To the Editor:—
The recent article by London et al. and the associated editorial were written in the context of perioperative medicine, perhaps obfuscating answers to their own questions.1,2The use of perioperative β blockers has now “…recently been highlighted as a ‘top tier' patient safety practice by the Institute of Medicine.”1Specifically: if the administration of perioperative β blockers “…should start as soon as the eligibility of high risk patients for surgery is confirmed. If possible, this should occur days to weeks before surgery,”2why are “high risk” patients NOT ALREADY ON perioperative β blockers when they present?
Admittedly, it is “recommended to follow the American College of Cardiology/American Heart Association guidelines and to perform coronary bypass grafting or percutaneous transluminal coronary angioplasty if they are indicated independently of the need for noncardiac surgery.”2If the lesson learned from coronary bypass grafting/percutaneous transluminal coronary angioplasty guidelines is to uncouple surgery from therapeutic need, isn't this also appropriate for perioperative β blockers? High-risk patients are typically referred to us after intervals by primary care physicians or internists, or ultimately surgeons! Why should primary care physicians even wait for surgery in high-risk patients? Are we guilty of enabling inferior care by assuming responsibility to initiate perioperative β blockers at the less opportune time of induction? Are these efforts misplaced or in need of redirection?
“Institution of perioperative β blockers before induction…may not be required if hemodynamics are well controlled. This contrasts to emergence when ischemia is particularly common.”1Apparently, careful administration of anesthetic agents provide stress mitigation intraoperatively, possibly equal to perioperative β blockers found in research protocols. The best anesthetic is one given frequently, and a sudden paradigm shift to acutely adding perioperative β blockers to typical induction drug regimens may increase the incidence of undesirable periods of hypotension. (Post)-induction hypotension may alone be the reason against adding yet another sympatholytic agent acutely at induction. Must something be removed or replaced to “make room” for perioperative β blockers?
Opioid administration historically (before modern beta blockers) emerged to mitigate stress responses at intubation and reduce minimum alveolar concentration requirements (hence the noticed “stability until emergence,” when respiratory depression becomes problematic, limiting further narcotic administration). However, there is no pain in an unconscious patient. Would restricting opioid use before the final 20 min of anesthesia (specifically treating only pain upon emergence, when painful stress responses develop), better maximize perioperative β blocker effects and utilization? What role do/should opioids play in modern anesthesia in the age of perioperative β blockers: postemergence pain therapy? What research is taking place in this direction?
Will potential dangers of widespread perioperative β blockers result from indiscriminant use in virtually all patients (i.e. , if good for high risk = beneficial to all; avoid malpractice litigation)? Will increased utilization of central venous pressure/pulmonary artery catheters to monitor filling pressures result, as perioperative β blocker induced hypotension and bradycardia would now encumber interpretation of classic signs of surgical hypovolemia? Will acute perioperative β blocker introduction at induction improve overall care or simply shift morbidity (i.e. , catheterization, hypotension)? Is “during surgery” a shortcoming of, and truly superfluous in, the title of the editorial? Are we really ready, willing, and if appropriate, able to take on this cause at induction now, based on the available choices, without randomized multicenter studies?
University of Pittsburgh, Presbyterian University Hospital, Pittsburgh, Pennsylvania. firstname.lastname@example.org