Pulmonary hypoxemia

In advanced COPD, airflow obstruction, damaged bronchioles and alveoli, and pulmonary vascular abnormalities lead to impaired gas exchange. This results in hypoxemia and eventually hypercapnia. Hypoxemia is initially present only during exercise but occurs at rest as the disease progresses. Inequality in the ventilation/perfusion ratio (VAQ) is the major mechanism behind hypoxemia in COPD. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

Respiratory alkalosis is characterized by an increased arterial pH, a primary decrease in the arterial PaC02 and, when present for sufficient time, a compensatory fall in the HCOf concentration. Respiratory alkalosis represents hyperventilation and is remarkably common. The most common etiologies of respiratory acidosis are listed in Table 25-7 and range from benign (anxiety) to life-threatening (pulmonary embolism). Some causes of hyperventilation and respiratory acidosis are remarkably common (hypoxemia or anemia). 

In a patient with chronic respiratory acidosis (e.g., chronic obstructive pulmonary disease), treatment is essentially similar to that for acute respiratory acidosis with a few important exceptions. Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg because the drive to breathe depends on hypoxemia rather than hypercarbia. 

The most common cause of acute respiratory failure in COPD is acute exacerbation of bronchitis with an increase in sputum volume and viscosity. This serves to worsen obstruction and further impair alveolar ventilation, resulting in worsening hypoxemia and hypercapnia. Additional causes are pneumonia, pulmonary embolism, left ventricular failure, pneumothorax, and CNS depressants. 

Symptoms Symptoms include acute onset of fever, chest tightness, cough, dyspnea, nausea, and arthralgias which occur four to eight hours after inhalational exposure. Airway necrosis and pulmonary capillary leak resulting in pulmonary edema would likely occur within eighteen to twenty-four hours, followed by severe respiratory distress and death from hypoxemia in thirty-six to seventy-two hours. 

At present, we suspect that toxin-LR causes heart failure in mice, perhaps due to suddenly increased resistance to pulmonary blood flow. Heart failure in mammals is known to cause engorgement of the liver with blood. Pulmonary vascular occlusion may also cause secondary hypoxemia and shock. However, biochemical pathways that are initiated by toxin-LR and that lead to the onset of discernable signs of illness after 30 min are unidentified. The 30 min asymptomatic period following toxin injection may be associated with a toxin-initiated cascade of biochemical events which lead to overt signs of illness. 

In another accidental exposure of five chlorine plant workers and 13 nonworkers, rales, dyspnea, and cyanosis were observed in the most heavily exposed and cough was present in nearly all the patients. Pulmonary function tests 24—48 hours after exposure showed airway obstruction and hypoxemia these conditions cleared within 3 months except in four of the chlorine workers, who still showed reduced airway flow and mild hypoxemia after 12-14 months. ... 

Two fatalities occurred after reentry of a home fumigated with sulfuryl fluoride. The male experienced severe dyspnea and cough, followed by generalized seizure and cardiopulmonary arrest within 24 hours. The female initially had weakness, nausea, and repeated vomiting within 4 days, there was severe hypoxemia and diffuse pulmonary infiltrates. Ventricular fibrillation and death occurred on day 6. The concentration of sulfuryl fluoride gas was not available, and the difference in time of death for the two individuals was not explainable. 

Puimonary reactions Pulmonary reactions characterized by acute dyspnea, hypoxemia, and interstitial infiltrates have been observed in neutropenic patients receiving amphotericin B and leukocyte transfusions. Separate the infusion as far as possible from the time of a leukocyte transfusion. 

Pulmonary - Pulmonary symptoms (especially a dry, nonproductive cough) or a nonspecific pneumonitis indicate a potentially dangerous lesion and require interruption of treatment and careful investigation. The typical patient presents with fever, cough, dyspnea, hypoxemia, and an infiltrate on chest x-ray. 

In conditions that lead to chronic hypoxemia, such as smoking and chronic obstructive pulmonary disease, an increased concentration of BPG In the RBCs promotes O2 dissociation from hemoglobin in tissues to support cellular function. 

Pulmonary eosinophilic syndrome, characterized by extreme hypoxemia, eosinophilia, interstitial pneumonitis, hilar lymphadenopathy, and pleural effusions, can be severe and can occur with as little as 7 to 9 days of therapy with the tetracyclines. In severe cases steroid therapy is required, but the outcome following drug discontinuation is nearly always good. 

NO itself can be used therapeutically. Inhalation of NO results in reduced pulmonary artery pressure and improved perfusion of ventilated areas of the lung. Inhaled NO is used for pulmonary hypertension, acute hypoxemia, and cardiopulmonary resuscitation, and there is evidence of short-term improvements in pulmonary function. 

Arevalo RP, Bullabh P, Krauss AN, Auld PAM, Spigland N. Octreotide-induced hypoxemia and pulmonary hypertension in premature neonates. J Pediatr Surg 2003 38 251-3. 

In children, capsaicin spray was demonstrated to cause a severe bronchospasm and pulmonary edema (Winograd, 1977 Bdlmire et al, 1996). In the Billmire study, a 4-week-old infant was exposed to 5% pepper spray after discharge from a self-defense device. The infant suffered respiratory failure and hypoxemia, requiring immediate extracorporeal membrane oxygenation. Inhaled capsaicin causes an immediate increase in airway resistance (Fuller, 1991). This dose-dependent bronchoconstriction after capsaicin inhalation in humans is the same as that demonstrated in asthmatics and smokers (Fuller et al, 1985). The capsaicin-induced bronchoconstriction and release of substance P is due to stimulation of nonmyelinated afferent C-fibers. 

The lethal effects of MIC were due to hypoxemia primarily because of pulmonary effects. HCN also causes... 

Lee, K.-N., Lee, H.-J., Shin, W.W., Webb, W.R. Hypoxemia and hver cirrhosis (hepatopulmonary syndrome) in eight patients comparison of the central and peripheral pulmonary vasculature. Radiology 1999 211 549-553... 

Pulmonary features of the adverse effects of aldesleukin include lung opacities, diffuse pulmonary interstitial edema, pleural effusions, alveolar edema, and hypoxemia, with full and rapid recovery after treatment withdrawal (29,30). 

Almitrine is a respiratory stimulant that improves hypoxemia in about 80% of patients with severe chronic obstructive pulmonary disease (SEDA-17, 212). Oral almitrine bimesilate (100 mg/day) increased Pa02 in patients with severe chronic obstructive pulmonary disease without altering mean pulmonary artery pressure (1). Adverse effects were rarely observed and it was concluded that long-term treatment was safe. In other studies, respiratory, digestive, and neurological symptoms have been noted but were often pre-existent (2,3). 

Hypoxemia has been incidentally reported (SEDA-15, 125) (24), and most probably resulted from an increase in right-to-left cardiac shunting (in a patient with a ventricular septal defect and pulmonary atresia). Atracurium (0.2 mg/kg) may have produced a fall in systemic vascular resistance, perhaps from histamine release pancuronium was subsequently given without incident. 

In pulmonary hypertension, both verapamil and nifedipine increase mean right atrial pressure in association with hypotension, chest pain, dyspnea, and hypoxemia the severe hemodynamic upset resulted in cardiac arrest in two patients after verapamil and death in another after nifedipine (54). A patient with pulmonary hypertension also developed pulmonary edema whilst taking nifedipine (55) and another seems to have developed this as an allergic reaction (56). 

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