LABORATORY INVESTIGATION CARDIOPULMONARY RESUSCITATION Potential adverse elfects of volume loading on perfusion of vital organs during closed-chest resuscitation

To determine whether expansion of blood volume improves vital organ perfusion pressures and blood flow during closed-chest cardiopulmonary resuscitation in dogs, we recorded intracranial and high-fidelity ascending aortic and right atrial pressures and measured total and regional blood flow with radioactive microspheres during cardiopulmonary resuscitation before and after rapid infusion of 1 liter of saline or dextran in 12 animals. Volume loading increased total forward blood flow from 327.1 50.9 to 692.7 + 105.9 ml/min (p < .01). However, blood flow to the cerebral hemispheres, cerebellum, brainstem, and ventricular myocardium all decreased significantly. For example, blood flow to the left cerebral hemisphere fell from 16.5 + 2.4 to 5.5 + 1.7 ml/min/100 g (p < .001), while left ventricular myocardial blood flow fell from 12.0 + 3.1 to 4.1 + 0.8 ml/min/100 g (p < .05). These changes in critical regional flow were accompanied by disproportionate increases in right atrial and intracranial pressures (relative to aortic pressure), which reduced the average pressure differences generated across the coronary and cerebral circulations from 1 l.0 + 2.5 to 3.7 + 1.3 mm Hg (p < .01) and from 16.1 ± 2.3 to 10.5 + 1.5 mm Hg (p < .01), respectively. The overall rise in forward flow was associated with a marked increase in extracranial, brachiocephalic blood flow. These findings suggest that large increments in blood volume can reduce vital organ perfusion during cardiopulmonary resuscitation despite an increase in total forward blood flow. Circulation 69, No. 1, 181-189, 1984. SEVERAL years ago, Harris et al. ' demonstrated that administration of intravenous fluid increases carotid blood flow and, in some cases, the arterial pressure generated by external chest compression. However, we suspected that these apparently beneficial effects might not be accompanied by improved vital organ perfusion for several reasons. First, coronary blood flow during cardiopulmonary resuscitation (CPR) is a function of the pressure difference generated across the coronary circulation2 and occurs primarily during the relaxation or release phase of each cycle of chest compression. 23 It seemed reasonable to expect that volume loading, by filling venous capacitance vessels, would raise right atrial as well as aortic pressure during this phase and that this effect would limit any improvement in the driving force for coronary blood flow. Second, From the Cardiology Division, Department of Medicine, University of Colorado Health Sciences Center, Denver. Supported in part by National Heart, Lung and Blood Institute New Investigator Research Award 1 R23 HL29219-01 and by Colorado Heart Association Grant-in-Aid 72-008-981. Address for correspondence: Roy V. Ditchey, M.D., Cardiology Division, Box B-130, University of Colorado Health Sciences Center, 4200 East Ninth Ave., Denver, CO 80262. Received March 8, 1983; revision accepted Sept. 22, 1983. Vol. 69, No. 1, January 1984 intracranial pressure rises more during chest compression when resting intracranial pressure is elevated.4 By increasing cerebral blood volume, volume loading would be expected to increase resting intracranial pressure, and therefore intracranial pressure during CPR. It seemed likely that this effect would limit any improvement in the driving force for cerebral blood flow. Increased carotid' and total forward blood flow after volume loading could be due entirely to enhanced flow through extrathoracic, extracranial vascular beds. The purpose of this study was to determine the effects of expansion of blood volume on vital organ perfusion pressures and blood flow during CPR. This was accomplished by recording ascending aortic, right atrial, and intracranial pressures and measuring total and regional blood flow with radioactive microspheres during CPR performed before and after rapid intravenous infusion of a large volume of saline or dextran.