To the Editor:
Kopp et al.'s recent study (1) adds to the body of evidence (1–5) that proves that respiratory depression, deep sedation, high block, and high vagal tone are not prerequisites for bradycardic arrest during neuraxial anesthesia. The remaining confounding aspect of the problem is the suddenness of onset. This suddenness poses the greatest hazard to patients and the greatest challenge to the clinician. As Caplan put it (6), “all of these cardiac arrests seemed to evolve with unexpected speed….”
In a letter, Brown et al. (7) claimed that it was “sudden recognition” rather than sudden bradycardia that was the problem. Subsequent case reports, however, even one co-authored by Brown et al. (5), included documentation, with rhythm strips (2), of truly abrupt severe bradycardia and asystole occurring in seconds, even describing cases of sudden unconsciousness while the patient was conversing with their anesthesiologist (2–3). Not all cases occur abruptly but some certainly do.
I would suggest that loss of compensatory vasoconstriction is a feature frequently neglected in the practice of spinal and epidural anesthesia. This compensation that we are so used to taking advantage of during ordinary states of bradycardia or hypovolemia is absent during neuraxial anesthesia. Thus, hypotension occurs at higher heart rates than ordinarily expected, even as high as the 50s, even in healthy young men with low baseline heart rates. My experience with spinal anesthesia is that when BP begins to drop, the rate of the usual HR slowing begins to accelerate. At that point, progression to bradycardic arrest with pulselessness and unconsciousness may progress with a rapidity on the order of seconds.
Unfortunately, few of the authors of recent studies have addressed the issue of the hemodynamic pattern in the 60–120 s preceding bradycardic arrest/asystole. Even Lesser et al. (8), who published an account of their cases as recorded by automated anesthesia record keepers, did not provide the above information. Granted, this would be difficult without continuous invasive arterial blood pressure monitoring.
The focus needs to shift to detailed analysis of the hemodynamics in the minute or two leading up to bradycardic arrest and asystole during neuraxial anesthesia. This is a time frame more than adequate in which to intervene to prevent calamities.
Leo I. Stemp, MD
Mercy Medical Center
1. Kopp SL, Horlocker TT, Warner ME, et al. Cardiac arrest during neuraxial anesthesia: frequency and predisposing factors associated with survival. Anesth Analg 2005;100:855–65.
2. Liguori GA, Sharrock NE. Asystole and severe bradycardia during epidural anesthesia in orthopedic patients. Anesthesiology 1997;86:250–7.
3. Geffin B, Sharpiro L. Sinus bradycardia and asystole during spinal and epidural anesthesia: a report of 13 cases. J Clin Anesth 1998;10:278–85.
4. Sprung J, Warner ME, Contreras MG, et al. Predictors of survival following cardiac arrest in patients undergoing noncardiac surgery: a study of 518,294 patients at a tertiary referral center. Anesthesiology 2003;99:259–69.
5. Mackey DC, Carpenter RL, Thompson GE, et al. Bradycardia and asystole during spinal anesthesia: a report of three cases without morbidity. Anesthesiology 1989;70:866–8.
6. Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988;68:5–11.
7. Brown DL, Carpenter RL, Moore DL, et al. Cardiac arrest during spinal anesthesia. Anesthesiology 1988;68:971–2.
8. Lesser JB, Sanborn KV, Valskys R, Kuroda M. Severe bradycardia during spinal and epidural anesthesia recorded by an anesthesia information management system. Anesthesiology. 2003;99:859–66.