Chapter 22 Cardiopulmonary Bypass and the Anesthesiologist
GOALS AND MECHANICS OF CARDIOPULMONARY BYPASS
Venous return may be decreased deliberately (as is done when restoring the patient’s blood volume before coming off bypass) by application of a venous clamp. From the reservoir, blood is pumped to an oxygenator and heat exchanger unit before passing through an arterial filter and returning to the patient. Additional components of the circuit generally include pumps and tubing for cardiotomy suction, venting, and cardioplegia delivery and recirculation, as well as in-line blood gas monitors, bubble detectors, pressure monitors, and blood sampling ports. A schematic representation of a typical bypass circuit is depicted in Figure 22-1.
PHYSIOLOGIC PARAMETERS OF CARDIOPULMONARY BYPASS
The primary objective of CPB is maintenance of systemic perfusion and respiration. Controversy arises with the question of whether systemic oxygenation and perfusion should be “optimal or maximal.” Remarkably, after more than one-half century of CPB, there is continued disagreement regarding the fundamental management of extracorporeal circulation. Clinicians and investigators disagree on what are the best strategies for arterial blood pressure goals, pump flow, hematocrit, temperature, blood gas management, or mode of perfusion (pulsatile vs. nonpulsatile) (Box 22-1). Additional considerations of what is best relate to other goals of CPB: maintenance of homeostasis, facilitation of surgery, and avoidance of complications.1
Perfusion Pressure during Cardiopulmonary Bypass
Between mean arterial pressures (MAP) of 50 and 150 mmHg, cerebral autoregulation maintains a relatively constant blood flow and oxygen delivery. During hypothermic CPB, the lower limit of cerebral autoregulation may be as low as 20 to 30 mmHg,2 affording some additional protection against hypoperfusion. Increasing perfusion pressure to alleviate the risk of hypoperfusion may lead to greater embolic load and worse outcomes. Ultimately, the selection of perfusion pressure during CPB will need to be based on clinical outcome studies.
Pump Flow during Bypass
Most perfusion teams also monitor mixed venous saturation, targeting levels of 70% or greater. Unfortunately, this level does not guarantee adequate perfusion of all tissue beds, because some (muscle, subcutaneous fat) may be functionally removed from circulationduring CPB. Hypothermic venous saturation may overestimate end-organreserves. Regionalperfusion of various end-organs (brain, kidney, small intestine, pancreas, and muscle) has been quantified with a fluorescent microsphere technique.3 Cerebral blood flow was unchanged at higher pump flows. Renal perfusion was maintained at flows of 1.9 and 1.6 L/min/m2. Perfusion to the pancreas was constant at all flows, and small bowel perfusion varied linearly with pump flow. Muscle bed flows were decreased at all flows.
Bypass Temperature Management Strategy
Effects on Central Nervous System
Several groups of investigators have assessed the effect of normothermic temperatures during bypass on perioperative central nervous system events in cardiac surgery patients.4 Mild hypothermia provides some magnitude of cerebral protection during CPB, whereas mildly hyperthermic temperatures (>37°C) exacerbate and amplify the ischemic injury associated with CPB.
Temperature Monitoring
Because the brain is vulnerable to hyperthermic temperatures, it is important to use the temperature-monitoring site most likely to reflect cerebral temperature. The most commonly used sites in cardiac surgery patients include esophageal, nasopharyngeal, tympanic, pulmonary arterial, rectal, urinary bladder, subcutaneous (or muscle), and cutaneous sites. Unfortunately, none of these monitoring locations has been demonstrated to reflect cerebral temperature reliably. With exposure of the brain, investigators have placed a thermocouple directly in the cerebral cortex. Brain temperature was compared with values obtained from sensors in eight locations.5 Investigators found a poor concordance between cerebral temperature and values obtained at the other monitoring sites. Locations hypothesized to best reflect core temperature—tympanic membrane, esophagus, nasopharynx, pulmonary artery—sometimes overestimated cerebral temperature or underestimated brain temperature. Because of the substantial variability noted in central temperature readings (Fig. 22-2) and lack of the concordance of central temperature measures in every patient, the investigators recommended the use of at least three measures of central or core temperature.
Acid-Base Strategy
The pH-stat approach to acid-base balance maintains a pH of 7.40 and PCO2 of 40 mmHg when corrected for body temperature, typically requiring the addition of CO2 during hypothermic CPB. This method of blood gas management was generally favored until the mid 1980s because it was believed that the potent vasodilatory effects of CO2 would provide increased cerebral blood flow and thereby minimize the risk of cerebral ischemia during CPB. It is now recognized that pH-stat management during hypothermia produces passive cerebral vasodilation, impairs autoregulatory responses to blood pressure changes and metabolic demands in the brain, and does not improve overall oxygen balance. In contrast, α-stat management preserves autoregulation and the relationship between cerebral blood flow and metabolism. Neither blood gas strategy has any significant effect on hypothermic cerebral metabolism. The increased CBF seen with pH-stat may also increase the risk of cerebral embolization or produce a steal phenomenon.6
Fluid Management
Several studies have investigated the differences between colloid and crystalloid priming solutions. In general, crystalloid solutions lead to decreased colloid osmotic pressure with a resultant increase in extracellular water retention, irrespective of the osmolarity of the pump prime. Albumin, unlike a pure crystalloid prime, can decrease the interaction of blood components with the bypass circuit by coating the fluid pathway surfaces. In their meta-analysis of 21 controlled trials enrolling 1346 patients, Russell and associates showed a notably smaller drop in on-bypass platelet counts in patients treated with albumin in the pump prime.7
END-ORGAN EFFECTS OF CARDIOPULMONARY BYPASS
Myocardial Injury
Most coronary revascularization procedures are completed with the assistance of CPB. Although the completion of coronary anastomoses is facilitated by CPB (i.e., the surgeon can operate on a quiet, nonbeating heart), the heart is subjected to a series of events leading to ischemic myocardium during extracorporeal circulation. The operation, which is designed to preserve and improve myocardial function, is sometimes associated with myocardial damage (Box 22-2). The extent and incidence of this injury are dependent on the sensitivity and specificity of the diagnostic methods being used. However, most patients who undergo cardiac operations sustain some degree of myocardial injury. Although patients with normal ventricular function may tolerate these minor amounts of injury without detectable sequelae, those with impaired ventricular function preoperatively may not be able to tolerate the slightest injury. As the patient population for CPB continues to become older and have greater degrees of concomitant illness, understanding the physiology of and developing effective preventive strategies for myocardial injury during CPB are increasingly important. Because myocardial damage influences early and long-term results, the identification and control of factors associated with myocardial injury are critical to ensuring good outcomes. Although injury may be linked to anesthetic and surgical management, myocardial injury usually is thought to occur from inadequate myocardial protection during CPB.
Mechanisms
Certain specific events during CPB are associated with myocardial ischemia and injury (Table 22-1). These events lead to ischemia by increasing oxygen demands, decreasing oxygen supply, or a combination of both. When these factors are present together they potentiate myocardial damage. For example, the distended, fibrillating ventricle with a low perfusion pressure is particularly susceptible to damage.
Table 22-1 Factors Associated with Myocardial Injury during Cardiopulmonary Bypass
Abnormal perfusate composition |
Persistent ventricular fibrillation |
Inadequate myocardial perfusion |
Ventricular distention |
Ventricular collapse |
Coronary embolism |
Catecholamines |
Aortic cross-clamping |
Reperfusion |
Myocardial Protection
Myocardial protection strategies can be summarized with four basic concepts:
Brain Injury
The brain is highly susceptible to injury during CPB. Many clinicians believe that cerebral injuries after cardiac surgery are the most devastating adverse outcomes associated with CPB. A study of 2400 patients undergoing elective coronary artery bypass grafting (CABG) from 24 U.S. centers reported that 6.1% of patients suffer adverse postoperative gross neurologic or psychiatric central nervous system events. These patients remain in the intensive care unit and hospital for greater periods of time, and 1 in every 3 surviving patients does not return home but requires continued long-term care and rehabilitation.8 (see chapter 23).
Renal Dysfunction
The effects of CPB on the renal system have significant health and economic impacts; however, despite intensive investigation into the pathogenesis and prevention of renal failure, there remains limited progress in the development of effective protective strategies in recent decades.9 Because intravascular volume depletion and hypoperfusion can lead to exacerbation of renal ischemia and accentuate the risk for postoperative acute renal failure, avoidance of nephrotoxic agents and close attention to intravascular volume, blood pressure, and cardiac output (CO) are central in the effort to reduce the occurrence of acute renal failure after cardiac surgery.
Gastrointestinal Effects
The effects of CPB on the gastrointestinal system are complex and not fully elucidated. Although most patients undergoing cardiac surgery do not suffer adverse changes in gastrointestinal function, subclinical perturbations including transient elevations in hepatocellular enzymes and hyperamylasemia have been observed after CPB. Although the incidence of gastrointestinal complications after CPB is low (range, 0.3% to 3.7%), they are associated with significant morbidity and remarkably high mortality (range, 11% to 67%) compared with cardiac surgery patients without postoperative gastrointestinal compromise. The frequently reported adverse gastrointestinal outcomes include gastroesophagitis, upper and lower gastrointestinal hemorrhage, hyperbilirubinemia, hepatic and splenic ischemia, colitis, pancreatitis, cholecystitis, diverticulitis, mesenteric ischemia, as well as intestinal obstruction, infarction, and perforation.10