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Ischemic cardiac morbidity is the most common cause of perioperative (and overall) death in the United States.[26] Myocardial ischemia results from an imbalance between myocardial oxygen supply and demand, for which there are many causes during the perioperative period.[123] The determinants of myocardial oxygen supply and demand are shown in Figure 52-5 . The most detrimental changes (tachycardia, hypervolemia, and anemia) are those that simultaneously decrease oxygen supply and increase oxygen demand. Tachycardia increases myocardial oxygen demand by increasing myocardial work, while at the
Figure 52-5
Determinants of myocardial oxygen supply and demand that
lead to myocardial ischemia. During the perioperative period, virtually every determinant
is altered by factors such as fluid shifts, blood loss, pain, catecholamines, altered
coagulability, and ventilatory insufficiency. (Adapted from Beattie C, Fleisher
LA: Perioperative myocardial ischemia and infarction. In
Beattie C, Fleisher LA [eds]: International Anesthesiology Clinics. Boston, Little,
Brown, 1992, pp 12–24.)
When the entire perioperative period is considered, myocardial ischemia occurs most commonly postoperatively, and less commonly preoperatively and intraoperatively.[125] [126] Postoperative myocardial ischemia is predominantly the ST depression type,[127] and is significantly associated with MI.[87] The low incidence of intraoperative ischemia may be due to anesthetic suppression of adrenergic tone,[128] and the minute-to-minute control of the hemodynamic and other determinants of myocardial oxygen supply and demand. In the early postoperative period, the patient is transferred from the highly controlled environment of the operating room to the postanesthetic care unit or intensive care unit, where the ratio of physician or nurse to patient is reduced, and control of hemodynamic variables is less complete. Postoperative ischemia often begins early in the postoperative period, a time associated with pain, tachycardia, hypertension, sympathetic discharge, and hypercoagulability.[128] Most postoperative myocardial ischemia is silent (clinically asymptomatic), as a result of masking by surgical pain or by opioid analgesia,[84] [129] [130] [131] and is usually associated with an increase in heart rate.[126] [127] The peak incidence of ischemia occurs during the early (days 0 to 3) versus late (days 4 to 7) postoperative period.[126] A study using continuous 12-lead electrocardiographic monitoring reported 67% of ischemic events started within 2 hours from the end of surgery and emergence from anesthesia.[127]
Table 52-8 summarizes eight studies showing the relative incidence of preoperative, intraoperative, and postoperative myocardial ischemia. The two studies[79] [132] with the lowest rates of intraoperative myocardial ischemia rigorously controlled intraoperative heart rate and blood pressure by protocol. Norris and associates[132] continued this "tight" hemodynamic control into the postoperative period and reported the lowest rate (15%) of postoperative myocardial ischemia. These studies suggest that good hemodynamic control perioperatively plays an important role in reducing myocardial ischemia. Unless a contraindication exists, I administer β-blockers liberally to keep the heart rate less than 80 beats/min throughout the perioperative period. Although it is commonly recommended to maintain the blood pressure within 20% of baseline, I use a more rational approach that better addresses patients with low or high baseline blood pressure ( Fig. 52-6 ).
Study | Preoperative | Intraoperative | Postoperative | Overall |
---|---|---|---|---|
Pasternack et al.[86] |
|
|
|
|
Aortic/lower extremity | 40 | 38 | 48 | 61 |
Carotid | 38 | 41 | 54 | 68 |
Ouyang et al.[84] | 13 | 21 | 63 |
|
McCann and Clements[726] | 14 |
|
38 |
|
Mangano et al.[87] | 20 | 25 | 41 |
|
Raby et al.[54] |
|
18 | 30 |
|
Christopherson et al.[79] | 8 | 11 | 40 | 40 |
Boylan et al.[302] |
|
|
35 |
|
Norris et al.[132] | 3 † | 4 † | 15 † | 16 |
Average | 19 | 23 | 42 | 43 |
Several clinical studies have increased our understanding of the clinical variables that precipitate myocardial ischemia. There has been a long-standing debate over whether the rate pressure product (heart rate × mean arterial blood pressure)[133] [134] or the pressure/rate quotient (mean arterial blood pressure divided by heart rate) [135] [136] is most correlated with ischemic episodes. Work by Buffington[137] supports the pressure/rate quotient, showing in a canine model that a quotient of less than 1.0 was associated with ischemia. In simpler terms, hypotension and tachycardia are a dangerous combination. In patients undergoing CABG
Figure 52-6
Nomogram used to determine minimum and maximum mean blood
pressure limits. The nomogram is used by reading the baseline mean arterial pressure
(MAP) from the left-hand axis horizontally onto the diagonal baseline mean pressure
line. The point of intersection on this line is then extended vertically to intersect
with the minimum and maximum allowable mean pressure curves. A patient with a baseline
MAP of 105 mm Hg, as illustrated, would have an allowable MAP range of 80 to 114
mm Hg. (From Norris EJ, Beattie C, Perler BA, et al: Double-masked randomized
trial comparing alternate combinations of intraoperative anesthesia and postoperative
analgesia in abdominal aortic surgery. Anesthesiology 95:1054–1067, 2001.)
The optimal hematocrit value for vascular surgery patients is unknown. In the mid 1980s, the tendency was to withhold transfusion to avoid the risk of human immunodeficiency virus and hepatitis infection. In 1988, the National Institutes of Health indicated that no "threshold" hemoglobin concentration could be defined for routine transfusion.[140] The American College of Physicians then stated that hemoglobin concentrations of greater than 7.0 g/dL are well tolerated in patients without cardiovascular disease.[141] These guidelines, however, did not include recommendations for patients with CAD or risk factors for CAD. Although there are no controlled trials, there appears to be an increased incidence of myocardial ischemia and cardiac morbidity in vascular surgery patients if hemoglobin concentrations are less than 9.0 g/dL in the early postoperative period.[142] [143] This evidence, along with our understanding of the effects of anemia on myocardial oxygen supply and demand,[124] supports the practice of maintaining hemoglobin concentrations above 9.0 g/dL in the vascular patient, especially patients at significant risk for ischemic cardiac morbidity.
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