Key result
In dogs with acute ischemic left ventricular failure, hypercapnia aggravated heart failure hemodynamics, which was reversed by normalizing pH, indicating pH rather than PaCO2 drives the deterioration.
Why the study?
Do changes in PaCO2 and pHa affect myocardial blood flow and central hemodynamics in dogs with acute ischemic left ventricular failure?
Do changes in PaCO2 and pHa affect myocardial blood flow and central hemodynamics in dogs with acute ischemic left ventricular failure?
In a canine model of acute ischemic left ventricular failure, hemodynamic deterioration during hypercapnia is driven by changes in pH rather than PaCO2.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for pH-targeted ventilation in acute HF; leaves open translation to human ischemic cardiomyopathy.
The present study was undertaken to examine the effects of changes in PaCO2 and pHa on myocardial blood flow and central hemodynamics during acute ischemic left ventricular failure. Six closed-chest dogs anesthetized with pentobarbital were hyperventilated, and CO2 was added to the inspiratory gas to induce: a) normocapnia, b) hypocapnia, c) hypercapnia, and d) hypercapnia with sodium carbonate given to correct pH. Embolization of the left coronary artery with 50-microns microspheres resulted in deterioration of left ventricular function, as indicated by increased left ventricular end-diastolic pressure and mean pulmonary arterial pressure, while cardiac output decreased. During hypocapnia with left ventricular failure, the central hemodynamics remained unchanged, while a minor but nonsignificant decrease in myocardial blood flow was observed. Hypercapnia aggravated the heart failure, as indicated by increased left ventricular end-diastolic pressure, mean right atrial pressure, and mean pulmonary arterial pressure; however, the pump function of the heart was unchanged, as demonstrated by the unaltered cardiac output, heart rate, and mean aortic blood pressure. The changes in the central hemodynamics were reversed when pH was normalized during hypercapnia. Thus, in the present study pH, and not PaCO2, was responsible for the hemodynamic deterioration observed during hypercapnia in the failing heart.
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Wexels et al. (1987) studied Acute ischemic left ventricular failure (n=6). Changes in PaCO2 and pHa (hypocapnia, hypercapnia, hypercapnia with sodium carbonate) vs. Normocapnia was evaluated on Myocardial blood flow and central hemodynamics. In dogs with acute ischemic left ventricular failure, hypercapnia aggravated heart failure hemodynamics, which was reversed by normalizing pH, indicating pH rather than PaCO2 drives the deterioration.
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