In Reply:—
I would first like to extend my appreciation to all of the individuals who have expressed interest in this area of medicine. 1Your insights and suggestions have been most appropriate.
In the first of the letters here, Drs. Hepner and Bader suggest anesthesiologists should assume a greater role as primary caregivers—specifically, as perioperative physicians. I could not agree more with my colleagues in this regard. Anesthesiologists truly are uniquely qualified to care for high-risk patients undergoing surgery because only with such specific training and experience can the clinician appropriately integrate diverse recommendations provided by multiple specialists, enabling synthesis of a comprehensive perioperative care plan. To suggest a preoperative assessment paradigm, for example, without a comprehensive understanding of the perioperative stress response—be it precipitated by sympathetic, inflammatory, thrombotic, or hydraulic phenomena—is not optimal. Thus, the anesthesiologist, as a unique caregiver in this setting, is truly the perioperative specialist—a role that we now have the opportunity of assuming and—I believe—that we have the responsibility of seizing, both for the benefit of our patients and for our specialty.
Regarding the suggestion that the type of surgery be considered in the overall assessment of risk, I fully agree. Clearly, there are a number of relatively minor operations that require only monitored anesthesia care, local anesthesia, or unconscious sedation. The stresses associated with emergence from such procedures certainly are less than those associated with more invasive procedures. For the most part, patients with stable symptomatology and reasonable functional capacity who undergo such minor procedures require little or no additional preoperative assessment or change in care. In contrast, however, for patients with progressive or unstable symptoms or current ventricular dysfunction, even “minor” stress responses associated with such procedures may trigger a cascade of untoward events, leading to irreversible injury. In such patients, it is difficult, if not impossible, to predict the degree of sympathetic, inflammatory, or thrombogenic stress that could “tip the scales”—that is, “destabilize the plaque.” Therefore, I believe that, for elective procedures, even if “minor,” stabilization of the disease state before surgery is prudent. For “nonminor” surgical procedures, which constitute the majority of surgeries, perioperative injury is not only determined by the preoperative disease state, but also by the type, magnitude, and duration of stresses associated with surgery. Thus, the optimal paradigm for care should address all of these considerations, and, in that sense, I agree with Drs. Hepner and Bader.
The comments of Dr. Lustik and Eichelberger also address surgery type, and, as such, the previous responses also apply. Regarding the importance of their second suggestion, intensive perioperative β-adrenergic blockade, I cannot help but agree with their conclusion that β blockade remains the only proven pharmacologic approach that allows reduction of perioperative morbidity and improvement of long-term survival after surgery. 2Interestingly, my colleagues suggest that intensive perioperative β blockade may be even more effective than use of sophisticated (and expensive) preoperative testing regimes. They may be right. However, I believe it is unwise to deemphasize the importance of preoperative risk assessment in light of the many benefits achieved by perioperative intensive β blockade–appropriately used, they may complement one another.
Our colleagues’ third comment addresses perioperative monitoring for ischemia. Although it is rational (and consistent with my personal biases), the application of such monitoring to even a subset of patients undergoing surgery is expensive, to say the least. For example, if applied to only 10% of patients undergoing surgery in the United States, we can surmise that at least $6 billion will be added to our health care bill annually. Nor can one suggest, without criticism, that such monitoring be applied only to patients undergoing major surgery. Clearly, patients with unstable disease, which indicates greater plaque instability, may be even more likely to have cardiovascular complications that those with stable disease who undergo far more invasive surgery. How, then, do we best tailor a cost-effective approach to individual patients, given the above limitations? Who merits more prolonged or more intensive (and more costly) monitoring after surgery? Perhaps the answer is not as complicated as we thought. We now know that patients who emerge from anesthesia and surgery without myocardial ischemia, regardless of the operation or the chronic disease state, will most likely not develop subsequent myocardial damage or ventricular dysfunction after surgery. In contrast, however, patients who do emerge with ischemia—again regardless of disease state or operation type—have a ninefold increase in risk for developing a serious adverse outcome during hospitalization 3and more than a twofold increase in risk of dying prematurely over the first 6 months after surgery. 4Thus, although I agree that the more invasive the surgery, the greater the stress response and the associated risk of perioperative ischemia, I believe that assessment of the emergence stress response will enable differentiation of patients and thereby provide rationale for selection of patients who require postoperative monitoring.
These authors also raised several considerations regarding the role of cardiac stress testing as a screening mechanism for cardiac catheterization and coronary angiography. Generally, a stepwise approach, including stress testing, is reasonable. However, in patients with severe or unstable symptomatology, proceeding directly to angiography is rational. Of greater concern, however, is appropriate selection of the stress test. It is clear that patients with stable exercise-related angina are most likely to have myocardial infarction precipitated by increases in oxygen demand, indicating that exercise treadmill or dobutamine stress testing may be most appropriate for these patients. Whereas for patients with unstable symptomatology, the choice of test is far less clear because untoward events can be precipitated by any one of a number of relatively dissimilar factors, including plaque instability, platelet aggregation, endothelial dysfunction, inflammation, or hypercoagulation. To model any of these stresses in awake, ambulatory patients is difficult, if not impossible. Furthermore, the relative importance of these factors varies by patient and by disease stage, making their relative contribution to perioperative injury difficult to predict. Thus, for this group of patients, selection of the most specific preoperative test enabling prediction of postoperative outcome is inherently limited.
Finally, I cannot fault our colleagues’ conservative approach to preoperative testing or their recommendation that comprehensive scientific data be amassed to allow rational selection of preoperative tests. However, as clinicians, we make decisions not only based on the comprehensive scientific data at hand, but also based on our individual experiences. Therefore, although the plea for more comprehensive databases is well-justified, we should recognize the critical importance of our clinical intuition as applied to medicine, for such is the art of its practice.
