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Circulation, Vol 84, 279-286, Copyright © 1991 by American Heart Association

ARTICLES

Vital organ perfusion during assisted circulation by manipulation of intrathoracic pressure

NC Chandra, R Beyar, HR Halperin, JE Tsitlik, E Wurmb, B Rayburn, AD Guerci and ML Weisfeldt
Peter Belfer Laboratory for Myocardial Research, Francis Scott Key Medical Center, Baltimore, MD 21224.

BACKGROUND. We have previously shown, in dogs with severe cardiac depression, that modest cyclic increases in intrathoracic pressure, starting synchronously with left ventricular isovolumic contraction, significantly increase aortic flow and pressure. However, little is known of changes in vital organ perfusion during this technique of assisted circulation. METHODS AND RESULTS. We studied regional organ flow using radioactive labeled microspheres in 13 20-25-kg mongrel dogs. In the control group, after chemical induction of cardiac depression with verapamil and propranolol, coronary flow fell from 129.1 +/- 14.4 to 51.6 +/- 11.3 ml/100 g/min (p less than 0.005) and continued to decline over a 14-minute time period (flow was 32.2 +/- 11.5 ml/100 g/min at 7 minutes and 20.7 +/- 9.5 ml/100 g/min at 14 minutes [n = 6]; all p less than 0.05). In the intervention group, regional blood flow was evaluated before and after the induction of cardiac depression and also during assisted circulation using 400-msec, 20-25-mm Hg intrathoracic pressure increases delivered by a circumthoracic pneumatic vest, starting synchronously with left ventricular isovolumic contraction. In the intervention group, coronary flow fell from 119 +/- 26.7 to 47.9 +/- 13.1 ml/100 g/min 1 minute after the induction of cardiac depression (p less than 0.005). With the initiation of assisted circulation, coronary flow increased to 55.8 +/- 19.2 ml/100 g/min at 7 minutes and fell to 23.1 +/- 15.9 ml/100 g/min on termination of assisted circulation at 14 minutes (p less than 0.05 and p = NS versus control group flows at 1 and 14 minutes, respectively). During assisted circulation, cerebral, renal, and small intestinal flows also increased (all p less than 0.05 versus flows during myocardial depression). No significant increase in hepatic flow was observed. CONCLUSIONS. In the canine model, manipulation of intrathoracic pressure appears to be an effective, short-term, noninvasive means of not only increasing aortic pressure but also increasing vital organ perfusion during cardiogenic shock. Further studies are needed to assess the usefulness of this technique of assisted circulation in humans.

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