Acute respiratory failure causes

UoshimaN, Yoshioka K, T )shi J, Wada S, Fujiwara Y. Acute respiratory failure caused hy vinorelbine tartrate in a patient with non-small cell lung cancer. Intern Med(2001) 40, TT9-82. 

Skeletal muscle dysfunction can cause myalgia, bone pain, weakness, and potentially fatal rhabdomyolysis. Respiratory muscle weakness and diaphragmatic contractile dysfunction can cause acute respiratory failure. 

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. 

The commonest form of lung damage is an interstitial alveolitis, although pneumonitis and bronchiolitis obhter-ans have also been reported, as have sohtary localized fibrotic lesions, non-cardiac pulmonary edema, pleural effusions, acute respiratory failure, acute pleuritic chest pain, and adult respiratory distress syndrome (SEDA-17, 220) (SEDA-18, 201) (66-68). Amiodarone has also been reported to cause impairment of lung function, even in patients who do not develop pneumonitis (69), and preexisting impairment of lung function may constitute a contraindication to amiodarone. 

In acute promyelocytic leukemia arsenic trioxide can cause a syndrome similar to the retinoic acid syndrome (15), with fever, skin rash, edema, pleural effusion, pericardial effusion, and acute respiratory failure. 

The clinical manifestations of serum phosphate depletion depend on the length and degree of the deficiency. Moderate hypophosphatemia of 1.5 to 2,4 mg/dL (0.48 to 0.77 mmol/L) is usually not associated with clinical signs and symptoms (unless chronic, when osteomalacia or rickets develops). Plasma concentrations less than 1.5 mg/dL (0.48 mmol/L) may produce clinical manifestations. Because phosphate is necessary for the formation of ATP, glycolysis and cellular function are impaired by low intracellular phosphate concentrations. Muscle wealmess, acute respiratory failure, and decreased cardiac output may occur in phosphate depletion. At very low serum phosphate (<1 mg/dL or <0.32 mmol/L), rhabdomyolysis may occur. Phosphate depletion in erythrocytes decreases erythrocyte 2,3-diphosphoglycerate, which causes tissue hypoxia because of increased affinity of hemoglobin for oxygen. Severe hypophosphatemia (serum phosphate concentration <0.5 mg/dL [<0.16 mmol/L]) may result in hemolysis of the red blood cells. Mental confusion and frank coma also may be secondary to the low ATP and tissue hypoxia. If hypophosphatemia is chronic, impaired mineralization of bone produces rickets in children and osteomalacia in adults. 

Doxapram is an analeptic that increases the depth of respirations (tidal volume) by stimulating the respiratory center in CNS respiratory rate may increase slightly. It may elevate BP by increasing cardiac output. Respiratory depression from opiates is reversed without affecting pain relief. It is indicated when one requires the stimulation of deep breathing in postoperative patients for reversal of respiratory depression caused by anesthesia (other than muscle relaxants) or drug overdose and as a temporary measure in acute respiratory failure in patients with chronic obstructive pulmonary disease (COPD) who are not undergoing mechanical ventilation. 

Flusser G, Gurman G, Zirkin H, et al. Desquamative interstitial pneumonitis causing acute respiratory failure, responsive only to immunosuppressants. Respiration 1991 58 324-326. 

The importance of respiratory failure associated with spinal cord injury depends on the level of the injury. High spinal cord injury, above C-3, causes diaphragm paralysis. This virtually always causes respiratory failure in infants and young children. NPPV can be tried in older children who have a sufficient respiratory autonomy for at least 8 to 10 hr/day. In patients with lower cervical cord injury, expiratory muscle function is severely compromised and thus cough is defective, and the clearance of bronchial secretions is greatly impaired. As a result, retention of secretions leading to atelectasis and bronchopneumonia frequently occurs in such patients and may require short periods of NPPV during episodes of acute respiratory failure. 

NPPV is also indicated when acute exacerbations caused by bronchitis or pneumonia precipitate the patient in acute respiratory failure. But ideally, NPPV should be initiated before an acute exacerbation, which does not represent an optimal physiological and psychological situation to start such a treatment. 

Casualties presented or were carried to emergency reception points without any evidence of physical trauma and apparently suffering from severe respiratory distress or total failure. The video footage did not show clear signs of acute respiratory failure in many of the cases although this must be assumed to be the cause of death in the cases of exposure to sarin. 

Lung disease is the cause of one in six deaths in the United States (American Lung Association, 2008), totahng close to 400,000 Americans each year. Unlike death rates from many other major diseases in the United States, death rates due to lung disease are increasing. The primary contributors to lung disease deaths are acute respiratory failure and chronic respiratory insufficiency. 

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