ROLE OF HYPOXEMIA AND HYPERCAPNIA IN ACUTE CARDIOVASCULAR-RESPONSE TOPERIODIC APNEAS IN SEDATED PIGS

The effects of hypoxemia and hypercapnia in acute cardiovascular respo nse to periodic non-obstructive apneas were explored in seven preinstr umented, sedated paralyzed and ventilated pigs under three conditions: room air breathing (RA), O-2 supplementation (O2), and supplementatio n with O-2 and CO2 (CO2). EEG monitoring showed no arousal under any c onditions. RA apneas increased mean arterial pressure (MAP, from basel ine 95.9 +/- 4.5 to late apnea 124.4 +/- 7.8 Torr, P < 0.01), left ven tricular end-diastolic pressure, end-diastolic and end-systolic myocar dial fiber lengths and systemic vascular resistance, but decreased car diac output (CO, 3.09 +/- 0.34-2.37 +/- 0.26 L/min, P < 0.01), heart r ate (HR, 115.1 +/- 7.5-102.0 +/- 7.8 bpm, P < 0.01), and stroke volume (SV, 29.6 +/- 0.7-21.1 +/- 1.8 ml, P < 0.01). O2 apneas produced simi lar decreases in HR (114.0 +/- 11.8-105.4 +/- 8.7 bpm, P < 0.05) as wi th RA apneas, but smaller increases in MAP (94.5 +/- 1.8-103.4 +/- 2.8 Torr, P < 0.01) and in the variables of pre-and after-load. CO and SV remained unchanged with O2 apneas. CO2 was associated with higher MAP , CO, and HR at baseline relative to RA, but similar cardiovascular re sponse during apneas in direction and magnitude to those of O2 apneas. We conclude that in this model hypoxemia is a major but not the sole determinant of the presser response during apneas. Hypercapnia cannot explain the presser response seen when hypoxemia is abolished. The HR fall during apneas is independent of hypoxemia, hypercapnia and the pr esser response. (C) 1998 Elsevier Science B.V. All rights reserved.