Preoperative Cardiac Evaluation of the Thoracic Surgical Patient
Jason C. Robins
Dan J. Fintel
It is neither possible nor appropriate to “clear” a patient for surgery during a preoperative evaluation. The principal goals of the preoperative evaluation are to estimate the risk for and minimize the incidence of postoperative cardiovascular complications. Additionally, it is valuable to recommend therapies that may reduce the long-term risk for cardiac events. The aim of this chapter is to outline a rational preoperative evaluation strategy and to discuss four principal postoperative cardiovascular complications: myocardial infarction (MI), congestive heart failure, arrhythmias, and hypertension.
In addition, the vexing problem of the perioperative management of antiplatelet therapy in patients with coronary stents is covered at the end of this chapter.
Thoracic surgery creates special challenges for the cardiac patient. In one study by Melendez and Carlon36 of 188 patients aged 15 to 87 years undergoing thoracic surgery, 14% had cardiovascular complications. Mangano and colleagues34 found that patients who have episodes of ischemia or who experience nonfatal MIs in the first week after surgery have a 2- to 20-fold risk for serious cardiovascular outcome in the 2 years after surgery. There are numerous physiologic reasons why the thoracic surgery patient is at especially high risk for cardiac complications. Significant atelectasis, decreased lung compliance, and decreased diffusing capacity after thoracic surgery may lead to hypoxia, hypercarbia, or increased work of breathing, which all decrease myocardial oxygen supply and increase myocardial oxygen demand. This mismatch may precipitate ischemia, which in turn can lead to arrhythmias, congestive heart failure, or even MI. Second, postoperative patients develop a hypercoagulable state that may exacerbate fixed coronary stenoses, contribute to new coronary plaque rupture, or place strain on the heart through the development of pulmonary emboli. Third, after major lung resections, the decrease in the pulmonary vascular bed results in increased preload, which can worsen congestive heart failure. Complicating matters further are the high catecholamine levels associated with pain and enormous fluid shifts found in many patients after thoracic surgery.
Preoperative Evaluation of Risk
The guiding principle in preoperative cardiac consultation is the same as in the everyday practice of medicine: order tests only if the results have a reasonable likelihood of changing management. To appreciate fully whether a test result may change management, an understanding of Bayes’ theorem is required. Bayes’ theorem states that the posttest probability of a person having a disease is related to the sensitivity and specificity of the test and the prevalence of that disease in the population being studied. For instance, if the clinical suspicion for a disease is high (pretest probability), a negative noninvasive test never rules out that disease. Here is a real-life example: In January 1993, a 37-year-old man—a long-time smoker with elevated cholesterol and a family history of coronary artery disease—presented to an emergency department in Sedgwick County, Kansas. He had complaints consistent with classic unstable angina. He had begun experiencing chest discomfort 2 days earlier while washing his car. He subsequently developed substernal chest tightness while loading boxes at work, which radiated to his arm and was associated with diaphoresis and shortness of breath. The symptoms resolved with 5 to 10 minutes of rest. On the surface, his physician performed all of the appropriate tests, admitting him overnight for observation, ruling out MI, and arranging for a treadmill stress test the next day. The patient exercised for 12 minutes without electrocardiographic changes and was discharged. Four days later, he died. His autopsy disclosed extensive three-vessel coronary stenoses. His widow sued, citing Bayes’ theorem, and was awarded a large sum. The jury went so far as to state that Bayes’ theorem is part of the medical standard of care.
Mangano and colleagues reported that morbidity and mortality due to cardiovascular disease are prevalent and costly for the 30 million patients who undergo noncardiac surgery annually, affecting >1 million of them. Some 10% of these patients have known coronary artery disease or are at significant risk.34 Several small clinical trials have investigated the effect of preoperative nitrates, calcium channel blockers, and alpha2 agonists with somewhat encouraging but not conclusive results. Because postoperative ischemic events are at least partially related to the persistently exaggerated sympathetic response commonly seen in these patients, beta-blocker therapy merits special examination. In fact, two studies have demonstrated significant benefits in terms of morbidity and mortality with the perioperative use of beta blockers. Mangano and associates34 randomized 200 patients to receive atenolol (a beta1-selective blocker) or placebo and followed them for 2 years. Atenolol was given
intravenously (10 mg) immediately before and after surgery and then orally (100 mg daily) until hospital discharge. A total of 30 patients (15.6%) died during the 2-year follow-up period; 21 of these deaths (12 of which were from cardiac causes) occurred in the placebo group compared with 9 (4 of which were from cardiac causes) in the atenolol group, resulting in a 55% reduction in overall mortality and a 65% reduction in cardiovascular mortality. Predictably, most of the beta-blocker benefit was seen during the first 6 to 8 months, when no cardiac deaths occurred in the atenolol group, compared with 7 cardiac deaths in the placebo group (p < 0.001). Poldermans and colleagues45 subsequently described a randomized trial of bisoprolol, another beta1-selective blocker, in patients undergoing major subdiaphragmatic vascular surgery who had evidence of dobutamine-induced hypokinesis (ischemia) by stress echocardiography. A total of 112 patients were followed for 30 days postoperatively after receiving perioperative bisoprolol plus standard care versus standard care alone. A dose of 5 mg was started at least 1 week before surgery and was increased as tolerated to 10 mg, with a goal heart rate of 60 bpm. Intravenous metoprolol was given postoperatively if patients were not able to take the oral medication. There were 2 (3.4%) cardiac deaths in the bisoprolol group versus 9 (17%) in the standard care group (p = 0.02); nonfatal infarcts were 0 versus 9 (17%) (p = 0.001); and the combined endpoint of death plus nonfatal infarct was 3.4% versus 34% (p = 0.001), with a relative risk of 0.09 [95% confidence interval (CI) of 0.02–0.37]. Note that chronic obstructive pulmonary disease (COPD) is no longer regarded as a contraindication to beta-blocker use. Gottlieb and coworkers20 demonstrated in an analysis of >40,000 patients with COPD after MI that these medications are both safe and effective. The 9,228 patients who received beta blockers had an absolute 2-year mortality rate of 16.8% but only a relative risk of 0.60 (CI, 0.57–0.63) compared with the 32,586 patients with COPD who did not receive beta blockers after infarction; that group had a 2-year mortality rate of 27.8%. Another medication that may be important in preventing postoperative cardiovascular complications is aspirin. This may be especially true in patients who have undergone vascular and cardiothoracic surgery. Mangano and associates34 prospectively studied 5,065 patients who survived at least 48 hours after coronary artery bypass surgery (CABG). Among the patients who received aspirin within the first 48 hours after surgery, the mortality rate was 1.3%, compared with 4.0% among patients who did not receive aspirin. The administration of aspirin before CABG has also been examined. Bybee and colleagues59,60 found that patients receiving preoperative aspirin (n = 1,316) had significantly lower postoperative in-hospital mortality compared with those not receiving preoperative aspirin (1.7% versus 4.4%; adjusted odds ratio [OR], 0.34; 95% CI, 0.15–0.75; p = 0.007). In addition, preoperative aspirin therapy was not associated with an increased risk of reoperation for bleeding (3.5% versus 3.4%; p = 0.96) or requirement for postoperative blood product transfusion (adjusted OR, 1.17; 95% CI, 0.88–1.54; p = 0.28). However, in a recent meta-analysis that examined the utility of preoperative aspirin in patients undergoing CABG, there was a significant increase in blood loss and transfusion of red blood cells and fresh frozen plasma in the aspirin group (p < 0.05). Therefore the routine administration of preoperative and postoperative aspirin requires further study before it can be universally recommended to patients undergoing noncardiac thoracic surgery.
intravenously (10 mg) immediately before and after surgery and then orally (100 mg daily) until hospital discharge. A total of 30 patients (15.6%) died during the 2-year follow-up period; 21 of these deaths (12 of which were from cardiac causes) occurred in the placebo group compared with 9 (4 of which were from cardiac causes) in the atenolol group, resulting in a 55% reduction in overall mortality and a 65% reduction in cardiovascular mortality. Predictably, most of the beta-blocker benefit was seen during the first 6 to 8 months, when no cardiac deaths occurred in the atenolol group, compared with 7 cardiac deaths in the placebo group (p < 0.001). Poldermans and colleagues45 subsequently described a randomized trial of bisoprolol, another beta1-selective blocker, in patients undergoing major subdiaphragmatic vascular surgery who had evidence of dobutamine-induced hypokinesis (ischemia) by stress echocardiography. A total of 112 patients were followed for 30 days postoperatively after receiving perioperative bisoprolol plus standard care versus standard care alone. A dose of 5 mg was started at least 1 week before surgery and was increased as tolerated to 10 mg, with a goal heart rate of 60 bpm. Intravenous metoprolol was given postoperatively if patients were not able to take the oral medication. There were 2 (3.4%) cardiac deaths in the bisoprolol group versus 9 (17%) in the standard care group (p = 0.02); nonfatal infarcts were 0 versus 9 (17%) (p = 0.001); and the combined endpoint of death plus nonfatal infarct was 3.4% versus 34% (p = 0.001), with a relative risk of 0.09 [95% confidence interval (CI) of 0.02–0.37]. Note that chronic obstructive pulmonary disease (COPD) is no longer regarded as a contraindication to beta-blocker use. Gottlieb and coworkers20 demonstrated in an analysis of >40,000 patients with COPD after MI that these medications are both safe and effective. The 9,228 patients who received beta blockers had an absolute 2-year mortality rate of 16.8% but only a relative risk of 0.60 (CI, 0.57–0.63) compared with the 32,586 patients with COPD who did not receive beta blockers after infarction; that group had a 2-year mortality rate of 27.8%. Another medication that may be important in preventing postoperative cardiovascular complications is aspirin. This may be especially true in patients who have undergone vascular and cardiothoracic surgery. Mangano and associates34 prospectively studied 5,065 patients who survived at least 48 hours after coronary artery bypass surgery (CABG). Among the patients who received aspirin within the first 48 hours after surgery, the mortality rate was 1.3%, compared with 4.0% among patients who did not receive aspirin. The administration of aspirin before CABG has also been examined. Bybee and colleagues59,60 found that patients receiving preoperative aspirin (n = 1,316) had significantly lower postoperative in-hospital mortality compared with those not receiving preoperative aspirin (1.7% versus 4.4%; adjusted odds ratio [OR], 0.34; 95% CI, 0.15–0.75; p = 0.007). In addition, preoperative aspirin therapy was not associated with an increased risk of reoperation for bleeding (3.5% versus 3.4%; p = 0.96) or requirement for postoperative blood product transfusion (adjusted OR, 1.17; 95% CI, 0.88–1.54; p = 0.28). However, in a recent meta-analysis that examined the utility of preoperative aspirin in patients undergoing CABG, there was a significant increase in blood loss and transfusion of red blood cells and fresh frozen plasma in the aspirin group (p < 0.05). Therefore the routine administration of preoperative and postoperative aspirin requires further study before it can be universally recommended to patients undergoing noncardiac thoracic surgery.
Preoperative Evaluation of Cardiovascular Risk
Preoperative cardiovascular evaluation does not routinely require a stress test before clearance for surgery. Which patients warrant noninvasive cardiac stress testing (treadmill test, stress echocardiography, or a nuclear stress test)? Which patients should proceed directly to coronary angiography? Who should have no testing at all? To answer these questions, it is important to understand that many patients will remain at high risk despite demonstrating no ischemia on noninvasive testing and others will remain at low risk despite an abnormal study. For example, an 80-year-old patient with diabetes who suffered a recent MI and has decompensated heart failure and high-grade atrioventricular block is still at high risk even with a stress test that is without evidence of ischemia. The purpose of noninvasive stress testing is to help stratify patients into low-, intermediate-, or high-risk categories. The American College of Cardiology/American Heart Association (ACC/AHA) published guidelines on preoperative testing in December 2001 that are drawn from the aforementioned principles of Bayesian analysis and of only ordering tests that have a reasonable likelihood of changing management. They recommend a stepwise approach to preoperative cardiac assessment that is logical and evidence based.
Step 1. Is the surgery emergent? If so, the task of the consultant may be to recommend perioperative beta blockade if ischemic heart disease is present or suspected. If left ventricular dysfunction is present, consider preoperative diuresis and possibly the utilization of a pulmonary artery catheter. In appropriate cases, a postoperative ischemia evaluation is indicated in patients whose need for surgery is urgent.
Step 2. Has the patient undergone a bypass within the last 5 years or percutaneous coronary intervention (PCI) from 6 months to 5 years previously? According to Mahar and coworkers, if the clinical symptoms have remained stable and there are no recurrent signs or symptoms of ischemia, the likelihood of a perioperative cardiac death or MI is extremely low. Further cardiac testing is generally not necessary.32
Step 3. Has the patient undergone a stress test or an angiogram in the past 2 years? If the patient has not experienced a change in symptoms since that examination, a repeat evaluation is not necessary.
Step 4. Does the patient have a major clinical predictor of risk? Examples of such clinical conditions include acute coronary syndromes, decompensated congestive heart failure, significant arrhythmias, or severe valvular disease. Usually, elective surgery is delayed until the acute cardiac problem is adequately treated (Table 21-1).15
Step 5. Does the patient have intermediate clinical predictors of risk? Examples include mild angina pectoris, prior MI, compensated or prior congestive heart failure, diabetes mellitus, or renal insufficiency. These patients can be stratified by their functional capacity (<4 metabolic equivalents (METs) by history) and the surgery-specific risk. Activities that require >4 METs include moderate cycling, climbing hills, ice-skating, roller-blading, singles tennis, and jogging. Most general thoracic surgeries are considered intermediate-risk procedures by the ACC/AHA task force unless the surgical procedure is anticipated to be prolonged with extensive
blood loss and large fluid shifts. Intermediate-risk procedures have a combined endpoint of the risk for MI or death between 1% and 5%. Low-risk procedures such as breast surgery and endoscopic procedures have a combined endpoint of <1%. High-risk procedures such as aortic and vascular surgery have a combined endpoint of >5%. Noninvasive testing is indicated only in those thoracic surgery patients who have intermediate clinical predictors and poor functional capacity.
Table 21-1 Clinical Predictors of Increased Perioperative Cardiovascular Risk (Myocardial Infarction, Heart Failure, Death)
Major
Unstable coronary syndromes
Acute or recent MIa with evidence of important ischemic risk by clinical symptoms or noninvasive study
Unstable or severeb angina (Canadian class III or IV)c
Decompensated heart failure
Significant arrhythmias
High-grade atrioventricular block
Symptomatic ventricular arrhythmias in the presence of underlying heart disease
Supraventricular arrhythmias with uncontrolled ventricular rate
Severe valvular disease
Intermediate
Mild angina pectoris (Canadian class I or II)
Previous MI by history or pathologic Q waves
Compensated or prior heart failure
Diabetes mellitus (particularly insulin-dependent)
Renal insufficiency
Minor
Advanced age
Abnormal ECG (left ventricular hypertrophy, left bundle-branch block, ST-T abnormalities)
Rhythm other than sinus (e.g., atrial fibrillation)
Low functional capacity (e.g., inability to climb one flight of stairs with a bag of groceries)
History of stroke
Uncontrolled systemic hypertension
ECG, electrocardiogram; MI, myocardial infarction.
aThe American College of Cardiology National Database Library defines recent MI as >7 days but ≤1 month (30 days); acute MI is within 7 days.
bMay include “stable” angina in patients who are unusually sedentary.
cCampeau L. Grading of angina pectoris. Circulation 1976;54:522.
Source: Eagle K, Berger P, Calkins H et al. ACC/AHA guideline update on perioperative cardiovascular evaluation for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery. Available at: http://www.acc.org/clinical/guidelines/perio/clean/perio_index. htm.
Step 6. Patients with intermediate clinical risk factors and moderate or excellent functional capacity (>4 METs) normally require no further testing before undergoing most general thoracic surgeries. However, if the surgery is complicated and the patient has two or more intermediate clinical risk factors, noninvasive testing should be considered.
Step 7. General thoracic operations are generally safe for patients with moderate or excellent functional capacity and no or only minor clinical risk factors. These patients warrant no further workup. If the functional capacity is poor and the surgical procedure high risk, a stress test should be considered.
Step 8. The results of noninvasive testing can be used to help the team to decide on the appropriate perioperative management, such as intensified medical therapy or coronary revascularization. CABG or PCI, in an effort to reduce the risk for surgery, should be recommended only if indicated. Thus, if an asymptomatic patient has a small amount of ischemia on a myocardial perfusion stress test and is found to have single-vessel disease at angiography, the recommendation is not to perform PCI.
In the setting of a nondiagnostic or borderline stress test, one may consider utilizing multislice computed tomography (MSCT) to further stratify the patient as to risk. While traditional coronary angiography is still considered the gold standard in detecting obstructive CAD, MSCT technology is emerging as a useful tool in patients with suspected disease in native, stented, or grafted coronary arteries. In addition, MSCT has the capacity to generate a functional cardiac assessment. Physicians should understand, however, that the rapid development of this technology means that the latest information is constantly changing. The noninvasive detection of stenosed or occluded coronary arteries and grafts by MSCT has become more reliable as the number of detectors has increased. The sensitivity and specificity of 16-slice MSCT for the detection of significant native artery stenosis has varied between studies, partly owing to differences in temporal resolution, cutoffs for significant stenosis, and reader protocols. The inability to evaluate all vessels because of motion artifact, partial volume, and poor contrast opacification (due to heart failure) plagued 16-slice MSCT. However the improved image quality of 64-slice MSCT has led to promising results in the detection of native coronary artery stenosis (Table 21-2). The sensitivity is high across the 64-slice studies (94%–99%), indicating that 64-slice MSCT is an excellent investigation for the exclusion of coronary artery stenosis. The varying selection of patients, technical parameters, and interpretation protocols between studies make direct comparison difficult. Undoubtedly
there will be further literature available in the near future on the promising diagnostic accuracy of 64-slice MSCT and its role in evaluation of preoperative risk.
there will be further literature available in the near future on the promising diagnostic accuracy of 64-slice MSCT and its role in evaluation of preoperative risk.
Table 21-2 64-Slice MSCT Studies of the Detection of Native Artery Stenosis39 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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Perioperative Management
There are times when patients with considerable risk will need an urgent operation and situations when a patient will develop a cardiac complication after operation. The management of cardiac conditions both before operation and during the perioperative period is similar.
Implantable Defibrillators and Pacemakers
No formal guidelines have been developed for the perioperative management of these devices. Adverse effects may occur primarily due to the interactions between the electrical currents of electrocautery, anesthetic agents, and the metabolic derangements so often present during thoracic surgery. Electrocautery is generally applied in a unipolar fashion between the cautery device and a plane perpendicular to the patient’s skin. The possibility of interference with an implanted device is related to the amount of current in the adjacent area. The interference can lead to a variety of responses by the device: (a) temporary or permanent resetting to a backup mode such as VOO or VVI pacing, (b) temporary or permanent inhibition of pacemaker output, (c) an increase in pacing rate due to the activation of a rate response sensor, (d) firing of an implanted cardioverter–defibrillator, and (e) myocardial injury that may cause failure to sense or capture. The probability of these events occurring has fallen considerably with the use of bipolar leads and improved pacemaker design. However, the following recommendations can still be made: pacemakers and implantable defibrillators should be interrogated before and after surgery. The defibrillator should be programmed off before the operation and then on immediately afterward. Pacemakers that are in a rate-responsive mode should be reprogrammed. All attempts should be made to avoid excessive electrocautery near the device whenever possible. If emergent cardioversion is required, the paddles should be placed as far as possible from the device, preferably in an anterioposterior position.
Myocardial Infarction
Perhaps the most feared postoperative complication is MI. The World Health Organization definition of MI requires that two of the following three conditions be met: (a) symptoms, (b) myocardial enzyme release, and (c) compatible electrocardiogram changes. However, this definition poses a dilemma to categorize the many postoperative patients who exhibit myocardial enzyme release but are devoid of symptoms or electrocardiographic changes. Most cardiologists consider a significant enzyme release as an MI despite the failure to meet strict criteria. It is worth noting that several conditions may result in the release of troponin I and T. These include blunt myocardial trauma, aortic dissection, pulmonary embolism, esophageal rupture, peptic ulcer disease, pancreatitis, and even cholecystitis.
After exclusion of these “impostors,” it is important, in order to assist with treatment strategies, to understand the various mechanisms that may result in myocardial injury. Myocardial injury is generally caused by significant mismatches in myocardial supply and demand (two notable exceptions are trauma and myocarditis). The usual mechanism for an MI in the nonpostoperative setting is coronary artery plaque rupture resulting in obstruction of a vessel causing myocardial damage due to this abrupt change in supply. The process, which leads to rupture, is atherosclerosis. This atherosclerosis is characterized primarily by intimal thickening due to the accumulation of cells and lipids, which starts out as a fatty streak and progresses to form fibroatheromas by developing a cap containing smooth muscle cells and collagen. Fatty streaks have been found in the intima of infants. These early lesions progress without compromising lumen diameter because of a compensatory vascular enlargement termed “remodeling.” It is important to realize that the culprit lesions in acute coronary syndromes are usually mildly stenotic and often not detectable even by angiography. In 1995, Falk and associates17 performed a meta-analysis of four studies of serial angiography before and after MI and demonstrated that fully 68% of culprit lesions were <50% stenotic, 18% were between 50% to 70%, and only 14% were >70% before plaque rupture. These studies were conducted in nonpostoperative settings. The typical lesion (plaque) that ruptures has a large lipid core, a thin fibrous cap, and a high content of inflammatory cells (mostly macrophages). These rupture-prone lesions are often called “soft” or “vulnerable” plaques. As the lesions mature, macrophages digest most of the lipid material, resulting in a diminished role of inflammatory cells and less release of cytokines. Additionally, the fibrous cap strengthens and thickens, which makes plaque rupture much less likely. Treatments for acute coronary syndromes (plaque ruptures) include antithrombotic regimens, therapies designed to decrease myocardial oxygen demand, and, when appropriate, myocardial revascularization. This is in distinction to “demand” MIs, in which no plaque rupture has occurred and hence there is a diminished role for antithrombotic agents. Most postoperative MIs are not the result of vulnerable plaque rupture but rather of increased myocardial oxygen demand or decreased supply secondary to blood loss. However, this distinction must be made on a case-by-case basis. Evidence for plaque rupture as the culprit must be sought after adequate control of blood pressure, heart rate, volume status, and anemia has been achieved. Such evidence may include recurrent chest pain, persistent electrocardiographic changes, ventricular arrhythmias, or refractory heart failure.
If in fact the MI is deemed the result of plaque rupture, then the various choices of antithrombotic agents or early cardiac catheterization should be considered with regard to their risk–benefit ratio. Unstable angina, non–ST-elevation MIs, and ST-elevation MIs represent a continuum of degree of coronary artery occlusion and amount of myocardial necrosis, with ST-elevation infarctions representing 100% occlusions and significant necrosis. ST-elevation MIs, which are exceedingly rare in the postoperative patient, are usually treated aggressively with aspirin, oxygen, beta blockers, morphine, intravenous nitroglycerin, and early cardiac catheterization with percutaneous intervention. Fibrinolytic therapy is contraindicated because of the presence of recent surgery. For acute non–ST-elevation MIs and unstable angina, the treatment is largely medical, only rarely requiring urgent percutaneous intervention. The risks for hemorrhage in the postoperative patient must be weighed against
the potential benefits of each therapy to make an informed decision as to which treatments to use.
the potential benefits of each therapy to make an informed decision as to which treatments to use.
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