Circulation, Vol 79, 1332-1342, Copyright © 1989 by American Heart Association
CL Schleien, RC Koehler, H Gervais, ID Berkowitz, JM Dean, JR Michael, MC Rogers and RJ Traystman
Pure alpha-adrenergic agonists, such as phenylephrine, and mixed alpha- and
beta-adrenergic agonists, such as epinephrine, raise perfusion pressure for
heart and brain during cardiopulmonary resuscitation (CPR). However, with
the high doses used during CPR, these drugs may directly affect vascular
smooth muscle and metabolism in brain and heart. We determined whether at
equivalent perfusion pressure, continuous infusion of phenylephrine (20
micrograms/kg/min) or epinephrine (4 micrograms/kg/min) leads to equal
organ blood flow, cerebral O2 uptake, and cerebral electrophysiologic
function. During 20 minutes of CPR initiated immediately upon ventricular
fibrillation in anesthetized dogs, left ventricular blood flow was similar
with epinephrine (45 +/- 9 ml/min/100 g) or phenylephrine (47 +/- 8
ml/min/100 g) infusion. The ratio of subendocardial to subepicardial blood
flow fell equivalently during CPR with either epinephrine (1.23 +/- 0.06 to
0.70 +/- 0.05) or phenylephrine (1.32 +/- 0.07 to 0.77 +/- 0.05)
administration. At similar levels of cerebral perfusion pressure (44 +/- 3
mm Hg), similar levels of cerebral blood flow were measured in both groups
(27 +/- 3 ml/min/100 g). Cerebral O2 uptake was maintained at prearrest
levels in both groups. Somatosensory-evoked potential amplitude was
modestly reduced during CPR, but it promptly recovered after
defibrillation. During CPR and at 2 hours after resuscitation, there were
no differences between drug groups in the level of regional cerebral or
coronary blood flow, cerebral O2 uptake, or evoked potentials. Therefore,
with minimal delay in the onset of CPR and with equipotent pressor doses of
phenylephrine and epinephrine, we found no evidence that one agent provides
superior coronary or cerebral blood flow or that epinephrine by virtue of
its beta-adrenergic properties adversely stimulates cerebral metabolism at
a critical time that would impair brain electrophysiologic function.
Moreover, epinephrine did not preferentially impair subendocardial blood
flow as might be expected if it enhanced the strength of fibrillatory
contractions.
ARTICLES
Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
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