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Canadian Journal of Anesthesia 51:404-405 (2004)
© Canadian Anesthesiologists' Society, 2004


Correspondence

Suppression of endogenous catecholamine release by anesthetics during cardiopulmonary resuscitation in the rabbit

Norikatsu Kii, MD, Naoto Adachi, MD PhD, Toshihiro Yorozuya, MD, Takumi Nagaro, MD and Tatsuru Arai, MD

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 mg•kg–1 plus 20 mg•kg–1•hr–1; n = 9). General anesthesia was supplemented with local anesthesia with lidocaine for surgery. After a left thoracotomy under mechanical ventilation, the rabbit’s ventricles were fibrillated electrically (1.0–1.5 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 10–40 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 Scheffé’s tests.

Before induction of ventricular fibrillation, the plasma concentration of epinephrine in the enflurane (1.7%) group was 0.77 µg•L–1. 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 AGo). 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 BGo). There were no differences in the recovery from ventricular fibrillation among the three groups.



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FIGURE Plasma concentrations of epinephrine (A) and norepinephrine (B) collected every two minutes. Enflurane 1.7% (empty circle), enflurane 2.7% (full circle), and pentobarbital 30 mg•kg–1 plus 20 mg•kg–1•hr–1 (triangle) groups. *P < 0.05, **P < 0.01 compared with the value in the enflurane 1.7% group. CPR = cardiopulmonary resuscitation; Vf = ventricular fibrillation.

 
In the present study, the increase in the epinephrine level was completely abolished by deep general anesthesia with 2.7% enflurane or high dose pentobarbital. However, several studies have shown marked increases in plasma catecholamine levels during CPR both in humans and animals.3,4 In subjects who experienced cardiac arrest requiring resuscitation in an intensive care unit, the epinephrine and norepinephrine levels increased 300fold and 32fold, respectively. Since these patients were not given any anesthetics, such increases may have been induced by acute stress.5 Hence, differences in the duration of circulatory arrest and anesthesia may be contributing factors in the elevation of endogenous catecholamine levels. Although there are reports suggesting that administration of epinephrine during CPR may not be helpful, this may not apply to patients who suffer cardiac arrest under general anesthesia.

References

1 Woodhouse SP, Lewis-Driver D, Eller H. Catecholamines during cardiopulmonary resuscitation for cardiac arrest. Resuscitation 1992; 24: 263–72.[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: 133–40.[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: 577–83.[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: E283–9.

5 Wortsman J, Frank S, Cryer PE. Adrenomedullary response to maximal stress in humans. Am J Med 1984; 77: 779–84.[Medline]





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