Acute systemic blood pressure elevation in obstructive and non
-obstructive breathhold in primates.
White, Sheila Goodnight, Eugene C. Fletcher, Charles C. Miller,.
DEPARTMENT OF MEDICINE, PULMONARY DISEASE AND CRITICAL CARE
SECTION, HOUSTON VETERANS ADMINISTRATION MEDICAL CENTER, BAYLOR
COLLEGE OF MEDICINE, HOUSTON, TEXAS 77030 and DEPARTMENT OF MEDICINE,
DIVISION OF RESPIRATORY AND ENVIRONMENTAL MEDICINE, UNIVERSITY OF
LOUISVILLE SCHOOL OF MEDICINE, LOUISVILLE, KY 40292
APStracts 2:0102A, 1995.
Previous authors have described phasic blood pressure (BP) response
dur ing obstructive apnea (OA) in human sleep consisting of a slow
incremental increase in BP to the point of apnea termination followed
by a rapid rise then fall in BP at the resumption of respiration.
This rise in BP has been attributed to post-apneic augmentation of
cardiac output (CO) resulting after release of the marked negative
intrathoracic pressure (NIP) of obstructed inspiration. Via
endotracheal tube, we created obstructed and non-obstructed
breathhold (apnea) in chloralose anesthesized baboons consisting of
fixed duration (30s, 45s, 60s), single OA's (mechanical obstruction)
and non-obstructive (paralysis, ventilator cessation) apneas (NOA) of
matched duration and arterial desaturation. Systemic BP was measured
prior to apnea (T0), during the last five seconds of apnea (T1), and
the first five seconds following resumption of respiration (T2).
Despite wide fluctuations in NIP and BP during the T0 to T1 phase of
OA, BP elevation in OA and NOA at T0, T1, or T2 did not differ for
any duration apnea. At the release of obstruction, when resolution of
NIP changes could theoretically increase cardiac output and
accentuate BP, there was no difference in T1 and T2 pressures between
the two conditions. We conclude that in this anesthesized animal
model, mechanical (NIP) changes don't play a major role in overall
maximum BP response to OA. Because of physiologic differences between
natural sleep in humans and the anesthetized state in animals, care
must be taken in extrapolating these results to human sleep apnea.
Received 22 July 1994; accepted in final form 3 March 1995.
APS Manuscript Number A752-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 21 March 1995.