Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine

C. L. Schleien, Raymond C Koehler, H. Gervais, Ivor David Berkowitz, J. M. Dean, J. R. Michael, M. C. Rogers, R. J. Traystman

Research output: Contribution to journalArticle

Abstract

Pure α-adrenergic agonists, such as phenylephrine, and mixed α- and β-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 determine whether at equivalent perfusion pressure, continuous infusion of phenylephrine (20 μg/kg/min) or epinephrine (4 μg/kg/min) leads to equal organ blood flow, cerebral O2 upake, and cerebral electrophysiologic function. During 20 minutes of CPR initiated immediately upon ventricular fibrillation in anesthetized dogs, left venricular 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 β-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.

Original languageEnglish (US)
Pages (from-to)1332-1342
Number of pages11
JournalCirculation
Volume79
Issue number6
StatePublished - 1989

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Cerebrovascular Circulation
Somatosensory Evoked Potentials
Cardiopulmonary Resuscitation
Phenylephrine
Epinephrine
Adrenergic Agonists
Brain
Perfusion
Pressure
Ventricular Fibrillation
Vascular Smooth Muscle
Evoked Potentials
Resuscitation
Pharmaceutical Preparations
Adrenergic Agents
Dogs

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine. / Schleien, C. L.; Koehler, Raymond C; Gervais, H.; Berkowitz, Ivor David; Dean, J. M.; Michael, J. R.; Rogers, M. C.; Traystman, R. J.

In: Circulation, Vol. 79, No. 6, 1989, p. 1332-1342.

Research output: Contribution to journalArticle

Schleien, CL, Koehler, RC, Gervais, H, Berkowitz, ID, Dean, JM, Michael, JR, Rogers, MC & Traystman, RJ 1989, 'Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine', Circulation, vol. 79, no. 6, pp. 1332-1342.
Schleien, C. L. ; Koehler, Raymond C ; Gervais, H. ; Berkowitz, Ivor David ; Dean, J. M. ; Michael, J. R. ; Rogers, M. C. ; Traystman, R. J. / Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine. In: Circulation. 1989 ; Vol. 79, No. 6. pp. 1332-1342.
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AU - Schleien, C. L.

AU - Koehler, Raymond C

AU - Gervais, H.

AU - Berkowitz, Ivor David

AU - Dean, J. M.

AU - Michael, J. R.

AU - Rogers, M. C.

AU - Traystman, R. J.

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N2 - Pure α-adrenergic agonists, such as phenylephrine, and mixed α- and β-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 determine whether at equivalent perfusion pressure, continuous infusion of phenylephrine (20 μg/kg/min) or epinephrine (4 μg/kg/min) leads to equal organ blood flow, cerebral O2 upake, and cerebral electrophysiologic function. During 20 minutes of CPR initiated immediately upon ventricular fibrillation in anesthetized dogs, left venricular 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 β-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.

AB - Pure α-adrenergic agonists, such as phenylephrine, and mixed α- and β-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 determine whether at equivalent perfusion pressure, continuous infusion of phenylephrine (20 μg/kg/min) or epinephrine (4 μg/kg/min) leads to equal organ blood flow, cerebral O2 upake, and cerebral electrophysiologic function. During 20 minutes of CPR initiated immediately upon ventricular fibrillation in anesthetized dogs, left venricular 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 β-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.

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