Cardiac Depressant Effect of CO2 and Its Reversal

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Abstract
Acute myocardial failure is observed when the denervated heart-lung preparation is rendered acidotic by increasing abruptly above 5% the CO2 concentration in a respiratory gas mixture of CO2 and O2. Evidences of this failing state include increased vena caval and left atrial pressures, decreased aortic pressure, diminished cardiac output against a constant resistance and acute cardiac dilatation. After production of acidotic failure by administration of 15% CO2 for 3–5 minutes (arterial ph = 7.14 ± 0.05, output negligible), values for these variables (with the exception of ph) can be returned to control levels by injecting 4 µg/min. of adrenaline or noradrenaline. Furthermore, the signs of CO2 failure do not appear if the adrenaline infusion is begun concomitant with high CO2 ventilation. These results were interpreted as indicating that in the intact dog, cardiac tolerance to hypercapnia may be the result of a stimulation of the sympatho-adrenal system, which counteracts the negative inotropic effect of CO2 on the myocardium. Reversal of CO2-induced failure was also observed within 5–10 minutes after injection of 0.1 mg of acetyl strophanthidin.