RESPIRATORY AND CIRCULATORY RESPONSES TO ACUTE CARBON MONOXIDE POISONING

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Abstract
No hyperpnea was observable during rest in either dogs or men when subjected to acute and severe CO poisoning. The CO2 combining capacity was unchanged, the arterial pCO2 was increased, and accordingly the pH was shifted toward the acid side. In severe CO poisoning the respiratory center was depressed. The cardiac output showed no more than slight increases with HbCO saturations ranging up to 30%. From that level up to 50% HbCO the cardiac output increased as much as one-half. The direct action on the respiratory center of the acute hypoxemia produced by CO poisoning that is severe yet compatible with life is purely depressive in nature. From the data given the O2 tension in venous blood can be calculated for various levels of HbCO.

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