Karl Wasserman, M.D., Ph.d., F.C.C.P.
Torrence, California
Division of Respiratory and Critical Care Phsiology and Medicine, Harbor-UCLA Medical Center.
Reprint requests: Dr. Wasserman, Harbor-UCLA Medical Center,
1000 West Carson, Torrence, California 90509
Age itself is a risk factor for surgical morbidity and morality. Maximal cardiovascular function decreases with aging. This is reflected in reduce maximal heart rate, stroke volume, and cardiac output and likely a reduced ability to readjust vascular tone to redistribute blood flow in response to regional metabolic stress. However, we all age at different rates, so that chronological aging is not the same as physiologic aging.1 Thus, it is not totally unexpected that age itself, or an assessment of a single component of cardiovascular function, would not be predictive of a patient’s cardiovascular reserve in response to metabolic stress, such as Hypermetabolic State of recovery from major surgery.
In a review of perioperative morbidity, Mangano2 notes that cardiac diseases are the leading cause of death following anesthesia and surgery, but risk of death, except with those patients with chronic heart failure, was difficult to assess. In an effort to select the elderly patients at greatest risk of complications following major abdominal surgery, Older and Smith3 used intensive care facilities for preoperative invasive measurements of hemodynamic, pulmonary, and renal function in 100 elderly patients prior to major abdominal surgery. They found a great variation in function, but no measurement was identified as a single indicator of cardiovascular risk.
In this issue of Chest (see page 701), Older and colleagues report the findings from their follow-up study of 187 elderly patients (mean age, 70 years) undergoing major abdominal surgery with an overall perioperative mortality rate of 7.5 percent. They found no relationship between perioperative mortality rate and age. In contrast, however, when they related perioperative mortality to the anaerobic threshold (AT) determined from gas exchange during noninvasive cardiopulmonary exercise testing, they identified the patients at greatest risk. They found an 18 percent mortality rate for those with an AT less than 11 ml/min/kg, (three times the basal metabolic VO2 rate). But a 0.8 percent mortality rate for those with an AT greater than 11 ml/min/kg. When they selected those patients with ECG evidence of ischemia and an AT less than 11 ml/min/kg, the perioperative mortality rate increased to 42 percent.
Del Guercio and Cohn,4 like Older and Smith,3 used preoperative cardiac catheterization with measurement of central hemodynamics and could not clearly stratify operative risk. Smith et al5 retrospectively used preoperative cardiopulmonary exercise testing on a cycle ergometer to identify those patients most likely to experience postoperative cardiovascular complications following thoracic surgery for lung cancer. They found good stratification between the patient’s maximal O2 uptake (VO2) and risk. Olsen et al6 and Nakagawa et al7 simultaneously measured central hemodynamics with right heart catheterization and pulmonary gas exchange during submaximal cycle ergometer exercise testing aided in assessment of risk. The present report of Older et al, thus, is especially relevant because of the large number of elderly patients studied and their finding that noninvasive incremental exercise testing in which gas exchange measurements of the subject’s AT (therefore, not requiring a maximal exercise effort) distinguished the patients at high risk for perioperative mortality from those at low risk.
We are thus presented with the question: Why should the AT separate those patients at greatest risk of perioperative death from those at least risk? Cardiac output and VO2 responses to any metabolic stress (e.g. exercise) are interrelated whether the subject is fit or unfit or has heart disease. Oxygen cannot be consumed by the cells in need unless the circulation delivers the oxygen to the cells. If VO2 equals the cellular O2 requirement, the circulation has responded appropriately (ie, the metabolic stress is below the AT). In contrast, if circulation cannot meet the O2 requirement of the cells, such as during exercise above the AT, VO2 does not reach a steady state.8 This shortfall in regeneration of high-energy PO4 by aerobic metabolism leads to an increase in cell and blood lactate, decrease in HCO3-, and increase in CO2 output (VCO2) relative to VO2 due to the release of CO2 from HCO3- as it buffers lactic acid. In this state of metabolic disequilibrium, muscular exercise cannot be indefinitely maintained.
Applying the same concept to the hypermetabolic state of surgery and postoperative tissue repair, cardiac output must increase to meet this increased metabolic stress. However, if an imbalance between oxygen supply and demand occurs because the circulation fails to supply all the cells with their oxygen requirement, the aerobic metabolic processes and cellular function will be impaired. Presumably, if enough of the body is anaerobic, the likelihood of perioperative mortality increases.
The AT measurement was originally developed as a test to detect the oxygen consumption above which the circulation fails to meet the metabolic requirement (ie, heart failure in the forward sense). An AT of 11 ml/min/kg is three times the normal basal metabolic rate. The present work of Older et al suggests that a reserve of twice the resting metabolic rate above the basal level is needed to reduce the subject’s risk of perioperative mortality to close to zero in elderly patients undergoing major abdominal surgery.
Exercise testing is used to determine the patient’s cardiovascular reserve, as it measures the ability of the cardiac output to increase in response to stress. In addition, it assesses the automatic control of the peripheral circulation and the ability to redistribute blood flow to the tissues in need. Thus, the use of exercise testing with gas exchange measurements is indeed a logical approach for evaluating cardiovascular reserve.
There are limitations to the use of exercise tests for determining the cardiovascular reserve to postoperative stress. For example, the bowel wall rather than the muscle may be the organ requiring more blood (hence, oxygen) flow; the former may not have the same tolerance to hypoxia as the latter. Also, postoperative edema would require that capillary PO2 be maintained at a higher value than in the non-edematous state to overcome the increased distance between red cells and mitochondria for oxygen diffusion. That the AT determined during exercise reflects the ability of the circulation to maintain oxygen delivery for homeostatic regulation of aerobic regeneration of adenosine triphospate in the perioperative period, as described by Older et al, is certainly an important and practical observation.
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