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148 Cards in this Set

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What is acute respiratory failure (ARF)?
a life-threatening state in which the cardiopulmonary system is unable to maintain adequate gas exchange.
ARF is caused by?
an imbalance in supply and demand.

Normally the cardiopulmonary system meets demands by increasing its work to supply adequate oxygen and rid the body of CO2. If the body demands become too high, the system fails, precipitating ARF.
What are restrictive disorders?
(aka interstitial lung diseases) Pulmonary problems associated with decreased/loss of lung compliance and decreased lung expansion

Problems that involve volume (the amount of air measured in mL or L that flows in and out of the lungs) rather than airflow (the rate or speed at which air moves into or out of the lungs).
What are S/s of restrictive pulmonary disorders?
-Increased RR
-Decreased TV*
-Decreased TLC* (total lung capacity)
-Normal to decreased PaO2
-SOB
-Cough
-Chest pain or discomfort
-Fatigue
-Hx of wt loss
What are obstructive disorders?
Pulmonary Problems That Hinder Expiratory Airflow or Limit Expiratory Airflow

Associated w/ increased lung compliance (hyperinflated lungs) accompanied by a loss of elastic recoil.
The V/Q ratio may be disturbed (normal V/Q ratio does not necessarily = healthy lungs.
What are examples of major obstructive disorders?
Major ones:
COPD - Emphysema*
Chronic Bronchitis
Asthma
Cystic Fibrosis
What are S/s (clinical manifestations) of obstructive pulmonary disorders?
-Mucus hypersecretion (except w/ pure emphysema)
-Wheezes, rhonchi
-Dyspnea (episodic or progressive)
-Dminished breath & heart sounds
-Barrel chest (increased AP diameter)
-Progressive hypercapnia & respiratory acidosis
-Progressive or episodic hypoxemia (particularly in later stages)
-Cor pulmonale* (pulmonary heart disease is enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs.)
-Accessory muscle use
-Increased expiratory time (expiration time longer than inspiration time)
-PFTs: Normal to increased TLC, increased FRC, decreased FEV, decreased VC
What are the components of ARF?
1. Failure of oxygenation
2. Failure of ventilation
What is the clinical definition (lab values) for dx ARF?
PaCO2 > 50 mmHg w/
pH < 7.30 &/or
PaO2 < 60 mmHg
What is the clinical definition (lab values) for the component "oxygenation failure" of ARF?
PaO2 < 60 mmHg
What are the clinical manifestations of the ARF component "oxygenation failure"?
Pulmonary: dyspnea, tachypnea, increased pulmonary vascular resistance

CV: increased BP, HR, cardiac dysrhythmias, cyanosis; weak, thready pulse

CNS: altered lvl of responsiveness; restlessness, confusion
What is the clinical definition/lab criteria for the ARF componenet "ventilation failure"?
PaCO2 > 50 mmHg w/
pH < 7.30 (acute respiratory acidosis)
What are the clinical manifestations of the ARF component "ventilation failure"?
Pulmonary: tachypnea
Vascular: H/A; flushed, wet skin
CV: bounding pulse, increased BP & HR

CNS: anesthetic effects of CO2: lethargy, drowsiness, coma (CO2 narcosis)
What is the primary problem of "failure of oxygenation" in ARF?
hypoxemia (from mild to severe)
What conditions commonly cause "oxygenation failure" ?
Restrictive pulmonary disorders (e.g. ARDS & pneumonia)
How does "oxygenation failure" in a pt w/ ARF develop "ventilatory failure"?
the rise of CO2 from hypoventilation as a result of worsening of restrictive pulmonary disorder such as ARDS & pneumonia in a pt, or if respiratory muscle fatigue develops
How do you tx/prevent "oxygenation failure" in ARF?
maintain PaO2 > = 60 mm Hg
What is "ventilatory failure" (acute respiratory acidosis) in ARF, caused by?
alveolar hypoventilation = the inability to move air adequately out of the alveoli, allowing a buildup of CO2.
What are the conditions for failure of ventilation in ARF?
Problems that interfere w/ movement of airflow:
-Neuromuscular disorders
-Respiratory muscle fatigue
-COPD
What is the primary problem in "ventilatory failure"?
hypercapnia - CO2 narcosis.
CO2 has a strong vasodilator effect, which causes many of the associated symptoms
What are the complications of ARF?
-Can Virtually Affect All Body Systems by causing organ hypoxia
-Decreased Cardiac Output
-Hypoperfusion––shock
-Hypercapnia leads to vasodilation causing
---Increased intracranial pressure
--Decreased cardiac output
--Decreased systemic vascular resistance
What is the pathogenesis of ARF?
-Presence of Disease Process That Interferes with Normal Lung Function
-Develops into V/Q Ratio Abnormalities with Decreasing PaO2
-Body Responds to Decreased PaO2 by Increasing Rate and Depth of Breathing

-Body’s Metabolic Rate Increases
---More oxygen is consumed
---More carbon dioxide is produced
-End Result
---Increased levels of PaCO2
---Decreased levels of PaO2
What are the two categories of risk factors for ARF?
-Ventilatory failure
-Oxygenation failure
Risk factors for ARF:
List the risk factors for ventilatory failure:
-Neuromuscular disorders, such as multiple scleosis, Guillain-Barre, spinal cord injuries & storke, that impair the client's rate & depth of respiration.
-Elevated intracranial pressure (closed head injuries, cerebral edema, hemorrhagic stroke)
-COPD
-Asthma
-Pulmonary embolism, pneumothorax
-ARDS
-Pulmonary edema
-Fibrosis of lung tissue
Risk factors for ARF:
List the risk factors for oxygenation failure:
-Low concentrations of O2 (CO poisoning, high altitude, smoke inhalation)
-Pneumonia
-Pul. edema
-hypoventilation
-hypovolemic shock
-low hgb
-ARDS
What is ARDS?
syndrome with a spectrum of increasing severity of lung injury defined by physiology and radiographic criteria in which wide spread damage to cells and structures of the alveolar capillary membrane occurs within hours to days of predisposing insult.

a systemic inflammatory response that injures the alveolar-capillary membrane. It becomes permeable to large molecules, and the lung space becomes filled with fluid. Surfactant activity is reduced, thus alveoli become unstable and collapse, leading to worsening edema.
What are the criterias for dx ARDS?
-Acute onset
-Bilateral infiltrates on chest x-ray (frontal view)
-PAWP 18 mmHg or less &/or no left atrial HTN (CHF)

Oxygenation status measure as PaO2/FiO2 ratio regardless of PEEP)
ALI = 300 mmHg or less
ARDS = 200 mmHg or less
What are the etiologic factors of ARDS?
-Comes from complication of systemic disease processes.
-Common to all predisposing factors: all are known to trigger a systemic inflammatory response that, if sufficiently strong, may involve the lungs --> leading to diffuse lung injury

-Gastric aspiration & septic shock: > 25% risk of ARDS
-Risk of ARDS is additive when multiple risk factors are present
-Genetic factors
Since ARDS s/s can mimic CHF, how do you differentiate between the two?
- PAWP: > 18 = CHF, < 18 = ARDS
- Bronchoalveolar lavage:
----In CHF: protein-poor and lacks inflammatory cells
----In ARDS: protein-rich and inflammatory cells
- Chest x-ray
----CHF: cardiomegaly, pulmonary infiltrates in dependent lung fields, pulmonary effusions
----ARDS: pulmonary infiltrates diffuse
What are the risk factors for ARDS?
May result from direct injury to lung tissue or effects of other systemic problems.
• Aspiration
• Pulmonary emboli (fat or amniotic fluid)
• Pneumonia and other pulmonary infections
• Sepsis
• Trauma
• Nervous system injury
• Smoke or toxic gas inhalation
• Drug ingestion (heroin, opioids, aspirin)
• Near-drowning victims
What is the pathogenesis of ARDS?
-Not a disease but a pattern of pathophysiological lung changes resulting in a corresponding pattern of clinical manifestations
-Diffuse inflammatory injury
-Disruption of pulmonary capillary endothelium and alveolar epithelium
• Allows plasma protein and fluid to escape into pulmonary interstitial spaces resulting in nonhydrostatic pulmonary edema
• Invasion of lung tissue by neutrophils > central to inflammatory response related to injury
What are the early clinical presentations of ARDS?
Early-
• Diagnosis w/in 48 hrs of insult
• Presence of hemorrhagic shock
• Increasing resp distress, tachypnea, and dyspnea
• Initial ABGs: respiratory alkalosis (secondary to hyperventilation)
• Death often from hemorrhagic shock
What are the late clinical presentations of ARDS?
Late-
• Diagnosis after 48 hrs of insult
• Multiple organ involvement
• Death from multiple organ dysfunction
What are the progressive manifestations/presentations of ARDS?
- Cough with sputum production
- ABG: increasing hypoxemia refractory to increasing concentration of oxygen
- cyanosis
-increasing use of accessory muscles
-pulmonary function tests: increasing pulmonary restriction (e.g. decreasing lung compliance, decreasing FRC).
How many phases of ARDS are there? How long does each phase last? List the phases.
Three:
1. Exudative phase (1-3)
2. Fibroproliferative phase (3-7 days)
3. "Repair & Recovery" phase (weeks-6 mo.)
Phases of ARDS:
Characteristics of Exudative phase?
diffuse microvascular injury and alveolar damage, invasion of inflammatory cells into interstitium, and development of hyaline membranes in alveolar spaces.
Phases of ARDS:
Characteristics of Fibroproliferative phase?
Lung repair period…
Degree of recovery is dependant on:
1. severity of primary lung injury
2. influence of secondary forms of injury (eg., barotraumas, nosocomial infection, O2 toxicity
Phases of ARDS:
Characteristics of "Repair & Recovery" phase?
- Process is slow and may reduce quality of life
- Clients may need to be evaluated for depression in coping with declined state of health
Phases of ARDS:
Pathology of Exudative phase
destruction of type 1 pneumocytes
Phases of ARDS:
Pathology of Fibroproliferative phase
-Hyperplasia of type 2 pneumocytes.
-Proliferation of fibroblasts in basement membrane of alveoli
• development of intra-alveolar and interstitial fibrosis
-Lung remodeling

Degree of lung repair is variable –
• Full repair of lung architecture
----Return to normal compliance and gas exchange over 6-12 month period
• Permanent damage to lung architecture
-----Occurs if basement membrane becomes disrupted – cannot repair correctly
What is pulmonary embolism?
Blockage of pulmonary blood vessel caused by lodging of a thromboembolism or other blood borne material that has passed through the venous system, into the right side of the heart, and into the pulmonary artery. Emboli lodges obstructing flow distal to the obstruction.
 Many are asymptomatic, others lead to rapid death.
 Blockage of pulmonary blood vessel caused by lodging of a thromboembolism or other blood borne material that has passed through the venous system, into the right side of the heart and into the pulmonary artery.
 Emboli become lodged into the lungs because of the natural blood flow of the venous system into the lungs for gas exchange through a decreasing-size pulmonary vascular system that begins at the pulmonary artery trunk and ends in the microvasculature of the pulmonary capillary system.
 This system acts as a filtering organ, stopping any material that is too large to squeeze through the tiny micovasculature.
 A variety of blood-borne material can flow through the system until it can no longer move forward, lodging and obstructing flow distal to the obstruction.
 Emboli lodges obstructing flow distal to the obstruction.
What are the four types of pulmonary emboli?
1. Thromoembolism
2. Fat embolism
3. Amniotic embolism
4. Venous air embolism (VAE)
Describe thromboemoblism
- Thrombus or blood clot usually from deep-vein thrombosis (DVT) in the lower extremities: thigh/pelvis areas
Describe fat embolism
- Fat gains access to circulatory system, usually via bone trauma or orthopedic surgery
- Usually occurs 12-36 hours after accident
- Patachiae, dyspnea, tachypnea, hemoptysis, neurologic decline, diffuse bilateral shadowing, fever, and tachycardia
Describe amniotic emoblism
- Occurs during birthing process when amniotic fluid mixes with maternal blood
- Mechanical obstruction that leads to obstruction of pulmonary vessels
- Creates pulmonary hypertension and hypoxemia
- Results: resolution, LV failure, or death
Describe venous air embolism (VAE)
- A bolus of air introduced into the venous circulation
- Rare but potentially lethal complication
- Predisposing factors:
---Venous or arterial intravenous catheters
---Cardiac pacemaker placement
---Penetrating chest trauma
What are the common predisposing factors of thromboembolism?
 >80% of PE originate as DVT in lower extremity deep veins. Many high-acuity patients are at risk for development of DVT and, therefore, for development of PE.


 Immobilization (3 or more consecutive days in the past month)
 Recent surgery (within past 3 months)
 Malignancy
 Prolonged travel (longer than 4h in past month)
 Previous history of thromophlebitis
What is the term to describe the 3 major factors that place a person at risk for developing DVT?
Virchow's Triad
What does the Virchow's Triad consist of?
1. Venous stasis
2. Hypercoagulability
3. Venous injury
Virchow's Triad:
Describe venous stasis
 Refers to slowing of blood flow.
 It most commonly results from significantly reduced mobility, such as is seen w/prolonged bedrest, severe illness, or major surgery; or immobility states, such as limb casts or paralysis.
 People w/polycythemia vera can also develop venous stasis because of a thickening of the blood (hyperviscosity) from a significantly elevated RBC count.
Virchow's Triad:
Describe hypercoagulability
 Abnormal tendency to form thrombi that can be inherited or acquired.
 Acquired causes include such conditions as cancer, oral contraceptives, sepsis, and others.
Virchow's Triad:
Describe venous injury
 Endothelial injury can occur either directly or indirectly.
 It can result from such predisposing agent as surgery or trauma, infection, and central catheters.
What are the three syndromes of PE presentation?
1. Pulmonary infarction syndrome
2. Isolated dyspnea syndrome
3. Circulatory collapse syndrome
What are the frequency/severity for pulmonary infarction syndrome in a pt. w/ PE?
Freq: 65%
Severity: Mild
What are the frequency/severity for isolated dyspnea syndrome in a pt. w/ PE?
Frequency: 22%
Severity: Moderate
What are the frequency/severity for circulatory collapse syndrome in a pt. w/ PE?
Frequency: 8%
Severity: Severe
What are the presenting defining characteristics of pulmonary infarction syndrome for a pt. w/ PE?
 Pleuritis pain
 Crackles (rales)
What are the presenting defining characteristics of isolated dyspnea syndrome for a pt. w/ PE?
 Dyspnea
 Absence of pleuritic pain & hemoptysis
What are the presenting defining characteristics of circulatory collapse syndrome for a pt. w/ PE?
 Tachycardia
 Hypotension or LOC (loss of consciousness)
 Complete right bundle branch block
 Cardiomegaly
 Absence or pleural effusion
What are common S/s of PE in order of frequency
 Dyspnea*
 Tachypnea
 Pleuritic pain
 Cough
 Unilateral leg pain and swelling (DVT findings; about 1/3 of PE cases)
 Wheezing
 Crackles (rales)
What are the risk factors for PE?
-Long-term immobility
-Oral contraceptive use, estrogen therapy
-Smoking
-Hypercoagulability (e.g. elevated platelet count)
-Obesity
-Surgery
-HF or chornic A-fib
-Autoimmune hemolytic anemia such as sickle cell disease
-Long bone fractures
-Advanced age
Describe the pathophysiology of PE
Severity of pulmonary embolism depends on degree of obstruction and location of embolus

DVT --> Part of thrombus breaks away --> embolus follows venous bl. flow into pulmonary artery --> embolus lodges in pulmonary artery system --> mech obstruction (loss of bl flow distal to blockage) & [stimulation of neurohumoral reflexes ->pulmonary vasoconstriction ->increase in pulmonary vascular resistance] --> decreased area of pulmonary vascular bed [& reflex bronchoconstriction in affected lung area] --> incre physiologic deadspace & decr surfactant production --> atelectasis --> incre V/Q mismatch & R-L shunt --> hypoxia w/ further vasoconstriction --> incre pulmonary vascular resistance --> pulmonary HTN --> Rt Heart Failure
What are clinical manifestations/ways to dx PE?
-Compression ultrasound - lower extremities to rule out DVT (observe for swelling, redness, tenderness, + Homan's sign)

-Chest x-ray - usually normal; not a good dx tool

-EKG - often normal, maybe sinus tach; not dx

-Pulmonary angiography - definitive dx test; able to pinpoint blockage

-ABG: Low PaO2, low PaCO2; not diagnostic but helpful in assessing hypoxia
What is SARS?
Severe acute respiratory syndrome is the result of a new viral infection from a family of viruses known as cornaviruses invading the pulmonary tissue, which leads to an inflammatory response, most commonly affecting upper respiratory tract
Etiology of SARS?
• Etiologies include: a novel coronavirus (the same family that can cause the common cold) possibly of mammalian or avian origin (its entire genome was sequenced by the end of May 2003)
What are the risk factors 10 days prior to illness for SARS?
o Travel to mainland China, Hong Kong, or Taiwan or close contact w/ someone ill w/ hx of travel to these areas
o Employment in occupation w/ possible exposure
o Atypical pneumonia w/o alternative dx
o People living in close direct contact w/ an infected person.
Describe the pathogenesis of SARS
• Coronaviruses have ribonucleic acid (RNA) as their genetic material & have many projections that look like a halo or “corona” when examined by electron microscopes. The new virus, known as SARS Co-V, is a mutated form of the coronavirus & is more virulent than most members of this virus family.
• Commonly infected area: Cells of the upper respiratory tract, triggering an inflammatory response. It stays in the respiratory passageways rather than spreading into the blood b/c it grows best at temperatures slightly lower than normal core body temp.
• Portals of entry: mucous membranes of the eyes, nose, & mouth.
What are the clinical presentations of SARS?
The hallmark symptoms are fever greater than 100.5 degrees F (38.0 degrees C) and cough, difficulty breathing, or other respiratory symptoms. Symptoms in the order of how commonly they appeared have included:
Common:
• Fever (>38oC/100.5F)
• myalgia (muscle pain)
• extreme weakness
• mild headache
• dry cough

Less Common:
• Dyspnea
• arthralgias
• nausea
• chills
• chest pain
• dizziness
• sore throat
• anxiety
What is the disease progression of SARS?
Disease Progression
• 25% progressed to ALI/ARDS
• 10 Percent Died Within First 28 Days
• Over Age 60, Mortality Rate of 43 Percent
How is SARS transmitted?
Airborne droplet (e.g. cough, secretions) or aerosol (e.g. humidifier). May Live Up to 24 Hours in Environment.
o When someone with SARS coughs or sneezes, infected droplets spray into the air. You can catch SARS if you breathe in or touch these particles. The SARS virus may live on hands, tissues, and other surfaces for up to 6 hours in these droplets and up to 3 hours after the droplets have dried.
o Live virus had even been found in the stool of people with SARS, where it has been shown to live for up to four days. And the virus may be able to live for months or years when the temperature is below freezing.
What are the two stages of SARS presentation?
o Incubation Period: 2–10 Days
o 2–7 Days Later: Dry Cough, SOB, Without Upper Respiratory Symptoms
o 7–10 Days Later: Radiographic Confirmation of Pneumonia
What is a pneumothorax?
the accumulation of air in the intrapleural cavity that leads to partial or complete lung collapse. The amount of air in the intrapleural space determines the degree of lung collapse.
What are the 3 subtypes of pneumothorax?
1. Spontaneous
2. Traumatic
3. Tension
Describe the pathophysiology of spontaneous-type pneumothorax

What are the two different types w/n spontaneous pneumothorax?
This type of pneumothorax occurs when there is the rupture of an air-filled bleb on the lung surface. This causes air leakage into the pleural spaces because the alveolar pressure is normally greater than the pleural pressure so air flows into the pleural space, which causes the lung to collapse. Hypoxia results from decreased total lung capacity, vital capacity, and lung compliance.

--Primary spontaneous: affects previously healthy people
(occurs most often in tall boys/men aged 10-30; also in smokers.)

--Secondary spontaneous: affects people w/ preexisting lung disease (e.g. COPD - emphysema; CF; TB; asthma)
Rupture of a bleb on the lung surface allows air to enter pleural space from airways.
What are the manifestations of spontaneous type pneumothorax?
-Abrupt onset
-Pleuritic chest pain
-Dyspnea, SOB
-Tachypnea, tachycardia
-Unequal lung excursion
-Decr breath sounds & hyperresonant percussion tone on affected side
Describe the pathophysiology of traumatic-type pneumothorax

What are 3 different types?
Trauma to the chest wall or pleura disrupts the pleural membrane.
--Open: occurs w/ penetrating chest trauma that allows air from the environment to enter the pleural space
--Closed: occurs w/ blunt trauma that allows air from the pleural space
--Iatroenic: involves laceration of visceral pleura during a procedure such as thoracentesis or central-line insertion
From Porth -
Open: occur when atmospheric air flows directly into the pleural cavity (under negative pressure). As the air pressure in the pleural cavity becomes positive, the lung on the affected side collapses, causing a decrease in lung capacity and can lead to hypoxia.

Closed: occurs when an opening is created between intrapleural space and the parenchyma of the lung. So air enters the pleural space from within the lung, causing increased pleural pressure and preventing lung expansion during inspiration
What are the manifestations of traumatic type pneumothorax?
-Pain
-Dyspnea
-Tachypnea, tachycardia
-Decreased respiratory excursion
-Absent breath sounds in affected area
-Air movement through an open wound
What can cause an open pneumothorax?
penetrating chest injury (stabbing, gunshot), insertion of a central venous catheter, chest surgery, transbronchial biopsy, thoracentesis
What can cause a closed pneumothorax?
blunt chest trauma, air leak from ruptured blebs, rupture from high intrathoracic pressures during mechanical ventilation, cancerous lesions that erode into pleural space
Describe the pathophysiology of tension-type pneumothorax
Air enters pleural space through chest wall or from airways but is unable to escape, resulting in rapid accumulation. Lung on affected side collapses. As intrapleural pressure increases, heart, great vessels, trachea, & esophagus shift toward the unaffected side
What are the manifestations of tension-type pneumothorax?
-Hypotension, shock
-Distended neck veins
-Severe dyspnea
-Tachypnea, tachycardia
-Decreased respiratory excursion
-Absent breath sounds on affected side
-Tracheal deviation toward unaffected side

**Most severe signs and symptoms occur with this type of pneumothorax
What can cause tension-type pneumothorax?
penetrating chest wound treated with an air-tight dressing, fractured ribs, mechanical ventilation, high level of peep that causes the alveolar blebs to rupture, chest tube occlusion.
The most severe S/s occur with which type of pneumothorax?
tension-type pneumothorax
What are general s/s of pneumothorax (of all types)?
sudden, sharp pleuritic chest pain, SOB, asymmetric chest wall expansion (overexpansion and rigidity on affected side), palpation may reveal subcutaneous emphysema (popping under skin), decreased vocal fremitus, hyperresonance on percussion on affected side, absent breath sounds on affected side
What is a hemothorax?
abnormal presence of blood in the intrapleural space.

Bleeding may arise from chest injury, complications of chest surgery, malignancies, or rupture of a great vessel (like an aortic aneurysm). Its usually diagnosed by the presence of blood in the pleural fluid. It usually requires drainage, and if the bleeding continues, surgery to control the bleeding may be required
Sedative-hypnotic agents:

What are the mech of action for BENZODIAZEPINES?
(e.g. diazepam & midazolam (Versed))
These drugs act on the limbic system and the RAS to make gamma-aminobutyric acid (GABA) more effective, causing interference with neuron firing. GABA stabilizes the post synaptic cells leads to an anxiolytic effect at doses lower than those required to induce sedation and hypnosis. Mechanism of action is not clearly known.
Sedative-hypnotic agents:

What are the mech of action for
BARBITURATES?
Are general CNS depressants that inhibit neuronal impulse conduction in the ascending RAS, depress the cerebral cortex, alter cerebellar function, and depress motor output.
Sedative-hypnotic agents:

What are the mech of action for
(Other) Meprobemate
Used to manage acute anxiety for up to four months. Works in the limbic system and the thalamus and has some anti convulsant properties and CNS muscle relaxing effects
Sedative-hypnotic agents:

What are the mech of action for
(Other) Chloral hydrate:
used to produce nocturnal sedation or preoperative sedation. Mechanism of action not known
Sedative-hypnotic agents:

What are the mech of action for
(Other) Zaleplon/Zolpidem:
Cause sedation, short term tx of insomnia. Work by affecting serotonin levels in sleep center near RAS.
Sedative-hypnotic agents:

What are the mech of action for
(Other) Eszopiclone (lunesta):
insomnia, reacts on GABA sites near benzodiazepine receptors.
Sedative-hypnotic agents:

What are the mech of action for
(Other) Antihistamines:
can be very sedating in some ppl. Used as preop medications and postop to decrease need for narcotics.
Sedative-hypnotic agents:

What are the mech of action for
(Other) Buspirone:
Mechanism of action is unknown
Sedative-hypnotic agents:

What are the mech of action for
(Other) Ramelteon:
Stimulates melatonin receptors, which are thought to be involved in the maintenance of circadian rhythm and sleep-wake cycle. Used for tx of insomnia.
What is the reversal agent for midazolam (Versed) OD/toxicity?
flumazenil (Romazicon)
Sedative-hypnotic agents:

What is the mech of action for
Propofol (Diprivan)
Short-acting hypnotic. Mech of action unknown. Produces amnesia. Has NO analgesic properties. Strictly SEDATION med.
Common examples of restrictive pulmonary disorder can be classified into what two types of problems
External problems
&
Internal problems
Common examples of external problems causing restrictive pulmonary disorders are:
Obesity
Neuromuscular diseases:
-Myasthenia gravis
-Muscular dystrophy
-Guillian-Barre syndrome
-Spinal cord trauma
Chest wall disorders:
-Extensive chest burns scoliosis
-Flail chest
Common ex. of internal problems causing restrictive pulmonary disorders are:
Pneumonia
Atelectasis
CHF
Pulmonary edema
Pulmonary fibrosis
Pulmonary tumors
Pneumothorax
Asbestosis
Restrictive pulmonary disorders are caused by
• Internal problems: Decreased number of functioning alveoli, lung tissue loss, such as a decrease in the # of functioning alveoli (e.g. atelectasis or pneumonia) or lung tissue loss (e.g. pneumonectomy or lung tumors)

• External problems: (e.g., chest burns or morbid obesity)
Obstructive pulmonary disorders are caused by
• Airway narrowing, such as bronchospasm, bronchoconstriction, & edema; OR
• By airway obstruction, such is seen w/ pooling of secretions or destruction of bronchioles & alveoli.
Restrictive & obstructive diseases differ in what areas
Differ in the effect on lung volumes, air flow, pathophysiology, blood gas disturbances & physical assessment
What are characteristics of restrictive disorders?
Decreased lung expansion
Decreased lung compliance
Normal airflow
What are characteristics of obstructive disorders?
Increased lung expansion
Decreased lung compliance
Decreased expiratory airflow; prolonged expiratory time
Pulmonary function testing for restrictive pulmonary disorders would show...
Decreased TLC
Decreased TV
Pulmonary function testing for obstructive pulmonary disorders would show...
Decreased FEVs
Pathologic disturbances for restrictive disorders involve:
Internal problems:
-Decreased functioning alveoli
-Loss of pulmonary tissue
-Loss of respiratory muscle strength

External problems
-Disorders that decrease lung compliance external to the lungs
Pathologic disturbance for obstructive pulmonary disorders involve:
Bronchoconstriction
Bronchospasm
Airway edema
Airway collapse
Pooling of copious secretions
Associated blood gas disturbances for restrictive pulm. disorders include:
Decreased PaO2
--Normal to low V/Q ratio
--Increased intrapulmonary shunt

Increased PaCO2 & decreased pH if ventilatory pump failure is present
Assoicated blood gas disturbances for obstructive pulm disorders include:
Increased PaCO2
Decreased pH (if not compensated)
Normal to decreased PaO2 (may stay stable until severe disease state)
Associated lung sounds heard in restrictive pulm. disorders include:
Crackles (most common)
Rhonchi, if secretions build up in large airways
Associated lung sounds heard in obstructive pulm. disorders include:
-Wheezes (most common)
-Rhonchi, if secretions build up in large airways
-Diminished breath sounds (severe bronchospasm)
What are racial differences in benzodiazipine & narcotic analgesic use for African Americans?
• Special care should be taken when benzodiazepines are used in African Americans.
• roughly 15-20% of African Americans are genetically predisposed to delayed metabolism of benzodiazepines and as a result they may develop high serum levels of these drugs resulting in increased sedation and increased incidence of adverse effects.
• If benzodiazepines are to be used in African Americans then the smallest possible dose should be used and the patient should be monitored very closely during the first week of treatment.
What are s/s of benzodiazepine withdrawal?
abrupt cessation may lead to w/d characterized by nausea, headache, vertigo, malaise (general feeling of unwellness), and nightmares.

– Agitation & anxiety, delirium, tremors, tachycardia, hypertenstion, cramping of skeletal muscles, pain, hypertension, tachypnea
What are ways to manage potential withdrawal s/s of benzodiazepine & narcotic analgesics?
- Best approach: prevention
- Daily periods of decreased sedation can offset withdrawal and slow weaning of agents after prolonged use will decrease withdrawal symptoms


Patients should take the medicine only if it is medically necessary, and they should not take larger doses than prescribed. If a person has been taking a prescribed benzodiazepine, that person should very gradually reduce the dose. Patients should never discontinue these medications abruptly if they have been taking them for more than a few weeks on a regular basis.
Even with gradual decrease of the dose, however, some patients may continue to have troubling symptoms. These patients can be treated with anticonvulsants. Alternatively, the person can start benzodiazepine treatment again, taking a long-acting type of the drug and then very gradually reducing the dose.
What are the four levels of sedation in order of increasing sedation?
Light
Moderate
Deep
General Anesthesia
Describe the sedation scale:
Light sedation
1. Normal response to verbal command but Cognition is impaired.
2. Ventilation unaffected
3. CV function unaffected
Describe the sedation scale:
Moderate sedation
1. Depressed LOC but able to respond to verbal commands.
2. No airway ventilation required.
3. CV function unaffected
Describe the sedation scale:
Deep sedation
1. Depressed LOC-not easy to awaken but does respond to repeated or painful stimuli.
2.Impaired ventilation which requires airway management.
3. CV function usually adequate.
Describe the sedation scale:
General anesthesia
1. Unarousable even to painful stimuli.
2. Requires airway management.
3. CV function may be impaired.
For when do you use the moderate sedation level?
Common with invasive uncomfortable procedures: bronchoscopy, elective cardioversion
For when do you use the deep sedation level?
ARDS patients may require deep sedation with analgesia during acute phase of disease if they are not tolerating ventilator therapy and are asynchronous with ventilator.
For when do you use the general anesthesia level?
EEG - –BIS (Bispectral Index System)
between 40 and 60 indicates a level for general anesthesia
What is the purpose/rationale for sedation scales?
Scales provide scoring system to assess and record levels of sedation.

a tool that can enhance accurate and consistent medication titration by clinicians, improve understanding and communication, and reduce the incidence of excessive drug-induced stupor.
What is/are the purpose/rationale for continuous EEG monitoring?
In the ICU, Continuous EEG monitoring is used to monitor neurological function & assess depth of sedation. Indications for using EEG monitoring are:

1. the patient is unable to tolerate ventilator therapy with sedatives and analgesics alone &
2. in the case of trauma pts. w/ elevated intracranial pressures that do not respond to conventional therapy .


Neuromuscular Blockade Agents are used in the ICU and the patients are monitored using the EEG.
How would you interpret/quantify a person w/ continuous EEG monitoring?
The EEG assigns a score to the level of sedation as do the previous mentioned scales. Modified EEG systems: monitor EEG signals via devices on pt forehead and calculate a score between 0-99 or 100.
• Lower score = deeper sedation level
– BIS (Bispectral Index System)
• value of 0 equals EEG silence
• near 100 is the expected value in a fully awake
• between 40 and 60 indicates a level for general anesthesia
When is Vercuronium (a neuromuscular blockade agent) used?

Is it short, immediate, or long acting?
(immediate acting drug) for short surgical procedures, intubation & mechanical ventilation.

These agents do not produce amnesia effect, reduce anxiety or provide pain relief.
When is Rocuronium (a neuromuscular blockade agent) used?
short surgical procedures, preferred for rapid intubation & short outpatient surgical procedures.

These agents do not produce amnesia effect, reduce anxiety or provide pain relief.
What is the mech of action for neuromuscular blockade agents in the ICU setting?
o Compete with acetylcholine at the neuromuscular junctions. The neuromuscular junction is the point at which a neuron communicates with a skeletal muscle fiber. These drugs are used to cause paralysis for the performance of surgical procedures, endoscopic diagnostic procedures or facilitation of mechanical ventilation as in the ICU and therefore EEG monitoring is necessary to monitor level of sedation.
What is the most commonly used neuromuscular blockade agent in the ICU?

Is it long, immediate, or short acting?
Pancuronium (Pavulon) - long acting agent
What other agents should be given in conjunction w/ paralytic agents (neuromuscular blockade agents such as Pancuronium, Vecuronium, or Rocuronium)?
It is vital that narcotic analgesics (usually fentanyl or morphine) and sedatives (usually midazolam or propofol) are given in conjunction with these paralytic agents.
What is a serious side effect of neuromuscular blockade agents?
malignant hyperthermia which is characterized by extreme muscle rigidity and severe hyperpyrexia.
What is the rationale for using Sedatives?
Used to calm patients and make them unaware of their environment.


•Clinical rationale for uses:
o Low doses:
 Anxiety
 Short term tx for insomnia
o Moderate sedation:
 invasive uncomfortable procedures: bronchoscopy, elective cardioversion
 mechanically vented pts
 neuro pts with brain injury
o High dose:
 Deep sedation:
 General anesthesia (high dose)
o ARDS patients may require deep sedation with analgesia during acute phase of disease if they are not tolerating ventilator therapy and are asynchronous with ventilator
What is the rationale for using Narcotic analgesics?
Used for severe acute or chronic pain, preoperative medication and analgesia during anesthesia
What is the rationale for using Paralytics aka. neuromuscular blockade meds?
o paralysis for surgical procedures and endoscopic diagnostic procedures when reflex muscle movement could interfere with the procedure
o facilitation of mechanical ventilation by preventing resistance to passing of the endotrachal tube and in situations when pts “fight” or resist respirator
o Indications for use in ICU:
 the patient is unable to tolerate ventilator therapy with sedatives and analgesics alone
 Elevated intracranial pressures that don’t respond to conventional therapy (trauma)

o These agents do not produce amnesia effect, reduce anxiety or provide pain relief
What are the reversal agents for sedative (i.e. Diazepam (Valium),Midazolam (Versed))
OD/toxicity?
Reversal agent: Flumazenil (Romazicon)
What are the reversal agents for Narcotics (i.e. morphine) OD/toxicity?
Reversal agent: Naloxone (Narcan)
What are the reversal agents for Paralytics (i.e. Pancuronium (Pavulon), Vecuronium (Norcuron), and Rocuronium (Zemuron))?
Reversal agent: Cholinesterase inhibitor (e.g. Neostigmine & Pyridostigmine)
What is/are examples of the main Sedation drugs used?
o Diazepam (Valium) = of the Benzodiazepines
o Propofol (Diprivan)
o Midazolam (Versed)
What is/are examples of Narcotic analgesics used?
Main narcotic: morphine
What is/are examples of Paralytics used?

**What are the special considerations for drug admin.?
• Main Paralytic drugs used in ICU:
o Pancuronium (Pavulon) long acting
o Vecuronium (Norcuron) or Rocuronium (Zemuron) intermediate acting

It is vital that narcotic analgesics (usually fentanyl or morphine) and sedatives (usually midazolam or propofol) are given in conjunction with these paralytic agents
What is delirium?
the reversible global impairment of cognitive processes.
What are some s/s of delirium?
impaired short term memory, altered sensory perception, abnormal thought processes, inappropriate behavior
Pt may be restless or agitated: Sundowner Syndrome, ICU psychosis
What is used to tx a pt w/ delirium?
Tx: Haloperidol (Haldol) stabilizes cerebral function & agitation; ICU psychosis & Sundowner's Syndrome = delirium
**need to monitor ECG for prolonged QT**
Delirum is one of the s/s of what condition?
opiate & benzodiazepine withdrawal
--> to avoid withdrawal symptoms: daily interruptions in the sedative infusion is common; daily periods of ↓ sedation can offset withdrawal and slow weaning of agents after prolonged use will ↓ withdrawal symptoms.
What is the mechanism of action for Haldol, used to tx Delirium?
dopamine, acetylcholine, histamine, and norepinephrine receptors in the brain and periphery are blocked. Inhibition of psychotic symptoms is believed to be a result of dopamine, blockade in the brain.
What do you need to monitor when taking Haloperidol (Haldol) while in the ICU?
Monitor ECG for prolonged QT interval w/ Haldol --> too prolonged QT causes flat vital signs
T/F: It only takes a few days to wean off sedative drugs such as Ativan, Propofol, Benzos, etc.).
False. It takes a pt. weeks to wean off these sedative drugs. Require method of withdrawal using daily periods of putting the pt on "sedation vacation"