Systemic and myocardial hemodynamics during periodic obstructive apneas in sedated pigs

The effects of periodic obstructive apneas on systemic and myocardial hemodynamics were studied in nine preinstrumented sedated pigs under four conditions: breathing room air (RA), breathing 100% O₂, breathing RA after critical coronary stenosis (CS) of the left anterior descending coronary artery, and breathing RA after autonomic blockade with hexamethonium (Hex). Apneas with RA increased mean arterial pressure (MAP; from baseline 103.0 ± 3.5 to late apnea 123.6 ± 7.0 Torr, P < 0.001) and coronary blood flow (CBF; late apnea 193.9 ± 22.9% of baseline, P < 0.001) but decreased cardiac output (CO; from baseline 2.97 ± 0.15 to late apnea 2.39 ± 0.19 l/min, P < 0.001). Apneas with O₂ increased MAP (from baseline 105.1 ± 4.6 to late apnea 110.7 ± 4.8 Torr, P < 0.001). Apneas with CS produced similar increases in MAP as apneas with RA but greater decreases in CO (from baseline 3.03 ± 0.19 to late apnea 2.1 ± 0.15 l/min, P < 0.001). In LAD-perfused myocardium, there was decreased segmental shortening (baseline 11.0 ± 1.5 to late apnea 7.6 ± 2.0%, P < 0.01) and regional intramyocardial pH (baseline 7.05 ± 0.03 to late apnea 6.72 ± 0.11, P < 0.001) during apneas with CS but under no other conditions. Apneas with Hex increased to the same extent as apneas with RA. Myocardial O₂ demand remained unchanged during apnea relative to baseline. We conclude that obstructive apnea-induced changes in left ventricular afterload and CO are secondary to autonomic-mediated responses to hypoxemia. Increased CBF during apneas is related to regional metabolic effects of hypoxia and not to autonomic factors. In the presence of limited coronary flow reserve, decreased O₂ supply during apneas can lead to myocardial ischemia, which in turn adversely affects left ventricular function.