Correspondence  |   May 2001
Did Anesthetics Trigger Cardiac Arrests in Patients with Occult Myopathies?
Author Notes
  • Children’s Hospital and Regional Medical Center, Seattle, Washington, and University of Washington School of Medicine, Seattle, Washington.
Article Information
Correspondence   |   May 2001
Did Anesthetics Trigger Cardiac Arrests in Patients with Occult Myopathies?
Anesthesiology 5 2001, Vol.94, 934-935. doi:
Anesthesiology 5 2001, Vol.94, 934-935. doi:
In Reply:—
Dr. Larach et al.  have reported that of the 25 cardiac arrest patients reported to The North American Malignant Hyperthermia (MH) Registry and MH Association of the United States Hotline from 1990–1993, 48% showed evidence for a previously unrecognized myopathy, and 32% had hyperkalemia-associated arrests. In contrast, 6.7% (10/150) of the Pediatric Perioperative Cardiac Arrest Registry patients were hyperkalemic at the time of arrest. All but one of these cases was associated with either massive transfusion (n = 5), reperfusion after liver transplant (n = 2), or renal insufficiency (n = 2). In one patient, succinylcholine administration resulted in hyperkalemia and cardiac arrest. This was a patient with severe neurologic deterioration from subacute sclerosing panencephalitis. No laboratory data or muscle biopsy data were provided to confirm the presence of a myopathy. The same was true for the 3 children found to have cardiomyopathy and for the 18 children whose arrest was assumed to be cardiovascular in origin but could not have a specific cause assigned.
The fact that fewer hyperkalemia-associated arrests have been reported to the Pediatric Perioperative Cardiac Arrest Registry than to The North American MH Registry is not surprising, given the different focus and entry criteria of the two registries. In fact, no cases of MH have been reported to the Pediatric Perioperative Cardiac Arrest Registry, perhaps because we have become more knowledgeable about MH prevention and therapy such that few MH-susceptible patients progress to cardiac arrest. In addition, the decreasing use of succinylcholine during the past decade as faster-acting nondepolarizing relaxants have become available may have resulted in the diagnosis of fewer patients with occult myopathy or MH susceptibility.
We agree with Dr. Larach et al.  that more information is required. As suggested in Dr. Rothstein’s editorial, 1 this sort of information can come only with a prospective multicenter epidemiologic study of anesthesia-related cardiac arrest.
Dr. Cote argues that we should not condemn halothane because it remains the most widely used anesthetic agent for children around the world, has a long track record of safety, and is inexpensive relative to other agents, such as sevoflurane. His points are well-taken. However, pediatric anesthesiologists recognize that halothane can cause bradycardia and hypotension in their patients, occasionally to the degree that cardiopulmonary resuscitation is required. The impact of halothane on heart rate, blood pressure, and cardiac output has been well-documented in many animal 2–4 and human 5–7 studies. Recently, studies comparing the cardiovascular responses in newborns, infants, and children to whom either halothane or sevoflurane was administered have suggested important differences, particularly with respect to heart rate and cardiac contractility and output. 8–10 As Dr. Cote points out, another important difference between these two agents is that it is possible to deliver roughly twice the number of minimum alveolar concentration multiples of halothane than of sevoflurane.
Halothane continues to be a frequently used agent in our institution, as in other institutions around the world that care for children. We hope that information provided by the Pediatric Perioperative Cardiac Arrest Registry about halothane’s role in contributing to occasional cardiac arrest will improve the safety of its use. As an example, the use of controlled ventilation was an associated factor in approximately half of the patients in which halothane-related cardiovascular depression caused cardiac arrest; the remainder had arrests during spontaneous or assisted ventilation. Thus, the classic teaching that spontaneously breathing patients do not have arrests caused by inhalation agent–induced cardiovascular depression is not always true.
As anesthetic agents with the promise of improved efficacy or fewer side effects become available, we would be remiss not to compare them with the gold standard. We do not know whether sevoflurane is associated with less risk compared with halothane, but there is reason to think this might be so. At the moment, each of us must apply an incomplete data set to our practices. Cost is certainly an issue and may be the decisive issue if sevoflurane is unaffordable. Those of us with the luxury of choice are charged with analyzing our outcomes as rigorously as possible and making the information available to others.
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