Comparative hemodynamic effects of periodic obstructive and simulated central apneas in sedated pigs.

It has been speculated that because of increased left ventricular (LV) afterload, decreased intrathoracic pressure (ITP) is responsible for decreased cardiac output (CO) in obstructive sleep apnea. If this were true, then obstructive apnea (OA) should have a greater effect on CO than would central apnea (CA). To assess the importance of decreased ITP during OA, we studied seven preinstrumented sedated pigs with OA and simulated CA that were matched for blood gases and apnea periodicities (with 15- or 30-s apnea duration). Compared with OA, CA with 30-s apnea duration produced comparable decreases in heart rate (from baseline to end apnea: OA, 106.6 +/- 4.8 to 93.4 +/- 4.4 beats/min, P < 0.01; and CA, 111.1 +/- 6.2 to 94.0 +/- 5.2 beats/min, P < 0.01) and comparable increases in LV end-diastolic pressure and LV end-diastolic myocardial segment length but greater increases in mean arterial pressure (97.1 +/- 3.7 to 107.7 +/- 4.3 Torr, P < 0.05; and 97.3 +/- 4.8 to 119.3 +/- 7.4 Torr, P < 0.01) and systemic vascular resistance (2,577 +/- 224 to 3,346 +/- 400 dyn . s . cm-5, P < 0.01; and 2,738 +/- 294 to 5,111 +/- 1,181 dyn . s . cm-5, P < 0.01) and greater decreases in CO (3.18 +/- 0.31 to 2.74 +/- 0.26 l/min, P < 0. 05; and 3.07 +/- 0.38 to 2.30 +/- 0.36 l/min, P < 0.01) and stroke volume (32.2 +/- 2.9 to 25.9 +/- 2.4 ml, P < 0.05; and 31.5 +/- 1.9 to 19.8 +/- 3.1 ml, P < 0.01). Only CA increased LV end-systolic myocardial segment length. Similar findings were observed with 15-s apnea duration. We conclude that CA produced greater depression of CO and greater changes of afterload-related LV dysfunction than did OA. Therefore, decreased ITP was not the dominant factor determining LV function with apneas.