In Reply:—
We thank Dr. Gallagher for his insightful comments regarding our review of hypertrophic cardiomyopathy (HCM),1and we are pleased to learn of his opinion that understanding the perianesthetic implications of HCM have been extended. The points raised by Dr. Gallagher are important and fundamental to the practice of anesthesiology, and we wish that we could have elaborated on some of those issues in our article, although space limitations did not allow us to touch on all aspects of perioperative care. The question remains: How can the practicing anesthesiologist preoperatively identify a complex disease such as HCM, which at the time of presentation for anesthesia and surgery may be unsuspected by the medical team as well as the patient? As pointed out by Dr. Gallagher, the study of Corrado et al. 2showed that a mass screening program in Italy of young competitive athletes (based largely on clinical history, physical examination, and 12-lead electrocardiogram) was an efficient means of detecting cardiac abnormalities, and ultimately led to the diagnosis of hypertrophic cardiomyopathy in an important minority of patients. Certainly, if such detailed preoperative examination was a standard part of the preoperative anesthetic examination, an increased number of HCM patients would be probably diagnosed before arrival in the operating room. To what extent the Italian athlete screening data, i.e. , the use of routine electrocardiograms, can be extrapolated to the general anesthesia population remains a difficult and unresolved issue, although this additional diagnostic test would permit anesthesiologists to make a potentially lifesaving diagnosis, as Dr. Gallagher has suggested.
In addition, clinical examinations, which include maneuvers to provoke the murmur of left ventricular tract obstruction (such as standing), characteristic of HCM, would be potentially helpful for diagnosis. The possible disastrous consequences of overlooking a preoperative diagnosis of HCM should heighten the index of suspicion and clinical vigilance on the part of the anesthesiologist in this regard.
With respect to the choice of induction agents, our article states: “The possibility of drug-induced hypotension or increased sympathetic activation upon initiating anesthesia should be considered when choosing an induction agent, and slow titration of these drugs should be used.”1More specifically, when inducing patients with diagnosed HCM, the anesthesiologist should consider the potential for global myocardial dysfunction besides focusing on the possibility of provoked left ventricular outflow tract obstruction. For example, an agent such as etomidate would be preferable to others (e.g. , propofol, ketamine) because of its relatively stable action on the cardiovascular system. Propofol produces direct myocardial depression and both arterial and venous dilatation, which potentiates systemic hypotension. Ketamine has cardiovascular-stimulating properties secondary to direct activation of the sympathetic nervous system and increases arterial blood pressure and heart rate, thereby negatively affecting the balance between myocardial oxygen supply and demand.
Etomidate produces minimal cardiac depression even in the presence of intrinsic myocardial disease and consequently would be considered the induction agent of choice for patients with HCM. Of note, etomidate does not effectively blunt the sympathetic response to laryngoscopy and intubation, and therefore, adjuvant methods (lidocaine, inhalational agents) should be considered to avoid an exaggerated sympathetic response during initiation of anesthesia.
The consideration (raised by Dr. Gallagher) regarding use of intraoperative 3- or 5-lead electrocardiogram does not seem particularly relevant to the potential identification of HCM. The diagnostic strategy of choice would be a 12-lead electrocardiogram obtained before induction.
*University of Miami, Miller School of Medicine, Miami, Florida. lpoliac@med.miami.edu
