Atropine, halothane, and pulseless electrical activity.
نویسنده
چکیده
C ardiovascular depression from halothane overdose is a well-described cause of cardiac arrest in children undergoing anesthesia. In Salem et al’s (1) report of cardiac arrests in infants and children, seven of 73 were related to overdose of halothane. In Keenan and Boyan’s (2) landmark article on cardiac arrest due to anesthesia, five of six pediatric arrests were due to halothane excess, with “Cardiac arrest . . . preceded by bradycardia in 26 of 27 patients.” (2) Thus, although halothane’s primary effect is negative inotropism (31, increasing alveolar concentrations of halothane are classically associated with decreased heart rate (HR), and overdose is typically heralded by bradycardia (4). However, in infants and children where atropine has already been given, halothane overdose can lead to profound hypotension despite a normal to high HR. Electrical HR is maintained by the effects of atropine, but ventricular function is all but abolished: electromechanical dissociation or pulseless electrical activity. Bradycardia in this setting occurs only after some time of low to no myocardial perfusion, and should not be awaited as the heralding sign of distress.
منابع مشابه
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عنوان ژورنال:
- Anesthesia and analgesia
دوره 80 3 شماره
صفحات -
تاریخ انتشار 1995