Pulmonary edema respiratory alkalosis

Respiratory alkalosis secondary to hyperventilation is usually observed secondary to CNS stimulation of ventilatory centers as a result of trauma, sepsis, or shock. Lung auscultation may reveal crackles (pulmonary edema) or absence of breath sounds (pneumothorax, hemothorax). Chest roentgenogram can confirm early suspicions or disclose an undetected abnormality such as pneumonia (pulmonary infiltrates). Continued insult to the lungs may result in adult respiratory distress syndrome. 

Nausea, vomiting, tinnitus, and hyperventilation are seen early in toxicity. As severity of toxicity increases, intractable vomiting, hyperthermia, hypotension, tachycardia, confusion, coma, seizures, pulmonary edema, acute renal failure, and death may occur. Hyperglycemia may be seen early, whereas hypoglycemia may occur later in toxicity. Acid-base disturbances such as respiratory alkalosis and/or metabolic acidosis may be noted. Signs and symptoms of salicylate toxicity may be noted as blood levels rise over 30mgdN. ... 

Acute toxicity manifests primarily in the CNS, cardiovascular system, and gastrointestinal system. CNS signs include restlessness, tremor, nervousness, headache, insomnia, tinnitus, confusion, delirium, psychosis, and seizures. Cardiac manifestations of overdose include sinus tachycardia, various dysrhythmias, asystole, and cardiovascular collapse. Other findings include tachypnea, nausea, vomiting, hematemesis, diarrhea, and fever. Case reports also include rhabdomyolysis and pulmonary edema. Laboratory findings include metabolic acidosis, respiratory alkalosis, ketosis, hypokalemia, and hyperglycemia. The estimated lethal dose in adults is 150-200 mg kg whereas doses of 10-15mgkg ... 

All patients developed a compensatory metabolic acidosis due to chronic hyperventilation. Respiratory alkalosis was thought to have developed because of capillary leak into the lungs producing borderline or frank pulmonary edema. After several days a superimposed normal anion gap acidosis developed from dilution by large volumes of saline fluid resuscitation. The authors found no defects in renal handling of calcium, phosphorous, or magnesium. There was no evidence of a renal acidification defect or renal tubular acidosis. 

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