In the last 10 years, there has been a growing body of literature regarding the prevention of perioperative cardiac complications with important strides toward minimizing postoperative cardiac events. That said, cardiac complications do occur, and this chapter addresses their demographics, risk factors, and management. It is divided into sections of postoperative myocardial infarction, congestive heart failure, atrial fibrillation, and ventricular arrhythmias.

Background

The combination of an aging, comorbid population with the rapid increase in surgical procedures has resulted in perioperative myocardial infarction (PMI) becoming a common and unfortunate reality. The incidence of PMI is dependent upon patient risk factors, the type of surgery, and the definition of MI. An early review of PMI in an unselected group of patients over the age of 40 years uncovered PMI rate of 1.4% compared to a 6.9% rate in patients selected for preoperative cardiac testing, presumably a higher-risk cohort. The largest study to date of operative cardiac outcomes, the PeriOperative Ischemic Evaluation (POISE) trial, found a 30-day MI rate of 5.7% in the control group undergoing noncardiac surgery. Meanwhile, the Coronary Artery Revascularization Prophylaxis (CARP) trial included a cohort of high-risk patients with known coronary artery disease undergoing vascular surgery and noted that 27% of patients experienced a postoperative troponin elevation. The overall risk and consequences of PMI are dependent upon patient- and procedure-related risk factors and it is thus imperative to risk assess (covered in Chapter 51), recognize, and appropriately manage PMI.

Diagnosis and Prognosis

Perioperative MI was traditionally difficult to diagnose because the key biomarker, creatinine kinase-MB is routinely elevated in postoperative patients due to skeletal muscle trauma. Additionally, the key symptom of chest pain is often masked at least partially by anesthesia, analgesia, and sedation. Furthermore, electrocardiograms (ECGs) are infrequently obtained, missing subtle or transient changes. As a result, PMI was routinely overlooked or not recognized until complications occurred, often as late as postoperative day 5. This played a significant role in the traditionally high rates of morbidity and mortality of PMI. Short-term mortality with PMI is directly correlated to the level of troponin elevation and ranges from 3.5 to 25%. Moreover, even postoperative troponin leak negatively impacts long-term survival.

The advent of troponin testing, sensitive and specific for myocardial injury, greatly enhances the ability to diagnose PMI. Coupling a rise of cardiac biomarkers with signs of myocardial ischemia—such as consistent symptoms, ECG changes, or findings on coronary imaging—allows PMI to be reliably diagnosed. Most PMIs occur within 24 hours of surgery, but about 10% occur more than 1 day postoperatively. The reasons for this dichotomy can be explained by the two different mechanisms of PMI.

Pathophysiology

Type 1 PMI

Traditional MIs result from an acute coronary syndrome (ACS). More to the point, a vulnerable plaque experiences a spontaneous rupture. This is often associated with plaque inflammation in the face of high emotional or physiologic stress situations. These stressors are common in the perioperative setting where sympathetic tone is high due to release of catecholamines. Additionally, hemodynamic instability is common, and coronary vasoconstriction may occur. The end result is that intracoronary plaques may rupture, initiating the coagulation cascade and the resultant type 1 PMI.

Type 2 PMI

Type 2 PMI is associated with myocardial oxygen supply and demand imbalances and is more common in operative than in nonoperative settings. The main driver for type 2 PMI is tachycardia. Patients with significant coronary artery disease (typically > 70% stenosis) and left ventricular hypertrophy (which increases myocardial demand) quickly overwhelm oxygenation delivery at elevated heart rates. The tachycardia is driven by myriad forces such as increased adrenergic tone, postoperative pain, systemic vasodilation, hypovolemia, and anemia. Electrocardiographically this presents as ST-depression rather than overt ST-elevation MI in the bulk of cases.

Type 2 PMI accounts for more than half of all PMIs. One study evaluating patients who died from PMI found that only 46% of patients had evidence of plaque rupture and thrombosis. The rest presumably died from complications of type 2 PMI. The pathophysiology of PMI explains why type 2 tends to occur within 3 days of surgery when the oxygen supply–demand balance is most impaired, whereas type 1 PMI from plaque rupture occurs with an even distribution over the 3 weeks following surgery.

Management

The management of PMI mirrors its pathophysiology. Type 1 PMI with true ST-elevation MI is uncommon and generally treated as a traditional ACS with the goal of revascularizing an acutely thrombosed artery. This management is complicated by increased risks of surgical site bleeding but generally involves anticoagulation and antiplatelet therapy along with coronary revascularization. These risks and benefits need to be carefully weighed with the surgical team prior to initiation of therapy. Beta-blockers and statin medications are also indicated.

Type 2 PMI is best treated by relieving the oxygen supply–demand imbalance. This includes reducing the adrenergic drive through pain control, beta-blockade, and maintenance of euvolemia. These former are best managed through the considered use of analgesics and beta-blockers to reduce the heart rate below 60 beats per minute, whereas the latter is accomplished by recognizing and treating the cause of hypovolemia.

Postoperative hypotension is commonly due to a combination of volume depletion and anesthetic agents and can be treated with IV fluids. However, other causes such as sepsis, arrhythmia, hemorrhage, cardiac failure, and pulmonary embolism should be considered and treated appropriately. Hypertension-induced type 2 PMI should be treated with beta-blockers and other antihypertensives as needed. Tachyarrhythmias such as atrial fibrillation with rapid ventricular response should be rate controlled or cardioverted as the situation dictates.

Postoperative anemia management to prevent and treat PMI is controversial as both postoperative anemia and liberal transfusion have been shown to “worsen outcomes.” For example, a retrospective study found preoperative hematocrit levels < 39% (hemoglobin ∼13 g/dL) were associated with increased cardiac complications and mortality. Conversely, the medical literature generally shows no benefit and potential harm in transfusing critically ill patients with hemoglobin levels above 7 g/dL. However, a subgroup analysis of these data revealed that patients with ischemic heart disease appeared to do better with more liberal transfusion policies (ie, transfusion to > 10 g/dL). Although not in the operative setting, another study found worse outcomes in patients who received a transfusion for hematocrit levels > 25% (hemoglobin ∼8 g/dL) in the setting of ACS. Furthermore, the protective effect of perioperative beta-blockers appears to be attenuated in the setting of surgical anemia where data support that beta-blocker use in the face of significant anemia worsens outcomes. While the data are murky, it appears a reasonable policy to transfuse patients with PMI or ACS and a hematocrit of < 25% (hemoglobin 8 g/dL). Of course, patients who are hemodynamically unstable due to hemorrhage require volume resuscitation and transfusion with close monitoring in a critical care setting.

Monitoring

There is little data to guide the use of postoperative monitoring for PMI. However, PMI is a strong predictor of short- and long-term mortality, and early intervention appears to improve outcomes. Further, the typical symptoms of MI are often masked by the surgical state. Thus it is reasonable to monitor high-risk patients for PMI. The ACC/AHA 2007 perioperative cardiac guideline recommends an electrocardiogram (ECG) at baseline, immediately postoperatively, as well as daily for the first 2 postoperative days in those at high risk (see Chapter 51 for determining cardiac risk) for PMI. They further recommend limiting postoperative cardiac enzyme testing to those with symptoms or ECG findings consistent with ACS. Positive findings should result in increased vigilance and initiation of appropriate therapy and secondary prevention.

Conclusion

Postoperative MI is an unfortunate reality that is driven by the increasing frequency of surgical procedures in our aging, comorbid population. Despite prudent preoperative assessment, PMI still occurs and is often masked by the operative state. PMI more often occurs from oxygen supply–demand imbalances than ACS and as such is most often treated with a return to homeostasis. High-risk patients should undergo at least limited postoperative monitoring for PMI.

Background