AJP - Heart and Circulatory Physiology, Vol 243, Issue 2 259-H267, Copyright © 1982 by American Physiological Society
Role of carotid artery resistance to collapse during high-intrathoracic-pressure CPR
F. C. Yin, J. M. Cohen, J. Tsitlik, B. Zola and M. L. Weisfeldt
The driving force for carotid artery flow during
high-intrathoracic-pressure cardiopulmonary resuscitation is a peripheral
arteriovenous pressure gradient resulting from differential transmission of
the high intrathoracic pressure to the carotid artery but not to the
jugular vein. To study the role of carotid artery resistance to collapse in
establishing this differential pressure transmission, we manipulated the
upstream, downstream, and surrounding pressures and measured the resultant
carotid artery flow in both intact dogs and in excised arteries. Stepwise
reductions in downstream pressure produced a narrowing near the outlet from
the high-pressure chamber (the thorax in vivo), but increments in flow
continued despite the presence of a positive (outside--inside) transmural
pressure gradient. Flow limitation occurred only when downstream pressure
was further decreased. Resistance to collapse was indexed by the transmural
pressure at the onset of flow limitation (Pcrit), which was 7.2 +/- 1.6
mmHg in eight intact dogs. After administration of norepinephrine Pcrit
increased by 2.6 +/- 0.7 mmHg, P less than 0.001). Seven excised carotid
arteries also demonstrated resistance to collapse which was enhanced
somewhat with norepinephrine. Thus resistance of the carotid artery to
collapse is a critical factor in maintaining forward flow during high
intrathoracic pressure. This resistance to collapse is also seen in vitro
and can be enhanced by vasoconstricting agents.
