain the same over several months. CSA results in only slight limitation of activity and is usually associated with a fixed atherosclerotic plaque. It is usually relieved by nitroglycerin or rest and often is managed with drug therapy. Rarely does CSA require aggressive treatment. (Ignatavicius 2013, p. 829)

Front 81

women
(CAD & MI)

Back 81

Many women with symptomatic ischemic heart disease or abnormal stress testing do not have normal coronary angiography (Shaw et al., 2009). Studies implicate microvascular disease or endothelial dysfunction or both as the causes for risk for CAD in women. Endothelial dysfunction is defined as the “inability of the arteries and arterioles to dilate due to inability of the endothelium to produce nitric oxide, a relaxant of vascular smooth muscle” (Bellasi et al., 2007).

Women typically have smaller coronary arteries and frequently have plaque that breaks off and travels into the small vessels to form an embolus (clot). “Positive remodeling” or outward remodeling (lesions that protrude outward) is more common in women (Bellasi et al., 2007). This outpouching may be missed on coronary angiography. (Ignatavicius 2013, p. 829)

Age is the most important risk factor for developing CAD in women. The older a women is, the more likely she will have the disease. When compared with men, women are usually 10 years older when they have CAD. In addition, women who have MIs have a greater risk for dying during hospitalization. When they are older than 40 years, women are more likely than men to die within 1 year after their MI (AHA, 2010). (Ignatavicius 2013, p. 831)

Premenopausal women have a lower incidence of MI than men. However, for postmenopausal women in their 70s or older, the incidence of MI equals that of men. Family history is also a risk factor for women; those whose parents had CAD are more susceptible to the disease. Women with abdominal obesity (androidal shape) and metabolic syndrome (described on p. 834) are also at increased risk for CAD (Bellasi et al., 2007). (Ignatavicius 2013, p. 831)

Front 82

cultural awareness
(CAD)

Back 82

Several groups have a higher genetic risk for CAD than others. African-American and Hispanic women have higher CAD risk factors than white women of the same socioeconomic status. Of American Indians and Alaskan Natives 18 years of age and older, about 64% of men and 81% of women have one or more CAD risk factors (hypertension [HTN], smoking, high cholesterol, excess weight, or diabetes mellitus). The leading cause of death for both men and women in the Euro-American population is cardiac disease, even though they may not have genetic predispositions to developing cardiovascular risk factors (AHA, 2010). (Ignatavicius 2013, p. 832)

Modifiable risk factors vary for people of different racial and ethnic backgrounds. Some of the differences may be explained by lack of access to health care for some groups or by genetic factors. American Indians, for example, have the highest percentage of smokers among women and men. However, many of these people have poor access to care or have language barriers in a predominantly English-speaking, Euro-American health care system. Nutritional preferences may also explain some of the differences. For instance, according to the AHA (2010), high cholesterol is more common in African-American and Hispanic populations. Diets higher in fat and cholesterol are often less expensive and may be a factor in explaining differences, and obesity is more common in these groups. Genetic factors may also contribute to the differences among ethnic groups. (Ignatavicius 2013, p. 834)

Front 83

health promotion & maintenance
(CAD)

Back 83

Ninety-five percent of sudden cardiac arrest victims die before reaching the hospital, largely because of ventricular fibrillation (“v fib”). To help combat this problem, automatic external defibrillators (AEDs) are found in many public places, such as in shopping centers and on airplanes. Employees are taught how to use these devices if a sudden cardiac arrest occurs. Some patients with diagnosed CAD have AEDs in their homes or at work. How to use this device is described on p. 738 in Chapter 36.

Health promotion efforts are directed toward controlling or altering modifiable risk factors for CAD. Some of these factors have a genetic basis, which is described elsewhere in this text. Common risk factors include:
--Elevated serum lipid levels
--Tobacco use
--Limited physical activity
--Hypertension
--Diabetes mellitus
--Obesity
--Excessive alcohol
--Stress (Ignatavicius 2013, pp. 831-832)

Front 84

pt education: self-management
(CAD)

Back 84

Smoking
--If you smoke, quit.
--If you don't smoke, don't start.

Diet
--Consume sufficient calories for your body to include:
----Less than 7% from saturated fats
----Avoiding trans fatty acids
--Limit your cholesterol intake to less than 200 mg/day.
--Limit your sodium intake as specified by your health care provider.

Cholesterol
--Have your lipid levels checked regularly.
--If your cholesterol and LDL levels are elevated, follow your health care provider's advice.

Physical Activity
--If you are middle-aged or older or have a history of medical problems, check with your health care provider before starting an exercise program.
--Appropriate exercise should be enjoyable, burn 400 calories per session, and sustain a heart rate of 120 to 150 beats/min, depending on your age.
--Exercise periods should be at least 20 to 30 minutes long with 10-minute warm-up and 5-minute cool-down periods.
--If you cannot exercise moderately three to five times each week, walk daily for 30 minutes at a comfortable pace.
--If you cannot walk 30 minutes daily, walk any distance you can (e.g., park farther away from a site than necessary; use the stairs, not the elevator, to go one floor up or two floors down).

Diabetes
--Manage your diabetes with your health care provider.

Blood Pressure
--Have your blood pressure checked regularly.
--If your blood pressure is elevated, follow your health care provider's advice.
--Continue to monitor your blood pressure at regular intervals.

Obesity
--Avoid severely restrictive or fad diets.
--Restrict intake of saturated fats, simple sugars, and cholesterol-rich foods.
--Increase your physical activity.

LDL, Low-density lipoprotein.
(Ignatavicius 2013, p. 832)

Front 85

complementary & alternative therapies
(CAD)

Back 85

Using Complementary and Alternative Therapies

Teach patients that adding omega-3 fatty acids from fish and plant sources has been effective for some patients in reducing lipid levels, stabilizing atherosclerotic plaques, and reducing sudden death from an MI. The preferred source of omega-3 acids is from fish three times a week or a daily fish oil nutritional supplement (1-2 g/day) containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (AHA, 2010). Plant sources (flaxseed, flaxseed oil, walnuts, and canola oil) contain α-linolenic acid, and the conversion of α-linolenic acid to EPA and DHA is not as efficient in patients who consume a typical Western diet (Surette, 2008). Lovaza (omega-3 fatty acids) is a new medication approved by the Federal Drug Administration (FDA) and is used to reduce very high triglycerides (>500 mg/dL) levels. Lovaza has not been proven to prevent heart attacks or stroke.

Garlic supplements may also have a small effect on reducing lipid levels, but they have not been shown to prevent MI. Patients often take a number of other supplements, such as vitamin E, coenzyme Q10, Pantesin, and vitamin B complex to decrease the risk for heart disease. None of these substances has been found to be helpful in reducing coronary artery disease. (Ignatavicius 2013, p. 833)

Front 86

tobacco use
(CAD)

Back 86

In the United States, an estimated 23% of men and 18% of women smoke cigarettes, putting them at increased risk for MI (AHA, 2010). About five million U.S. men and women chew tobacco, with the highest rates in the South and rural areas. Tobacco use and passive smoking from “second-hand smoke” (also called environmental smoke) substantially reduce blood flow in the coronary arteries.

Tobacco use, especially cigarette smoking, accounts for over one third of deaths from CAD. It enhances the process of atherosclerosis through mechanisms that are still poorly understood. Nicotine begins the release of catecholamines, resulting in an increased heart rate and peripheral vasoconstriction. This action causes increases in blood pressure (BP), cardiac afterload, and oxygen consumption. Cigarette smoking has also been found to cause endothelial dysfunction and increased vessel wall thickness. This process increases the risk for clot formation and vessel occlusion. The resulting hypertension may exacerbate the atherosclerotic process by increasing vessel wall permeability. Another problem with cigarette smoking is the production of carbon monoxide, which has been found to decrease the oxygen content in arterial blood. The good news is that when cigarette smoking is stopped, the risk for CAD decreases. A person who stops smoking may decrease the risk for CAD by as much as 80% in 1 year. Reducing the tar and nicotine content of the cigarettes smoked does not reduce the risk for CAD (AHA, 2010).

Ask about tobacco use, and advise the tobacco user and family members who smoke to quit using this harmful substance. Teach all patients to avoid environmental tobacco smoke at work and at home if at all possible. (Ignatavicius 2013, p. 833)

Front 87

physical activity
(CAD)

Back 87

Physical inactivity may be the most important risk factor for the general population. Less-active, less-fit people have a 30% to 50% greater risk for developing high blood pressure (BP), which predisposes to CAD. Physical inactivity is more common among women than men, among African Americans and Hispanics than Euro-Americans, among older adults than younger adults, and among the less affluent than the more affluent (AHA, 2010). The causes for these differences are not known. Teach patients that regular physical activity helps maintain body weight and muscle mass while improving BP and lipid values.

Moderate-intensity activities like walking are associated with a major reduction in CAD risk. However, intense exercising may contribute to plaque rupture and increase the number of cardiac episodes. Teach people that participating in exercise for 30 minutes a day can reduce hypertension and increase secretions of endorphins. It also leads to decreased smoking and eating, improved metabolism, and a stronger feeling of well-being. Other benefits include decreased blood clotting and higher plasma HDL levels, increased heart volume, increased cardiac capillary blood flow, and decreased heart rate. Physical activity does not increase collateral circulation or reduce the size of existing plaques. (Ignatavicius 2013, p. 833)

Front 88

managing other factors
(CAD)

Back 88

One in three Americans has hypertension (HTN). This disease increases the workload of the heart, which increases the risk for MI. The cause of primary HTN is not known. However, it is easily detected and usually controllable. About half of patients having a first MI have a BP greater than 160/95 mm Hg. Ways to manage hypertension and therefore reduce the risk for CAD are described in Chapter 38.

Diabetes mellitus (DM) is a major risk factor for heart disease. A woman with diabetes mellitus is twice as likely to develop CAD than a woman without DM. Heart disease is the leading cause of diabetic-related death in both men and women. Most adults with diabetes also have hypertension. Chapter 67 discusses vascular complications of diabetes in detail.

Obesity is strongly associated with the development of hypertension, diabetes, and increased serum lipid levels. Women with fat deposited around their waists are at the highest risk for CAD. Teach the importance of weight management to help prevent these chronic and potentially life-threatening diseases.

Alcohol may help prevent or contribute to the development of CAD, depending on the amount consumed. Excessive consumption, described as having more than 3 ounces (90 mL) per day, can lead to increased heart disease, hypertension, and metabolic syndrome, described in the next section. A lower amount may help prevent CAD (Suzuki et al., 2009).

A person's response to emotional stress may also be associated with heart disease. Work stress, in particular, may be associated with left ventricular hypertrophy. During times of stress, increased heart rate increases the work of the heart, thus causing changes in the left ventricle.

Metabolic syndrome, also called syndrome X, has been recognized as a risk factor for cardiovascular (CV) disease and is being aggressively researched. Patients who have three of the factors in Table 40-1 are diagnosed with metabolic syndrome. This health problem increases the risk for developing diabetes and CAD. About 47 million people in the United States have metabolic syndrome (AHA, 2010). This increase is likely due to physical inactivity and the current obesity epidemic. Management is aimed at reducing risks, managing hypertension, and preventing complications.

Elevated levels of serum homocysteine, an amino acid, have been associated with an increased incidence of CAD. However, research findings are not consistent regarding its risk. Vitamin B supplements have been thought to decrease homocysteine. Recent studies suggest that vitamin B is not effective as secondary prevention, but few studies have been conducted on vitamin B as a primary preventive measure (Ebbing et al., 2008).

Patients with multiple modifiable risk factors have several times the risk for CAD as those without these characteristics. Although many factors place a person at risk for heart disease, there are well-documented, effective ways of promoting cardiovascular health. The most important interdisciplinary intervention is health teaching.
(Ignatavicius 2013, pp. 833-834)

Front 89

assessment
(CAD & MI)

Back 89

History

If symptoms of CAD are present at the time of the interview, delay collecting data until interventions for symptom relief, vital sign instability, and dysrhythmias are started and discomfort resolves. If the patient had pain, ask about how he or she has managed the discomfort and other symptoms and which drugs he or she may be taking. When the patient is pain-free, obtain information about family history and modifiable risk factors, including eating habits, lifestyle, and physical activity levels. Ask about a history of smoking and how much alcohol is consumed each day. Collaborate with the dietitian to assess current body mass index (BMI) and weight.

Physical Assessment/Clinical Manifestations

Rapid assessment of the patient with chest pain or other presenting symptoms is crucial. It is important to differentiate among the types of chest pain and to identify the source. Question the patient to determine the characteristics of the discomfort. Patients may deny pain, however, and report that they feel “pressure.” Appropriate questions to ask concerning the discomfort include onset, location, radiation, intensity, duration, and precipitating and relieving factors.

If pain is present, ask the patient if the pain is in the chest, epigastric area, jaw, back, shoulder, or arm. Ask him or her to rate the pain on a scale of 0 to 10, with 10 being the highest level of discomfort. Some patients describe the discomfort as tightness, a burning sensation, pressure, or indigestion.

Because angina pain is ischemic pain, it usually improves when the imbalance between oxygen supply and demand is resolved. For example, rest reduces tissue demands and nitroglycerin improves oxygen supply. Discomfort from a myocardial infarction (MI) does not usually resolve with these measures. Also ask about any associated symptoms, including nausea, vomiting, diaphoresis, dizziness, weakness, palpitations, and shortness of breath.

Assess blood pressure and heart rate. Interpret the patient's cardiac rhythm and presence of dysrhythmias. Sinus tachycardia with premature ventricular contractions (PVCs) frequently occurs in the first few hours after an MI.

Next assess distal peripheral pulses and skin temperature. The skin should be warm with all pulses palpable. In the patient with unstable angina or MI, poor cardiac output may be manifested by cool, diaphoretic (“sweaty”) skin and diminished or absent pulses. Auscultate for an S3 gallop, which often indicates heart failure—a serious and common complication of MI. Assess the respiratory rate and breath sounds for signs of heart failure. An increased respiratory rate is common because of anxiety and pain, but crackles or wheezes may indicate left-sided heart failure. An S4 heart sound is a common finding in the patient who has had a previous MI or hypertension. Assess for the presence of jugular venous distention and peripheral edema.

The patient with MI may experience a temperature elevation for several days after infarction. Temperatures as high as 102° F (38.9° C) may occur in response to myocardial necrosis, indicating the inflammatory response.

Psychosocial Assessment

Denial is a common early reaction to chest discomfort associated with angina or MI. On average, the patient with an acute MI waits more than 2 hours before seeking medical attention. Often he or she rationalizes that symptoms are due to indigestion or overexertion. In some situations, denial is a normal part of adapting to a stressful event. However, denial that interferes with identifying a symptom such as chest discomfort can be harmful. Explain the importance of reporting any discomfort to the health care provider.

Fear, depression, anxiety, and anger are other common reactions of many patients and their families. Assist in identifying these feelings. Encourage them to explain their understanding of the event, and clarify any misconceptions. (Ignatavicius 2013, pp. 834-835)

Front 90

lab & diagnostics
(CAD & MI)

Back 90

Laboratory Assessment

Although there is no single ideal test to diagnose MI, the most common laboratory tests include troponins T and I, creatine kinase-MB (CK-MB), and myoglobin. These cardiac markers are specific for MI and cardiac necrosis. Troponins T and I and myoglobin rise quickly. CK-MB is the most specific marker for MI but does not peak until about 24 hours after the onset of pain. These tests are described in more detail in Chapter 35.

Imaging Assessment

Unless there is associated cardiac dysfunction (e.g., valve disease) or heart failure, a chest x-ray is not diagnostic for angina or MI.

Thallium scans use radioisotope imaging to assess for ischemia or necrotic muscle tissue related to angina or myocardial infarction (MI). Areas of decreased or absent perfusion, referred to as cold spots, identify ischemia or infarction. Thallium may be used with the exercise tolerance test. Dipyridamole (Persantine) thallium scanning (DTS) may also be used.

Contrast-enhanced cardiovascular magnetic resonance (CMR) may also be done as a noninvasive approach to detect MI. Echocardiography may be used to visualize the structures of the heart.

Use of the 64-slice computed tomography coronary angiography (CTCA) has been found to be helpful in diagnosing coronary artery disease in symptomatic patients identified as having a “low- or intermediate-pretest probability” risk for CAD. This new generation of high-speed computed tomography (CT) scanners is becoming a highly reliable, noninvasive way to evaluate CAD (Weustink et al., 2010).

Other Diagnostic Assessment

Twelve-lead electrocardiograms (ECGs) allow the health care provider to examine the heart from varying perspectives. By identifying the lead(s) in which ECG changes are occurring, the health care provider can identify both the occurrence and the location of ischemia (angina) or necrosis (infarction). In addition to the traditional 12-lead ECG, the health care provider may request a “right-sided” or 18-lead ECG to determine whether ischemia or infarction has occurred in the right ventricle.

An ischemic myocardium does not repolarize normally. Thus 12-lead ECGs obtained during an angina episode reveal ST depression, T-wave inversion, or both. Variant angina, caused by coronary vasospasm (vessel spasm), usually causes elevation of the ST segment during angina attacks. These ST and T-wave changes usually subside when the ischemia is resolved and pain is relieved. However, the T wave may remain flat or inverted for a period of time. If the patient is not experiencing angina at the moment of the test, the ECG is usually normal unless he or she has evidence of an old MI.

When infarction occurs, one of three ECG changes is usually observed: ST-elevation MI (STEMI), T-wave inversion, or non–ST-elevation MI (NSTEMI). An abnormal Q wave (wider than 0.04 seconds or more than one-third the height of the QRS complex) may develop, depending on the amount of myocardium that has necrosed. Women having an MI often present with an NSTEMI or T-wave inversion.

The Q wave may develop because necrotic cells do not conduct electrical stimuli. Hours to days after the MI, the ST-segment and T-wave changes return to normal. However, when the Q wave exists, it may become permanent. The Q waves may disappear after a number of years, but their absence does not necessarily mean that the patient has not had an MI.

After the acute stages of an angina episode or MI, the health care provider often requests an exercise tolerance test (stress test) on a treadmill to assess for ECG changes consistent with ischemia, evaluate medical therapy, and identify those who might benefit from invasive therapy. Pharmacologic stress-testing agents such as dobutamine (Dobutrex) may be used instead of the treadmill. Treadmill exercise testing is only moderately accurate for women when compared with men (Bellasi et al., 2007). In women with suspected CAD, stress echocardiography or single photon emission computed tomography (SPECT) should be performed.

Cardiac catheterization may be performed to determine the extent and exact location of coronary artery obstructions. It allows the cardiologist and cardiac surgeon to identify patients who might benefit from percutaneous transluminal coronary angioplasty (PTCA) and stent placement or from coronary artery bypass grafting (CABG). Each of the diagnostic tests in this section is described in detail in Chapter 35. (Ignatavicius 2013, pp. 835-836)

Front 91

analysis, planning, & implementation
(CAD & MI)

Back 91

Analysis

The patient with coronary artery disease (CAD) may have either angina or MI. If MI is suspected or cannot be completely ruled out, the patient is admitted to a telemetry unit for continuous monitoring or to a critical care unit if hemodynamically unstable.

The priority problems for most patients with CAD are:

1 Acute Pain related to imbalance between myocardial oxygen supply and demand

2 Inadequate tissue perfusion (cardiopulmonary) related to interruption of arterial blood flow

3 Activity Intolerance related to fatigue caused by imbalance between oxygen supply and demand

4 Ineffective Coping related to effects of acute illness and major changes in lifestyle

For the patient experiencing an MI, additional problems include:

1 Potential for dysrhythmias

2 Potential for heart failure

3 Potential for recurrent symptoms and extension of injury

Planning and Implementation

Astute assessment skills, timely analysis of troponin, and analysis of the 12-lead ECG (or 18-lead ECG for a suspected right ventricular infarction) are essential to ensure appropriate patient care management. This is particularly important since the average time a patient waits before seeking treatment is 2 hours and 20 minutes. This delay lessens the 4- to 6-hour window of opportunity for the most advantageous treatment with percutaneous intervention. (Ignatavicius 2013, p. 836)

Front 92

managing acute pain
(CAD & MI)

Back 92

Managing Acute Pain

Patients with diabetes mellitus and coronary artery disease (CAD) may not experience chest pain or pressure because of diabetic neuropathy. In this patient population, the onset of acute myocardial infarction (AMI) may be signaled by new onset of atrial fibrillation. With new-onset atrial fibrillation, a cardiac workup should be done to rule out myocardial infarction.

Planning: Expected Outcomes

The expected outcome is that the patient will verbalize a report of decreased pain and discomfort as a result of prompt collaborative interventions.

Interventions

The purpose of patient-centered collaborative care is to eliminate discomfort by providing pain relief measures, decreasing myocardial oxygen demand, and increasing myocardial oxygen supply.

Emergency Care

Evaluate any report of pain, obtain vital signs, ensure an IV access, and notify the health care provider of the patient's condition. Chart 40-3 summarizes the emergency interventions for the patient with symptoms of CAD.

Pain relief helps increase the oxygen supply and decrease myocardial oxygen demand. The American Heart Association (AHA) recommends several pain management strategies, including morphine sulfate and oxygen. Give morphine as the priority in managing pain in patients having an MI! (Ignatavicius 2013, p. 836)

Front 93

angina drug therapy
(CAD & MI)

Back 93

At home or in the hospital, the patient may take nitroglycerin to relieve episodic anginal pain. Aspirin 325 mg, an antiplatelet drug, may also be taken daily to prevent clots that further block coronary arteries.

Nitroglycerin (NTG), a nitrate often referred to as “nitro,” increases collateral blood flow, redistributes blood flow toward the subendocardium, and dilates the coronary arteries. In addition, it decreases myocardial oxygen demand by peripheral vasodilation, which decreases both preload and afterload. Teach the patient to hold the tablet under the tongue and drink 5 mL of water, if necessary, to allow the tablet to dissolve. NTG spray is also available and is more quickly absorbed. Pain relief should begin within 1 to 2 minutes and should be clearly evident in 3 to 5 minutes. After 5 minutes, recheck the patient's pain intensity and vital signs. If the BP is less than 100 mm Hg systolic or 25 mm Hg lower than the previous reading, lower the head of the bed and notify the health care provider. If the patient is experiencing some but not complete relief and vital signs remain stable, another NTG tablet or spray may be used. In 5-minute increments, a total of three doses may be administered in an attempt to relieve angina pain. If the patient uses NTG spray instead of the tablet, teach him or her to sit upright and spray the dose under the tongue. NTG topical patches should be placed below the nipple line to decrease discomfort.

Angina usually responds to NTG. The patient typically states that the pain is relieved or markedly diminished. When simple measures, such as taking three sublingual nitroglycerin tablets one after the other, do not relieve chest discomfort, the patient may be experiencing an MI.

In a specialized unit, the health care provider may prescribe IV NTG for management of the chest pain. Begin the drug infusion slowly, checking the BP and pain level every 3 to 5 minutes. The nitroglycerin dose is increased until the pain is relieved, the BP falls excessively, or the maximum prescribed dose is reached (Chart 40-4).

When pain or other symptoms have subsided and the patient is stabilized, the health care provider may change the drug to an oral or topical nitrate. During administration of long-term oral and topical nitrates, an 8- to 12-hour nitrate-free period should be maintained to prevent tolerance. The patient may initially report a headache. Give acetaminophen (Tylenol, Exdol ) before the nitrate to ease some of this discomfort.

The health care provider usually prescribes morphine sulfate (MS) to relieve discomfort that is unresponsive to nitroglycerin. Morphine relieves MI pain, decreases myocardial oxygen demand, relaxes smooth muscle, and reduces circulating catecholamines. It is usually administered in 2- to 10-mg doses IV every 5 to 15 minutes until the maximum prescribed dose is reached or the patient experiences relief or signs of toxicity. Monitor for adverse effects of morphine, which include respiratory depression, hypotension, bradycardia, and severe vomiting. Treatment for morphine toxicity is naloxone (Narcan) 0.2 to 0.8 mg IV, vasopressor drugs, IV fluids, and oxygen therapy. Monitor the patient's vital signs and cardiac rhythm every few minutes.

These strategies are often enough to relieve the pain. If they are not adequate, additional interventions identified in the Improving Cardiopulmonary Tissue Perfusion section below may be attempted.
(Ignatavicius 2013, pp. 836-838)

Front 94

other angina interventions
(CAD & MI)

Back 94

Several other interventions may be used with drug therapy to relieve chest pain. Supplemental oxygen increases the amount of oxygen available to myocardial tissue. Therefore oxygen is often prescribed and administered at a flow of 2 to 4 L/min by nasal cannula titrated to maintain an arterial oxygen saturation (SaO2) of 95% or higher. If the BP is stable, assist the patient in assuming any position of comfort. Placing the patient in semi-Fowler's position often enhances comfort and tissue oxygenation. A quiet, calm environment and explanations of interventions often reduce anxiety and help relieve chest pain. If needed, remind the patient to take several deep breaths to increase oxygenation. (Ignatavicius 2013, p. 838)

Front 95

emergency angina care
(CAD & MI)

Back 95

Emergency Care of the Patient with Chest Discomfort

--Assess airway, breathing, and circulation (ABCs). Defibrillate as needed.
--Provide continuous ECG monitoring.
--Obtain the patient's description of pain or discomfort.
--Obtain the patient's vital signs (blood pressure, pulse, respiration).
--Assess/provide vascular access.
--Consult chest pain protocol or notify the physician or Rapid Response Team for specific intervention.
--Obtain a 12-lead ECG within 10 minutes of reports of chest pain.
--Provide pain relief medication and aspirin as prescribed.
--Administer oxygen therapy to maintain oxygen saturation ≥95%.
--Remain calm. Stay with the patient if possible.
--Assess the patient's vital signs and intensity of pain 5 minutes after administration of medication.
--Remedicate with prescribed drugs (if vital signs remain stable), and check the patient every 5 minutes.
--Notify the physician if vital signs deteriorate. (Ignatavicius 2013, p. 838)


***Nursing Safety Priority Critical Rescue***

If the patient is experiencing an MI, prepare the patient for transfer to a specialized unit where close monitoring and appropriate management can be provided. If the patient is at home or in the community, call 911 for transfer to the closest emergency department. (Ignatavicius 2013, p. 838)

Front 96

aspirin therapy
(CAD & MI)

Back 96

Aspirin (ASA) therapy is recommended by the American College of Cardiology and the American Heart Association (AHA). It inhibits both platelet aggregation and vasoconstriction, thereby decreasing the likelihood of thrombosis. If the patient has new-onset angina at home, teach him or her to chew aspirin 325 mg (4 “baby aspirins” that are 81 mg each) immediately and call 911! The antiplatelet effect of ASA begins within 1 hour of use and continues for several days. Administer 162 to 325 mg non–enteric-coated aspirin every day to all patients with suspected CAD unless absolutely contraindicated. Instruct the patient to chew and swallow the drug and continue taking the drug unless adverse effects occur. (Ignatavicius 2013, pp. 838-839)

Front 97

improving cardiopulmonary tissue perfusion
(CAD & MI)

Back 97

Planning: Expected Outcomes

The primary outcome is that the patient will have increased myocardial perfusion as evidenced by an adequate cardiac output, normal sinus rhythm, and vital signs within normal limits.

Interventions

Because myocardial infarction (MI) is a dynamic process, restoring perfusion to the injured area (usually within 4 to 6 hours) often limits the amount of extension and improves left ventricular function. Complete, sustained reperfusion of coronary arteries in the first few hours after an MI has decreased mortality rates. (Ignatavicius 2013, p. 838)

Front 98

reperfusion therapy
(CAD & MI)

Back 98

As time passes, myocardial tissue can become increasingly ischemic and necrotic. Therefore, based on the location and skill set of the health care institution, one of two reperfusion strategies should be employed to open a blocked artery in a patient experiencing AMI.

Thrombolytic therapy using fibrinolytics dissolves thrombi in the coronary arteries and restores myocardial blood flow. Examples of these agents, which target the fibrin component of the coronary thrombosis, include:
--Tissue plasminogen activator (t-PA, alteplase [Activase]) (IV or intracoronary)
--Reteplase (Retavase) (IV or intracoronary)
--Tenecteplase (TNK) (IV push [IVP])

Intracoronary fibrinolytics may be delivered during cardiac catheterization. Thrombolytic agents are most effective when administered within the first 6 hours of a coronary event. They are used in men and women, young and old.

Thrombolytic therapy is given in a unit where the patient can be continuously monitored. It is indicated for chest pain of longer than 30 minutes’ duration that is unrelieved by nitroglycerin, with indications of transmural ischemia and injury as shown by the ECG. Contraindications include recent abdominal surgery or stroke, because bleeding may occur when fresh clots are lysed (broken down or dissolved). Table 40-2 lists the current contraindications to thrombolytic therapy.

Patients who weigh less than 143 pounds (65 kg) may need to have their dose of thrombolytic adjusted to lessen the likelihood of bleeding. (Ignatavicius 2013, pp. 839-840)

Front 99

percutaneous transluminal coronary angioplasty (PTCA)
(CAD & MI)

(AKA percutaneous coronary angioplasty (PCI) or just angioplasty)

Back 99

For some patients having an MI, primary percutaneous transluminal coronary angioplasty (PTCA) with stent (metallic mesh) placement may be used to reopen the clotted coronary artery. Percutaneous intervention has been associated with excellent return of blood flow through the coronary artery when it can be performed by an interventional cardiologist within 2 to 3 hours of the onset of symptoms. Many community hospitals can now perform emergent PTCA. When primary PTCA is not available, patients should receive immediate thrombolytic agents if they are appropriate candidates and then be transferred to a facility that can perform PTCA. This procedure is described in detail on p. 844 of this chapter.

Patients who receive fibrinolytics require PTCA for more definitive treatment such as stent placement. Therefore, if criteria for PTCA are met, it is more advantageous to go directly to the catheterization laboratory where definitive treatment, not just clot resolution, can be performed.

Monitor the patient for indications that the clot has been lysed (dissolved) and the artery reperfused. These indications include:
--Abrupt cessation of pain or discomfort
--Sudden onset of ventricular dysrhythmias
--Resolution of ST-segment depression/elevation or T-wave inversion
--A peak at 12 hours of markers of myocardial damage

After clot lysis with thrombolytics, large amounts of thrombin are released into the system, increasing the risk for vessel reocclusion. To maintain the patency of the coronary artery after thrombolytic therapy, the health care provider usually prescribes aspirin and IV heparin. Maintain the heparin infusion for 3 to 5 days as prescribed, and monitor the activated partial thromboplastin time (aPTT). The target aPTT range is usually 1.5 to 2.5 times the control sample. The heparin antifactor Xa assay (heparin assay) test may be used instead of the aPTT in some clinical facilities. Low–molecular-weight heparin (LMWH) (enoxaparin [Lovenox]) may be substituted for IV heparin. Therapeutic dosing of LMWH in this patient population should be based on weight (1 mg/kg). (Ignatavicius 2013, p. 840)

Front 100

percutaneous transluminal coronary angioplasty (PTCA)
(cardiac surgeries)

Back 100

Percutaneous transluminal coronary angioplasty (PTCA), most commonly done before stent placement, is an invasive but nonsurgical technique. It is performed to reduce the frequency and severity of discomfort for patients with angina and to bridge patients to coronary artery bypass graft (CABG) surgery. Because of the artery's normal elasticity and “memory” to retain its original shape, the artery often re-occludes if a stent is not used as part of the procedure.

Patients who are most likely to benefit from PTCA have single- or double-vessel disease with discrete, proximal, noncalcified lesions (clots). This procedure often does not work for complex clots. When identifying which lesions are treatable with PTCA, the cardiologist considers the clot's complexity and location, as well as the amount of myocardium at risk. Although treating lesions located in the left main artery places a large amount of myocardial tissue at risk if the vessel closes quickly, these lesions are now being treated more with PTCA and stent placement. In the past, coronary artery bypass grafting (CABG) was the intervention used for these patients. PTCA may also be used for the patient with an evolving acute MI, either alone or with thrombolytic therapy or glycoprotein (GP) IIb/IIIa inhibitor, to reperfuse the damaged myocardium.

Before the procedure, the patient receives an initial dose of a thienopyridine (clopidogrel [Plavix]) or prasugrel [Effient]), antiplatelet drugs. If there are any concerns that the patient may require CABG, the thienopyridine is held until postprocedure. The inhibition of the platelets is permanent and increases the risk for postoperative bleeding. Patients should wait 5 (clopidogrel) to 7 (prasugrel) days after dosing with a thienopyridine before undergoing CABG. If the patient has received thrombolytic therapy, clopidogrel (Plavix) is the preferred thienopyridine. The physician performs the angioplasty under fluoroscopic guidance in the cardiac catheterization laboratory. A balloon-tipped catheter is introduced through a guidewire to the coronary artery occlusion. The physician activates a compressor that inflates the balloon to force the plaque against the vessel wall, thus dilating the wall, and reduces or eliminates the occluding clot. Balloon inflation may be repeated until angiography indicates a decrease in the stenosis (narrowing) to less than 50% of the vessel's diameter (Fig. 40-3).

During the procedure, the patient may receive boluses of IV heparin or a continuous infusion of bivalirudin (Angiomax). Heparin is used to maintain an elevated activated clotting time and prevent clotting on wires and catheters during the procedure. Heparin is discontinued before removal of the catheters. Bivalirudin (Angiomax) is a directed thrombin inhibitor and is frequently used as an alternative to IIb/IIIa inhibitors and heparin. Bivalirudin has a short half-life (25 minutes) and is less dependent on renal function. IV or intracoronary nitroglycerin or diltiazem (Cardizem) is given to prevent coronary vasospasm. PTCA initially reopens the vessel in most appropriately selected patients. Within the first 24 hours, however, a small percentage of patients have re-stenosis. At 6 months, a larger number have one or more blockages.

The health care provider usually prescribes a long-term nitrate and dual antiplatelet therapy with aspirin and a thienopyridine for patients after PTCA. A beta blocker and an ACE inhibitor or ARB are added for patients who have had primary angioplasty after an MI. Patients who do not receive a thienopyridine continue to have infusions of GP IIb/IIIa inhibitors during the initial hours after PTCA. Some may experience hypokalemia after the procedure and require careful monitoring and potassium supplements. The nursing interventions for patients receiving these drugs are described in Chart 40-4. Provide careful explanations of drug therapy and any recommended lifestyle changes. (Ignatavicius 2013, pp. 844-845)

Front 101

stent
(cardiac surgeries)

Back 101

Other techniques being used to ensure continued patency of the vessel are laser angioplasty (the laser breaks up the clot), atherectomy, and stents. Atherectomy devices can either excise and retrieve plaque or emulsify it. One of the advantages of this procedure is that it creates a less bulky vessel with better elastic recoil. Stents are expandable metal mesh devices that are used to maintain the patent lumen created by angioplasty or atherectomy. Bare metal or drug-eluting stents (DES) (drug-coated) may be used. By providing a supportive scaffold, these devices prevent closure of the vessel from arterial dissection or vasospasm. A thienopyridine and aspirin (antiplatelet agents) are prescribed for 12 months after a stent has been placed (Moser & Riegel, 2008). Fig. 40-4 shows a stent positioned in a coronary artery. (Ignatavicius 2013, p. 845)

Front 102

coronary artery bypass graft surgery (CABG)

Back 102

Over 500,000 coronary artery bypass graft (CABG) surgeries are performed in the United States each year. It is the most common type of cardiac surgery and the most common procedure for older adults. Almost half of all CABGs are done for patients older than 65 years (AHA, 2010). The occluded coronary arteries are bypassed with the patient's own venous or arterial blood vessels or synthetic grafts. The internal mammary artery (IMA) is the current graft of choice because it has a 90% patency rate at 12 years after the procedure.

CABG is indicated when patients do not respond to medical management of CAD or when disease progression is evident. Because of the development of drug-eluting stents (DESs), patients who previously had no option other than CABG have been able to have their vessels revascularized without surgery. The decision for surgery is based on the patient's symptoms and the results of cardiac catheterization. Candidates for surgery are patients who have:
--Angina with greater than 50% occlusion of the left main coronary artery that cannot be stented
--Unstable angina with severe two-vessel disease, moderate three-vessel disease, or small-vessel disease in which stents could not be introduced
--Ischemia with heart failure
--Acute MI with cardiogenic shock
--Signs of ischemia or impending MI after angiography or PTCA
--Valvular disease
--Coronary vessels unsuitable for PTCA

The vessels to be bypassed should have proximal clots blocking more than 70% of the vessel's diameter but with good distal runoff. Bypass of less occluded vessels may result in poor perfusion through the graft and early obstruction. CABG is most effective when adequate ventricular function remains and the ejection fraction is close to or greater than 50%. Patients with lower ejection fractions are subject to develop more complications.

For most patients, the risk is low and the benefits of bypass surgery are clear. Surgical treatment of CAD does not appear to affect the life span. Left ventricular function is the most important long-term indicator of survival. CABG improves the quality of life for most patients. Most are pain-free at 1 year after surgery and remain so at 5 years after the procedure. The percentage of patients experiencing some pain increases sharply after 5 years. (Ignatavicius 2013, pp. 845-846)

Front 103

pre-op care
(CABG)

Back 103

CABG surgery may be planned as an elective procedure or performed as an emergency. It may be done as a traditional operative technique or performed as a minimally invasive surgical (MIS) technique. Patients undergoing elective surgery are admitted on the morning of surgery. Preoperative preparations and teaching are completed during prehospitalization interviews. Teach patients that their drugs will be changed after surgery. Ensure that the necessary drugs have been administered before surgery.

Familiarize the patient and family with the cardiac surgical–critical care unit (sometimes referred to as the “open heart” unit), and prepare them for postoperative care. If the procedure is elective, demonstrate and have the patient return a demonstration of how to splint the chest incision, cough, deep breathe, and perform arm and leg exercises. Stress that:

• The patient should report any pain to the nursing staff.

• Most of the pain will be in the site where the vessel was harvested. (With the use of endovascular vessel harvesting [EVH] and one or two small incisions, the pain and edema are less than for previously performed procedures.)

• Analgesics will be given for pain.

• Coughing and deep breathing are essential to prevent pulmonary complications.

• Early ambulation is important to decrease the risk for venous thrombosis and possible embolism.

For the traditional surgical procedure, explain that the patient will have a sternal incision; possibly a large leg incision; one, two or three chest tubes; an indwelling urinary catheter; pacemaker wires; and hemodynamic monitoring. An endotracheal tube will be connected to a ventilator for several hours postoperatively. Tell the patient and family that the patient will not be able to talk while the endotracheal tube is in place. When describing the postoperative course, emphasize that close monitoring and the use of sophisticated equipment are standard treatment.

Preoperative anxiety is common. An appropriate nursing assessment should identify the level of anxiety and the coping methods patients have used successfully in the past. Some patients may find it helpful to define their fears. Common sources of fear include fear of the unknown, fear of bodily harm, and fear of death.

In elective procedures, patients may benefit from detailed information about the surgery. Others may feel overwhelmed by so much material. Some patients need to discuss their feelings in detail or describe the experiences of people they know who have undergone CABG. Assess patients’ anxiety level and help them cope. (Ignatavicius 2013, p. 846)

Front 104

post-op care
(CABG)

Back 104

After traditional surgery, the patient is transported to a post–open heart surgery unit and undergoes mechanical ventilation for 3 to 6 hours. He or she requires highly skilled nursing care from a nurse qualified to provide post–cardiac surgery care, including routine postoperative care described in Chapter 18. Be sure to use sterile technique when changing sternal or donor-site dressings.

Connect the mediastinal tubes to water seal drainage systems, and ground the epicardial pacer wires by connecting them to the pacemaker generator. Monitor pulmonary artery and arterial pressures, as well as the heart rate and rhythm, which are displayed on a monitor.

Closely assess the patient for dysrhythmias, such as bradydysrhythmias, atrial fibrillation, or heart block. Manage symptomatic dysrhythmias according to unit protocol or the health care provider's prescription. Hypoxemia and hypokalemia are frequent causes of ventricular dysrhythmias. If the patient has symptomatic bradydysrhythmias or heart block, turn on the pacemaker and adjust the pacemaker settings as prescribed. Monitor for, report, and document other complications of CABG, including:
--Fluid and electrolyte imbalance
--Hypotension
--Hypothermia
--Hypertension
--Bleeding
--Cardiac tamponade
--Decreased level of consciousness
--Anginal pain

(Ignatavicius 2013, p. 847)

Front 105

valvular heart disease

Back 105

Acquired valvular dysfunctions include mitral stenosis, mitral regurgitation, mitral valve prolapse, aortic stenosis, and aortic regurgitation (Chart 37-6). The tricuspid valve is not affected often and may occur following endocarditis in IV drug abusers. (Ignatavicius 2013, p. 758)

Front 106

aortic stenosis
(valvular heart disease)

Back 106

Aortic Stenosis

Aortic stenosis is the most common cardiac valve dysfunction in the United States and is often considered a disease of “wear and tear.” In aortic stenosis, the aortic valve orifice narrows and obstructs left ventricular outflow during systole. This increased resistance to ejection or afterload results in ventricular hypertrophy. As stenosis worsens, cardiac output becomes fixed and cannot increase to meet the demands of the body during exertion. Symptoms then develop. Eventually the left ventricle fails, blood backs up in the left atrium, and the pulmonary system becomes congested. Right-sided HF can occur late in the disease. When the surface area of the valve becomes 1 cm or less, surgery is indicated on an urgent basis!

Congenital bicuspid or unicuspid aortic valves are the primary causes for aortic stenosis in many patients. Rheumatic aortic stenosis occurs with rheumatic disease of the mitral valve and develops in young and middle-aged adults. Atherosclerosis and degenerative calcification of the aortic valve are the major causative factors in older adults. Aortic stenosis has become the most common valvular disorder in all countries with aging populations.

The classic symptoms of aortic stenosis result from fixed cardiac output: dyspnea, angina, and syncope occurring on exertion. When cardiac output falls in the late stages of the disease, the patient experiences marked fatigue, debilitation, and peripheral cyanosis. A narrow pulse pressure is noted when the BP is measured. A diamond-shaped, systolic crescendo-decrescendo murmur is usually noted on auscultation.
(Ignatavicius 2013, pp. 759-760)

Front 107

aortic regurgitation
(valvular heart disease)

Back 107

In patients with aortic regurgitation, the aortic valve leaflets do not close properly during diastole and the annulus (the valve ring that attaches to the leaflets) may be dilated, loose, or deformed. This allows flow of blood from the aorta back into the left ventricle during diastole. The left ventricle, in compensation, dilates to accommodate the greater blood volume and eventually hypertrophies.

Aortic insufficiency usually results from nonrheumatic conditions such as infective endocarditis, congenital anatomic aortic valvular abnormalities, hypertension, and Marfan syndrome (a rare, generalized, systemic disease of connective tissue).

Patients with aortic regurgitation remain asymptomatic for many years because of the compensatory mechanisms of the left ventricle. As the disease progresses and left ventricular failure occurs, the major symptoms are exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Palpitations may be noted with severe disease, especially when the patient lies on the left side. Nocturnal angina with diaphoresis often occurs.

On palpation, the nurse notes a “bounding” arterial pulse. The pulse pressure is usually widened, with an elevated systolic pressure and diminished diastolic pressure. The classic auscultatory finding is a high-pitched, blowing, decrescendo diastolic murmur. (Ignatavicius 2013, p. 760)

Front 108

assessment
(valvular heart disease)

Back 108

A patient with valvular disease may suddenly become ill or slowly develop symptoms over many years. Collect information about the patient's family health history, including valvular or other forms of heart disease to which he or she may be genetically predisposed. Question about attacks of rheumatic fever and infective endocarditis, the specific dates when these occurred, and the use of antibiotics to prevent recurrence of these diseases. Also question the patient about a history of IV drug abuse, a common cause of infective endocarditis. Discuss the patient's fatigue level and tolerated activity level, the presence of angina or dyspnea, and the occurrence of palpitations, if present.

As part of the physical assessment, obtain vital signs, inspect for signs of edema, palpate and auscultate the heart and lungs, and palpate the peripheral pulses. Assessment findings are summarized in Chart 37-6.

Echocardiography is the noninvasive diagnostic procedure of choice to visualize the structure and movement of the heart. The more invasive transesophageal echocardiography (TEE) or transthoracic echocardiography (TTE) is also performed to assess most valve problems. Exercise tolerance testing (ETT) and stress echocardiography are sometimes done to evaluate symptomatic response and assess functional capacity. With either mitral or aortic stenosis, cardiac catheterization may be indicated to assess the severity of the stenosis and its other effects on the heart.

In patients with mitral stenosis, the chest x-ray shows left atrial enlargement, prominent pulmonary arteries, and an enlarged right ventricle. In those with mitral regurgitation (insufficiency), the chest x-ray reveals an increased cardiac shadow, indicating left ventricular and left atrial enlargement.

In the later stages of aortic stenosis, the chest x-ray may show left ventricular enlargement and pulmonary congestion. Left atrial and left ventricular dilation appear on the chest x-ray of patients with aortic regurgitation (insufficiency). If HF is present, pulmonary venous congestion is also evident.

The health care provider also requests an ECG to assess abnormalities such as left ventricular hypertrophy, as seen with mitral regurgitation and aortic regurgitation, or right ventricular hypertrophy, as seen in severe mitral stenosis. Atrial fibrillation is a common finding in both mitral stenosis and mitral regurgitation and may develop in aortic stenosis because of left atrial dilation. (Ignatavicius 2013, p. 760)

Front 109

interventions
(valvular heart disease)

Back 109

Management of valvular heart disease depends on which valve is affected and the degree of valve impairment. Some patients can be managed with yearly monitoring and drug therapy, whereas others require invasive procedures or heart surgery. (Ignatavicius 2013, p. 760)

Front 110

noninvasive heart valve reparative procedures
(valvular heart disease)

Back 110

Reparative procedures are becoming more popular because of continuing problems with thrombi, endocarditis, and left ventricular dysfunction after valve replacement. Reparative procedures do not result in a normal valve, but they usually “turn back the clock,” resulting in a more functional valve and an improvement in cardiac output. Turbulent blood flow through the valve may persist, and degeneration of the repaired valve is possible.

Balloon valvuloplasty, an invasive nonsurgical procedure, is possible for stenotic mitral and aortic valves; however, careful selection of patients is needed. It may be the initial treatment of choice for people with noncalcified, mobile mitral valves. Patients selected for aortic valvuloplasty are usually older and are at high risk for surgical complications or have refused operative treatment. The benefits of this procedure for aortic stenosis tend to be short lived, rarely lasting longer than 6 months.

When performing mitral valvuloplasty, the physician passes a balloon catheter from the femoral vein, through the atrial septum, and to the mitral valve. The balloon is inflated to enlarge the mitral orifice. For aortic valvuloplasty, the physician inserts the catheter through the femoral artery and advances it to the aortic valve, where it is inflated to enlarge the orifice. The procedure usually offers immediate relief of symptoms because the balloon has dilated the orifice and improved leaflet mobility. The results are comparable with those of surgical commissurotomy for appropriately selected patients.

***Nursing Safety Priority Action Alert***

After valvuloplasty, observe the patient closely for bleeding from the catheter insertion site and institute post-angiogram precautions. Bleeding is likely because of the large size of the catheter. Assess for signs of a regurgitant valve by closely monitoring heart sounds, CO, and heart rhythm. Because vegetations (thrombi) may have been dislodged from the valve, observe for any indication of systemic emboli (see the Infective Endocarditis section, p. 763). (Ignatavicius 2013, p. 761)

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surgical management
(valvular heart disease)

Back 111

Surgeries for patients with valvular heart disease include invasive reparative procedures and replacement. These procedures are performed after symptoms of left ventricular failure have developed but before irreversible dysfunction occurs. Surgical therapy is the only definitive treatment of aortic stenosis and is recommended when angina, syncope, or dyspnea on exertion develops.

Invasive Heart Valve Reparative Procedures

Direct (open) commissurotomy is accomplished with cardiopulmonary bypass during open heart surgery. The surgeon visualizes the valve, removes thrombi from the atria, incises the fused commissures (leaflets), and débrides calcium from the leaflets, widening the orifice.

Mitral valve annuloplasty (reconstruction) is the reparative procedure of choice for most patients with acquired mitral insufficiency. To make the annulus (the valve ring that attaches to and supports the leaflets) smaller, the surgeon may suture the leaflets to an annuloplasty ring or take tucks in the patient's annulus. Leaflet repair is often performed at the same time. Elongated leaflets may be shortened, and shortened leaflets may be repaired by lengthening the chordae that bind them in place. Perforated leaflets may be patched with synthetic grafts.

Annuloplasty and leaflet repair result in an annulus of the appropriate size and in leaflets that can close completely. Thus regurgitation is eliminated or markedly reduced.

Heart Valve Replacement Procedures

The development of a wide variety of prosthetic (synthetic) and biologic (tissue) valves has improved the surgical therapy and prognosis of valvular heart disease. Each type has advantages and disadvantages. An aortic valve can be replaced only with a prosthetic valve for symptomatic adults with aortic stenosis and aortic insufficiency. A biologic valve cannot be used because of the high pressure within the aorta.

Biologic valve replacements may be xenograft (from other species), such as a porcine valve (from a pig) (Fig. 37-3) or a bovine valve (from a cow). Because tissue valves are associated with little risk for clot formation, long-term anticoagulation is not indicated. Xenografts are not as durable as prosthetic valves and usually must be replaced every 7 to 10 years. The durability of the graft is related to the age of the recipient. Calcium in the blood, which is present in larger quantities in younger patients, breaks down the valves. The older the patient, the longer the xenograft will last.

Valves donated from human cadavers and pulmonary autographs (relocation of the patient's own pulmonary valve to the aortic position [Ross procedure]) are also being used for valve replacement.

Patients having a valve replacement have open heart surgery similar to the procedure for a coronary artery bypass graft (CABG) (see Chapter 40). Ideally, surgery is an elective and planned procedure. Inform the patient and family about the management of postoperative pain, incision care, and strategies to prevent respiratory complications (see Chapters 16 and 18). Teach patients receiving oral anticoagulants to stop taking them before surgery, usually at least 72 hours before the procedure. Patients also need to have a preoperative dental examination. If dental caries or periodontal disease is present, these problems must be resolved before valve replacement.

Postoperative nursing interventions for patients with valve replacement are similar to those for a CABG (see Chapter 40).

Patients with valve replacements are also more likely to have significant reductions in cardiac output (CO) after surgery, especially those with aortic stenosis or left ventricular failure from mitral valve disease. Carefully monitor cardiac output (CO) and assess for indications of heart failure (HF). Report any manifestations of HF to the surgeon immediately and prepare for collaborative management (see earlier discussion on heart failure in this chapter).
(Ignatavicius 2013, pp. 761-762)

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infective endocarditis

Back 112

Infective endocarditis (previously called bacterial endocarditis) is a microbial infection (e.g., viruses, bacteria, fungi) of the endocardium. The most common infective organism is Streptococcus viridans or Staphylococcus aureus.

Infective endocarditis occurs primarily in patients who abuse IV drugs, have had valve replacements, have experienced systemic infection, or have structural cardiac defects. With a cardiac defect, blood may flow rapidly from a high-pressure area to a low-pressure zone, eroding a section of endocardium. Platelets and fibrin adhere to the denuded endocardium, forming a vegetative lesion. During bacteremia, bacteria become trapped in the low-pressure “sinkhole” and are deposited in the vegetation. Additional platelets and fibrin are deposited, which causes the vegetative lesion to grow. The endocardium and valve are destroyed. Valvular insufficiency may result when the lesion interferes with normal alignment of the valve. If vegetations become so large that blood flow through the valve is obstructed, the valve appears stenotic and then is very likely to embolize (i.e., cause emboli to be released into the systemic circulation) (McCance et al., 2010).

Possible ports of entry for infecting organisms include:
--The oral cavity (especially if dental procedures have been performed)
--Skin rashes, lesions, or abscesses
--Infections (cutaneous, genitourinary, GI, systemic)
--Surgery or invasive procedures, including IV line placement (Ignatavicius 2013, p. 763)

Front 113

assessment
(infective endocarditis)

Back 113

Because the mortality rate remains high, early detection of infective endocarditis is essential. Unfortunately, many patients (especially older adults) are misdiagnosed. Clinical manifestations typically occur within 2 weeks of a bacteremia (Chart 37-8).

Most patients have recurrent fevers from 99° to 103° F (37.2° to 39.4° C). As a result of physiologic changes associated with aging, however, older adults may be afebrile. The severity of symptoms may depend on the virulence of the infecting organism.

Diagnostic Assessment

The most reliable criteria for diagnosing endocarditis include positive blood cultures, a new regurgitant murmur, and evidence of endocardial involvement by echocardiography.

A positive blood culture is a prime diagnostic test. Both aerobic and anaerobic specimens are obtained for culture. Some slow-growing organisms may take 3 weeks and require a specialized medium to isolate. Low hemoglobin and hematocrit levels may also be present.

Echocardiography has improved the ability to diagnose infective endocarditis accurately. Transesophageal echocardiography (TEE) allows visualization of cardiac structures that are difficult to see with transthoracic echocardiography (TTE; see Chapter 35). (Ignatavicius 2013, p. 764)

Front 114

clinical manifestations
(infective endocarditis)

Back 114

Key Features:
--Fever associated with chills, night sweats, malaise, and fatigue
--Anorexia and weight loss
--Cardiac murmur (newly developed or change in existing)
--Development of heart failure
--Evidence of systemic embolization
--Petechiae
--Splinter hemorrhages
--Osler's nodes (on palms of hands and soles of feet)
--Janeway's lesions (flat, reddened maculae on hands and feet)
--Positive blood cultures

Assess the patient's cardiovascular status. Almost all patients with infective endocarditis develop murmurs. Carefully auscultate the precordium, noting and documenting any new murmurs (usually regurgitant in nature) or any changes in the intensity or quality of an old murmur. An S3 or S4 heart sound also may be heard.

Heart failure (HF) is the most common complication of infective endocarditis. Assess for right-sided HF (as evidenced by peripheral edema, weight gain, and anorexia) and left-sided HF (as evidenced by fatigue, shortness of breath, and crackles on auscultation of breath sounds). See discussion of HF earlier in this chapter.

Arterial embolization is a major complication in up to half of patients with infective endocarditis. Fragments of vegetation break loose and travel randomly through the circulation. When the left side of the heart is involved, vegetation fragments are carried to the spleen, kidneys, GI tract, brain, and extremities. When the right side of the heart is involved, emboli enter the pulmonary circulation.

Splenic infarction with sudden abdominal pain and radiation to the left shoulder can also occur. When performing an abdominal assessment, note rebound tenderness on palpation. The classic pain described with renal infarction is flank pain that radiates to the groin and is accompanied by hematuria (red blood cells in the urine) or pyuria (white blood cells in the urine). Mesenteric emboli cause diffuse abdominal pain, often after eating, and abdominal distention.

About a third of patients have neurologic changes, others have signs and symptoms of pulmonary problems. Emboli to the central nervous system cause either transient ischemic attacks (TIAs) or a stroke. Confusion, reduced concentration, and aphasia or dysphagia may occur. Pleuritic chest pain, dyspnea, and cough are symptoms of pulmonary infarction related to embolization.

Petechiae (pinpoint red spots) occur in many patients with endocarditis. Examine the mucous membranes, the palate, the conjunctivae, and the skin above the clavicles for small, red, flat lesions. Assess the distal third of the nail bed for splinter hemorrhages, which appear as black longitudinal lines or small red streaks. (Ignatavicius 2013, pp. 763-764)

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interventions
(infective endocarditis)

Back 115

Interventions

Care of the patient with endocarditis usually includes antimicrobials, rest balanced with activity, and supportive therapy for HF. If these interventions are successful, surgery is usually not required.

Nonsurgical Management

The major component of treatment for endocarditis is drug therapy. Other interventions help prevent the life-threatening complications of the disease.

Antimicrobials are the main treatment, with the choice of drug depending on the specific organism involved. Because vegetations surround and protect the offending microorganism, an appropriate drug must be given in a sufficiently high dose to ensure its destruction. Antimicrobials are usually given IV, with the course of treatment lasting 4 to 6 weeks. For most bacterial cases, the ideal antibiotic is one of the penicillins or cephalosporins.

Patients may be hospitalized for several days to institute IV therapy and then are discharged for continued IV therapy at home. After hospitalization, most patients who respond to therapy may continue it at home when they become afebrile, have negative blood cultures, and have no signs of HF or embolization.

Anticoagulants do not prevent embolization from vegetations. Because they may result in bleeding, these drugs are avoided unless they are required to prevent thrombus formation on a prosthetic valve.

The patient's activities are balanced with adequate rest. Consistently use appropriate aseptic technique to protect the patient from contact with potentially infective organisms. Continue to assess for signs of HF (e.g., rapid pulse, fatigue, cough, dyspnea) throughout the antimicrobial regimen and report significant changes.

Surgical Management

The cardiac surgeon may be consulted if antibiotic therapy is ineffective in sterilizing a valve, if refractory HF develops secondary to a defective valve, if large valvular vegetations are present, or if multiple embolic events occur. Current surgical interventions for infective endocarditis include:

• Removing the infected valve (either biologic or prosthetic)

• Repairing or removing congenital shunts

• Repairing injured valves and chordae tendineae

• Draining abscesses in the heart

Preoperative and postoperative care of patients having surgery involving the valves is similar to that described earlier for valve replacement (pp. 761-762).

Community-Based Care

Community-based care for patients with infective endocarditis is essential to resolve the problem, prevent relapse, and avoid complications. Patients and families need to be willing and have the knowledge, physical ability, and resources to administer IV antibiotics at home. Collaborate with the home care nurse to complete health teaching started in the hospital and to monitor patient adherence and health status as directed by The Joint Commission's National Patient Safety Goals.

In collaboration with the case manager, the home care nurse and pharmacist arrange for appropriate supplies to be available to the patient at home. Supplies include the prepared antibiotic, IV pump with tubing, alcohol wipes, IV access device, normal saline solution, and a saline flush solution drawn up in syringes. A saline lock, peripherally inserted central catheter (PICC) line, or central catheter is positioned at a venous site that is easily accessible to the patient or a family member.

Teach the patient and family how to administer the antibiotic and care for the infusion site while maintaining aseptic technique. The patient or family member should demonstrate this technique before the patient is discharged from the hospital. Emphasize the importance of maintaining a blood level of the antibiotic by administering the antibiotics as scheduled. After stabilization at home, the case manager or other nurse contacts the patient every week to determine whether he or she is adhering to the antibiotic therapy and whether any problems have been encountered.

Encourage proper oral hygiene. Advise patients to use a soft toothbrush, to brush their teeth at least twice per day, and to rinse the mouth with water after brushing. They should not use irrigation devices or floss the teeth because bacteremia may result. Teach them to clean any open skin areas well and apply an antibiotic ointment.

***Nursing Safety Priority Action Alert***

Patients must remind health care providers (including their dentists) of their endocarditis. Teach patients to request prophylactic antibiotics for every invasive procedure, especially dental care.

Instruct patients to note any indications of recurring endocarditis such as fever. Remind them to monitor and record their temperature daily for up to 6 weeks. Teach them to report fever, chills, malaise, weight loss, increased fatigue, sudden weight gain, or dyspnea to their primary care provider.
(Ignatavicius 2013, pp. 764-765)

Front 116

rheumatic carditis

Back 116

Rheumatic carditis, also called rheumatic endocarditis, is a sensitivity response that develops after an upper respiratory tract infection with group A beta-hemolytic streptococci. It occurs in almost half of patients with rheumatic fever. The precise mechanism by which the infection causes inflammatory lesions in the heart is not established; however, inflammation is evident in all layers of the heart. The inflammation results in impaired contractile function of the myocardium, thickening of the pericardium, and valvular damage.

Rheumatic carditis is characterized by the formation of Aschoff bodies (small nodules in the myocardium that are replaced by scar tissue). A diffuse cellular infiltrate also develops and may be responsible for the resulting heart failure (HF). The pericardium becomes thickened and covered with exudate, and a serosanguineous pleural effusion may develop. The most serious damage occurs to the endocardium, with inflammation of the valve leaflets developing. Hemorrhagic and fibrous lesions form along the inflamed surfaces of the valves, resulting in stenosis or regurgitation of the mitral and aortic valves (McCance et al., 2010). (Ignatavicius 2013, p. 766)

Front 117

collaborative care
(rheumatic carditis)

Back 117

Rheumatic carditis is one of the major indicators of rheumatic fever. The common manifestations are:
--Tachycardia
--Cardiomegaly (enlarged heart)
--Development of a new murmur or a change in an existing murmur
--Pericardial friction rub
--Precordial pain
--Electrocardiogram (ECG) changes (prolonged PR interval)
--Indications of heart failure (HF)
--Evidence of an existing streptococcal infection

Primary prevention is extremely important. Teach all patients to remind their health care providers to provide appropriate antibiotic therapy if they develop the indications of streptococcal pharyngitis:
--Moderate to high fever
--Abrupt onset of a sore throat
--Reddened throat with exudate
--Enlarged and tender lymph nodes

Penicillin is the antibiotic of choice for treatment. Erythromycin (Eryc, Erythromid ) is the alternative for penicillin-sensitive patients.

Once a diagnosis of rheumatic fever is made, antibiotic therapy is started immediately. Teach the patient to continue the antibiotic administration for the full 10 days to prevent reinfection. Suggest ways to manage fever, such as maintaining hydration and taking antipyretics. Encourage the patient to get adequate rest. (Ignatavicius 2013, pp. 766-767)

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dysrhythmias

Back 118

Cardiac dysrhythmias are abnormal rhythms of the heart's electrical system that can affect its ability to effectively pump oxygenated blood throughout the body. Some dysrhythmias are life threatening, and others are not. They are the result of disturbances of cardiac electrical impulse formation, conduction, or both. When the heart does not work effectively as a pump, perfusion and oxygenation to vital organs and peripheral tissues can be impaired, resulting in organ dysfunction or failure.

Many health problems, especially coronary artery disease (CAD), electrolyte imbalances, changes in oxygenation, and drug toxicity, can cause abnormal heart rhythms. Dysrhythmias can occur in people of any age but occur most often in older adults. To provide collaborative patient-centered care using best practices, a basic understanding of cardiac electrophysiology, the conduction system of the heart, and the principles of electrocardiography is needed as a medical-surgical nurse. Specialty nurses and advanced practice nurses have a more in-depth knowledge as they manage patients with these cardiac problems in critical care areas. (Ignatavicius 2013, p. 711)

Front 119

cardiac conduction system

Back 119

The cardiac conduction system consists of specialized myocardial cells (Fig. 36-1). The electrophysiologic properties of those cells regulate heart rate and rhythm and possess unique properties: automaticity, excitability, conductivity, and contractility.

Automaticity (pacing function) is the ability of cardiac cells to generate an electrical impulse spontaneously and repetitively. Normally, only primary pacemaker cells (sinoatrial [SA] node) can generate an electrical impulse. Under certain conditions, such as myocardial ischemia (decreased blood flow), electrolyte imbalance, hypoxia, drug toxicity, and infarction (cell death), any cardiac cell may produce electrical impulses independently and create dysrhythmias. Disturbances in automaticity may involve either an increase or a decrease in pacing function.

Excitability is the ability of non-pacemaker heart cells to respond to an electrical impulse that begins in pacemaker cells and to depolarize. Depolarization occurs when the normally negatively charged cells within the heart muscle develop a positive charge.

Conductivity is the ability to send an electrical stimulus from cell membrane to cell membrane. As a result, excitable cells depolarize in rapid succession from cell to cell until all cells have depolarized. The wave of depolarization causes the deflections of the electrocardiogram (ECG) waveforms that are recognized as the P wave and the QRS complex. Disturbances in conduction result when conduction is too rapid or too slow, when the pathway is totally blocked, or when the electrical impulse travels an abnormal pathway.

Contractility is the ability of atrial and ventricular muscle cells to shorten their fiber length in response to electrical stimulation, causing sufficient pressure to push blood forward through the heart. In other words, contractility is the mechanical activity of the heart.

Specialized cells of the myocardium are responsible for cardiac conduction. They consist of the sinoatrial node, atrioventricular junctional area, and bundle branch system.

Conduction begins with the sinoatrial (SA) node (also called the sinus node), located close to the surface of the right atrium near its junction with the superior vena cava. The SA node is the heart's primary pacemaker. It can spontaneously and rhythmically generate electrical impulses at a rate of 60 to 100 beats per minute and therefore has the greatest degree of automaticity.

The SA node is richly supplied by the sympathetic and parasympathetic nervous systems, which increase and decrease the rate of discharge of the sinus node, respectively. This process results in changes in the heart rate.

Impulses from the sinus node move directly through atrial muscle and lead to atrial depolarization, which is reflected in a P wave on the ECG. Atrial muscle contraction should follow. Within the atrial muscle are slow and fast conduction pathways leading to the atrioventricular (AV) node.

The atrioventricular (AV) junctional area consists of a transitional cell zone, the AV node itself, and the bundle of His. The AV node lies just beneath the right atrial endocardium, between the tricuspid valve and the ostium of the coronary sinus. Here T-cells (transitional cells) cause impulses to slow down or to be delayed in the AV node before proceeding to the ventricles. This delay is reflected in the PR segment on the ECG. This slow conduction provides a short delay, allowing the atria to contract and the ventricles to fill. The contraction is known as “atrial kick” and contributes additional blood volume for a greater cardiac output. The AV node is also controlled by both the sympathetic and the parasympathetic nervous systems. The bundle of His connects with the distal portion of the AV node and continues through the interventricular septum.

The bundle of His extends as a right bundle branch down the right side of the interventricular septum to the apex of the right ventricle. On the left side, it extends as a left bundle branch, which further divides.

At the ends of both the right and the left bundle branch systems are the Purkinje fibers. These fibers are an interweaving network located on the endocardial surface of both ventricles, from apex to base. The fibers then partially penetrate into the myocardium. Purkinje cells make up the bundle of His, bundle branches, and terminal Purkinje fibers. These cells are responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and the subsequent ventricular muscle contraction. A few nodal cells in the ventricles also occasionally demonstrate automaticity, giving rise to ventricular beats or rhythms. (Ignatavicius 2013, pp. 711-713)

Front 120

electrocardiogram (ECG, EKG)

Back 120

The electrocardiogram (ECG) provides a graphic representation, or picture, of cardiac electrical activity. The cardiac electrical currents are transmitted to the body surface. Electrodes, consisting of a conductive gel on an adhesive pad, are placed on specific sites on the body and attached to cables connected to an ECG machine or to a monitor. The cardiac electrical current is transmitted via the electrodes and through the lead wires to the machine or monitor, which displays the cardiac electrical activity.

A lead provides one view of the heart's electrical activity. Multiple leads, or views, can be obtained. Electrode placement is the same for male and female patients.

Lead systems are made up of a positive pole and a negative pole. An imaginary line joining these two poles is called the lead axis. The direction of electrical current flow in the heart is the cardiac axis. The relationship between the cardiac axis and the lead axis is responsible for the deflections seen on the ECG pattern:
--The baseline is the isoelectric line. It occurs when there is no current flow in the heart after complete depolarization and also after complete repolarization. Positive deflections occur above this line, and negative deflections occur below it. Deflections represent depolarization and repolarization of cells.
--If the direction of electrical current flow in the heart (cardiac axis) is toward the positive pole, a positive deflection (above the baseline) is viewed (Fig. 36-2, A).
--If the direction of electrical current flow in the heart (cardiac axis) is moving away from the positive pole toward the negative pole, a negative deflection (below the baseline) is viewed (Fig. 36-2, B).
--If the cardiac axis is moving neither toward nor away from the positive pole, a biphasic complex (both above and below baseline) will result (Fig. 36-2, C). (Ignatavicius 2013, p. 713)

Front 121

electrocardiographic complexes, segments, and intervals

Back 121

Complexes that make up a normal ECG consist of a P wave, a QRS complex, a T wave, and possibly a U wave. Segments include the PR segment, the ST segment, and the TP segment. Intervals include the PR interval, the QRS duration, and the QT interval (Fig. 36-5).

The P wave is a deflection representing atrial depolarization. The shape of the P wave may be a positive, negative, or biphasic (both positive and negative) deflection, depending on the lead selected. When the electrical impulse is consistently generated from the sinoatrial (SA) node, the P waves have a consistent shape in a given lead. If an impulse is then generated from a different (ectopic) focus, such as atrial tissue, the shape of the P wave changes in that lead, indicating that an ectopic focus has fired.

The PR segment is the isoelectric line from the end of the P wave to the beginning of the QRS complex, when the electrical impulse is traveling through the atrioventricular (AV) node, where it is delayed. It then travels through the ventricular conduction system to the Purkinje fibers.

The PR interval is measured from the beginning of the P wave to the end of the PR segment. It represents the time required for atrial depolarization as well as the impulse delay in the AV node and the travel time to the Purkinje fibers. It normally measures from 0.12 to 0.20 second (five small blocks).

The QRS complex represents ventricular depolarization. The shape of the QRS complex depends on the lead selected. The Q wave is the first negative deflection and is not present in all leads. When present, it is small and represents initial ventricular septal depolarization. When the Q wave is abnormally present in a lead, it represents myocardial necrosis (cell death). The R wave is the first positive deflection. It may be small, large, or absent, depending on the lead. The S wave is a negative deflection following the R wave and is not present in all leads.

The QRS duration represents the time required for depolarization of both ventricles. It is measured from the beginning of the QRS complex to the J point (the junction where the QRS complex ends and the ST segment begins). It normally measures from 0.04 to 0.10 second (up to three small blocks).

The ST segment is normally an isoelectric line and represents early ventricular repolarization. It occurs from the J point to the beginning of the T wave. Its length varies with changes in the heart rate, the administration of medications, and electrolyte disturbances. It is normally not elevated more than 1 mm or depressed more than 0.5 mm from the isoelectric line. Its amplitude is measured at a point 1.5 to 2 mm after the J point. ST elevation or depression can be caused by myocardial injury, ischemia or infarction, conduction abnormalities, or the administration of medications.

The T wave follows the ST segment and represents ventricular repolarization. It is usually positive, rounded, and slightly asymmetric. If an ectopic stimulus excites the ventricles during this time, it may cause ventricular irritability, lethal dysrhythmias, and possible cardiac arrest in the vulnerable heart. This is known as the R-on-T phenomenon. T waves may become tall and peaked, inverted (negative), or flat as a result of myocardial ischemia, potassium or calcium imbalances, medications, or autonomic nervous system effects.

The U wave, when present, follows the T wave and may result from slow repolarization of ventricular Purkinje fibers. It is of the same polarity as the T wave, although generally it is smaller. It is not normally seen in all leads and is more common in lead V3. An abnormal U wave may suggest an electrolyte abnormality (particularly hypokalemia) or other disturbance. Correct identification is important so that it is not mistaken for a P wave. If in doubt, notify the health care provider and request that a potassium level be obtained.

The QT interval represents the total time required for ventricular depolarization and repolarization. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. This interval varies with the patient's age and gender and changes with the heart rate, lengthening with slower heart rates and shortening with faster rates. It may be prolonged by certain medications, electrolyte disturbances, Prinzmetal's angina, or subarachnoid hemorrhage. A prolonged QT interval may lead to a unique type of ventricular tachycardia called torsades de pointes.

Artifact is interference seen on the monitor or rhythm strip, which may look like a wandering or fuzzy baseline. It can be caused by patient movement, loose or defective electrodes, improper grounding, or faulty ECG equipment, such as broken wires or cables. Some artifact can mimic lethal dysrhythmias like ventricular tachycardia (with tooth brushing) or ventricular fibrillation (with tapping on the electrode). Assess the patient to differentiate artifact from actual lethal rhythms! Do not rely only on the ECG monitor. (Ignatavicius 2013, pp. 715-717)

Front 122

ECG rhythm analysis

Back 122

Analysis of an ECG rhythm strip requires a systematic approach using a six-step method facilitated by use of a measurement tool called an ECG caliper:

1 Determine the heart rate. If the atrial and ventricular rhythms are regular, use any of the methods previously described to calculate the heart rate. If the rhythms are irregular, use the 6-second strip method for accuracy. Normal heart rates fall between 60 and 100 beats/min. A rate less than 60 beats/min is called bradycardia. A rate greater than 100 beats/min is called tachycardia.

2 Determine the heart rhythm. Heart rhythms can be either regular or irregular. Irregular rhythms can be regularly irregular, occasionally irregular, or irregularly irregular. Check the regularity of the atrial rhythm by assessing the PP intervals, placing one caliper point on a P wave and placing the other point on the precise spot on the next P wave. Then move the caliper from P wave to P wave along the entire strip (“walking out” the P waves) to determine the regularity of the rhythm. P waves of a different shape (ectopic waves), if present, create an irregularity and do not walk out with the other P waves. A slight irregularity in the PP intervals, varying no more than three small blocks, is considered essentially regular if the P waves are all of the same shape. This alteration is caused by changes in intrathoracic pressure during the respiratory cycle.

Check the regularity of the ventricular rhythm by assessing the RR intervals, placing one caliper point on a portion of the QRS complex (usually the most prominent portion of the deflection) and the other point on the precise spot of the next QRS complex. Move the caliper from QRS complex to QRS complex along the entire strip (walking out the QRS complexes) to determine the regularity of the rhythm. QRS complexes of a different shape (ectopic QRS complexes), if present, create an irregularity and do not walk out with the other QRS complexes. A slight irregularity of no more than three small blocks between intervals is considered essentially regular if the QRS complexes are all of the same shape.

3 Analyze the P waves. Check that the P wave shape is consistent throughout the strip, indicating that atrial depolarization is occurring from impulses originating from one focus, normally the SA node. Determine whether there is one P wave occurring before each QRS complex, establishing that a relationship exists between the P wave and the QRS complex. This relationship indicates that an impulse from one focus is responsible for both atrial and ventricular depolarization. The nurse may observe more than one P wave shape, more P waves than QRS complexes, absent P waves, or P waves coming after the QRS, each indicating that a dysrhythmia exists. Ask these five questions when analyzing P waves:
--Are P waves present?
--Are the P waves occurring regularly?
--Is there one P wave for each QRS complex?
--Are the P waves smooth, rounded, and upright in appearance, or are they inverted?
--Do all the P waves look similar?

4 Measure the PR interval. Place one caliper point at the beginning of the P wave and the other point at the end of the PR segment. The PR interval normally measures between 0.12 and 0.20 second. The measurement should be constant throughout the strip. The PR interval cannot be determined if there are no P waves or if P waves occur after the QRS complex. Ask these three questions about the PR interval:
--Are PR intervals greater than 0.20 second?
--Are PR intervals less than 0.12 second?
--Are PR intervals constant across the ECG strip?

5 Measure the QRS duration. Place one caliper point at the beginning of the QRS complex and the other at the J point, where the QRS complex ends and the ST segment begins. The QRS duration normally measures between 0.04 and 0.10 second. The measurement should be constant throughout the entire strip. Check that the QRS complexes are consistent throughout the strip. When the QRS is narrow (0.10 second or less), this indicates that the impulse was not formed in the ventricles and is referred to as supraventricular or above the ventricles. When the QRS complex is wide (greater than 0.10 second), this indicates that the impulse is either of ventricular origin or of supraventricular origin with aberrant conduction, meaning deviating from the normal course or pattern. More than one QRS complex pattern or occasionally missing QRS complexes may be observed, indicating a dysrhythmia.

Ask these questions to evaluate QRS intervals:
--Are QRS intervals less than or greater than 0.12 second?
--Are the QRS complexes similar in appearance across the ECG paper?

6 Interpret the rhythm. Using steps 1 to 5, you can interpret the cardiac rhythm and differentiate normal and abnormal cardiac rhythms. (Ignatavicius 2013, p. 718)

Front 123

normal sinus rhythm

Back 123

Normal sinus rhythm (NSR) is the rhythm originating from the sinoatrial (SA) node (dominant pacemaker) that meets these ECG criteria (Fig. 36-7):
--Rate: Atrial and ventricular rates of 60 to 100 beats/min
--Rhythm: Atrial and ventricular rhythms regular
--P waves: Present, consistent configuration, one P wave before each QRS complex
--PR interval: 0.12 to 0.20 second and constant
--QRS duration: 0.04 to 0.10 second and constant

Sinus arrhythmia is a variant of NSR. It results from changes in intrathoracic pressure during breathing. In this context, the term arrhythmia does not mean an absence of rhythm, as the term suggests. Instead, the heart rate increases slightly during inspiration and decreases slightly during exhalation. This irregular rhythm is frequently observed in healthy children as well as adults.

Sinus arrhythmia has all the characteristics of NSR except for its irregularity. The PP and RR intervals vary, with the difference between the shortest and the longest intervals being greater than 0.12 second (three small blocks):
--Rate: Atrial and ventricular rates between 60 and 100 beats/min
--Rhythm: Atrial and ventricular rhythms irregular, with the shortest PP or RR interval varying at least 0.12 second from the longest PP or RR interval
--P waves: One P wave before each QRS complex; consistent configuration
--PR interval: Normal, constant
--QRS duration: Normal, constant

Sinus arrhythmias occasionally are due to nonrespiratory causes, such as digitalis or morphine. These drugs enhance vagal tone and cause decreased heart rate and irregularity unrelated to the respiratory cycle. (Ignatavicius 2013, pp. 718-719)

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dysrhythmias

Back 124

Any disorder of the heartbeat is called a dysrhythmia. Historically, the term arrhythmia has been used in the literature. Although the terms are often used interchangeably, dysrhythmia is more accurate. Dysrhythmias result from:
--A disturbance in the relationship between electrical conductivity and the mechanical response of the myocardium
--A disturbance in impulse formation (either from an abnormal rate or from an ectopic focus)
--A disturbance in impulse conduction (delays and blocks)
--The combination of several mechanisms

Although many dysrhythmias have no clinical manifestations, many others have serious consequences if not treated. A summary of key features is found in Chart 36-1.

Dysrhythmia Terminology

Tachydysrhythmias are heart rates greater than 100 beats per minute. They are a major concern in the adult patient with coronary artery disease (CAD). Coronary artery blood flow occurs mostly during diastole when the aortic valve is closed and is determined by diastolic time and blood pressure in the root of the aorta. Tachydysrhythmias are serious because they:
--Shorten the diastolic time and therefore the coronary perfusion time (the amount of time available for blood to flow through the coronary arteries to the myocardium).
--Initially increase cardiac output and blood pressure. However, a continued rise in heart rate decreases the ventricular filling time because of a shortened diastole, decreasing the stroke volume. Consequently, cardiac output and blood pressure will begin to decrease, reducing aortic pressure and therefore coronary perfusion pressure.
--Increase the work of the heart, increasing myocardial oxygen demand.

The patient with a tachydysrhythmia may have:
--Palpitations
--Chest discomfort (pressure or pain from myocardial ischemia or infarction)
--Restlessness and anxiety
--Pale, cool skin
--Syncope (“blackout”) from hypotension

Tachydysrhythmias may also lead to heart failure. Presenting symptoms of heart failure may include dyspnea, lung crackles, distended neck veins, fatigue, and weakness (see Chapter 37).

Bradydysrhythmias occur when the heart rate is less than 60 beats per minute. These rhythms can also be significant because:
--Myocardial oxygen demand is reduced from the slow heart rate, which can be beneficial.
--Coronary perfusion time may be adequate because of a prolonged diastole, which is desirable.
--Coronary perfusion pressure may decrease if the heart rate is too slow to provide adequate cardiac output and blood pressure; this is a serious consequence.

Therefore the patient may tolerate the bradydysrhythmia well if the blood pressure is adequate. If the blood pressure is not adequate, symptomatic bradydysrhythmias may lead to myocardial ischemia or infarction, dysrhythmias, hypotension, and heart failure.

Premature complexes are early rhythm complexes. They occur when a cardiac cell or cell group, other than the sinoatrial (SA) node, becomes irritable and fires an impulse before the next sinus impulse is produced. The abnormal focus is called an ectopic focus and may be generated by atrial, junctional, or ventricular tissue. After the premature complex, there is a pause before the next normal complex, creating an irregularity in the rhythm. The patient with premature complexes may be unaware of them or may feel palpitations or a “skipping” of the heartbeat. If premature complexes, especially those that are ventricular, become more frequent, the patient may experience symptoms of decreased cardiac output.

Premature complexes may occur repetitively in a rhythmic fashion:
--Bigeminy exists when normal complexes and premature complexes occur alternately in a repetitive two-beat pattern, with a pause occurring after each premature complex so that complexes occur in pairs.
--Trigeminy is a repeated three-beat pattern, usually occurring as two sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in triplets.
--Quadrigeminy is a repeated four-beat pattern, usually occurring as three sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in a four-beat pattern.

Such patterns may occur with atrial, junctional, or ventricular premature complexes. Patients may be unaware of the premature beats, or they may feel palpitations.

Classification of Dysrhythmias

Dysrhythmias are classified according to their site of origin. The sites include the SA node, atrial tissue, AV node, junctional tissue, and ventricular tissue. Dysrhythmias may be caused by a disturbance in impulse formation or by conduction delays or blocks. The incidence and the prevalence of dysrhythmias are not known because they usually result from an underlying condition, such as heart disease. This chapter is limited to the most common dysrhythmias and those that are potentially life threatening. (Ignatavicius 2013, pp. 719-720)

Front 125

sinus dysrhythmias

Back 125

The sinus node is the pacemaker in all sinus dysrhythmias. Innervation from sympathetic and parasympathetic nerves is normally in balance to ensure a normal sinus rhythm (NSR). An imbalance increases or decreases the rate of SA node discharge either as a normal response to activity or physiologic changes or as a pathologic response to disease. (Ignatavicius 2013, p. 720)

Front 126

sinus tachycardia

Back 126

Sympathetic nervous system stimulation or vagal (parasympathetic) inhibition results in an increased rate of SA node discharge, which increases the heart rate. When the rate of SA node discharge is more than 100 beats per minute, the rhythm is called sinus tachycardia (Fig. 36-8, A). Sinus tachycardia, with temporary heart rates of 200 to 220 beats per minute, may be normal in infants and children. The rate gradually decreases until age 10 years. From age 10 years to adulthood, the heart rate normally does not exceed 100 beats per minute except in response to activity, and then usually does not exceed 160 beats per minute. Rarely does the heart rate reach 180 beats per minute.

Sinus tachycardia initially increases cardiac output and blood pressure. However, continued increases in heart rate decrease coronary perfusion time, diastolic filling time, and coronary perfusion pressure while increasing myocardial oxygen demand.

Increased sympathetic stimulation is a normal response to physical activity but may also be caused by anxiety, pain, stress, fear, fever, anemia, hypoxemia, hyperthyroidism, and pulmonary embolism. Drugs such as epinephrine, atropine, caffeine, alcohol, nicotine, aminophylline, and thyroid medications may also increase the heart rate. In some cases, sinus tachycardia is a compensatory response to decreased cardiac output or blood pressure, as occurs in hypovolemic shock, myocardial infarction (MI), infection, and heart failure.

The patient may be asymptomatic except for an increased pulse rate. However, if the rhythm is not well tolerated, he or she may have symptoms.

The desired outcome is to decrease the heart rate to normal levels by treating the underlying cause. Teach the patient to remain on bedrest if the tachycardia is causing hypotension or weakness.

***Nursing Safety Priority Action Alert***

For patients with sinus tachycardia, assess for fatigue, weakness, shortness of breath, orthopnea, decreased oxygen saturation, and decreased blood pressure. Also assess for restlessness and anxiety from decreased cerebral perfusion and for decreased urine output from impaired renal perfusion. The patient may also have anginal pain and palpitations. The ECG pattern may show T-wave inversion or ST-segment elevation or depression in response to myocardial ischemia.

(Ignatavicius 2013, p. 720)

Front 127

sinus bradycardia

Back 127

Excessive vagal (parasympathetic) stimulation to the heart causes a decreased rate of sinus node discharge. It may result from carotid sinus massage, vomiting, suctioning, Valsalva maneuvers (e.g., bearing down for a bowel movement or gagging), ocular pressure, or pain. Increased parasympathetic stimuli may also result from hypoxia, inferior wall MI, and the administration of drugs such as beta-adrenergic blocking agents, calcium channel blockers, and digitalis.

The stimuli slow the heart rate and decrease the speed of conduction through the heart. When the sinus node discharge rate is less than 60 beats/min, the rhythm is called sinus bradycardia (Fig. 36-8, B). Sinus bradycardia increases coronary perfusion time, but it may decrease coronary perfusion pressure. However, myocardial oxygen demand is decreased. Well-conditioned athletes who are bradycardic have a hypereffective heart, in which the strong heart muscle provides an adequate stroke volume and a low heart rate to achieve a normal cardiac output.

The patient with sinus bradycardia may be asymptomatic except for the decreased pulse rate. At times, however, the rhythm may not be well tolerated. Assess the patient for:
--Syncope (“blackouts” or fainting)
--Dizziness and weakness
--Confusion
--Hypotension
--Diaphoresis (excessive sweating)
--Shortness of breath
--Chest pain

If the patient has any of these symptoms and the underlying cause cannot be determined, the treatment is to administer drug therapy, increase intravascular volume via IV fluids, and apply oxygen. If the heart rate does not increase sufficiently, pacing may be needed to increase the heart rate. (Ignatavicius 2013, pp. 720-721)

Front 128

atrial fibrillation

Back 128

Atrial fibrillation (AF) is the most common dysrhythmia seen in clinical practice. It impairs quality of life, causes considerable morbidity and mortality, and imposes a large economic burden on health care systems (Dagres & Anastasiou-Nana, 2010).

AF is associated with atrial fibrosis and loss of muscle mass. A mutation in the lamin AC (LMAC) gene has been linked to atrial fibrosis and dilation (Hardin & Steele, 2008). These structural changes are common in heart diseases such as hypertension, heart failure, and coronary artery disease. As AF progresses, cardiac output decreases by as much as 20 to 30 percent.

Currently, approximately 2.3 million people in the United States are diagnosed with AF; it is estimated that more than 12 million people will have AF by the year 2050 (Tedrow et al., 2010). The incidence of AF increases with age; AF causes serious problems in older people, leading to stroke and/or heart failure. Risk factors include hypertension (HTN), previous ischemic stroke, transient ischemic attack (TIA) or other thromboembolic event, coronary heart disease, diabetes mellitus, heart failure, and mitral valve disease (Holding et al., 2009).

In addition to advanced age, obesity, Caucasian race, and excessive alcohol have been identified as risk factors for AF (see the Evidence-Based Practice box on p. 727). About half of obese adults may develop AF (Chilukuri et al., 2010). Caucasians are more at risk for AF than African Americans and other ethnic groups, perhaps because of the larger left atrial diameter in Caucasians (Marcus et al., 2010). AF that is temporary and reversible is associated with excessive alcohol consumption (sometimes called holiday heart syndrome) (McDonough, 2009).

In patients with AF, multiple rapid impulses from many atrial foci depolarize the atria in a totally disorganized manner at a rate of 350 to 600 times per minute; ventricular response is usually 120 to 200 beats per minute. The result is a chaotic rhythm with no clear P waves, no atrial contractions, loss of atrial kick, and an irregular ventricular response (Fig. 36-9). The atria merely quiver in fibrillation (commonly called “A fib”). Often the ventricles beat with a rapid rate in response to the numerous atrial impulses. Heart dilation and blood pooling in the atria can lead to thrombus formation, and this increases the risk for stroke or other embolic events. The rapid and irregular ventricular rate decreases ventricular filling and reduces cardiac output, further impairing the heart's perfusion ability. (Ignatavicius 2013, p. 726)

Front 129

collaborative care
(a fib)

Back 129

AF may be intermittent or chronic. Symptoms depend on the ventricular rate. If the ventricular rate is rapid, the presenting symptoms may be similar to those described earlier for supraventricular tachycardia. Because of loss of atrial kick, however, the patient in uncontrolled AF is at greater risk for an inadequate cardiac output. Assess the patient for fatigue, weakness, shortness of breath, dizziness, anxiety, syncope, palpitations, chest discomfort or pain, and hypotension. Some patients may be asymptomatic.

The loss of coordinated atrial contractions in AF can lead to stagnation of blood resulting in thrombus formation. The patient is at risk for pulmonary embolism. Thrombi may form within the right atrium and then move through the right ventricle to the lungs. In addition, the patient is at risk for systemic emboli, particularly an embolic stroke, which may cause severe neurologic impairment or death. Patients with AF who have valvular disease are particularly at risk for venous thromboembolism (VTE). Monitor patients carefully for these complications (see Chapter 38).

Traditional interventions for AF include antidysrhythmic drugs to slow the ventricular conduction or to convert the AF to normal sinus rhythm (NSR). Examples of these drugs are calcium channel blockers like diltiazem (Cardizem) or, for more difficult-to-control AF, amiodarone (Cordarone). Dronedarone (Multaq) is a new drug similar to amiodarone, yet better tolerated by patients, for maintenance of sinus rhythm after cardioversion (Cheng, 2010). However, dronedarone should not be used in patients with a history or current congestive heart failure because it can cause an exacerbation of cardiac symptoms.

Beta blockers, such as metoprolol (Toprol, Dutoprol) and esmolol (Brevibloc), may also be used to slow ventricular response. Digoxin (Lanoxin, Novo-Digoxin ) is given for patients with heart failure and AF.

Anticoagulants, such as heparin, enoxaparin (Lovenox), and warfarin (Coumadin), may also be given for patients at high risk for emboli. Because of the unpredictable drug response, laboratory monitoring (e.g., international normalized ratio [INR]), and many food/drug interactions with warfarin, clinical trials are ongoing for newer, more effective medications (Garlitski & Estes, 2010). When taking warfarin, teach patients the importance of avoiding high vitamin K foods and avoiding herbs, such as ginger, ginseng, goldenseal, Ginkgo biloba, and St. John's wort, which could interfere with the drug's action. Chapter 38 describes anticoagulant therapy in detail on p. 800.

Because of the problems associated with warfarin, alternative anticoagulant agents may be given on a long-term basis to prevent strokes associated with AF. Examples include antiplatelet drugs, such as aspirin and clopidogrel (Plavix), or one of the newer direct thrombin inhibitors, such as dabigatran (Pradaxa). These drugs should be used cautiously in patients over 75 years of age due to their risk of falls (Sellers & Newby, 2011).

Cardioversion is the electrical treatment of choice when drugs are not effective. Before elective cardioversion, the health care provider prescribes anticoagulation therapy for about 6 weeks to prevent a thromboembolic event if the rhythm is successfully converted. To assess for the presence of atrial clots, a contraindication for cardioversion, the physician may order a transesophageal echocardiogram (TEE) before attempting emergency cardioversion (see Chapter 35). When AF has persisted more than 12 months, it is not likely to convert to a sinus rhythm by drug therapies and may fail to respond to electrical cardioversion, which is discussed on p. 737.

AF resistant to medical therapies may be treated with percutaneous radiofrequency catheter ablation. Pulmonary vein ablation creates scar tissue that blocks impulses and disconnects the pathway of the abnormal rhythm. The evidence indicates an increase in the number and complexity of catheter ablation procedures for AF. Data from 85 international centers indicated an 80% success rate defined as freedom from AF with or without drugs, and a complication rate of 4.5%. The United States is establishing the Safety of AF Ablation Registry Initiative to collect data that should be a valuable source of statistics on the safety and efficacy of AF ablation procedures (Garlitski & Estes, 2010). Patients with AF with a rapid ventricular rate not responsive to drug therapy may have AV nodal ablation performed to totally disconnect the conduction from the atria to the ventricles. However, this treatment requires implantation of a permanent ventricular pacemaker.

Bi-ventricular pacing may be another alternative for patients with heart failure and conduction disorders. Bi-atrial pacing, anti-tachycardia pacing, and implantable atrial defibrillators are other methods used to suppress or resolve AF. All of these methods are discussed on p. 733.

Patients in AF with heart failure (discussed in Chapter 37) may benefit from the surgical maze procedure, an open-chest surgical technique often performed with coronary artery bypass grafting (CABG). Before this procedure, electrophysiologic mapping studies are done to confirm the diagnosis of AF. The surgeon places a maze of sutures in strategic places in the atrial myocardium, pulmonary artery, and possibly the superior vena cava to prevent electrical circuits from developing and continuing AF. Sinus impulses can then depolarize the atria before reaching the AV node and preserve the atrial kick. Postoperative care is similar to that after other open-heart surgical procedures (see Chapter 40).

The catheter maze procedure is done by inserting a catheter through a leg vein into the atria and dragging a heated ablating catheter along the atria to create lines (scars) of conduction block. Patients having this minimally invasive form of the procedure have fewer complications, less pain, and a quicker recovery than those with the open, surgical maze procedure.

***Nursing Safety Priority Drug Alert***

Teach patients taking any type of anticoagulant drug to report bruising, bleeding nose or gums, and other signs of bleeding to their health care provider immediately. Also remind them to take aspirin with food to prevent GI distress.

(Ignatavicius 2013, pp. 726-728)

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ventricular dysrhythmias

Back 130

Ventricular Dysrhythmias

Ventricular dysrhythmias are potentially more life threatening than atrial dysrhythmias because the left ventricle pumps oxygenated blood throughout the body to perfuse vital organs and other tissues. The most common or life-threatening ventricular dysrhythmias include:
--Premature ventricular complexes
--Ventricular tachycardia
--Ventricular fibrillation
--Ventricular asystole
(Ignatavicius 2013, p. 728)

Front 131

premature ventricular complexes

Back 131

Premature Ventricular Complexes

Premature ventricular complexes (PVCs), also called premature ventricular contractions, result from increased irritability of ventricular cells and are seen as early ventricular complexes followed by a pause. When multiple PVCs are present, the QRS complexes may be unifocal or uniform, meaning that they are of the same shape (Fig. 36-10, A), or multifocal or multiform, meaning that they are of different shapes (Fig. 36-10, B). PVCs frequently occur in repetitive rhythms, such as bigeminy (two), trigeminy (three), and quadrigeminy (four). Two sequential PVCs are a pair, or couplet. Three or more successive PVCs are usually called nonsustained ventricular tachycardia (NSVT).

Premature ventricular contractions are common, and their frequency increases with age. They may be insignificant or may occur with problems such as myocardial infarction, chronic heart failure, chronic obstructive pulmonary disease (COPD), and anemia. PVCs may also be present in patients with hypokalemia or hypomagnesemia. Sympathomimetic agents, anesthesia drugs, stress, nicotine, caffeine, alcohol, infection, or surgery can also cause PVCs, especially in older adults. Postmenopausal women often find that caffeine causes palpitations and PVCs.

The patient may be asymptomatic or experience palpitations or chest discomfort caused by increased stroke volume of the normal beat after the pause. Peripheral pulses may be diminished or absent with the PVCs themselves because the decreased stroke volume of the premature beats may decrease peripheral perfusion.

If there is no underlying heart disease, PVCs are not usually treated other than by eliminating any contributing cause (e.g., caffeine, stress). With acute myocardial ischemia or MI, PVCs are managed by administering oxygen and amiodarone (Cordarone) as prescribed. Potassium is given for replacement therapy if hypokalemia is the cause. People with more than 5000 PVCs in a 24-hour period are usually placed on beta blockers.

***Nursing Safety Priority Action Alert***

Because other dysrhythmias can cause widened QRS complexes, assess whether the premature complexes perfuse to the extremities. Palpate the carotid, brachial, or femoral arteries while observing the monitor for widened complexes or auscultating apical heart sounds. With acute MI, PVCs may be considered as a warning, possibly triggering life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF).

(Ignatavicius 2013, p. 728)

Front 132

ventricular tachycardia

Back 132

Ventricular Tachycardia

Ventricular tachycardia (VT), sometimes referred to as “V tach,” occurs with repetitive firing of an irritable ventricular ectopic focus, usually at a rate of 140 to 180 beats/min or more (Fig. 36-11). VT may result from increased automaticity or a re-entry mechanism. It may be intermittent (nonsustained VT) or sustained, lasting longer than 15 to 30 seconds. The sinus node may continue to discharge independently, depolarizing the atria but not the ventricles, although P waves are seldom seen in sustained VT.

Ventricular tachycardia may occur in patients with ischemic heart disease, MI, cardiomyopathy, hypokalemia, hypomagnesemia, valvular heart disease, heart failure, drug toxicity, hypotension, or ventricular aneurysm. In patients who go into cardiac arrest, VT is commonly the initial rhythm before deterioration into ventricular fibrillation (VF) as the terminal rhythm!

Clinical manifestations of sustained VT partially depend on the ventricular rate. Slower rates are better tolerated.

Current Advanced Cardiac Life Support (ACLS) guidelines state that elective cardioversion is highly recommended for stable VT. The physician may prescribe an oral antidysrhythmic agent, such as mexiletine (Mexitil) or sotalol (Betapace, Sotacor ), to prevent further occurrences. Unstable VT without a pulse is treated the same way as ventricular fibrillation, described next.

***Nursing Safety Priority Critical Rescue***

In some patients, VT causes cardiac arrest. Assess the patient's airway, breathing, circulation, level of consciousness, and oxygenation level. For the stable patient with sustained VT, administer oxygen and confirm the rhythm via a 12-lead ECG. Amiodarone, lidocaine, or magnesium sulfate may be given.
(Ignatavicius 2013, pp. 728-729)

Front 133

ventricular fibrillation

Back 133

Ventricular fibrillation (VF), sometimes called “V fib,” is the result of electrical chaos in the ventricles and is life threatening! Impulses from many irritable foci fire in a totally disorganized manner so that ventricular contraction cannot occur. There are no recognizable ECG deflections (Fig. 36-12, A). The ventricles merely quiver, consuming a tremendous amount of oxygen. There is no cardiac output or pulse and therefore no cerebral, myocardial, or systemic perfusion. This rhythm is rapidly fatal if not successfully ended within 3 to 5 minutes.

VF may be the first manifestation of coronary artery disease (CAD). Patients with myocardial infarction (MI) are at great risk for VF. It may also occur in those with hypokalemia, hypomagnesemia, hemorrhage, antidysrhythmic therapy, rapid supraventricular tachycardia (SVT), or shock. Surgery or trauma may also cause VF.

Emergency Care: Ventricular Fibrillation

When VF begins, the patient becomes faint, immediately loses consciousness, and becomes pulseless and apneic (no breathing). There is no blood pressure, and heart sounds are absent. Respiratory and metabolic acidosis develop. Seizures may occur. Within minutes, the pupils become fixed and dilated and the skin becomes cold and mottled. Death results without prompt intervention.

The desired outcomes of collaborative care are to resolve VF promptly and convert it to an organized rhythm. Therefore the priority is to defibrillate the patient immediately according to ACLS protocol. If a defibrillator is not readily available, CPR must be continued until the defibrillator arrives. An automatic external defibrillator (AED) is frequently used because it is simple for both medical and lay personnel. Defibrillation is discussed on p. 737.

If the VF does not end after one defibrillator shock, the nurse and resuscitation team resume high-quality CPR and provide airway management. The team also gives oxygen and drug therapy, which could include vasopressin, epinephrine, amiodarone, lidocaine, and magnesium sulfate, alternating with defibrillation. If VF is successfully converted to an organized rhythm, supportive therapy is continued. (Ignatavicius 2013, pp. 729-730)

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ventricular asystole

Back 134

Ventricular asystole, sometimes called ventricular standstill, is the complete absence of any ventricular rhythm (Fig. 36-12, B). There are no electrical impulses in the ventricles and therefore no ventricular depolarization, no QRS complex, no contraction, no cardiac output, and no pulse, respirations, or blood pressure. The patient is in full cardiac arrest. The sinoatrial (SA) node, in some cases, may continue to fire and depolarize the atria, with only P waves seen on the ECG. The sinus impulses, however, do not conduct to the ventricles, and QRS complexes remain absent. In most cases, the entire conduction system is electrically silent, with no P waves seen on the ECG.

Ventricular asystole usually results from myocardial hypoxia, which may be a consequence of advanced heart failure. It may also be caused by severe hyperkalemia and acidosis. If P waves are seen, asystole is likely because of severe ventricular conduction blocks.

Emergency Care: Ventricular Asystole

The expected outcome of treatment is to restore cardiac electrical activity.

Collaborate with the resuscitation team to manage the airway and administer oxygen, epinephrine, and atropine. The prognosis for patients with asystole is poor. Health care providers should consider ending resuscitation efforts if there is no response after standard interventions have been implemented and when cessation is approved by an authorized physician.

An emerging clinical practice is allowing or encouraging family presence at resuscitation attempts. This can be a positive experience for family members and significant others because it promotes closure after the death of a loved one. Although there may be staff resistance and some limits to family presence, overall it is a beneficial practice that should be considered in all resuscitation attempts.

***Nursing Safety Priority Critical Rescue***

If asystole occurs, call for assistance and begin high-quality CPR immediately (unless there is a do-not-resuscitate [DNR] order). Check another ECG lead to ensure the rhythm is asystole and not fine VF, which requires immediate defibrillation. Do NOT shock asystole! (Ignatavicius 2013, pp. 730-731)

Front 135

assessment
(dysrhythmia)

Back 135

Patients may or may not realize they have a dysrhythmia, and some patients who have a dysrhythmia may be asymptomatic. Therefore assessment of the patient's past and current history is essential because dysrhythmias are associated with acute and chronic health problems and medical/surgical therapies. Assessment also includes taking vital signs and placing the patient on an ECG monitor. Continuous monitoring of the patient's ECG rhythm is needed to assess for manifestations associated with dysrhythmias, such as abnormal pulse rate and rhythm, palpitations, chest pain, syncope, decreased blood pressure, and dyspnea. When these manifestations are present, the patient is “symptomatic.” Assessment findings were discussed earlier in this chapter for each specific type of dysrhythmia.

It is also important to assess the psychosocial impact of dysrhythmias on patients and families and the effectiveness of their coping skills. Patients with any type of dysrhythmia are often very anxious and fearful that their heart will stop functioning. (Ignatavicius 2013, p. 731)

Front 136

interventions
(dysrhythmia)

Back 136

The nurse's major priority for care is to assess for complications and monitor the patient for response to treatment (Chart 36-3). Interventions are specific to the type of dysrhythmia, the cause, the effect it has on cardiac output, and the risk it presents to the patient.

Assess the patient's apical and radial pulses for a full minute for any irregularity, which may occur with problems such as premature beats, atrial fibrillation (AF), and second-degree heart blocks. If the apical pulse rate differs from the radial pulse rate, a pulse deficit exists and suggests that the heart is not pumping adequately to perfuse the body. Clinical manifestations of sustained tachydysrhythmias and bradydysrhythmias are summarized in Chart 36-1. Review the interpretation of the patient's 12-lead ECG and other diagnostic assessment. (Ignatavicius 2013, pp. 731-732)

--Assess vital signs at least every 4 hours and as needed.
--Monitor patient for cardiac dysrhythmias.
--Evaluate and document the patient's response to dysrhythmias.
--Encourage the patient to notify the nurse when chest pain occurs.
--Assess chest pain (e.g., location, intensity, duration, radiation, and precipitating and alleviating factors).
--Assess peripheral circulation (e.g., palpate for presence of peripheral pulses, edema, capillary refill, color, and temperature of extremity).
--Provide antidysrhythmic therapy according to unit policy (e.g., antidysrhythmic medication, cardioversion, or defibrillation), as appropriate.
--Monitor and document patient's response to antidysrhythmic medications or interventions.
--Monitor appropriate laboratory values (e.g., cardiac enzymes, electrolyte levels).
--Monitor the patient's activity tolerance and schedule exercise/rest periods to avoid fatigue.
--Observe for respiratory difficulty (e.g., shortness of breath, rapid breathing, labored respirations).
--Promote stress reduction.
--Offer spiritual support to the patient and/or family (e.g., contact clergy), as appropriate. (Ignatavicius 2013, p. 731)

Front 137

drug therapy
(dysrhythmia)

Back 137

Drug therapy for dysrhythmias often includes those from one or more classes of antidysrhythmic agents (see Chart 36-2). The Vaughn-Williams classification is commonly used to categorize drugs according to their effects on the action potential of cardiac cells (classes I though IV). Other drugs also have antidysrhythmic effects but do not fit the Vaughn-Williams classification.

Class I antidysrhythmics are membrane-stabilizing agents used to decrease automaticity. The three subclassifications in this group include type IA drugs, which moderately slow conduction and prolong repolarization, prolonging the QT interval. These drugs are used to treat or to prevent supraventricular and ventricular premature beats and tachydysrhythmias, but they are not as commonly used as other drugs. An example is procainamide hydrochloride (Pronestyl). Type IB drugs shorten repolarization. These drugs are used to treat or prevent ventricular premature beats, ventricular tachycardia (VT), and ventricular fibrillation (VF). Examples include lidocaine and mexiletine hydrochloride (Mexitil). Type IC drugs markedly slow conduction and widen the QRS complex. These agents are used primarily to treat or to prevent recurrent, life-threatening ventricular premature beats, VT, and VF. Examples include flecainide acetate (Tambocor) and propafenone hydrochloride (Rythmol).

Class II antidysrhythmics control dysrhythmias associated with excessive beta-adrenergic stimulation by competing for receptor sites and thereby decreasing heart rate and conduction velocity. Beta-adrenergic blocking agents, such as propranolol (Inderal) and esmolol hydrochloride (Brevibloc), are class II drugs. They are used to treat or to prevent supraventricular and ventricular premature beats and tachydysrhythmias. Sotalol hydrochloride (Betapace, Sotacor ) is an antidysrhythmic agent with both non-cardioselective beta-adrenergic blocking effects (class II) and action potential duration prolongation properties (class III). It is an oral agent that may be used for the treatment of documented ventricular dysrhythmias, such as VT, that are life threatening.

Class III antidysrhythmics lengthen the absolute refractory period and prolong repolarization and the action potential duration of ischemic cells. Class III drugs include amiodarone (Cordarone) and ibutilide (Corvert) and are used to treat or prevent ventricular premature beats, VT, and VF.

Class IV antidysrhythmics slow the flow of calcium into the cell during depolarization, thereby depressing the automaticity of the sinoatrial (SA) and atrioventricular (AV) nodes, decreasing the heart rate, and prolonging the AV nodal refractory period and conduction. Calcium channel blockers, such as verapamil hydrochloride (Calan, Isoptin ) and diltiazem hydrochloride (Cardizem), are class IV drugs. They are used to treat supraventricular tachycardia (SVT), atrial flutter, and atrial fibrillation (AF) to slow the ventricular response.

Other drugs, such as digoxin, atropine, adenosine, and magnesium sulfate, may be used to treat dysrhythmias. Digoxin (Lanoxin, Novodigoxin ) increases vagal tone, slowing AV nodal conduction. It is useful in treating chronic AF by controlling the rate of ventricular response. However, digoxin does not convert AF to sinus rhythm. Atropine is a parasympatholytic or vagolytic agent used to treat vagally-induced symptomatic bradydysrhythmias. Adenosine is an endogenous nucleoside that slows AV nodal conduction to interrupt re-entry pathways. Magnesium sulfate is an electrolyte administered to treat refractory VT or VF because these patients may be hypomagnesemic, with increased ventricular irritability. The drug is also used for a life-threatening VT called torsades de pointes that can result from certain antidysrhythmics, such as amiodarone.

In addition to antidysrhythmics, several other drugs are used during cardiac arrest (Chart 36-4). Epinephrine (Adrenalin) is usually a first-line agent in all cardiac arrests. It is given mainly for its alpha-adrenergic effects to increase vasomotor tone for myocardial and cerebral perfusion. Its beta-adrenergic effects may stimulate the heart and increase myocardial contractility to improve cardiac output. Recent evidence suggests that epinephrine may be problematic during cardiopulmonary resuscitation because the alpha-adrenergic actions caused an increase in cerebral ischemia (Ristagno et al., 2009). Another study by Grigoriyan et al. (2009) found poorer survival rates for patients who received vasopressors before cardiac arrest. Vasopressin has potent vasoconstricting effects and is equivalent to epinephrine in VF and pulseless VT. It has a long half-life and is given one time as an IV bolus of 40 units. Dopamine hydrochloride (Intropin) is generally used for its beta-adrenergic effects after cardiac arrest but may be used for its alpha-adrenergic effects during resuscitation. Dobutamine hydrochloride (Dobutrex) is a beta-adrenergic agent used to improve myocardial contractility and increase cardiac output.

Norepinephrine (Levophed) or phenylephrine hydrochloride (Neo-Synephrine) may be used for its alpha-adrenergic effects to increase vasomotor tone and increase perfusion pressure. Sodium bicarbonate, along with regular insulin and calcium chloride, may be administered during cardiac arrest for patients who are hyperkalemic. It may also be used, if necessary, to treat a documented base deficit metabolic acidosis, as occurs in diabetic ketoacidosis or tricyclic antidepressant overdose. In addition to hyperkalemia, calcium chloride is given for hypocalcemia or calcium channel blocker toxicity because the conditions may cause cell damage and cerebrovascular vasospasm. Isoproterenol (Isuprel) is indicated to increase the heart rate in heart transplant patients, but pacing is preferred. (Ignatavicius 2013, pp. 732-734)

Front 138

vagal maneuvers

Back 138

Vagal maneuvers induce vagal stimulation of the cardiac conduction system, specifically the SA and AV nodes. Although not as common today, vagal maneuvers may be attempted to treat supraventricular tachydysrhythmias and include carotid sinus massage and Valsalva maneuvers. The results of these interventions, however, are often temporary and may cause “rebound” tachycardia or severe bradycardia. Further therapy must be initiated.

In carotid sinus massage, the physician massages over one carotid artery for a few seconds, observing for a change in cardiac rhythm. This intervention causes vagal stimulation, slowing SA and AV nodal conduction. Prepare the patient for the procedure, instruct him or her to turn the head slightly away from the side to be massaged, and observe the cardiac monitor for a change in rhythm. An ECG rhythm strip is recorded before, during, and after the procedure. After the procedure, assess vital signs and the level of consciousness. Complications include bradydysrhythmias, asystole, VF, and cerebral damage. Because of these risks, carotid massage is not commonly performed. A defibrillator and resuscitative equipment must be immediately available during the procedure.

To stimulate a vagal reflex, the health care provider instructs the patient to bear down as if straining to have a bowel movement. Assess the patient's heart rate, heart rhythm, and blood pressure; observe the cardiac monitor; and record an ECG rhythm strip before, during, and after the procedure to determine the effect of therapy. (Ignatavicius 2013, p. 734)

Front 139

pacemaker

Back 139

An invasive temporary pacemaker system consists of an external battery-operated pulse generator and pacing electrodes, or lead wires. These wires attach to the generator on one end and are in contact with the heart on the other end (Fig. 36-13). Electrical pulses, or stimuli, are emitted from the negative terminal of the generator, flow through a lead wire, and stimulate the cardiac cells to depolarize. The current seeks ground by returning through the other lead wire to the positive terminal of the generator, thus completing a circuit. The intensity of electrical current is set by selecting the appropriate current output, measured in milliamperes.

Patients do not usually feel invasive pacemaker stimuli. However, they occasionally feel an uncomfortable sensation from the stimuli if strong electrical currents (high milliamperage) are delivered by the pacemaker. The discomfort may be alleviated by decreasing the generator current if possible (Fig. 36-14).

Monitor for these complications of invasive temporary pacing, which may be serious and include:

• Infection or hematoma at the pacemaker wire insertion site

• Ectopic complexes (usually premature ventricular complexes [PVCs]) caused by irritability from the pacing wire in the ventricle, use of high current, or undersensing with pacemaker competition

• Loss of capture, noted by the presence of a pacing stimulus or spike but no QRS complex

• Undersensing or pacemaker competition, noted when pacing stimuli occur at a fixed rate in the presence of an adequate intrinsic rhythm

• Oversensing, noted when the pacemaker fails to fire in the presence of an inadequate intrinsic rhythm

• Electromagnetic interference, noted by altered generator variables

• Stimulation of the chest wall or diaphragm, noted by rhythmic contraction of the chest wall muscles or hiccups with the use of high current or from lead wire perforation, which could cause cardiac tamponade (Ignatavicius 2013, pp. 735-736)
Ignatavicius, Workman. (2013). Medical-Surgical Nursing: Patient-Centered Collaborative Care, 7th Edition. W.B. Saunders Company. Retrieved from <vbk:978-1-4377-2801-9#outline(45.6.3.1)>.

Front 140

cardioversion

Back 140

Cardioversion is a synchronized countershock that may be performed in emergencies for unstable ventricular or supraventricular tachydysrhythmias or electively for stable tachydysrhythmias that are resistant to medical therapies. If the patient has been taking digoxin, the drug is withheld for up to 48 hours before an elective cardioversion. Digoxin increases ventricular irritability and puts the patient at risk for VF after the countershock. For elective cardioversion for atrial flutter or fibrillation, the patient must take anticoagulants for 4 to 6 weeks before the procedure to prevent clots from moving from the heart to the brain or lungs.

The shock depolarizes a large amount of myocardium during the cardiac depolarization. It is intended to stop the re-entry circuit and allow the sinus node to regain control of the heart. Emergency equipment must be available during the procedure. The physician, advanced practice nurse, or other qualified nurse explains the procedure to the patient and family. Assist the patient in signing a consent form unless the procedure is an emergency for a life-threatening dysrhythmia. Because he or she is usually conscious, a short-acting anesthetic agent should be administered for sedation.

One electrode is placed to the left of the precordium, and the other is placed on the right next to the sternum and below the clavicle. The defibrillator should be set in the synchronized mode. This avoids discharging the shock during the T wave, which may increase ventricular irritability, causing ventricular fibrillation (VF). Charge the defibrillator to the energy level requested, usually starting at a low rate.

After cardioversion, assess the patient's response and heart rhythm. Therapy is repeated, if necessary, until the desired result is obtained or alternative therapies are considered. If the patient's condition deteriorates into VF after cardioversion, check to see that the synchronizer is turned off so that immediate defibrillation can be administered.

Nursing care after cardioversion includes:
--Maintaining a patent airway
--Administering oxygen
--Assessing vital signs and the level of consciousness
--Administering antidysrhythmic drug therapy, as prescribed
--Monitoring for dysrhythmias
--Assessing for chest burns from electrodes
--Providing emotional support
--Documenting the results of cardioversion

***Nursing Safety Priority Critical Rescue***

For safety before cardioversion, turn oxygen off and away from patient; fire could result. Shout “CLEAR” before shock delivery for electrical safety!
(Ignatavicius 2013, p. 738)

Front 141

defibrillation

Back 141

Defibrillation, an asynchronous countershock, depolarizes a critical mass of myocardium simultaneously to stop the re-entry circuit, allowing the sinus node to regain control of the heart.

Continue effective CPR until a defibrillator is available. The defibrillator is charged to 120 to 200 joules (biphasic) or 360 joules (monophasic) for one countershock from the defibrillator. Before defibrillation, loudly and clearly command all personnel to clear contact with the patient and the bed and check to see they are clear before the shock is delivered. Resume CPR immediately after the shock, and continue CPR for 5 cycles or about 2 minutes. Then reassess the rhythm, and if VF or pulseless VT continues, charge the defibrillator to give a second shock at the same energy level previously used. Resume CPR after the shock, and continue with the ACLS protocol. Nursing care for defibrillation is the same as for cardioversion. (Ignatavicius 2013, p. 738)

Front 142

implantable cardioverter/defibrillator (ICD)

Back 142

The implantable cardioverter/defibrillator (ICD) is indicated for patients who have experienced one or more episodes of spontaneous sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) not caused by an MI. Collaborate with the physician and the electrophysiology nurse to prepare the patient for this procedure. A psychological profile is done to determine whether the patient can cope with the discomfort and fear associated with internal defibrillation from the ICD. Many patients report anxiety, depression, and decreased quality of life, which dissipates for the majority of patients after 12 months (Hallas et al., 2010).

The leads of the device are introduced through the skin, and the generator is implanted in the left pectoral area, similar to a permanent pacemaker insertion procedure. This procedure is performed in the electrophysiology laboratory. If ICD therapies are not successful and the patient remains in VF or pulseless VT, the qualified nurse or health care provider must promptly externally defibrillate.

The generator may be activated or deactivated by the physician placing a magnet over the implantation site for a few moments. The patient requires close monitoring in the postoperative period for dysrhythmias and complications such as bleeding and cardiac tamponade. The nurse must know whether the ICD is activated or deactivated. Care of the patient is similar to that after implantation of a permanent pacemaker.

Some patients use a lightweight, automatic wearable cardioverter/defibrillator (WCD), approved since 2002. This external vest-like device is worn 24 hours a day except when the patient showers or bathes. One popular brand is the Zoll Lifecor LifeVest, which is programmed to monitor ventricular tachycardia (VT) and ventricular fibrillation (VF). If the patient is conscious while experiencing VT, he or she can press a button to prevent a shock. This precaution is an advantage over implantable devices because ICDs are programmed to always deliver a shock when VT or VF occurs (Morrison & Smith, 2009).

When external chest compressions and ACLS measures are unsuccessful in resuscitating the patient in cardiac arrest, the physician may perform open-chest cardiac massage using a thoracotomy or sternotomy approach in post–cardiac surgery patients. Internal defibrillation may also be performed. This procedure is a drastic measure that frequently results in devastating consequences for the patient and is therefore used as a last resort. (Ignatavicius 2013, p. 739)

Front 143

shock

Back 143

A continuous supply of oxygen is needed by all organs, tissues, and cells to function properly. The lungs first bring oxygen into the body, and the cardiovascular system (heart, blood, and blood vessels) delivers oxygen to all tissues and removes cellular wastes (Fig. 39-1). Shock is widespread abnormal cellular metabolism that occurs when oxygenation and tissue perfusion needs are not met to the level necessary to maintain cell function (McCance et al., 2010). It is a condition rather than a disease and represents the “whole-body” response that occurs when too little oxygen is delivered to the tissues. All body organs are affected by shock and either work harder to adapt and compensate for reduced oxygenation (see Fig. 39-1) or fail to function because of hypoxia. Shock is a “syndrome” because the cellular, tissue, and organ events occur in a predictable sequence.

Any problem that impairs oxygen delivery to tissues and organs can start the syndrome of shock and lead to a life-threatening emergency. Most often, shock is a result of cardiovascular problems and changes. Patients in acute care settings are at higher risk, but shock can occur in any setting. For example, older patients in long-term care settings are at risk for sepsis and shock related to urinary tract infections. When the body's adaptive adjustments (compensation) or health care interventions are not effective and shock progresses, severe hypoxia can lead to cell loss, multiple organ dysfunction syndrome (MODS), and death.

Shock is classified by the functional impairment it causes into the categories of hypovolemic shock, cardiogenic shock, distributive shock (which includes septic shock, neurogenic shock, and anaphylactic shock), and obstructive shock. Table 39-1 describes the functional impairment classification and common causes of shock.

Most manifestations of shock are similar regardless of what starts the process or which tissues are affected first. These common manifestations result from physiologic adjustments (compensatory mechanisms) in the attempt to ensure continued oxygenation of vital organs. These adjustment actions are performed by the sympathetic nervous system, triggering the stress response and activating the endocrine and cardiovascular systems. Manifestations unique to any one type of shock result from specific tissue dysfunction. (Ignatavicius 2013, p. 810)

Front 144

manifestations
(shock)

Back 144

Cardiovascular Manifestations
--Decreased cardiac output
--Increased pulse rate
--Thready pulse
--Decreased blood pressure
--Narrowed pulse pressure
--Postural hypotension
--Low central venous pressure
--Flat neck and hand veins in dependent positions
--Slow capillary refill in nail beds
--Diminished peripheral pulses

Respiratory Manifestations
--Increased respiratory rate
--Shallow depth of respirations
--Increased PaCO2
--Decreased PaO2
--Cyanosis, especially around lips and nail beds

Neuromuscular Manifestations
Early
--Anxiety
--Restlessness
--Increased thirst
Late
--Decreased central nervous system activity (lethargy to coma)
--Generalized muscle weakness
--Diminished or absent deep tendon reflexes
--Sluggish pupillary response to light

Kidney Manifestations
--Decreased urine output
--Increased specific gravity
--Sugar and acetone present in urine

Integumentary Manifestations
--Cool to cold
--Pale to mottled to cyanotic
--Moist, clammy
--Mouth dry; pastelike coating present

Gastrointestinal Manifestations
--Decreased motility
--Diminished or absent bowel sounds
--Nausea and vomiting
--Constipation

PaCO2, Partial pressure of arterial carbon dioxide; PaO2, partial pressure of arterial oxygen. (Ignatavicius 2013, p. 811)

Front 145

types of shock

Back 145

Types of shock and their causes vary because shock is a manifestation of a pathologic condition rather than a disease state (see Table 39-1). More than one type of shock can be present at the same time. For example, trauma caused by a car crash may trigger hemorrhage (leading to hypovolemic shock) and a myocardial infarction (leading to cardiogenic shock).

Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease, resulting in inadequate total body oxygenation. Common problems leading to hypovolemic shock are hemorrhage and dehydration. A complete discussion of the pathophysiology and management of hypovolemic shock begins on p. 812.

Cardiogenic shock occurs when the actual heart muscle is unhealthy and pumping is directly impaired. Myocardial infarction is the most common cause of direct pump failure (Held & Sturtz, 2009). Other causes are listed in Table 39-1. Any type of pump failure decreases cardiac output and MAP. Chapter 40 discusses the pathophysiology and care for the person with cardiogenic shock from myocardial infarction.

Distributive shock occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot circulate and deliver oxygen. It can be caused by a loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, and increased capillary leak. All these factors can decrease mean arterial pressure (MAP) and may be started by nerve changes (neural-induced) or the presence of some chemicals (chemical-induced).

Neural-induced distributive shock is a loss of MAP that occurs when sympathetic nerve impulses controlling blood vessel smooth muscle are decreased and the smooth muscles relax, causing vasodilation. This blood vessel dilation can be a normal local response to injury, but shock results when vasodilation is widespread (King & Olson, 2007). Problems leading to loss of sympathetic tone are listed in Table 39-1.

Chemical-induced distributive shock has three common origins: anaphylaxis, sepsis, and capillary leak syndrome. It occurs when certain body chemicals or foreign substances in the blood and vessels start widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside the body), but this type of shock also can be induced by substances normally found in the body (endogenous), such as excessive amounts of the mediator histamine.

Anaphylaxis is one result of type I allergic reactions. It begins within seconds to minutes after exposure to a specific allergen in a susceptible person. The result is widespread loss of blood vessel tone and decreased cardiac output. Table 22-2 (in Chapter 22) lists common allergens that can cause anaphylaxis. Chapter 22 describes the pathophysiology, prevention, and care of the patient with anaphylactic shock.

Sepsis is a widespread infection that triggers a whole-body inflammatory response. It leads to distributive shock when infectious microorganisms are present in the blood. This form of shock is most commonly called septic shock. A complete discussion of the pathophysiology, prevention, and collaborative care for the patient with sepsis and septic shock begins on p. 819.

Capillary leak syndrome is the response of capillaries to the presence of biologic mediators that change blood vessel integrity and allow fluid to shift from the blood vessels into the interstitial tissues. Once in the interstitial tissue, these fluids are stagnant and cannot deliver oxygen or remove tissue waste products. Fluid shifts result from increased size of capillary pores, loss of plasma osmolarity, and increased hydrostatic pressure in the blood. Problems causing fluid shifts include severe burns, liver disorders, ascites, peritonitis, paralytic ileus, severe malnutrition, large wounds, hyperglycemia, kidney disease, hypoproteinemia, and trauma.

Obstructive shock is caused by problems that impair the ability of the normal heart muscle to pump effectively. The heart itself remains normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. The most common causes of obstructive shock are pericarditis and cardiac tamponade (see Table 39-1). Care of the person with cardiac tamponade is presented in detail in Chapter 37 (pericarditis) and Chapter 40 (as a complication after cardiac bypass graft surgery).

Although the causes and initial manifestations associated with the different types of shock vary, eventually the effects of hypotension and anaerobic cellular metabolism (metabolism without oxygen) result in the common key features of shock (Ignatavicius 2013, pp. 811-812)

Front 146

stages of shock

Back 146

The syndrome of shock progresses in four stages when the conditions that cause shock remain uncorrected and poor cellular oxygenation continues. These stages are:

1 Initial stage

2 Nonprogressive stage

3 Progressive stage

4 Refractory stage

The stages are defined on the basis of how well compensatory mechanisms are working, the severity of the clinical manifestations, and whether tissue damage is reversible.

Initial Stage of Shock (Early Stage)

The initial (early) stage of shock is present when the patient's baseline MAP is decreased by less than 10 mm Hg. During this stage, compensatory mechanisms are so effective at returning systolic pressure to normal that oxygenated blood flow to vital organs is maintained. The cellular change in this stage is increased anaerobic metabolism with production of lactic acid, although overall metabolism is still aerobic. The compensation responses of vascular constriction and increased heart rate are effective, and both cardiac output and MAP are maintained within the normal range. Because vital organ function is not disrupted, the manifestations of shock are difficult to detect. A heart and respiratory rate increased from the patient's baseline level or a slight increase in diastolic blood pressure may be the only objective manifestation of this early stage of shock.

Nonprogressive Stage of Shock (Compensatory Stage)

The nonprogressive (compensatory) stage of shock occurs when MAP decreases by 10 to 15 mm Hg from baseline. Kidney and hormonal compensatory mechanisms are activated because cardiovascular responses alone are not enough to maintain MAP and supply oxygen to vital organs.

The kidneys and baroreceptors sense an ongoing decrease in MAP and trigger the release of renin, antidiuretic hormone (ADH), aldosterone, epinephrine, and norepinephrine to start kidney compensation. Renin, secreted by the kidney, causes decreased urine output, increased sodium reabsorption, and widespread blood vessel constriction (see Fig. 13-6 in Chapter 13). ADH increases water reabsorption in the kidney, further reducing urine output, and also causes blood vessel constriction in the skin and other less vital tissue areas. Together these actions compensate for shock by maintaining the fluid volume within the central blood vessels.

Tissue hypoxia occurs in nonvital organs (e.g., skin, GI tract) and in the kidney, but it is not great enough to cause permanent damage. Because some metabolism is anaerobic, acid-base and electrolyte changes occur in response to the buildup of metabolites. Changes include acidosis (low blood pH) and hyperkalemia (increased blood potassium level).

Manifestations of the nonprogressive stage of shock include both subjective and objective changes resulting from decreased tissue perfusion. Subjective changes include thirst and anxiety. Objective changes include restlessness, tachycardia, increased respiratory rate, decreased urine output, falling systolic blood pressure, rising diastolic blood pressure, narrowing pulse pressure, cool extremities, and a 2% to 5% decrease in oxygen saturation measured by pulse oximetry. Comparing these changes with the values and manifestations obtained earlier is critical to identifying this stage of shock.

If the patient is stable and compensatory mechanisms are supported by medical and nursing interventions, he or she can remain in this stage for hours without having permanent damage. Stopping the conditions that started the shock at this stage and providing supportive interventions can prevent the shock from progressing. The cellular effects of this stage are reversible when nurses recognize the problem and coordinate with the health care team to start appropriate interventions (Mattiace, 2008; Stricker, 2010).

Progressive Stage of Shock (Intermediate Stage)

The progressive stage of shock occurs when there is a sustained decrease in MAP of more than 20 mm Hg from baseline. In this stage, compensatory mechanisms are functioning but can no longer deliver sufficient oxygen, even to vital organs. Vital organs develop hypoxia, and less vital organs become anoxic (no oxygen) and ischemic (cell dysfunction or death from lack of oxygen). As a result of poor oxygenation and a buildup of toxic metabolites, some tissues have severe cell damage and die.

Manifestations of the progressive stage of shock include a worsening of subjective and objective changes resulting from decreased tissue perfusion. Continuous monitoring and comparison with earlier findings are critical to assess therapy effectiveness. Subjective changes include severe thirst sensation and deeper anxiety. The patient may express a sense of “something bad” (impending doom) about to happen. He or she may seem confused. Objective changes are a rapid, weak pulse; low blood pressure; pallor to cyanosis of oral mucosa and nail beds; cool and moist skin; anuria; and a 5% to 20% decrease in oxygen saturation. Laboratory data at this stage may show a low blood pH, along with rising lactic acid and potassium levels.

The progressive stage of shock is a life-threatening emergency. Vital organs can tolerate this situation for only a short time before being damaged permanently. Immediate interventions are needed to reverse the effects of this stage of shock. Tolerance varies from person to person and depends on age and health. The patient's life usually can be saved if the conditions causing shock are corrected within 1 hour or less of the onset of the progressive stage.

Refractory Stage of Shock (Irreversible Stage)

The refractory stage or irreversible stage of shock occurs when too much cell death and tissue damage result from too little oxygen reaching the tissues. Vital organs have overwhelming damage. The body can no longer respond effectively to interventions, and shock continues. Therapy is not effective in saving the patient's life, even if the cause of shock is corrected and MAP temporarily returns to normal. So much tissue damage has occurred with widespread release of toxic metabolites and enzymes that cell damage in vital organs continues despite aggressive interventions. Manifestations are a rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation. (Ignatavicius 2013, pp. 813-815)

Front 147

hypovolemic shock

Back 147

The basic problem of hypovolemic shock is a loss of blood volume from the vascular space, resulting in a decreased mean arterial pressure (MAP) (see Fig. 39-2) and a loss of oxygen-carrying capacity from the loss of circulating red blood cells (RBCs). The reduced MAP slows blood flow, resulting in decreased tissue perfusion. The loss of RBCs decreases the ability of the blood to oxygenate the tissue it does reach. These oxygenation and perfusion problems lead to cellular anaerobic (without oxygen) conditions and abnormal cellular metabolism.

The main trigger leading to hypovolemic shock is a sustained decrease in MAP that results from decreased circulating blood volume. A decrease in MAP of 5 to 10 mm Hg below the patient's normal baseline value is detected by pressure-sensitive nerve receptors (baroreceptors) in the aortic arch and carotid sinus. This information is transmitted to brain centers, which stimulate adjustments (compensatory mechanisms) that help ensure continued blood flow and oxygen delivery to vital organs while limiting blood flow to less vital areas. The movement of oxygenated blood into selected areas while bypassing others (“shunting”) results in some shock manifestations.

If the events that caused the initial decrease in MAP are halted now, compensatory mechanisms provide adequate oxygenation and perfusion without outside intervention. If the initiating events continue and MAP decreases further, some tissues function under anaerobic conditions. This condition increases lactic acid levels and other harmful metabolites (e.g., protein-destroying enzymes, oxygen free radicals). These substances cause electrolyte and acid-base imbalances with tissue-damaging effects and depressed heart muscle activity. These effects are temporary and reversible if the cause of shock is corrected within 1 to 2 hours after onset. When shock conditions continue for longer periods without help, the resulting acid-base imbalance, electrolyte imbalances, and increased metabolites cause so much cell damage in vital organs that multiple organ dysfunction syndrome (MODS) occurs and recovery from shock is no longer possible. Table 39-2 summarizes the responses during the progression of shock. (Ignatavicius 2013, pp. 812-813)

Etiology

Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease that prevents total body oxygenation. Common problems leading to hypovolemic shock are hemorrhage (external or internal) and dehydration.

Hypovolemic shock from external hemorrhage is common after trauma and surgery. Hypovolemic shock from internal hemorrhage occurs with blunt trauma, GI ulcers, and poor control of surgical bleeding. Hemorrhage also can be caused by any problem that reduces the levels of clotting factors (see Table 39-1). Hypovolemia as a result of dehydration can be caused by any problem that decreases fluid intake or increases fluid loss (see Table 39-1).

Incidence/Prevalence

The exact incidence of hypovolemic shock is not known because it is a response rather than a disease. It is a common complication among hospitalized patients in emergency departments and after surgery or invasive procedures.

Health Promotion and Maintenance

Hypovolemic shock from most causes can be prevented. Teach all people to prevent dehydration by having an adequate fluid intake during exercise and when in hot, dry environments. Urge people to prevent trauma and hemorrhage by using proper safety equipment and seat belts and being aware of hazards in the home or workplace.

Secondary prevention of hypovolemic shock is a major nursing responsibility. Keep in mind that just being a patient in the acute care setting is a risk factor. Identify patients at risk for dehydration, and assess for early manifestations. This is especially important for those who have reduced cognition or reduced mobility or who are on NPO status.

Assess all patients who have invasive procedures or trauma for obvious or occult bleeding. Compare pulse quality and rate with baseline. Compare urine output with fluid intake. Check vital signs for patients who have persistent thirst. Assess for shock in any patient who develops a change in mental status, an increase in pain, or an increase in anxiety. (Ignatavicius 2013, p. 815)

Front 148

interventions
(hypovolemic shock)

Back 148

Medical and nursing interventions for patients in hypovolemic shock focus on reversing the shock, restoring fluid volume to the normal range, and preventing complications through supportive and drug therapies. Monitoring is critical to determine whether the patient is responding to therapy or whether shock is progressing and a change in intervention is needed. Surgery may be needed to correct the cause of shock.

Best Practice for Patient Safety & Quality Care

The Patient in Hypovolemic Shock
--Ensure a patent airway.
--Start an IV catheter, or maintain an established catheter.
--Administer oxygen.
--Elevate the patient's feet, keeping his or her head flat or elevated to no more than a 30-degree angle.
--Examine the patient for overt bleeding.
--If overt bleeding is present, apply direct pressure to the site.
vAdminister drugs as prescribed.
--Increase the rate of IV fluid delivery.
--Do not leave the patient. (Ignatavicius 2013, pp. 817-818)

Front 149

septic shock

Back 149

Septic shock is the stage of sepsis and SIRS when multiple organ failure is evident and uncontrolled bleeding occurs (see Fig. 39-4). Even with appropriate intervention, the death rate among patients in this stage of sepsis exceeds 50% (Toussaint & Gerlach, 2009). Severe hypovolemic shock and hypodynamic cardiac function are present as a result of an inability of the blood to clot because the platelets and clotting factors were consumed earlier. Capillary leak continues and cardiac contractility is poor from cellular ischemia. The clinical manifestations resemble the late stage of hypovolemic shock.

Etiology

The major cause of sepsis is a bacterial infection that escapes local control, although in immunocompromised patients, fungal infections also cause sepsis. Common organisms causing sepsis include gram-negative bacteria (Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae) and gram-positive bacteria (Staphylococcus and Streptococcus). Table 39-4 lists some of the health problems that increase the risk for sepsis and septic shock.

Incidence/Prevalence

Sepsis and septic shock are common events in the United States. More than 750,000 cases occur annually and result in over 200,000 deaths. Although sepsis management has improved, the incidence is increasing as a result of more drug-resistant organisms and the fact that patients are discharged from the hospital “quicker and sicker.” Sepsis takes time to develop, and the patient may be discharged before manifestations are obvious.

Health Promotion and Maintenance

Prevention is the best management strategy for sepsis and septic shock. Evaluate all patients for their risk for sepsis, especially older adults, because the death rate from sepsis in people older than 65 years is nearly twice that of younger adults (El Solh et al., 2008). Table 39-4 lists some of the health problems that increase the risk for septic shock. Use aseptic technique during invasive procedures and when working with nonintact skin and mucous membranes in immunocompromised patients. Remove indwelling urinary catheters and IV access lines as soon as they are no longer needed.

Early detection of sepsis before progression to septic shock is a major nursing responsibility. Because sepsis can be a complication of many conditions found in acute care settings, always consider its possibility. Assess vital signs often (at least twice per shift) for changes from baseline levels. Review laboratory data for changes in serum lactate levels, in total white blood cell (WBC) count, and in the differential. The hallmark of sepsis is an increasing serum lactate level, a normal or low total WBC count, and a decreasing segmented neutrophil level with a rising band neutrophil level. This change is called a left shift (see Chapter 19).

Early detection can be made by patients and families, as well as health care personnel. This is especially important for patients discharged to home after invasive procedures or surgery. Teach patients the manifestations of local infection (local redness, pain, swelling, purulent drainage, loss of function) and of early sepsis (fever, urine output less than intake, light-headedness). Teach them how to use a thermometer and to take the temperature twice a day and whenever they are not feeling well. Urge those with symptoms of early sepsis to immediately contact their health care provider. Teach them that if antibiotics are prescribed, to take these drugs as prescribed and to complete the entire course. (Ignatavicius 2013, p. 822)

Front 150

interventions
(septic shock)

Back 150

Interventions for sepsis and septic shock focus on identifying the problem as early as possible, correcting the conditions causing it, and preventing complications. The use of a sepsis resuscitation bundle for treatment of sepsis is the standard of practice. A bundle is a group of two or more specific interventions that have been shown to be effective when applied together or in sequence. The sepsis resuscitation and management bundles are presented in Table 39-6.

Oxygen therapy is useful whenever poor tissue perfusion and poor oxygenation are present. Oxygen is delivered in the same ways as for hypovolemic shock. However, the patient with septic shock is more likely to be mechanically ventilated. Care of the patient being mechanically ventilated is discussed in detail in Chapter 34.

Drug therapy to enhance cardiac output and restore vascular volume is essentially the same as that used in hypovolemic shock (see Chart 39-4). In addition, drug therapy is needed to combat sepsis, adrenal insufficiency, hyperglycemia, and clotting problems.

Although septic shock can be caused by any organism, the most common agents are gram-negative bacteria. IV antibiotics with known activity against gram-negative bacteria are given before organisms are identified, preferably within 1 hour of a sepsis diagnosis. Multiple drugs with wide activity are prescribed, based on the site of infection and the most common geographic infections, until the actual causative organism is known. Drugs and drug categories commonly used for septic shock include vancomycin, aminoglycosides, systemic penicillin or cephalosporins, macrolides, and quinolones.

The stress of severe sepsis can cause adrenal insufficiency. Adrenal support involves providing the patient with low-dose corticosteroids during the treatment period for at least 7 days. Drugs used for this purpose are IV hydrocortisone and oral fludrocortisone (Florinef).

Patients with sepsis or septic shock usually have elevated blood glucose levels (>150 mg/dL), which is associated with a poor outcome. Insulin therapy is used to maintain blood glucose levels as close to normal as possible (80 to 110 mg/dL) or at least lower than 150 mg/dL.

During severe sepsis, patients have microvascular abnormalities and form many small clots. Heparin therapy has been used to limit clotting and to prevent the consumption of clotting factors. Additional therapy involves the use of activated protein C to manage microvascular abnormalities and prevent bleeding.

Synthetic activated protein C has been shown to stop the inflammatory responses during sepsis, preventing small clot formation and halting the progression of the disorder before septic shock occurs. Drotrecogin alfa (Xigris) is given as a continuous infusion over 4 days in patients who are considered at high risk for death. The drug has many serious complications and, because it disrupts clotting activity, is not given to patients with other bleeding problems. In addition, the drug is very expensive, with a single dose costing over $7000.

Blood replacement therapy is used when hemorrhage occurs and may include clotting factors, fresh frozen plasma (FFP), whole blood, or packed red blood cells. Chapter 42 discusses in detail the care of the patient during blood replacement. (Ignatavicius 2013, pp. 825-826)

Front 151

anaphylactic shock

Back 151

Anaphylaxis, the most dramatic and life-threatening example of a type I hypersensitivity reaction, occurs rapidly and systemically. It affects many organs within seconds to minutes after allergen exposure. Anaphylaxis is not common, although the incidence appears to be rising along with the general increase in the incidence of allergic reactions. The episodes can vary in severity, and it can be fatal. The major factor in fatal outcomes for anaphylaxis is a delay in the administration of epinephrine (Walker et al., 2010; Watson, 2010; White, 2010). Many substances can trigger anaphylaxis in a susceptible person (Table 22-2). Drugs and dyes are more common causes of anaphylaxis in acute care settings; food and insect stings/bites are more common causes of anaphylaxis in community settings.

Health Promotion and Maintenance

Anaphylaxis has a rapid onset and a potentially fatal outcome (even with appropriate medical intervention); thus prevention is critical. Teach the patient with a history of allergic reactions to avoid allergens whenever possible, to wear a medical alert bracelet, and to alert health care personnel about specific allergies. Some patients must carry an emergency anaphylaxis kit (e.g., a kit with injectable epinephrine, sometimes called a “bee sting kit”) or an epinephrine injector, such as the EpiPen or Twinject automatic injector. The EpiPen device is a spring-loaded injector that delivers 0.3 mg of epinephrine per 2-mL dose (Fig. 22-2). Teach patients who have been prescribed the device how to care for and use it (Chart 22-1).

The medical records of patients with a history of anaphylaxis should prominently display the list of specific allergens. Ask the patient about drug allergies before giving any drug or therapeutic agent. If he or she has a known allergy, be sure to document this response in the medical record and communicate the allergy to other members of the health care team. Skin tests should be performed before giving any substance that has a high incidence of causing anaphylactic reactions, such as iodine-containing dyes. Be aware of common cross-reacting agents. For example, a patient who is allergic to penicillin is also likely to react to cephalosporins because both have a similar chemical structure. People who have an allergy to bananas, avocados, and some nuts are more likely to have a latex allergy, although this is not universal. (Ignatavicius 2013, pp. 387-388)

Front 152

interventions
(anaphylactic shock)

Back 152

Assess respiratory function first. Emergency respiratory management is critical during an anaphylactic reaction, because the severity of the reaction increases with time. Not only can the upper airway be affected, but also bronchoconstriction of the lower airways can quickly impair airflow and lead to hypoxemic arrest. Immediately establish or stabilize the airway. If an IV drug is suspected to be causing the anaphylaxis, stop the drug immediately but do not remove the venous access because restarting an IV may be very difficult if the patient experiences a rapid decline in blood pressure. Instead, change the IV tubing and hang normal saline. More emergency interventions for patients with anaphylaxis are listed in Chart 22-3.

The patient with anaphylaxis is usually anxious or frightened and often expresses a sense of impending doom. Stay with the patient and reassure him or her that the appropriate interventions are being instituted.

Epinephrine (1:1000) 0.3 to 0.5 mL is the first-line drug for anaphylaxis. It is given IM or IV when symptoms of anaphylaxis appear (see Chart 22-3). This drug constricts blood vessels, improves cardiac contraction, and dilates the bronchioles. The same dose may be repeated every 5 minutes if needed.

*Best Practice for Patient Safety & Quality Care*

Emergency Care of the Patient with Anaphylaxis
--Immediately assess the respiratory status, airway, and oxygen saturation of patients who show any symptom of an allergic reaction.
--Call the Rapid Response Team.
--Ensure that intubation and tracheotomy equipment is ready.
--Apply oxygen using a high-flow, non-rebreather mask at 90% to 100%.
--Immediately discontinue the IV drug of a patient having an anaphylactic reaction to that drug. Do not discontinue the IV, but change the IV tubing and hang normal saline.
--If the patient does not have an IV, start one immediately and run normal saline.
--Be prepared to administer epinephrine IV or IM.
----Epinephrine 1:1000 concentration, 0.3 to 0.5 mL IV push
----Repeat as needed every 5 minutes until the patient responds
--Keep the head of the bed elevated about 10 degrees if hypotension is present; if blood pressure is normal, elevate the head of the bed to 45 degrees or higher to improve ventilation.
--Raise the feet and legs.
--Stay with the patient.
--Reassure the patient that the appropriate interventions are being instituted. (Ignatavicius 2013, pp. 389-390)

Front 153

cardiogenic shock

Back 153

Class IV heart failure is cardiogenic shock. In cardiogenic shock, necrosis of more than 40% of the left ventricle occurs. Most patients have a stuttering pattern of chest pain, resulting in piecemeal extension of the MI.

***Nursing Safety Priority Critical Rescue***

Monitor for, report, and document manifestations of cardiogenic shock immediately. These signs and symptoms include:
--Tachycardia
--Hypotension
--BP less than 90 mm Hg or 30 mm Hg less than the patient's baseline
--Urine output less than 30 mL/hr
--Cold, clammy skin with poor peripheral pulses
--Agitation, restlessness, or confusion
--Pulmonary congestion
--Tachypnea
--Continuing chest discomfort

Early detection is essential because diagnosed cardiogenic shock has a high mortality rate! (Ignatavicius 2013, p. 843)