CARDIOPULMONARY RESUSCITATION Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 + 1% to 46 ± 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 1 50/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of compression, but not on rates of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression. We conclude that intrathoracic pressure fluctuations generate blood flow during manual CPR. Circulation 73, No. 3, 539-550, 1986. THERE IS continuing controversy concerning the mechanisms of blood flow during cardiopulmonary resuscitation. In 1960, Kouwenhoven et al.' proposed, but never proved, that blood moved due to direct comFrom the Peter Belfer Laboratory for Myocardial Research, Cardiology Division, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore. Supported by Ischemic Heart Disease SCOR grant 5P50-HL-17655 from the National Heart, Lung, and Blood Institute, and an NIH training grant 2T32-HL-70227. Address for correspondence: Henry R. Halperin, M.D., Cardiology Division, The Johns Hopkins Hospital, 600 N. Wolfe St., Baltimore, MD 21205. Received March 26, 1985; revision accepted Nov. 29, 1985. *Present address: Beijing Medical School, Beijing, People's Republic of China. pression of the heart between the sternum and vertebral column. If this mechanism is correct, stroke volume should be determined by the amount of cardiac deformation, and prolongation of compression beyond the time necessary to squeeze the heart will have no effect on stroke volume because ejection ceases as soon as sternal displacement is maximal. At constant sternal displacement, increases in the rate of compression will augment flow because a fixed stroke volume is pumped into the systemic arteries more frequently per unit time. Early evidence pointed to the fact that heart compression alone could not account for the equivalence of Vol. 73, No. 3, March 1986 539 by gest on O cber 5, 2017 http://ciajournals.org/ D ow nladed from