Organ Protection during Cardiopulmonary Bypass

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Chapter 23 Organ Protection during Cardiopulmonary Bypass

Modern cardiac surgery, heralded by the advent of cardiopulmonary bypass (CPB) more than 5 decades ago, continues to be challenged by the risk of organ dysfunction and the morbidity and mortality that accompanies it. Catastrophic organ system failure was common in the early days of CPB, but advances in perfusion, anesthesia, and surgical techniques have allowed most patients to undergo surgery without major morbidity or mortality. However, organ dysfunction ranging in severity from the most subtle to the most severe still occurs, manifesting most frequently in patients with decreased functional reserves or extensive comorbidities. With more than 1 million patients worldwide undergoing various cardiac operations annually, understanding organ dysfunction and developing perioperative organ protective strategies are of paramount importance.

A number of injurious common pathways may account for the organ dysfunction typically associated with cardiac surgery. CPB itself initiates a whole-body inflammatory response with the release of various injurious inflammatory mediators. Add to this the various preexisting patient comorbidities and the potential for organ ischemic injury due to embolization and hypoperfusion and it becomes clear why organ injury can occur. Most cardiac surgery, due to its very nature, causes some degree of myocardial injury. Other body systems can be affected by the perioperative insults associated with cardiac surgery (particularly CPB), including the kidneys, lungs, gastrointestinal tract, and central nervous system.

CENTRAL NERVOUS SYSTEM INJURY

Incidence and Significance of Injury

Central nervous system dysfunction after CPB represents deficits ranging from neurocognitive deficits, occurring in 25% to 80% of patients, to overt stroke, occurring in 1% to 5% of patients. The significant disparity between studies in the incidence of these adverse cerebral outcomes relates in part to their definition and to numerous methodologic differences in the determination of neurologic and neurocognitive outcome. Retrospective versus prospective assessments of neurologic deficits account for a significant portion of this inconsistency, as does the experience and expertise of the examiner. The timing of postoperative testing also affects determinations of outcome. For example, the rate of cognitive deficits is as high as 80% for patients at discharge, between 10% and 35% at 6 weeks or longer after coronary artery bypass grafting (CABG), and 10% to 15% more than a year after surgery. Higher rates of cognitive deficits recur 5 years after surgery, when as many as 43% of patients have documented deficits.

Although the incidence of this dysfunction varies greatly, the significance of these injuries cannot be overemphasized. Cerebral injury is a most disturbing outcome of cardiac surgery. To have a patient’s heart successfully treated by the planned operation but discover that the patient no longer functions as well cognitively or is immobilized from a stroke can be devastating. There are enormous personal, family, and financial consequences of extending a patient’s life with surgery, only to have the quality of the life significantly diminished. Mortality after CABG, although having reached relatively low levels in the past decade (approximately 1% overall), is increasingly attributable to cerebral injury.1

Risk Factors for Central Nervous System Injury

Successful strategies for perioperative cerebral and other organ protection begin with a thorough understanding of the risk factors, causes, and pathophysiology. Risk factors for central nervous system injury can be considered from several different perspectives. Most studies outlining risk factors take into account only stroke. Few describe risk factors for neurocognitive dysfunction. Although it is often assumed that their respective risk factors are similar, few studies have consistently reported the preoperative risks of cognitive loss after cardiac surgery. Factors such as a poor baseline (preoperative) cognitive state, years of education (i.e., more advanced education is protective), age, diabetes, and CPB time are frequently described.

Stroke is better characterized with respect to risk factors. Although studies differ somewhat as to all the risk factors, certain patient characteristics consistently correlate with an increased risk for cardiac surgery–associated neurologic injury. In a study of 2108 patients from 24 centers in a study conducted by the Multicenter Study of Perioperative Ischemia, incidence of adverse cerebral outcome after CABG surgery was determined and the risk factors analyzed.2 Two types of adverse cerebral outcomes were defined. Type I included nonfatal stroke, transient ischemic attack (TIA), stupor or coma at time of discharge, and death caused by stroke or hypoxic encephalopathy. Type II included new deterioration in intellectual function, confusion, agitation, disorientation, and memory deficit without evidence of focal injury. A total of 129 (6.1%) of the 2108 patients had an adverse cerebral outcome in the perioperative period. Type I outcomes occurred in 66 (3.1%) of 2108 patients, with type II outcomes occurring in 63 (3.0%) of 2108 patients. Stepwise logistic regression analysis identified eight independent predictors of type I outcomes and seven independent predictors of type II outcomes (Table 23-1).

Table 23-1 Risk Factors for Adverse Cerebral Outcomes after Cardiac Surgery

Risk Factor Type I Outcomes Type II Outcomes
Proximal aortic atherosclerosis 4.52 [2.52 to 8.09]*  
History of neurologic disease 3.19 [1.65 to 6.15]  
Use of IABP 2.60 [1.21 to 5.58]  
Diabetes mellitus 2.59 [1.46 to 4.60]  
History of hypertension 2.31 [1.20 to 4.47]  
History of pulmonary disease 2.09 [1.14 to 3.85] 2.37 [1.34 to 4.18]
History of unstable angina 1.83 [1.03 to 3.27]  
Age (per additional decade) 1.75 [1.27 to 2.43] 2.20 [1.60 to 3.02]
Admission systolic BP > 180 mm Hg   3.47 [1.41 to 8.55]
History of excessive alcohol intake   2.64 [1.27 to 5.47]
History of CABG   2.18 [1.14 to 4.17]
Arrhythmia on day of surgery   1.97 [1.12 to 3.46]
Antihypertensive therapy   1.78 [1.02 to 3.10]

BP = blood pressure; CABG = coronary artery bypass graft surgery; IABP = intra-aortic balloon pump.

* Adjusted odds ratio [95% confidence intervals] for type I and type II cerebral outcomes associated with selected risk factors from the Multicenter Study of Perioperative Ischemia.

From Arrowsmith JE, Grocott HP, Reves JG, et al: Central nervous system complications of cardiac surgery. Br J Anaesth 84:378, 2000.

Of all the factors in the Multicenter Study of Perioperative Ischemia analysis, age appears to be the most overwhelmingly robust predictor of stroke and of neurocognitive dysfunction after cardiac surgery. Age has a greater impact on neurologic outcome than it does on perioperative myocardial infarction or low cardiac output states after cardiac surgery (Fig. 23-1).

image

Figure 23-1 The relative effect of age on the predicted probability of neurologic and cardiac morbidity after cardiac surgery.

(From Tuman KJ, McCarthy RJ, Najafi H, et al: Differential effects of advanced age on neurologic and cardiac risks of coronary artery operations. J Thorac Cardiovasc Surg 104:1510, 1992.)

Atheromatous disease of the ascending, arch, and descending thoracic aorta has been consistently implicated as a risk factor for stroke in cardiac surgical patients. The increased use of transesophageal echocardiography (TEE) and epiaortic ultrasonography has added new dimensions to the detection of aortic atheromatous disease and the understanding of its relation to stroke risk. These imaging modalities have allowed the diagnosis of atheromatous disease to be made in a more sensitive and detailed manner, contributing greatly to the information regarding potential stroke risk. Studies have consistently reported higher stroke rates for patients with increasing atheromatous aortic involvement (particularly the ascending and arch segments). This relationship is outlined in Figure 23-2.

image

Figure 23-2 Stroke rate 1 week after cardiac surgery as a function of atheroma severity. Atheroma was graded by transesophageal echocardiography as follows: I, normal; II, intimal thickening; III, plaque < 5 mm thick; IV, plaque > 5 mm thick; V, any plaque with a mobile segment.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Hartman GS, Yao FS, Bruefach M 3rd, et al: Severity of aortic atheromatous disease diagnosed by transesophageal echocardiography predicts stroke and other outcomes associated with coronary artery surgery: A prospective study. Anesth Analg 83:701, 1996.)

Cause of Perioperative Central Nervous System Injury

Because central nervous system dysfunction represents a wide range of injuries, differentiating the individual causes of these different types of injuries becomes somewhat difficult (Box 23-1). They are frequently grouped together and superficially discussed as representing different severities on a continuum of similar injury. This likely misrepresents the different causes of these injuries. The following section addresses stroke and cognitive injury (Table 23-2).

Table 23-2 Causes of Cognitive Dysfunction after Cardiac Surgery

Cause Possible Settings
Cerebral microemboli Generated during cardiopulmonary bypass (CPB); mobilization of atheromatous material or entrainment of air from the operative field; gas injections into the venous reservoir of the CPB apparatus
Global cerebral hypoperfusion Hypotension, occlusion by an atheromatous embolus leading to stroke
Inflammation (systemic and cerebral) Injurious effects of CPB, such as blood interacting with the foreign surfaces of pump-oxygenator; upregulation of proinflammatory cyclooxygenase mRNA
Cerebral hyperthermia Hypothermia during CPB; hyperthermia during and after cardiac surgery, such as aggressive rewarming
Cerebral edema Edema from global cerebral hypoperfusion or from hyponatremia; increased cerebral venous pressure from cannula misplacement
Blood-brain barrier dysfunction Diffuse cerebral inflammation; ischemia from cerebral microembolization or increased intracranial pressure
Pharmacologic influences Anesthetic-related cognitive damage; necrosis of neonatal brains; proteomic changes
Genetic influences Effects of single nucleotide polymorphisms on risk for Alzheimer’s disease or for acute coronary syndromes and other thrombotic disorders

Neuroprotective Strategies

Management of Aortic Atherosclerosis

A combination of epiaortic scanning and atheroma avoidance techniques (with respect to cannulation, clamping, and vein graft anastomosis placement) have been used to attempt to reduce neurocognitive deficits.4 The incidence of cognitive decline may be lower in patients who had an avoidance technique guided by epiaortic scanning compared with no epiaortic scanning. It is an area that requires more investigation. One of the difficulties in interpreting studies that have evaluated atheroma avoidance strategies is the absence of any form of blinding of the investigators. For the most part, a strategy is chosen based on the presence of known atheroma, and the results of these patients are compared with historical controls. Multiple techniques can be used to minimize atheromatous material liberated from the aortic wall from getting into the cerebral circulation. These range from optimizing placement of the aortic cannula in the aorta to an area relatively devoid of plaque to the use of specialized cannulas that reduce the sandblasting of the aortic wall. Alternative aortic cannulas and using different locations possess the ability to decrease embolization of atheromatous plaque. The avoidance of partial occlusion clamping for proximal vein graft anastomosis using a single-step automated anastomotic device and the use of alternatives to cross-clamping all possess the ability to mitigate injury due to embolization.

Glucose Management

Hyperglycemia is a common occurrence during the course of cardiac surgery. Administration of cardioplegia containing glucose and stress response–induced alterations in insulin secretion and resistance increase the potential for significant hyperglycemia. Hyperglycemia has been repeatedly demonstrated to impair neurologic outcome after experimental focal and global cerebral ischemia. The explanation for this adverse effect likely relates to the effects that hyperglycemia have on anaerobic conversion of glucose to lactate, which ultimately cause intracellular acidosis and impair intracellular homeostasis and metabolism. A second injurious mechanism relates to an increase in the release of excitotoxic amino acids in response to hyperglycemia in the setting of cerebral ischemia. If hyperglycemia is injurious to the brain, the threshold for making injuries worse appears to be 180 to 200 mg/dL.

The appropriate type of perioperative serum glucose management and whether it adversely affects neurologic outcome in patients undergoing CPB remain unclear. The major difficulty in hyperglycemia treatment is the relative ineffectiveness of insulin therapy. Using excessive amounts of insulin during hypothermic periods may lead to rebound hypoglycemia after CPB. Chaney and associates6 attempted to maintain normoglycemia during cardiac surgery with the use of an insulin protocol and came to the conclusion that even with aggressive insulin treatment, hyperglycemia is often resistant and may actually predispose to postoperative hypoglycemia. Attempting to mediate injury may actually predispose to additional injury.

Off-Pump Cardiac Surgery

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