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Correspondence |
Ehime, Japan
To the Editor:
Generally, during cardiopulmonary resuscitation (CPR), epinephrine is administered to restore circulation. However, several reports suggest abandoning exogenous catecholamine administration because of sufficient concentrations of endogenous catecholamines during CPR.1,2 On the other hand, general anesthetics have been shown to alter autonomic nervous system responses and catecholamine levels. Thus, recommendations regarding the administration of exogenous catecholamines may not hold true in the setting of cardiac arrest under general anesthesia.
This study was approved by the Committee on Animal Experimentation at Ehime University School of Medicine, Ehime, Japan. Twenty-one Japanese white rabbits (3.0 kg) were divided into three groups: 1.7% enflurane (n = 5), 2.7% enflurane (n = 7), and pentobarbital (30 mgkg1 plus 20 mgkg1hr1; n = 9). General anesthesia was supplemented with local anesthesia with lidocaine for surgery. After a left thoracotomy under mechanical ventilation, the rabbits ventricles were fibrillated electrically (1.01.5 V, 60 Hz). During ventricular fibrillation, mechanical ventilation was stopped. Four minutes after ventricular fibrillation, mechanical ventilation and cardiac massage were started. When ventricular fibrillation spontaneously converted to sinus rhythm within five minutes, cardiac massage was stopped. When ventricular fibrillation continued for five minutes, electrical defibrillation was carried out at 10 J. When successful conversion was not observed, additional shocks were delivered at 1040 J (maximum six times) and cardiac massage continued for 11 min. When resuscitation was not successful within 11 min, CPR was stopped. Blood samples were collected every two minutes from the right carotid artery, and the plasma concentrations of catecholamines were determined by a high-performance liquid chromatography system. The data were analyzed by two-way repeated measures analysis of variance, followed by Scheffés tests.
Before induction of ventricular fibrillation, the plasma concentration of epinephrine in the enflurane (1.7%) group was 0.77 µgL1. The epinephrine levels in the enflurane (2.7%) and pentobarbital groups were decreased to 3% and 6% of that in the enflurane (1.7%) group, respectively. In the enflurane (1.7%) group, a marked increase in the epinephrine level was observed during CPR after ventricular fibrillation, and the value reached 780% in five minutes (Figure A
). Afterwards, the plasma epinephrine concentration decreased gradually. In the enflurane (2.7%) and pentobarbital groups, no increase was observed in the epinephrine levels during CPR. Plasma concentrations of norepinephrine did not increase during CPR in the three groups (Figure B
). There were no differences in the recovery from ventricular fibrillation among the three groups.
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References
1 Woodhouse SP, Lewis-Driver D, Eller H. Catecholamines during cardiopulmonary resuscitation for cardiac arrest. Resuscitation 1992; 24: 26372.[Medline]
2 Little RA, Frayn KN, Randall PE, et al. Plasma catecholamines in patients with acute myocardial infarction and in cardiac arrest. Q J Med 1985; 54: 13340.[Medline]
3 Duan YF, Winters RW, McCabe PM, Green EJ, Schneiderman N. Basal and reactive plasma catecholamine levels under stress and anesthesia in rabbits. Physiol Behav 1994; 56: 57783.[Medline]
4 Foley PJ, Tacker WA, Wortsman J, Frank S, Cryer PE. Plasma catecholamine and serum cortisol responses to experimental cardiac arrest in dogs. Am J Physiol 1987; 253: E2839.
5 Wortsman J, Frank S, Cryer PE. Adrenomedullary response to maximal stress in humans. Am J Med 1984; 77: 77984.[Medline]
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