Left ventricular function was assessed in six patients with essentially normal cardiopulmonary function, in five patients with primary myocardial disease, and in 16 patients with chronic obstructive pulmonary disease by determining the response of the ventricle to an increased resistance to ejection. Studies were performed at the time of cardiac catheterization and increased resistance to left ventricular ejection was produced by the intravenous infusion of methoxamine. In the control patients, methoxamine produced an increase in stroke volume index (SVI), in stroke work index (SWI), and stroke power index (SPI), whereas left ventricular end-diastolic pressure (LVEDP) increased only moderately. In contrast SVI, SWI, and SPI fell, whereas LVEDP increased inordinately in the patients with myocardiopathy. The patients with chronic obstructive pulmonary disease responded to the infusion with an increase in SVI, SWI, SPI, and LVEDP comparable to the control patients. Furthermore, in this latter group of patients, a quantitatively similar response was observed in those with essentially normal resting hemodynamics, in those with resting pulmonary hypertension, and in those whose disease had progressed to the stage of right ventricular failure. This study provides no evidence that chronic obstructive pulmonary disease results in chronic impairment of left ventricular function, but on the contrary, has demonstrated that the left ventricle responds normally to an increased pressure load in these patients.

Adult↗

PubMed1968

Effect of acute hypoxia and hypercapnic acidosis on the development of acetylstrophanthidin-induced arrhythmias.

The effect of acutely induced hypoxia, hypercapnic acidosis, and the combination of the two on the amount of acetylstrophanthidin (AS) required to produce cardiac arrhythmias was determined in anesthetized dogs. Each animal was studied during ventilation with room air and again during ventilation with gas mixtures of appropriate concentrations; 24 hr separated the study periods. AS was infused intravenously at a rate of 5 mug/kg per min. Significantly less AS was required to produce arrhythmias during hypoxia and hypercapnic acidosis together than during the period with normal arterial Po(2), Pco(2), and pH (10 animals). Included in this group were two animals which had undergone previous bilateral adrenalectomy and four animals in which heart rate was maintained at the same frequency during both study periods. A significant reduction in the toxic dose of AS also was demonstrated in eight animals, two with constant heart rate, during hypoxia with normal arterial Pco(2) and pH. Hypercapnic acidosis alone (eight animals) did not significantly alter the toxic dose of AS. After the administration of propranolol (six animals) or hexamethionium (six animals), no significant difference was observed between the toxic dose of AS during hypoxia and that during ventilation with room air. Thus although hypoxia and hypercapnic acidosis together do reduce the amount of AS required to produce arrhythmias, it is the hypoxia which exerts the predominant effect on the development of this increased sensitivity to AS. Furthermore, this effect of hypoxia occurs primarily as a result of reflexly augmented sympathetic stimulation of the heart.

Adrenal Medulla↗

PubMed1967