Role of carotid artery resistance to collapse during high-intrathoracic-pressure CPR

Abstract

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.