Over the past two decades, much had been learned about perioperative cardiac issues and the resultant short- and long-term complications. This chapter addresses their demographics, risk factors, and management. It is divided into sections of the most commonly encountered postoperative cardiac complications; postoperative myocardial infarction, congestive heart failure, atrial fibrillation, and ventricular arrhythmias.
POSTOPERATIVE MYOCARDIAL INFARCTION
Postoperative myocardial infarction (PMI) is a distinct clinical entity from nonpostoperative myocardial infarction (MI). Compared with patients presenting to emergency departments with MI, patients with PMI die nearly twice as often. The incidence of PMI is dependent upon patient risk factors and the type of surgery and the technique used. Reported rates of PMI and associated mortality have varied widely in the literature because of differences in patient selection, changes over time in surgical and anesthetic techniques, differences in screening strategies and definitions of PMI, and the ever-increasing sensitivity of biomarkers for myocardial necrosis. Nonetheless, PMI remains a common and devastatingly morbid postoperative complication.
There are three major conditions associated with the rise of cardiac biomarkers in the perioperative period. Two of these are defined by Third Universal Definition of Myocardial Infarction Consensus, published in 2012, which describes Type I PMI as infarction secondary to plaque rupture and intracoronary thrombus formation and Type II PMI as an infarction secondary to a mismatch between the supply of oxygen and the metabolic demands of the myocardium. The third cause of biomarker rise has generated several names, most recently described as nonischemic myocardial injury with necrosis.
Traditional MIs result from an acute coronary syndrome (ACS). More to the point, a vulnerable plaque experiences a spontaneous rupture, fissuring, erosion, or other event leading to intracoronary thrombus and downstream infarction. In the perioperative period, a number of contributing mechanisms exist including an increase in inflammation with an associated hypercoagulable state and an increase catecholamine secretion leading to increase shear stress on preexistent coronary plaques. The end result is intracoronary plaque rupture, which initiates the coagulation cascade, leading to thrombus and infarction. Electrocardiographically there may be ST segment elevations, Q waves, or less specific ST segment depressions or T-wave changes.
Type 2 PMI is associated with myocardial oxygen supply and demand imbalances and occurs in operative and nonoperative settings. The main driver for type 2 PMI is tachycardia secondary to factors such as increased adrenergic tone, postoperative pain, systemic vasodilation, hypovolemia, anemia, and the withholding of chronic β-receptor blocking medications. Patients with fixed coronary disease and increased left ventricular mass possess increased risk for this mechanism of injury. Electrocardiographically this presents with ST-depression, nonspecific T-wave changes or even a normal electrocardiogram (ECG) much more commonly than ST-segment elevation.
Nonischemic myocardial injury with necrosis