COMPARATIVE HEMODYNAMIC-EFFECTS OF PERIODIC OBSTRUCTIVE AND SIMULATEDCENTRAL 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 (GO) 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 I TP during OA, we studied seven preinstrumented sedated pigs with Oh an d simulated CA that were matched for blood gases and apnea periodiciti es (with 15- or 30-s apnea duration). Compared with OA, CA with 30-s a pnea duration produced comparable decreases in heart rate (from baseli ne 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 compa rable increases in LV end-diastolic pressure and LV end-diastolic myoc ardial 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 5,1 11 +/- 1,181 dyn.s.cm(-5), P < 0.01) and greater decreases in CO (3.18 +/- 0.31 to 2.74 +/- 0.26 1/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 findi ngs were observed with 15-s apnea duration. We conclude that CA produc ed greater depression of CO and greater changes of afterload-related L V dysfunction than did OA. Therefore, decreased ITP was not the domina nt factor determining LV function with apneas.