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Acidosis In Cardiopulmonary Arrest

ponent of arrests and that vigorous attention to the arterial pH was necessary for successful treatment [1,2]. This assumption appeared well founded because acidosis should theoretically develop rapidly during cardiopulmonary arrest. Metabolic acidosis is caused by tissue hypoxia with conversion to anaerobic metabolism; respiratory acidosis is caused by the cessation of spontaneous ventilation. Clearly, acidosis is undesirable during CPR because it has been shown to depress cardiac contractility and automaticity, as well as decrease the ventricular fibrillation threshold and the chronotropic and pres-