Smoking, birth control, hx of DVT, HTN, HF, COPD, dehydration, ^ Age, major operations (hip, knee, abd, pelvic procedures) and traveling in cramped quarters or sitting for long periods of time.

(Black p. 1591)

Tachypnea, dyspnea, anxiety or fretfulness, chest pain, tachycardia, hypoxemia, crackles, coughing, diaphoresis, syncopy, hemoptysis, and fever.

(Black p. 1592)

Chest X-Ray, V/Q lung scan, spiral CT scan of the chest and Pulmonary angiography. D-dimer can rule out PE but not definitively diagnose PE.

(Black p. 1592)

• Monitor for hypoxemia, respiratory compromise, and assess vital signs, adventitious lung sounds frequently, ABG or oximetry values, and manifestations of right-sided heart failure.
• Auscultate heart sounds frequently, assessing for murmurs or extra heart sounds. Check for peripheral edema, distended neck veins, and liver engorgement.
• To facilitate breathing, elevate the head of the bed and apply oxygen.
• PE is thrombus from the lower legs, elevate the legs with caution to avoid severe flexure of the hips as it increases the risk of new thrombi.
• Fear with the sudden onset of severe chest pain and inability to breathe leads to anxiety, restlessness, and apprehension. Emotional support can reduce anxiety and lessen dyspnea.
• Analgesics are given as needed to reduce pain and anxiety. Morphine is the most common agent. Anxiety and pain increase oxygen demand and dyspnea. Administer oral care with soft brushes or rinses while oxygen is in use, especially if the client breathes through the mouth.

(Black p. 1593)

• Treatment of pneumonia should include organism-specific antibiotic therapy, respiratory support as needed, nutritional support, and fluid and electrolyte management.
• Initial drug therapy should consist of empirical broad-spectrum antibiotics until the specific organism has been identified through sputum culture analysis.
• Oxygen should be administered as ordered, and bronchodilator medications, postural drainage, chest physiotherapy, and nasotracheal suctioning may be used to maintain airway patency.

(Black  p. 1600)

 Respiratory failure is a broad, nonspecific clinical diagnosis indicating that the respiratory system is unable to supply the oxygen necessary to maintain metabolism or cannot eliminate sufficient carbon dioxide.

(Black p. 1635)

Hypoxemic respiratory failure may be caused by diffuse problems such as pulmonary edema; near-drowning; adult (acute) respiratory distress syndrome (ARDS); or localized problems such as pneumonia, bleeding into the chest, or lung tumors.

(Black p. 1635)

Pulmonary edema occurs when capillary hydrostatic pressure is increased, promoting movement of fluid into the interstitial space of the alveolar-capillary membrane. Initially, increased lymphatic flow removes the excess fluids, but continued leakage eventually overwhelms this mechanism. Gas exchange becomes impaired by the thick membrane. Increasing interstitial fluid pressure ultimately causes leaks into the alveolar sacs, impairing ventilation and gas exchange.
(Black p. 1636)

• Correct Hypoxemia: oxygen therapy at high FiO2 levels.  Positive- pressure ventilation such as continuous positive airway pressure (CPAP) or mechanical ventilation.
• Reduce Preload: Place pt in an upright position.  Diuretics are prescribed to promote fluid excretion. Nitrates, such as nitroglycerin, are used for their vasodilating properties, decreasing the workload of the heart muscle.
• Reduce Afterload: Afterload is reduced to diminish workload on the left ventricle. Antihypertensive agents are prescribed. Angiotensin-converting enzyme (ACE) inhibitors are considered essential in the treatment of pulmonary edema from congestive heart failure. ACE inhibitors reduce afterload and improve stroke volume and cardiac output. There is also a slight reduction in preload when renal perfusion is improved and diuresis begins. Morphine is prescribed to reduce the sympathetic nervous system response and to reduce anxiety from the dyspnea.
• Support Perfusion: The left ventricle is supported by using inotropic medications such as dobutamine, dopamine, and norepinephrine.  Urine output is monitored closely to determine whether renal perfusion is adequate. An intra-aortic balloon pump (IABP) may be required with severe heart failure and pulmonary edema.

(Black p. 1637)

Ventilatory failure is the inability of the body to sustain respiratory drive or the inability of the chest wall and muscles to mechanically move air in and out of the lungs.

The hallmark of ventilatory failure is an elevated CO2 level.

(Black p. 1638)

• Headache, dyspnea, confusion, decreased level of consciousness, restlessness, agitation, dizziness, tremors, and initial hypertension, followed by hypotension and tachycardia.
• Early signs include rapid, shallow breathing with increased inspiratory muscle movement. Late findings include cyanosis, nasal flaring, and sternal and intercostal retractions.
• The increased work of breathing may lead to cool, clammy skin (diaphoresis), dysrhythmias, and decreased capillary refill.

(Copstead p. 530)

• Disorders of the neuromuscular chest apparatus (poliomyelitis, Guillain-Barré syndrome, quadriplegia, hemiplegia, ALS and MS).
• Disorders affecting the chest skeletal system (kyphoscoliosis), and chest trauma (rib and sternal fractures).
• Shock (e.g., septic, hypovolemic), PE, and pulmonary edema.
• Extreme obesity may lead to alveolar hypoventilation.
• Lung diseases: advanced emphysema, pneumonia, asthma, COPD, cysticfibrosis and ARDS.
• CNS: Drug overdose, TIA, brain trauma, hypothyroidism, CNS infection and brain tumor.

(Copstead p. 530)

• Decreased O₂ affinity.
• Release of O₂ from the hemoglobin molecule.
• Moves O₂ from the blood to the tissues.
• The pH is acidotic generally below 7.2.
• Acidosis, hyperthermia, increased PaCO2, anemia, chronic hypoxia and hyperthyroidism leading to increased end product of RBC metabolism.

(Copstead p. 527)

• Increased O₂ affinity.
• Binding of O₂ to the hemoglobin molecule.
• Moves O₂ from the tissues to the blood (hypoxia).
• The pH is alkalotic generally above 7.6.
• May be caused by alkalosis, hypothermia, decreased PaCO2, increased end product of RBC metabolism and CO poisoning.

(Copstead p. 527)

 Sudden, progressive form of respiratory failure characterized by severe dyspnea, refractory hypoxemia, and diffuse bilateral infiltrates. It follows acute and massive lung injury that results from a variety of clinical states, often occurring in previously healthy people.

(Black p. 1652)

• Viral, bacterial, or fungal pneumonias
• Fat embolus
• Aspiration (e.g., foreign material, drowning, vomitus)
• Inhaled toxins/smoke
• Prolonged exposure to high concentrations of oxygen (ventilator)
• Sepsis/Shock/Multisystem trauma
• Disseminated intravascular coagulation (DIC)
• Pancreatitis
• Uremia
• Drug overdose
• Anaphylaxis
• Prolonged heart bypass surgery
• Massive blood transfusions
• Pregnancy-induced hypertension
• Increased intracranial pressure
• Radiation therapy

(Black p. 1653)

•  Seen approximately 24 hours after the initial insult and consists of damage to the capillary endothelium and leakage of fluid into the pulmonary interstitium.
• Microemboli also develop and cause a further increase in pulmonary artery pressures.
• Inflammatory responses accompany the pulmonary parenchymal damage, leading to the release of toxic mediators, the activation of complement, the mobilization of macrophages, and the release of vasoactive substances from mast cells.
• There is further damage to the basement membrane, interstitial space, and alveolar epithelium.
• Fibrin, blood, fluid, and protein exude into the interstitial spaces around the alveoli and increase the distance across the capillary membrane.

(Black p. 1653)

• Begins about 7 to 10 days after inital insult.
• Type I and type II alveolar cells are ultimately damaged, resulting in decreased surfactant production, alveolar collapse, and atelectasis, leading to further impairment in gas exchange.
• Significant hypoxemia is present because of decreased surfactant production, intrapulmonary shunting, and V/Q mismatch.

(Black p. 1653)

•  Occurs about 2 to 3 weeks after inital insult.
• There is irreversible deposition of fibrin into the lung, resulting in pulmonary fibrosis, further decreasing lung compliance and worsening hypoxemia.
• The end result is a significant V/Q imbalance and profound arterial hypoxemia.

(Black p. 1653)

• Mechanical ventilation, ET intubation, and PEEP are usually required to maintain adequate blood oxygen levels.
• The goal of ventilatory support is to use the least amount of FiO2 and PEEP possible to maintain oxygen saturation at or above 90% while decreasing the potential of oxygen toxicity.
• PEEP will also be used to decrease intrapulmonary shunting and to recruit collapsed alveoli.
• Nitric oxide (NO) is now being used more often in the treatment of ARDS. NO causes selective vasodilation in the pulmonary vascular system and is a powerful bronchodilator. Inhaled NO dilates the capillary bed of the lungs, which in turn reduces the pressure in the pulmonary arteries without lowering systemic blood pressure.
• Antioxidants, scavengers of oxygen free radicals, are also being used. N-Acetylcysteine and procysteine have been effective in reducing the degradative effect of the proteases. Steroids have been used with improvement in pulmonary function.
• The prone position has been used to improve oxygenation by changing the distribution of perfusion. The belief is that ARDS does the greatest damage in the gravity-dependent parts of the lungs. By placing the client in a prone position, there is a change in the dependent portions of the lung, resulting in increased perfusion to the less damaged portions of the lungs and decreased pulmonary shunting. Prone positioning is also thought to reduce compression of the lung by the heart, improve chest wall compliance, and result in better draining of bronchial secretions.
• Placing a client in prone position has side effects including hypotension, desaturation, and dysrhythmias, although these appear to be short term. 
• Kinetic therapy via continuously rotating beds can also be used to improve ventilation. The constant postural drainage assists in removing airway plugs. To be effective, the movement must be at least 45 degrees from side to side, which is best accomplished by a rotation bed.

(Black p. 1654)

 Lung fibrosis. 

Complications arising during supportive management may include cardiac dysrhythmias caused by hypoxemia, oxygen toxicity, renal failure, thrombocytopenia, gastrointestinal bleeding secondary to stress ulcers, sepsis from invasive lines, and disseminated intravascular coagulation (DIC).

(Black p. 1656)

Positive End-Expiratory Pressure

Applied during mechanical ventilation.

Applies positive airway pressure that keeps the alveoli open and reduces the amount of shunting with the goal that the FiO2 may be reduced to the lowest possible level to maintain gas exchange and to prevent oxygen toxicity

(Black p. 1643)

Continuous Positive Airway Pressure

Applied to a client with spontaneous respiration
Applies positive airway pressure that keeps the alveoli open and reduces the amount of shunting with the goal that the FiO2 may be reduced to the lowest possible level to maintain gas exchange and to prevent oxygen toxicity.

(Black p. 1643)

In the ideal state, 4 L/min of alveolar ventilation is matched to 5 L/min of capillary blood flow in the lungs, creating a normal alveolar ventilation-to-perfusion ratio (V_A/Q) of 0.8  Two major factors that affect this normal V_A/Q ratio are right-to-left shunt, and regional ventilation and perfusion changes. Other factors influencing the ratio are position changes, exercise, bed rest, and lung disease.

(Copstead p. 525)

• Underperfusion.
• Conceptually related to physiologic dead space, in which the alveolar unit is ventilated, but not perfused.
• Low PCO₂ and normal PAO₂ and can be viewed as a respiratory reserve, which can be used if perfusion is restored.
• Deadspace

(Copstead p. 526)

• Underventilated
• Lower PaO₂ (hypoxemia)
• Occurs regionally in areas where the airways are partially obstructed and airflow rates are low.
• Responsive to treatment with oxygen because the airways are only partially obstructed, so it is possible for oxygen to enter the alveoli by diffusion.

• No Ventilation.
• Functionally equivalent to right-to-left shunt, contributes to lowering of PaO2
• In patients with acute respiratory failure (ARF), physiologic shunt may rise to more than 50%.
• Although physiologic shunt is similar to low V_A/Q in affecting low oxygen levels, shunt is not responsive to oxygen therapy because the alveoli are collapsed or consolidated and oxygen cannot gain entry into them.

(Copstead p. 526)

RSV

Respiratory Syncytial Virus

• Acute viral infection with maximum effect at the bronchiolar level. The infection occurs primarily in winter and spring.
•  Related to parainfluenza virus.
• RSV affects the epithelial cells of the respiratory tract. The ciliated cells swell, protrude into the lumen, and lose their cilia.
• RSV produces a fusion of the infected cell membrane with cell membranes of adjacent epithelial cells, thus forming a giant cell with multiple nuclei.
• At the cellular level this fusion results in multinucleated masses of protoplasm, or syncytia.

(Hockenberry p. 1334)

• Bronchiolar mucosa swells, and lumina are subsequently filled with mucus and exudate.
• The walls of the bronchi and bronchioles are infiltrated with inflammatory cells, and peribronchiolar interstitial pneumonitis is usually present.
• Luminal epithelial cells are shed into the bronchioles when they die, the lumina are frequently obstructed, particularly on expiration.
• The varying degrees of obstruction produced in small air passages lead to hyperinflation, obstructive emphysema resulting from partial obstruction, and patchy areas of atelectasis.
• Dilation of bronchial passages on inspiration allows sufficient space for intake of air, but narrowing of the passages on expiration prevents air from leaving the lungs.
• Thus air is trapped distal to the obstruction and causes progressive overinflation (emphysema).

(Hockenberry p. 1335)

•  Direct contact with respiratory secretions, mainly as a result of inoculation from hand to eye, nose, or other mucous membranes; by direct inoculation by large-particle aerosols; or by self-inoculation from contaminated fomites.
• RSV in secretions can survive for hours on countertops, gloves, paper tissues, and cloth, and for half an hour on skin; it remains infectious when transferred from hands or objects.

(Hockenberry p. 1335)

• Classic manifestations include signs of altered air exchange, such as wheezing, retractions, crackles, dyspnea, tachypnea, diminished breath sounds, rhinorrhea, pharyngitis, coughing, sneezing, possible ear or eye infection, intermittent fever.
• As Illness Progresses: Increased coughing and wheezing, air hunger, tachypnea and retractions, and cyanosis.
• Severe Illness: Tachypnea >70 breaths/min, listlessness, apneic spells, poor air exchange and poor breath sounds.

(Hockenberry p. 1335)

• Bronchiolitis is treated symptomatically with cool humidified oxygen, adequate fluid intake, airway maintenance, and medications.
• Most children with bronchiolitis can be managed at home.
• Hospitalization is usually recommended for children with respiratory distress or those who cannot maintain adequate hydration.
• Other reasons for hospitalization include complicating conditions, such as underlying lung or heart disease or associated debilitated states, or a caregiver whose adequacy is questionable.
• The child who is tachypneic or apneic, has marked retractions, seems listless, or has a history of poor fluid intake should be admitted.

(Hockenberry p. 1336)

• Respiratory syncytial virus immunoglobulin (RSV-IGIV, or RespiGam).
• RespiGam is an IV preparation of immunoglobulin G that provides neutralizing antibodies against subtype A and B strains of RSV.
• The drug is given on an inpatient or outpatient basis before or during the RSV epidemic season via IV. Subsequent doses are given every month to maintain protection.
• RespiGam is used to prevent RSV infection in high-risk infants.
• RespiGam is not approved by the Food and Drug Administration for patients with congenital heart disease and should not be used in patients with cyanotic congenital heart disease.

(Hockenberry p. 1336)

• Palivizumab (Synagis).
• It is a genetically engineered RSV monoclonal antibody.
• Palivizumab is favored over RSV-IGIV because it can be given monthly in an IM injection, it has none of the risks of complications associated with IV administration of human immunoglobulin products, and it does not interfere with the measles-mumps-rubella and varicella vaccines.
• Palivizumab is appropriate for prophylaxis for high-risk infants, including those with congenital heart disease.

(Hockenberry p. 1336)