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120 Cards in this Set
- Front
- Back
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The severity of bleeding when dealing with an upper GI bleed depends upon whether the origin is venous, arterial, or capillary. Bleeding from arterial is profuse, and the blood is bright red, which indicates that it has not been in contact with the stomach’s acid. If the blood is black and tarry (melena) it means that it has taken a long time for the blood to make its way through the intestines, meaning an upper GI bleed
Most bleeding ulcers are related to the presence of H. pylori or drug use. Immediate vitals and baselines need to be created. The case and treatment methods can be explored and discussed after the initial emergency care is given. Pulse, cap refill, respiratory rate, BP, and symptoms of shock are all vital Epinephrine can be a vital tool in saving this person’s life. Capillay and Venous- slow oozing Arterial- squirting |
common etiology, clinical manifestations, collaborative care, and nursing management of upper GI bleeding
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usually a result of sever retching or vomiting. The tear occurs in the esophageal mucosa at the junction of the esophagus and stomach and results in bleeding. This is an upper GI bleed, so the blood does not become black or discolored.
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Mallory-Weiss tear
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Superficial; smooth margins; round, oval, or cone shaped
Predominately antrum, also in body and fundus of stomach Normal to decreased gastric secretion 1 Greater in women 2 Peak age 50-60 3 More common in persons of lower socioeconomic status 4 Increased w/ smoking, drug, and alcohol 5 Increased with incompetent pyloric schincter and bile reflux 6 Increased with stress ulcers after burns, head trauma, and major surgery 12 Burning or gaseous pressure in high left epigastrum and back and upper abdomen 13 Pain 1-2 hrs. after meals; if penetrating ulcer, aggravation of discomfort w food 14 Occasional nausea and vomiting, weight loss 18 High recurrance rate 20 complications: Hemorrhage, perforation, outlet obstruction, intractability |
Duodenal ulcers
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Penetrating (associated with deformity of duodenal bulb from healing of recurrent ulcers)
First 1-2 cm of duodenum Increased gastric secretion 7 Greater in men, hppns to women postmenopausal 8 Peak age 35-45 9 Psychological stress 10 Increased with drug, smoking, alcohol use 11 Associated with other diseases: COPD, Pancreatic disease, hyperparathyroidism 15 Burning, cramping, pressure like pain across midepigastric and upper abdomen; back pain w/ posterior ulcers 16 Pain 2-4 hr after meals and midmorning, midafternoon, middle of night, periodic and episodic 17 Pain relief with antacids and food; occasional nausea and vomit 19 High incidence rate complications:21 Hemorrhage, perforation, obstruction |
gastric ulcers
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Etiology and Pathophysiology
Predisposing factors Hiatal hernia Incompetent lower esophageal sphincter (LES) Decreased esophageal clearance Decreased gastric empyting Acidic gastric secretions reflux and cause irritation and inflammation Clinical Manifestations Heartburn Burning Tight sensation felt beneath the lower sternum and spreads upward Heartburn occurring more than once a week, becomes more severe, or occurs at night and wakes a person from sleep should be evaluated by a health care professional May also report: Wheezing, Coughing, Dyspnea, Hoarseness, Sore Throat, Lump in Throat, or Choking Regurgitation is common Described as hot, bitter, or sour liquid coming into the mouth or throat Gastric symptoms Early satiety, postemal bloating, nausea, and vomiting Related to delayed gastric emptying Diagnostic Studies Barium swallow Endoscopy Biopsy and cytologic specimens to differentiate carcinoma from Barrett’s esophagus Esophageal manometric studies Collaborative Care Lifestyle modifications Nutritional therapy Decreases high-fat foods, avoid milk at night Drug Therapy H2 receptor blockers Proton pump inhibitors Antacids Sucralfate Prokinetic drugs Nursing Management Avoid factors that cause reflux Stop smoking, avoid acid or acid producing foods Elevate HOB 30 Do not lie down 2 to 3 hrs after eating Patient teaching Drug therapy Evaluate effectiveness Observe for side effects |
clinical manifestations, treatments for, and nursing management of GERD?
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Are frequently used to manage peptic ulcer disease. Block the action of histamine of the H2 receptor and thus reduce HCL acid secretion. Decreases conversion of pepsinogen to pepsin.
Cimetidine (Tagamet) Ranitidine (Zantac) Famotidine (Pepcid) Nizatidine (Axid) |
Histamine-2 receptor blockers
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Omeprazole (Prilosec)
Lansoprazole (Prevacid) Esomeprazole (Nexium) Pantoprazole (Protonix) Block ATPase enzymes that Is important for the blockers in reducing gastric acid secretion and promoting ulcer healing. PPI’s are also used in combination with antibiotics to treat ulcers caused by H. pylori |
PPI
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Sucralfate (Carafate)
These drugs protect the esophagus, stomach, and duodenum. The way this drug works is that it creates a protective barrier that does not allow for erosion from pepsin, acid, or bile salts. |
Cytoprotective
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Misoprostol (Cytotec)
This drug has some antisecretory effects on gastric mucosa. This drug does not interfere with the therapeutic effects of NSAID’s and Aspirin |
Antisecretory and Cytoprotective
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Identify patients at risk
Early detection and decrease morbidity Encourage patients to take ulcerogenic drugs with food or milk Physical and emotional rest are conductive to ulcer healing Have a careful diet that promotes healing: non-spicy food, avoid alcohol, and other things of that nature |
patient education is important for peptic ulcer disease
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This occurs when there is a large influx of fluid and other stuff that is too much for the small intestine to deal with.
Direct result of surgical removal of large portion of stomach and pyloric sphincter Decreases reservoir capacity of stomach Associated with meals having a hyperosmolar composition Experienced by 1/3 to ½ of patients after peptic ulcer surgery |
dumping syndrome
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is the presence of a productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded
It is excessive production of mucous in the bronchi accompanied by a recurrent cough. (1) hyperplasia of mucous-secreting glands (2) increase in goblet cells; (3) disappearance of cilia; (4) chronic inflammatory changes and narrowing of small airways; (5) altered function of alveolar macrophages, leading to increased bronchial infections Polycythemia Bronchospasms Dyspnea Collaborative Care Oxygen therapy |
chronic bronchitis
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is an abnormal permanent enlargement of the airspaces distal to the terminal bronchioles.
Structural changes in emphysema include: (1) hyperinflation of alveoli, (2) destruction of alveolar walls; (3) destruction of alveolar capillary walls; (4) narrowed, tortuous, small airways; (5) loss of lung elasticity clincal manifestation:Dyspnea Minimal coughing Flattened Diaphragm Hypoxemia collaborative care: oxygen therapy |
emphysema
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Smoking is the number one cause of all lung diseases
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cigarette smoking and chronic lung disease
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Oxygen therapy, not overdoing activity, having treatments around in case of an acute exacerbation. That kind of stuff. It wasn’t listed in the book really. Inhalers, STOP SMOKING
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nursing management of the patient with chronic bronchitis and emphysema.
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Raises PO2 in inspired air
Treats hypoxemia Classified as high or low-flow systems Simple face mask for oxygen administration Humidification is commonly used because O2 can be drying Nebs provide humidified oxygen |
indications for O2 therapy,
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Nasal cannula
Regular Oxygen conserving Reservoir cannula Store oxygen in a small reservoir during exhalation and can reduce flow requirements by 50% Encourage patient to remain as active as possible |
delivery system for O2
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Chest x-rays early in the disease may not show abnormalilites
History and physical exam Pulmonary function studies Spirometry Typical findings include reduced FEV/FVC and increased residual volume and total lung capacity Ratio of <70% suggests presence of obstructive lung disease ABGs Decreased Pa02 Increased PaCO2 Decreased pH Increased Bicarbonate level found in late stages COPD Exercise test to determine oxygen saturation in the blood and pulse oximetry ECG can show signs of right ventricular failure |
diagnostic results of a person with COPD
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Postural drainage
Uses gravity to assist in bronchial drainage Drainage positions are determined by involved areas of lung Percussion Performed in the appropriate postural drainage position Hands in a cup-like position, creating an air pocket between the patient’s chest and the hand Hollow sound should be heard with flexion and extension of the wrist Facilitates movement of thick mucous Should not be performed over kidneys, sternum, spinal cord, or any tender area Vibration Tensing the hand and arm muscles repeatedly Pressing mildly with the flat of the hang on the affected area while the patient slowly exhales a deep breath Facilitates movement of secretions of larger airways Mild vibrations tolerated better than percussion |
actions are indicated to promote airway clearance for the patient with COPD
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Breathing retraining
Pursed lip breathing Prolongs exhalation and prevents bronchiolar collapse and air trapping Diaphragmatic breathing -Focuses on using diaphragm instead of accessory muscles to achieve maximum inhalation and slow respiratory rate -Can be achieved by assuming semi-Fowler’s position and placing one hang on the abdomen and the other on the chest and observing which moves Effective coughing Huff coughing Can easily be taught May help clear secretions ineffective coughing patterns do not Chest physiotherapy Postural drainage Percussion Vibration Helps bring secretion into larger, more central airways |
copd
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Impaired gas exchange related to alveolar hypoventilation as manifested by headache on awakening, PaCO2 ≥ 45 mm HG and abnormal for patient’s baseline, PaO2 <60 mm Hg, or SaO2 < 90% at rest.
Subjective Data: Long term exposure to chemical pollution, respiratory irritants, occupational fumes, dust; recurrent respiratory infections; previous hospitalizations, medications, smoking, family history of respiratory disease, anorexia, weight loss or gain, fatigue, inability to perform ADLs; palpitations, swelling of feet; progressive dyspnea, especially on exertion; wheezing; recurrent cough; sputum production with changes in color, odor, viscosity, amount; orthopnea, constipation, gas, bloating Objective Data: Rapid shallow breathing; inability to speak; prolonged expiratory phase;pursed-lip breathing; wheezing; rhonchi, crackles, use of accessory muscles; tachycardia, arrhythmias, right-sided S3 (cor pumonale), ascites, ↑ anteroposterior diameter (barrel-chest), abnormal ABG’s |
assessment findings indicate impaired gas exchange in a person with COPD
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Role of O2 therapy related to COPD is the treat the hypoxemia cause by the low levels of oxygen in the blood. It is also used to decrease the work load of heart and to decrease the work of breathing
- Delivery methods depend on the Factors of Inspired air, (FIO2), mobility, comfort, and patient cooperation. à Can be low flow (NC, face tent, face mask) or high flow (venturi mask) Complications include CO2 narcosis (receiving high amounts of O2 may decrease the patients drive to breath) and O2 toxicity (high concentrations may inactivate the pulmonary surfactant and lead to the development of ARDS) |
Role of O2 therapy in the management of COPD
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Class- Beta adrenergic agonist/ bronchodilator
àRoute of Admission- Nebulizer, oral tab àMech. of Action- Selectively stimulates Beta 2 receptors, relaxes smooth muscle producing bronchodilation àSide effects- Tachycardia, nervousness, N/V, hypokalemia, hypotension, bronchospasm |
albuterol
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Class- anticholenergic, bronchodilator
à Route of Admission- Nebulizer, MDI à Mech. of Action- Inhibits interaction of acetylcholine at receptor sites on bronchial smooth muscle. à Side effects- palpitation, anxiety, N/V, cough, bronchospasm |
Ipratroprium
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Class- bronchodilator
à Route of Admission- PO à Mech. of Action- unknown, relaxes smooth muscle of respiratory system by blocking phosphodiesterase which increases cAMP à Side effects- seizures, muscle twitching, sinus tachycardia, hypotension, tachypnea, increase resp. rate |
Aminophylline
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Class- spasmolytic
à Mech of Action- relaxes smooth muscle of respiratiory system by blocking phosphodiesterase. à Side effects- N/V, anxiety, seizures, tremors, palpitations, increased resp. rate, hyperglycemia. à Route of Admission- PO |
Theophylline
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(inhaled) (475, L 649)
àAction- decrease inflammation by inhibiting mast cells macrophages, and leukotrienes. Anti inflammatory and vasoconstrictor properties àRole- to decrease the inflammation and decrease congestion related to allergies; has immunosuppressive effects. Decreases edema in bronchial airways |
Fluticasone
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àAction- decrease inflammation by the suppression of migration of polymorphonuclear leukocytes
à Role- decreases edema in bronchial airways, decrease mucus secretion; has inflammatory and immunosuppressive effects. Because IV, it produces systemic side effects taking away from the therapeutic actions |
Methylprednisone (IV)
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Action, decrease inflammation and capillary permeability
à Oral corticosteroids are indicated for treatment of acute asthma. |
prednisone-oral
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used to decrease inflammation in order to make breathing easier
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Corticosteroids
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is the enlargement of the right ventricle and secondary to diseases of lung, thorax, and pulmonary circulation; follows preexisting condition- pulmonary HTN
àWhen a patient has , it is not the primary issue. The initial cause of right sided heart failure and is chronic hypoxemia causing polycythemia and an increase in total blood volume and viscosity. treated by treating the primary pulmonary problem. Low flow, long term O2 is used to correct the hypoxemia and to reduce the vasoconstriction. Fluid, e-lyte, and acid- base imbalances must be corrected. |
Cor Pulmonale
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à Clinical manifestations- dyspnea, chronic productive cough, wheezy respirations, substernal pain, fatigue.
may be triggered by an acute respiratory tract infection. à If heart failure accompanies may have peripheral edema, weight gain, distended neck veins, bounding pulse, and an enlarged liver. |
Cor Pulmonale
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is targeted by first treating the condition that caused it initially; usually a pulmonary problem.
à Low flow O2 is used to correct the hypoxemia and decrease the vasoconstriction in chronic states of respiratory disorders. à Diuretics and low Na+ diets will help decrease the plasma volume and load on the heart. à If the problem is obstructive, bronchodilator therapy is used |
Collaborative care for Cor Pulmonale
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is an infection of the endocardial surface of the heart (innermost layer; pericardium = outermost). Occurs when blood flow turbulence within the heart allows the causative organism (usually bacteria) to infect previously damaged valves or surfaces.
Principal risk factors: cardiac lesion, prosthetic valve, acquired valvular disease, mitral valve prolapse, prior endocarditis. - previously rheumatic heart disease was most common cause. Also r/t IV drug use, aging (people tend to undergo more invasive procedures), Increased survival of children with congenital heart disease |
Infective Endocarditis
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check serum antibiotic level periodically
- check blood cultures to assess effectiveness of antibiotics - arthralgia is common (check ROM/muscle tenderness) - check temperature often… infection |
nursing priorities for infective endocarditis
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accurate identification of the infecting organism is key
Tx of Streptococcal endocarditis - IV or IM Rocephin; IV/IM ceftriaxone + gentamicin; IV/IMceftriaxone followed by oral amoxicillin Antibiotic prophylaxis is recommended for patients with nonspecific cardiac conditions before dental/surgical procedures (resp. tract, GI, GU) or increased risk p/t who is to have drainage of infective tissue, an indwelling cardiac pacemaker, dialysis or a shunt. |
antibiotic therapy for infective endocarditis
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The hallmark finding in acute pericarditis is the pericardial friction rub (a scratching, grating, high-ptiched sound).
However, ECG changes are key diagnostic clues and evolve over hours, days, to weeks. ST segment changes are present in all ECG leads except Vr and Vi (MI involves only localized ST segment changes) See pg 894 for detailed EGC explination |
Most useful serial diagnostic marker for pericarditis
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CT develops as the pericardial effusion increases in size and occurs because of an increase in intrapericardial pressure cause by fluid accumulation in the pericardial space: result is compression of the heart
speed of fluid accumulation affects severity of clinical manifestations P/t is often confused, agitated, restless Tachycardia/Tachypena Neck veins are markedly distended b/c of jugular venous pressure elevation Significant pulsus paradoxus is present * P/t with slow onset of CT my only have dyspnea |
Major s/s of cardiac tamponade
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an inspiratory drop in systolic drop in systolic BP > 10 mm Hg
- Take BP as normal - Deflate cuff slowly until systolic sounds are heard on expiration, note pressure - Deflate cuff until systolic sounds are heard thru-out the respiratory cycle, note pressure. - Determine difference eg. – Sound heart at expiration 110 mm Hg Sound heard thru-out cycle 82 mm Hg -------------------- Amt. of paradox 28 mm Hg See Table 36-10 for clarification |
Pulsus paradoxus
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* This is considered a primary nursing considering (including p/t anxiety)
The pain and inflammation of acute pericarditis are usually treated with NSAID’s (Indocin) or high dose Salicylates (300-900 mg orally 4x daily) Assessment of amount, quality, location of pain is important Maintain bed rest and bed elevated at 45 degrees Provide padded overbed table for p/t to lean on |
Interventions by nurse to ease pain associated with pericarditis
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important to assess valvular, congenital, or syphilitic cardiac disease (including valve repair or replacement), previous endocarditis, childbirth, staphylococcal or streptococcal infections, nosocomial bactreremia. IT is also important to note any immunosuppressent therapy medications and recent obstetric or gynecologic procedures, invasive techniques including catherization, cystoscopy, intravascular procedures and recent dental or surgical procedure. As far as functional health patterns one would note IV drug abuse, alcohol abuse, malaise, wt. gain or los, chills, diaphoresis, bloody urine, exercise intolerance, generalized weakness, fatigue, cough, dyspnea on exertion, orthopnea, palpitations, night sweats, chest back or abdominal pain, headache, joint tenderness and muscle tenderness. Thats the history- as far as objective data goes- see table 36-7 on page 890. (most importantly Osler nodes, Janeway's lesions, fever, tachypenia)
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hx. of patients with infective endocarditis
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important to note recent beta-hemolytic streptococcal infection, previous rheumatic fever or rheumatic heart disease. As far as functional health patterns go, one would look for family history, malaise, anorexia, weight loss, palpitations, weakness, fatigue, ataxia, chest pain, abdominal pain, migratory joint pain and tenderness- especially large joints. Thats the history- see table 36-15 on page 899 for objective data. (most importantly ployarthritis, chorea, erythma marginatum, subcutaneous nodules, chorea, polyarthritis)
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hx. of patients with rheumatic heart disease
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A person who has had rheumatic fever is more susceptible to a second attack after a streptococcal infection. The best prevention is monthly injections of penicillin. Alternative treatment is administration of oral penicillin or erythromcin on or two times a day. This treatment should continue fr life in individuals who had rheummatic heart disease. Rehumatic fever without carditis after age 18 may require only five years of prophylactic antibiotic therapy, or therapy may continue forever in patients with frequent exposure to group A Streptococcus. Additional prophylaxis is necessary if a patient with known rheumatic heart disease has dental or surgical procedures involving the upper respiratory, GI, or GU tract.
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teachings needs related to prophylactic antibiotic therapy for persons with a history of RHD (rheumatic heart disease
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dyspnea, hemoptysis, fatigue, palpitations, loud accentuated S1 opening snap, low pitched rumbling diastolic murmur.
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clinical manifestations mitral valve stenosis
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palpitations, dyspnea, chest pain, activity intolerance, syncope, mobile misdystolic nonejection click and a late or holosystolic murmur
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clinical manifestations mitral valve prolapse
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is the enlargement of the right ventricle and secondary to diseases of lung, thorax, and pulmonary circulation; follows preexisting condition- pulmonary HTN
àWhen a patient has , it is not the primary issue. The initial cause of right sided heart failure and is chronic hypoxemia causing polycythemia and an increase in total blood volume and viscosity. treated by treating the primary pulmonary problem. Low flow, long term O2 is used to correct the hypoxemia and to reduce the vasoconstriction. Fluid, e-lyte, and acid- base imbalances must be corrected. |
Cor Pulmonale
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à Clinical manifestations- dyspnea, chronic productive cough, wheezy respirations, substernal pain, fatigue.
may be triggered by an acute respiratory tract infection. à If heart failure accompanies may have peripheral edema, weight gain, distended neck veins, bounding pulse, and an enlarged liver. |
Cor Pulmonale
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is targeted by first treating the condition that caused it initially; usually a pulmonary problem.
à Low flow O2 is used to correct the hypoxemia and decrease the vasoconstriction in chronic states of respiratory disorders. à Diuretics and low Na+ diets will help decrease the plasma volume and load on the heart. à If the problem is obstructive, bronchodilator therapy is used |
Collaborative care for Cor Pulmonale
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is an infection of the endocardial surface of the heart (innermost layer; pericardium = outermost). Occurs when blood flow turbulence within the heart allows the causative organism (usually bacteria) to infect previously damaged valves or surfaces.
Principal risk factors: cardiac lesion, prosthetic valve, acquired valvular disease, mitral valve prolapse, prior endocarditis. - previously rheumatic heart disease was most common cause. Also r/t IV drug use, aging (people tend to undergo more invasive procedures), Increased survival of children with congenital heart disease |
Infective Endocarditis
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|
check serum antibiotic level periodically
- check blood cultures to assess effectiveness of antibiotics - arthralgia is common (check ROM/muscle tenderness) - check temperature often… infection |
nursing priorities for infective endocarditis
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|
accurate identification of the infecting organism is key
Tx of Streptococcal endocarditis - IV or IM Rocephin; IV/IM ceftriaxone + gentamicin; IV/IMceftriaxone followed by oral amoxicillin Antibiotic prophylaxis is recommended for patients with nonspecific cardiac conditions before dental/surgical procedures (resp. tract, GI, GU) or increased risk p/t who is to have drainage of infective tissue, an indwelling cardiac pacemaker, dialysis or a shunt. |
antibiotic therapy for infective endocarditis
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The hallmark finding in acute pericarditis is the pericardial friction rub (a scratching, grating, high-ptiched sound).
However, ECG changes are key diagnostic clues and evolve over hours, days, to weeks. ST segment changes are present in all ECG leads except Vr and Vi (MI involves only localized ST segment changes) See pg 894 for detailed EGC explination |
Most useful serial diagnostic marker for pericarditis
|
|
|
CT develops as the pericardial effusion increases in size and occurs because of an increase in intrapericardial pressure cause by fluid accumulation in the pericardial space: result is compression of the heart
speed of fluid accumulation affects severity of clinical manifestations P/t is often confused, agitated, restless Tachycardia/Tachypena Neck veins are markedly distended b/c of jugular venous pressure elevation Significant pulsus paradoxus is present * P/t with slow onset of CT my only have dyspnea |
Major s/s of cardiac tamponade
|
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|
an inspiratory drop in systolic drop in systolic BP > 10 mm Hg
- Take BP as normal - Deflate cuff slowly until systolic sounds are heard on expiration, note pressure - Deflate cuff until systolic sounds are heard thru-out the respiratory cycle, note pressure. - Determine difference eg. – Sound heart at expiration 110 mm Hg Sound heard thru-out cycle 82 mm Hg -------------------- Amt. of paradox 28 mm Hg See Table 36-10 for clarification |
Pulsus paradoxus
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|
* This is considered a primary nursing considering (including p/t anxiety)
The pain and inflammation of acute pericarditis are usually treated with NSAID’s (Indocin) or high dose Salicylates (300-900 mg orally 4x daily) Assessment of amount, quality, location of pain is important Maintain bed rest and bed elevated at 45 degrees Provide padded overbed table for p/t to lean on |
Interventions by nurse to ease pain associated with pericarditis
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|
|
important to assess valvular, congenital, or syphilitic cardiac disease (including valve repair or replacement), previous endocarditis, childbirth, staphylococcal or streptococcal infections, nosocomial bactreremia. IT is also important to note any immunosuppressent therapy medications and recent obstetric or gynecologic procedures, invasive techniques including catherization, cystoscopy, intravascular procedures and recent dental or surgical procedure. As far as functional health patterns one would note IV drug abuse, alcohol abuse, malaise, wt. gain or los, chills, diaphoresis, bloody urine, exercise intolerance, generalized weakness, fatigue, cough, dyspnea on exertion, orthopnea, palpitations, night sweats, chest back or abdominal pain, headache, joint tenderness and muscle tenderness. Thats the history- as far as objective data goes- see table 36-7 on page 890. (most importantly Osler nodes, Janeway's lesions, fever, tachypenia)
|
hx. of patients with infective endocarditis
|
|
|
important to note recent beta-hemolytic streptococcal infection, previous rheumatic fever or rheumatic heart disease. As far as functional health patterns go, one would look for family history, malaise, anorexia, weight loss, palpitations, weakness, fatigue, ataxia, chest pain, abdominal pain, migratory joint pain and tenderness- especially large joints. Thats the history- see table 36-15 on page 899 for objective data. (most importantly ployarthritis, chorea, erythma marginatum, subcutaneous nodules, chorea, polyarthritis)
|
hx. of patients with rheumatic heart disease
|
|
|
A person who has had rheumatic fever is more susceptible to a second attack after a streptococcal infection. The best prevention is monthly injections of penicillin. Alternative treatment is administration of oral penicillin or erythromcin on or two times a day. This treatment should continue fr life in individuals who had rheummatic heart disease. Rehumatic fever without carditis after age 18 may require only five years of prophylactic antibiotic therapy, or therapy may continue forever in patients with frequent exposure to group A Streptococcus. Additional prophylaxis is necessary if a patient with known rheumatic heart disease has dental or surgical procedures involving the upper respiratory, GI, or GU tract.
|
teachings needs related to prophylactic antibiotic therapy for persons with a history of RHD (rheumatic heart disease
|
|
|
dyspnea, hemoptysis, fatigue, palpitations, loud accentuated S1 opening snap, low pitched rumbling diastolic murmur.
|
clinical manifestations mitral valve stenosis
|
|
|
palpitations, dyspnea, chest pain, activity intolerance, syncope, mobile misdystolic nonejection click and a late or holosystolic murmur
|
clinical manifestations mitral valve prolapse
|
|
|
is the enlargement of the right ventricle and secondary to diseases of lung, thorax, and pulmonary circulation; follows preexisting condition- pulmonary HTN
àWhen a patient has , it is not the primary issue. The initial cause of right sided heart failure and is chronic hypoxemia causing polycythemia and an increase in total blood volume and viscosity. treated by treating the primary pulmonary problem. Low flow, long term O2 is used to correct the hypoxemia and to reduce the vasoconstriction. Fluid, e-lyte, and acid- base imbalances must be corrected. |
Cor Pulmonale
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|
|
à Clinical manifestations- dyspnea, chronic productive cough, wheezy respirations, substernal pain, fatigue.
may be triggered by an acute respiratory tract infection. à If heart failure accompanies may have peripheral edema, weight gain, distended neck veins, bounding pulse, and an enlarged liver. |
Cor Pulmonale
|
|
|
is targeted by first treating the condition that caused it initially; usually a pulmonary problem.
à Low flow O2 is used to correct the hypoxemia and decrease the vasoconstriction in chronic states of respiratory disorders. à Diuretics and low Na+ diets will help decrease the plasma volume and load on the heart. à If the problem is obstructive, bronchodilator therapy is used |
Collaborative care for Cor Pulmonale
|
|
|
is an infection of the endocardial surface of the heart (innermost layer; pericardium = outermost). Occurs when blood flow turbulence within the heart allows the causative organism (usually bacteria) to infect previously damaged valves or surfaces.
Principal risk factors: cardiac lesion, prosthetic valve, acquired valvular disease, mitral valve prolapse, prior endocarditis. - previously rheumatic heart disease was most common cause. Also r/t IV drug use, aging (people tend to undergo more invasive procedures), Increased survival of children with congenital heart disease |
Infective Endocarditis
|
|
|
check serum antibiotic level periodically
- check blood cultures to assess effectiveness of antibiotics - arthralgia is common (check ROM/muscle tenderness) - check temperature often… infection |
nursing priorities for infective endocarditis
|
|
|
accurate identification of the infecting organism is key
Tx of Streptococcal endocarditis - IV or IM Rocephin; IV/IM ceftriaxone + gentamicin; IV/IMceftriaxone followed by oral amoxicillin Antibiotic prophylaxis is recommended for patients with nonspecific cardiac conditions before dental/surgical procedures (resp. tract, GI, GU) or increased risk p/t who is to have drainage of infective tissue, an indwelling cardiac pacemaker, dialysis or a shunt. |
antibiotic therapy for infective endocarditis
|
|
|
The hallmark finding in acute pericarditis is the pericardial friction rub (a scratching, grating, high-ptiched sound).
However, ECG changes are key diagnostic clues and evolve over hours, days, to weeks. ST segment changes are present in all ECG leads except Vr and Vi (MI involves only localized ST segment changes) See pg 894 for detailed EGC explination |
Most useful serial diagnostic marker for pericarditis
|
|
|
CT develops as the pericardial effusion increases in size and occurs because of an increase in intrapericardial pressure cause by fluid accumulation in the pericardial space: result is compression of the heart
speed of fluid accumulation affects severity of clinical manifestations P/t is often confused, agitated, restless Tachycardia/Tachypena Neck veins are markedly distended b/c of jugular venous pressure elevation Significant pulsus paradoxus is present * P/t with slow onset of CT my only have dyspnea |
Major s/s of cardiac tamponade
|
|
|
an inspiratory drop in systolic drop in systolic BP > 10 mm Hg
- Take BP as normal - Deflate cuff slowly until systolic sounds are heard on expiration, note pressure - Deflate cuff until systolic sounds are heard thru-out the respiratory cycle, note pressure. - Determine difference eg. – Sound heart at expiration 110 mm Hg Sound heard thru-out cycle 82 mm Hg -------------------- Amt. of paradox 28 mm Hg See Table 36-10 for clarification |
Pulsus paradoxus
|
|
|
* This is considered a primary nursing considering (including p/t anxiety)
The pain and inflammation of acute pericarditis are usually treated with NSAID’s (Indocin) or high dose Salicylates (300-900 mg orally 4x daily) Assessment of amount, quality, location of pain is important Maintain bed rest and bed elevated at 45 degrees Provide padded overbed table for p/t to lean on |
Interventions by nurse to ease pain associated with pericarditis
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important to assess valvular, congenital, or syphilitic cardiac disease (including valve repair or replacement), previous endocarditis, childbirth, staphylococcal or streptococcal infections, nosocomial bactreremia. IT is also important to note any immunosuppressent therapy medications and recent obstetric or gynecologic procedures, invasive techniques including catherization, cystoscopy, intravascular procedures and recent dental or surgical procedure. As far as functional health patterns one would note IV drug abuse, alcohol abuse, malaise, wt. gain or los, chills, diaphoresis, bloody urine, exercise intolerance, generalized weakness, fatigue, cough, dyspnea on exertion, orthopnea, palpitations, night sweats, chest back or abdominal pain, headache, joint tenderness and muscle tenderness. Thats the history- as far as objective data goes- see table 36-7 on page 890. (most importantly Osler nodes, Janeway's lesions, fever, tachypenia)
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hx. of patients with infective endocarditis
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important to note recent beta-hemolytic streptococcal infection, previous rheumatic fever or rheumatic heart disease. As far as functional health patterns go, one would look for family history, malaise, anorexia, weight loss, palpitations, weakness, fatigue, ataxia, chest pain, abdominal pain, migratory joint pain and tenderness- especially large joints. Thats the history- see table 36-15 on page 899 for objective data. (most importantly ployarthritis, chorea, erythma marginatum, subcutaneous nodules, chorea, polyarthritis)
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hx. of patients with rheumatic heart disease
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A person who has had rheumatic fever is more susceptible to a second attack after a streptococcal infection. The best prevention is monthly injections of penicillin. Alternative treatment is administration of oral penicillin or erythromcin on or two times a day. This treatment should continue fr life in individuals who had rheummatic heart disease. Rehumatic fever without carditis after age 18 may require only five years of prophylactic antibiotic therapy, or therapy may continue forever in patients with frequent exposure to group A Streptococcus. Additional prophylaxis is necessary if a patient with known rheumatic heart disease has dental or surgical procedures involving the upper respiratory, GI, or GU tract.
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teachings needs related to prophylactic antibiotic therapy for persons with a history of RHD (rheumatic heart disease
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dyspnea, hemoptysis, fatigue, palpitations, loud accentuated S1 opening snap, low pitched rumbling diastolic murmur.
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clinical manifestations mitral valve stenosis
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palpitations, dyspnea, chest pain, activity intolerance, syncope, mobile misdystolic nonejection click and a late or holosystolic murmur
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clinical manifestations mitral valve prolapse
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angina pectoris, syncope, heart failure, normal or soft S1 prominent S, crescendo, decrescendo murmur
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Aortic valve stenosis
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Mechanical valves are more durable and last longer but have an increased risk of thromboembolism so pts. need to use long term anticoagulants. Therefore women of childbearing age should not use a mechanical valve (can't take anticoagulant therapy). A mechanical valve may be considered for a younger patient because it is more durable and last longer. For pt's over the age of 65, durability is less important, but the risk of compliance or hemorrhage from anticoagulants may be greater so biological may work better for them
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mechanical or biological valve replacement
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Recommend antibiotic prophylaxis for endocarditis before undergoing certain dental or surgical procedures if the patient has MVP with regurgitation.
(2) Monitor the patient treated with beta-adrengeric blockers to control palpitations. (3) Advise the pt. to have healthy eating patterns- like avoiding caffeine, don’t take diet pills. (4)Take OTC drugs with caution (5) Develop aerobic exercise program |
patient teaching is appropriate for a person with valvular heart disease
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digoxin helps control the rate of the heart- increases the force of contraction and slows the rate of the heart.
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role of digoxin in the management of valvular heart disease
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reduces the workload of the heart which can reduce chest pain.
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nitroglycerin
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is contraindicated with stenosis because it reduces preload, which is necessary with stenosis to free stiffened valve so they can open. It can cause really low blood pressure which is a bad thing!
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Nitroglycerin
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In the healthy lung the airsacs look like a bunch of grapes. Ventilation is the movement of air in and out of these airsacs. Each airsac is surrounded by blood vessels. Perfusion is the movement of blood through these vessels. The area where the airsacs and blood vessels meet is where the exchange of oxygen and carbon dioxide occur. Air is inhaled. The oxygen moves from the airsacs of the lung to the blood. It then travels to the cells of the body. Carbon dioxide travels from the cells of the body to the airsacs of the lung through the blood.
The term COPD is an abbreviation for Chronic Obstructive Pulmonary Disease. COPD is a general term used to describe the chronic lung disease linked with cigarette smoking. When the lungs are affected by COPD there is a relatively irreversible decrease in airflow and permanent destruction of the airsacs in the lung. Over time this creates some areas where there is a blood supply without any airsac. This is considered a ventilation-perfusion mismatch. Ventilation perfusion mismatch occurs along a spectrum: on one end alveoli are ventilated but not perfused (pure dead space ventilation), and on the other end alveoli are perfused but not ventilated (pure shunt). The best ventilation perfusion (V/Q) ratios occur in dependent regions of the lung, due to the preferential effect of gravity on both ventilation and perfusion. The non dependent regions are relatively better ventilated than perfused (alveolar dead space). Extensive ventilation perfusion mismatch occurs due to lung injuries, whether due to consolidation (filling alveoli with exudates), perioperative atelectasis, or “acute lung injury” where there is alveolar edema and capillary microthrombosis. Hypoxemia due to ventilation-perfusion mismatch can usually be reversed with application of supplemental oxygen. Where there is extensive atelectasis due to gas absorption or mucus plugging, the treatment is oxygen, bronchial toilet and perhaps CPAP,to recruit collapsed airways. |
ventilation-perfusion mismatch that occurs with atelectasis, pulmonary embolus, COPD?
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cyanosis, paradoxic chest movement with respiratory cycle (abdomen and chest move in opposite manner), coma arrhythmias, hypotension, tremor seizures
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late signs Acute respiratory failure
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tachycardia and mild hypertension, increased respiratory rate, srestlessness, change in persons mental status, because of inadequate delivery of oxygen to teh brain, severe morning headache
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early signs acture respiratory failure
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Inadequate oxygen transfer between the alveoli and pulmonary capillary bed.
The ABG's would be: PaO2 of 60 mm or less (normal is 80-100), and inspired O2 concentration of 60% or greater. |
hypoxemic (oxygenation failure
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happens from an imbalance between ventilatory supply and ventilatory demand. When ventilatory demand does exceed ventilatory supply, the PaCO2 can no longer be sustaind within normal limits and hypercapnia occurs. The ABG's would be: paCO@ above normal (greater than 45), and acidemia (ph less than 7.35)
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hypercapnia (ventilatory failure)-
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Disorders that compromise lung ventilation and CO2 removal include drug overdoses with central nervous system depressants, neuro diseases, trauma or diseases involving the spinal cord and its role in lung ventilations
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hypercapnic respiratory failure-
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Disorders that interfere with oxygen transfer into the blood include pneumonia, pulmonary emboli and alveolar injury related to inhalation of toxic gases. Low cardiac output can also cause this.
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hypoxemic respiratory failure
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respiratory) dyspnea, tachypnea, prolonged expiration, intercostal muscle retraction, use of accessory muscles in respiration, decrease in SpO2, paradoxic chest movent, cyanosis
(Cerebral) agitation, disorientation, deliruim, restless, confusion, decreased loc, coma (late) (caridac)- tachycardia, hypertension, cool clammy skin, arrhythmias and hypotension (late) (other) unable to speak w/o pausing, tired |
hypoxemia-
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respiratory)- dyspnes decresased resp rate or increased rate with cshallow respirations, decreased tidal volume
(cerebral)-morning headache, disorient, somnolence, coma (late) (cardiac)- arrhythmias, hypertension, tachycardia, bounding pulse (neuro)- muscle weakess, decrease in tendon reflexes, tremor, late seizures (other)-pursed lip breathing, tripod position |
hypercapnia
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At the time of the initial injury, and for several hours to one to two days afterward, the patient may not experience respiratory symptoms or the patient may exhibit only dyspena, tachypnea, couch and restlessness. Chest auscultation may be normal or reveal fine, scattered crackles. abg's usually indicate mild hypoxemia and resp. alkalosis caused by hyperventilation. The chest x-ray may be normal or exhibit evident of minimal scattered intersitital infiltrates.
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early signs of ARDS
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sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid. The alveoli fill with fluid, resulting in severe dyspnea, hypoxemia refractory to supplemental oxygen, reduced lung compliance and diffuse pulmonary infiltrates
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pathophysiology of ARDS
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PEEP therapy is used during mechanical ventilation (as in someone with ARDS) to compensate or loss of glottic function caused by the endotracheal tube. Levels typically range from 10-20cm H2O for patients with ARDS. This level allows for the collapsed alveoli to be reopened and the FIO2 to return to a level of 60%.
Some patients with ARDS show an improvement in PaO2 levels when turned to prone positioning. Early in ARDS, fluid moves throughout the lung and because of gravity, will pool in dependent regions (air will be on top). When a patient is supine the heart and mediastinal contents place even more pressure on the lungs and the patient is predisposed to atelectasis. Therefore, when the patient is placed in the prone position, the air-filled non-atelectic alveoli in the ventral portion of the lung become dependent. This allows for perfusion to better match ventilation. Not all patients respond the same/well to the prone position and there is no way of predicting who will respond. |
role of PEEP therapy and prone positioning in the treatment of ARDS?
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Nosocomial pneumonia: this can result from the impaired hosts defenses, contaminated equipment, invasive devices, aspiration and prolonged ventilations. Will present with signs of infection/pneumonia (fever, increased WBC, crackles/course lung sounds, etc.)
Barotrauma: results from rupture of overdistended alveoli during mechanical ventilation. The high peak pressures required in pts. with ARDS predispose to this complication. Barotrauma results in presence of alveolar air in locations where it is not usually found. This can lead to pulmonary interstitial emphysema, pneumothorax, subut. Emphysema, pneumoperitoneum, pneumomediastinum and tension pneumothorax. Volu-pressure Trauma: occurs in pts with ARDS when large tidal volumes are used to ventilate noncompliant lungs. This results in alveolar fractures and movement of fluids and proteins into the alveolar spaces. ( I would assume that this would present like pneumonia as there is fluid in the spaces in the lungs, possibly causing pockets of crap. The book doesn’t go into more detail) PEEP therapy can cause compromise venous return to the right side of the heart, decreasing preload, cardiac output and blood pressure. It can also cause hyperinflation of the alveoli, compression of the pulmonary capillary bed, a reduction in blood return to the left side of the heart and a dramatic reduction in blood pressure. It, in itself can cause barotraumas and volu-pressure trauma. |
complications and associated manifestations of positive pressures ventilation and PEEP therapy
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Indicated primarily for those who (1) has a chronic illness such as lung and heart disease and diabetes mellitus, (2) is recovering from a sever illness, (3) is 65+ y/o (4) is in a long-term care facility. There is significant d/t rate of drug-resistant S. pneumoniae infections increasing. Can be given with other vaccines just at a separate site. Pneumococcal vaccine is good for a lifetime, however those that are immunosuppressed and run the risk for fatal consequences of the infection should be re-vaccinated q5years.
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recommendation guidelines for Pneumococcal vaccination
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Oxygen therapy is an appropriate first step in reversing hypoxemia caused by a V/Q mismatch. If the mismatch is caused by a shunt, a mechanical ventilator may be required. Diffusion limitations may cause hypoxemia during exercise. Enough O2 should be administered to keep PaO2 at 55-60mm Hg or an SaO2 at 90% or more
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actions by the nurse are appropriate to correct hypoxemia or O2 desaturation of a patient
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presents with frequent awakening at night, insomnia, excessive daytime sleepiness, and witnessed apneic episodes. Other symptoms include loud snoring, morning headaches (from hypercapnia), personality changes, and irritability. Patient will describe effects of chronic sleep loss (i.e. inability to concentrate, impaired memory, etc)
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sleep apnea
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applies a nasal mask that maintains positive pressure in the airway during inspiration and expiration to prevent airway collapse. The pt. may also undergo a uvulopalatopharyngoplasty (UPPP or UP3) and genioglossal advancement and hyoid myoltomy (GAHM). UP3 involves removal of the tonsillar pillars, uvula, and posterior soft palate. GAHM involves advancing the attachment of the muscular part of the tongue on the mandible (usually performed in conjunction with the UP3). Non-surgical measures include avoiding sedatives and alcohol 3-4 hrs prior to sleep, weight loss, using an oral appliance during sleep to prevent airflow obstruction
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CPAP
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Dry mouth – Salagen (pilocarpine hydrochloride) increases saliva production and should be started before radiation starts. Pt. can also increase fluids, chewing sugarless gum or candy, using nonalcoholic mouth rinses and using artificial saliva.
Stomatitis – irritation, ulceration and pain are common. Rinses of water and hydrogen peroxide or baking soda and water can be used. Commercial mouthwashes and hot or spicy foods should be avoided. If severe, a mixture of antacid, benadryl and lidocaine can be used. Reddened skin – avoid all exposure to the sun |
side effects of radiation therapy for treatment of laryngeal cancer
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removal of vocal cords) pt. should be informed about the loss of regular speech. Patient may be advised of alternative modes of speech. Pt. should also be advised that they will have a permanent tracheostomy. It should also be explained that the patient will not be eating, that they will be given tube feedings via a nasogastric, nasointestinal, or gastrostomy tube
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total laryngectomy
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(removal of part of the vocal cords or structures above true vocal cords) pt. will need a temporary tracheostomy in each case. The voice will be preserved, but the quality is breathy and hoarse. Parenteral nutrition will be required initially, but patient can resume normal diet in future. Patient with supraglottic laryngectomy will have to relearn how to swallow so as not to aspirate food
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Partial or supraglottic laryngectomy
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Maintenance of patent airway is imperative. Frequent suctioning via the laryngectomy tube will be required immediately following surgery. Monitor the type and amount of secretions. If the mucus is too thick, saline may be instilled into airway to loosen secretions enough to clear the airway. (this practice is not recommended by RT) Pt. will be placed in semi-Fowler’s position to decrease edema and limit tention on suture lines. VS should be monitored frequently. Wound suction may be used, so drainage should be monitored (drg should be serosanguineous and gradually decrease in volume over 24 hours). Patency of drainage tubes should be monitored. Area around tubes should be monitored for redness/swelling. An exercise program should be implemented to maintain strength and movement in the affected shoulder and neck. The patient may need support of the neck to move the head after surgery
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nursing care for the patient post-laryngectomy and measures the nurse takes to prevent potential complications
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TB tests are determined to be positive based on the size of the induration (or wheel) and the group you fall into. Some groups are positive with an induration of only 5mm. Others who have a low risk of exposure are not positive unless their induration is 15mm or more.
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interpretation of a positive PPD
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Patients are more likely to have a false-negative if they were infected with TB many years ago and persons with an active current infection. False positives may occur in people such as healthcare workers or those who have decreased response to allergens which often warrant them to have a second PPD test, the response may be accelerated and misinterpreted as positive
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patients are more likely to have a false negative PPD? False positive PPD
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While the pt has active TB, should be placed on respiratory isolation until they are considered noninfectious (effective dx therapy, improving clinically, 3 negative AFB smears). The pt. should be taught to cover the nose and mouth with a paper tissue every time he or she coughs, sneezes or produces sputum. The tissues should be thrown into a paper bag and disposed of with the trash, burned or flushed down the toilet. The patient should be taught careful hand washing. The pt. should also be instructed on the importance of taking the medications as prescribed, when prescribed. The pt should be taught to recognize signs/symptoms of relapses and factors that could reactivate TB (immunosuppressive therapy, malignancy and prolonged illness
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teaching is indicated for the patient with TB to prevent transmission
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Respiratory isolation is used in hospitals via a negative pressure isolation room that offers 6 or more exchanges per hour. UV radiation of the air in the upper part of the room is another option. HEPA masks are used to filter particles but must be molded to tightly fit the face
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measures are taken to reduce transmission in the hospital or institutional setting
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Latent TB occurs when an individual becomes infected with TB but does not become acutely ill. Drug therapy can be used to prevent infection from developing into a clinical disease. In latent TB, there is a significant reaction to tuberculin skin test, negative bacteriologic studies, no x-ray findings compatible with TB, no clinical evidence of TB. An active case would manifest in x-ray and clinical findings as well as with the tuberculin test.
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How does latent TB infection differ from active TB
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Myobacterium tuberculosis and kills more people than any other infectious disease. It is spread via airborne droplets from speaking and sneezing, making it difficult to avoid. It cannot be spread by hands or objects. During the activation of the immune system response, the bacteria can easily spread to lymph nodes, causing further problems.
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TB
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In the case of a latent TB infection, INH is the drug of choice, and should be continuously used for 6-9 months, and longer in patients with HIV. In the case of an active TB disease, the drugs of choice are INH, Rifamate, Pyrazinimide, Streptomycin, and Myambutol. What is important to remember is that often, four of these drugs will be given aggressively to reduce the risk of drug resistant TB. This is also done for 6-9 months.
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the first line pharmacologic therapy in management of latent TB infection
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Adverse reactions for some of the drugs include hepatitis, therefore baseline liver function tests are important to monitor. The nurse needs to teach the patient to cover mouth when sneezing or coughing, and hand washing after handling sputum soiled tissues, also to complete the full prescription of medications and do not stop taking them when symptoms disappear
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major adverse reactions of first-line TB drugs
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Directly observed therapy (DOT) is important for patients at risk for noncompliance with their medications. The nurse must follow up on her care to ensure that the patient adheres to the drug regimen
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the role of directly observed therapy in the management of TB
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Lung cancer is the leading cause of cancer related deaths, and it most commonly occurs in individuals over 50 and those with a history of cigarette smoking. Tobacco smoke contains 60 carcinogens, which cause destruction of bronchial epithelium. Environmental tobacco smoke is also a concern, as it leads to a 35% increased risk of lung cancer among non-smokers
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major risk factors for lung cancer and what is the effect of cumulative exposure to carcinogens
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The most common surgical procedure is a lobectomy, or a removal of one or more lobes of the lung. Less commonly used is a pneumonectomy, which involves the removal of an entire lung. Other procedures are segmental resection and wedge resection, in which a small part of the lung is removed.
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types of surgical procedures are used in the treatment of lung cancer
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Early symptoms include persistent cough with sputum, local or unilateral chest pain, dyspnea, and an auscultory wheeze. Later symptoms sometimes show and include anorexia, fatigue, hoarse voice, and dysphagia.
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symptoms of lung cancer
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results from multiple rib fractures, causing instability of the chest wall. The chest wall cannot provide the bony structure necessary to maintain ventilation. The chest will suck in on inhalation, and protrude out during exhalation. It can usually be seen on visual examination of the patient.
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flail chest
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shows rapid accumulation of air in the pleural space causing severely high pressure which results in tension of the heart. Air can enter but not escape. It is an emergency in which the patient is likely to die from hypoxemia, so a large-bore needle must be inserted into the chest wall to release trapped air.
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tension pneumothorax
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shows fluid in the pleural space, and is not a disease itself but an indication of other disease, such as infection
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pleural effusion
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Immediately ensure patent airway, administer a high flow of oxygen with a non rebreather, begin fluid resuscitation if necessary, cover chest wound with dressing taped on three sides, stabilize impaled objects with dressing but do not remove the object. After this has been performed, then place patient in semi-Fowler’s position if spine injury has been ruled out.
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initial emergency interventions for chest trauma
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Priorities include monitoring chest drainage, monitor respirations, administer oxygen, help client to change positions regularly, and promote ambulation. Also assess for anxiety and pain control, giving pain medications as necessary.
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nursing care priorities for the patient post-pneumonectomy
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Both involve removal of fluid from the chest, and post-procedure it is important to instruct patient to be on NPO status until gag reflex returns and monitor for laryngeal edema, also monitor for recove
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post-procedure care of the patient following thoracentesis and bronchoscopy
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