The prevalence of cardiovascular disease increases with advancing age. Moreover, the number of patients older than 65 years of age is expected to increase by 25% to 35% over the next two decades. Cardiovascular complications are estimated to account for 25% to 50% of deaths following noncardiac surgery. Perioperative myocardial infarction (MI), pulmonary edema, systolic and diastolic heart failure, arrhythmias, stroke, and thromboembolism are the most common diagnoses in patients with preexisting cardiovascular disease. The relatively high prevalence of cardiovascular disorders in surgical patients has given rise to attempts to define cardiac risk or the likelihood of intraoperative or postoperative fatal or life-threatening cardiac complications.
The ACC/AHA Task Force Report provides guidelines for perioperative cardiovascular evaluation. The guidelines state that the patient’s medical history is critical in determining the requirements for preoperative cardiac evaluation and that certain conditions (eg, unstable coronary syndromes and decompensated heart failure) warrant cardiology intervention prior to all but emergency procedures. The preoperative history should also address any past procedures, such as cardioverter defibrillator implants, coronary stents, and other interventions. Additionally, the patient’s ability to perform the tasks of daily living should be assessed as a guide to determine functional capacity. A patient with a history of cardiac disease and advanced age, but good exercise tolerance, will likely have a lower perioperative risk than a similar individual with dyspnea after minimal physical activity (Table 21–1).
TABLE 21–1Estimated energy requirements for various activities.1 ||Download (.pdf) TABLE 21–1 Estimated energy requirements for various activities.1
The patient should be queried about other disease processes that frequently accompany heart disease. Cardiac patients often present with obstructive pulmonary disease, reduced kidney function, and diabetes mellitus.
A physical examination should be performed on all patients, and the heart and lungs should be auscultated. The physical examination is especially useful in patients with certain conditions. For example, if a harsh systolic murmur suggestive of aortic stenosis is detected in a candidate for elective surgery, additional ultrasound evaluation will likely be warranted, as aortic stenosis substantially increases the risks in patients undergoing noncardiac surgery.
The following conditions are associated with increased risk:
Ischemic heart disease (history of MI, evidence on electrocardiogram [ECG], chest pain)
Congestive heart failure (dyspnea, pulmonary edema)
Cerebral vascular disease (stroke)
High-risk surgery (vascular, thoracic)
Preoperative creatinine greater than 2 mg/dL
The ACC/AHA guidelines identify conditions that are a major cardiac risk and warrant intensive management prior to all but emergent surgery. These conditions include unstable coronary syndromes (recent MI, unstable angina), decompensated heart failure, significant arrhythmias, and severe valvular heart disease. The ACC/AHA guidelines identify an MI within 7 days, or one within 1 month with myocardium at risk for ischemia, as “active” cardiac conditions. On the other hand, evidence of past MI with no myocardium thought at ischemic risk is considered a low risk for perioperative infarction after noncardiac surgery. The ACC/AHA guidelines classify recommendations into four categories, as class I (benefit >>> risk), class IIa (benefit >> risk), class IIb (benefit ≥ risk), and class III (no benefit or harm). Additionally, they grade the strength of the evidence upon which the recommendations is based as A (multiple randomized trials), B (limited trials, nonrandomized studies), and C (consensus of experts, case studies).
Class I recommendations are as follows:
Patients who have a need for emergency noncardiac surgery should proceed to the operating room with perioperative surveillance and postoperative risk factor management
Patients with active cardiac conditions should be evaluated by a cardiologist and treated according to ACC/AHA guidelines
Patients undergoing low-risk procedures should proceed to surgery
Patients with poor exercise tolerance (<4 metabolic equivalents [METs]) and no known risk factors should proceed to surgery
The ACC/AHA guidelines use an algorithmic approach to discern risks of major adverse cardiac events (MACE; eg, perioperative death or myocardial infarction). Risks accrue secondary both to the nature of surgery and because of patient characteristics. The ACC/AHA suggest various risk calculators that are available online (eg, American College of Surgeons risk calculator, www.surgicalriskcalculator.com) to estimate patient risk of perioperative major adverse cardiac events (Figure 21–1).
Stepwise approach to perioperative cardiac assessment for coronary artery disease (CAD). Colors correspond to the following classes of recommendations: class I, green; class IIa, yellow; class IIb, orange; class III, red. Step 1: In patients scheduled for surgery with risk factors for or known CAD, determine the urgency of surgery. If an emergency, then determine the clinical risk factors that may influence perioperative management and proceed to surgery with appropriate monitoring and management strategies based on the clinical assessment (see Section 2.1 of the ACC/AHA guidelines for more information on CAD). (For patients with symptomatic heart failure [HF], valvular heart disease [VHD], or arrhythmias, see Sections 2.2, 2.4, and 2.5 of the guidelines for information on evaluation and management.) Step 2: If the surgery is urgent or elective, determine if the patient has an acute coronary syndrome (ACS). If yes, then refer patient for cardiology evaluation and management according to guideline-directed medical therapy (GDMT) according to the UA/NSTEMI and STEMI clinical practice guidelines (CPGs). Step 3: If the patient has risk factors for stable CAD, then estimate the perioperative risk of major adverse cardiac event (MACE) on the basis of the combined clinical/surgical risk. This estimate can use the American College of Surgeons NSQIP risk calculator (http://www.surgicalriskcalculator.com) or incorporate the Revised Cardiac Risk Index (RCRI) with an estimation of surgical risk. For example, a patient undergoing very low-risk surgery (eg, ophthalmologic surgery), even with multiple risk factors, would have a low risk of MACE, whereas a patient undergoing major vascular surgery with few risk factors would have an elevated risk of MACE (see Section 3 of the ACC/AHA guidelines). Step 4: If the patient has a low risk of MACE (<1%), then no further testing is needed, and the patient may proceed to surgery (see Section 3 of the guidelines). Step 5: If the patient is at elevated risk of MACE, then determine functional capacity with an objective measure or scale such as the Duke Activity Status Index (DASI). If the patient has moderate, good, or excellent functional capacity (>4 METs), then proceed to surgery without further evaluation (see Section 4.1 of the ACC/AHA guidelines). Step 6: If the patient has poor (<4 METs) or unknown functional capacity, then the clinician should consult with the patient and perioperative team to determine whether further testing will impact patient decision making (eg, decision to perform original surgery or willingness to undergo coronary artery bypass graft or percutaneous coronary intervention, depending on the results of the test) or perioperative care. If yes, then pharmacological stress testing is appropriate. In those patients with unknown functional capacity, exercise stress testing may be reasonable to perform. If the stress test is abnormal, consider coronary angiography and revascularization depending on the extent of the abnormal test. The patient can then proceed to surgery with GDMT or consider alternative strategies, such as noninvasive treatment of the indication for surgery (eg, radiation therapy for cancer) or palliation. If the test is normal, proceed to surgery according to GDMT (see Section 5.3 of the guidelines). Step 7: If testing will not impact decision making or care, then proceed to surgery according to GDMT or consider alternative strategies, such as noninvasive treatment of the indication for surgery (eg, radiation therapy for cancer) or palliation. MET, metabolic equivalent; NB, No Benefit; NSQIP, National Surgical Quality Improvement Program; STEMI, ST-elevation myocardial infarction; UA/NSTEMI, unstable angina/non–ST-elevation myocardial infarction. (Reproduced with permission from Fleisher LA, Fleischman KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol. 2014 Dec 9;64(22):e77-e137.)
The ACC/AHA guidelines also provide specific recommendations regarding various preexistent cardiac conditions (eg, heart failure, valvular heart disease, arrhythmias) likely to be encountered perioperatively. Recommendations regarding supplemental preoperative evaluation are presented in Table 21–2.
TABLE 21–2Summary of recommendations for supplemental preoperative evaluation.1 ||Download (.pdf) TABLE 21–2 Summary of recommendations for supplemental preoperative evaluation.1
|Recommendations ||COR2 ||LOE |
|The 12-lead ECG |
|Preoperative resting 12-lead ECG is reasonable for patients with known coronary heart disease or other significant structural heart disease, except for low-risk surgery ||IIa ||B |
|Preoperative resting 12-lead ECG may be considered for asymptomatic patients, except for low-risk surgery ||IIb ||B |
|Routine preoperative resting 12-lead ECG is not useful for asymptomatic patients undergoing low-risk surgical procedures ||III: No Benefit ||B |
|Assessment of LV function |
|It is reasonable for patients with dyspnea of unknown origin to undergo preoperative evaluation of LV function ||IIa ||C |
|It is reasonable for patients with HF with worsening dyspnea or other change in clinical status to undergo preoperative evaluation of LV function ||IIa ||C |
|Reassessment of LV function in clinically stable patients may be considered ||IIb ||C |
|Routine preoperative evaluation of LV function is not recomended ||III: No Benefit ||B |
|Exercise stress testing for myocardial ischemia and functional capacity |
|For patients with elevated risk and excellent functional capacity, it is reasonable to forgo further exercise testing and preceed to surgery ||IIa ||B |
|For patients with elevated risk and unknown functional capacity it may be reasonable to perform exercise testing to assess for functional capacity if it will change management ||IIb ||B |
|For patients with elevated risk and moderate to good functional capacity, it may be reasonable to forgo further exercise testing and proceed to surgery ||IIb ||B |
|For patients with elevated risk and poor or unknown functional capacity, it may be reasonable to perform exercise testing with cardiac imaging to assess for myocardial ischemia ||IIb ||C |
|Routine screening with noninvasive stress testing is not useful for low-risk noncardiac surgery ||III: No Benefit ||B |
|Cardiopulmonary exercise testing |
|Cardiopulmonary exercise testing may be considered for patients undergoing elevated risk procedures ||IIb ||B |
|Noninvasive pharmacological stress testing before noncardiac surgery |
|It is reasonable for patients at elevated risk for noncardiac surgery with poor functional capacity to undergo either DSE or MPI if it will change management ||IIa ||B |
|Routine screening with noninvasive stress testing is not useful for low-risk noncardiac surgery ||III: No Benefit ||B |
|Preoperative coronary angiography |
|Routine preoperative coronary angiography is not recommended ||III: No Benefit ||C |
The ACC/AHA guidelines suggest that 60 days or more should elapse after an MI before noncardiac surgery in patients who were not treated with a coronary intervention. Moreover, an MI within 6 months of surgery is associated with increased perioperative mortality. Increased patient age and frailty are likewise associated with greater risk for acute coronary syndromes and stroke. Recently, studies have found a surprising number of asymptomatic patients with elevated levels of troponin after surgery. Such findings are indicative of myocardial injury despite there being no other evidence suggestive of MI. Nevertheless, these patients are at considerably increased risk. The specific management of these patients remains controversial.
Patients with hypertension frequently present for elective surgical procedures. Some will have been effectively managed, but unfortunately, many others will not have been. Hypertension is a leading cause of death and disability in most Western societies and the most prevalent preoperative medical abnormality in surgical patients, with an overall prevalence of 20% to 25%. Long-standing uncontrolled hypertension accelerates atherosclerosis and hypertensive organ damage. Hypertension is a major risk factor for cardiac, cerebral, renal, and vascular disease. Complications of hypertension include MI, congestive heart failure, stroke, renal failure, peripheral occlusive disease, and aortic dissection. The presence of concentric left ventricular hypertrophy (LVH) in hypertensive patients may be an important predictor of cardiac mortality. However, systolic blood pressures below 180 mm Hg, and diastolic pressures below 110 mm Hg, have not been associated with increased perioperative risks. When patients present with systolic blood pressures greater than 180 mm Hg and diastolic pressures greater than 110 mm Hg, anesthesiologists face the dilemma of delaying surgery to allow optimization of oral antihypertensive therapy, but adding the risk of a surgical delay versus proceeding with surgery and achieving blood pressure control with rapidly acting intravenous agents. The incidence of adverse cardiac events in patients treated and operated upon may be similar to that in patients delayed to allow for better long-term blood pressure control. Of note, patients with preoperative hypertension are more likely than others to develop intraoperative hypotension.
Blood pressure measurements are affected by many variables, including posture, time of day, emotional state, recent activity, and drug intake, as well as the equipment and technique used. A diagnosis of hypertension cannot be made with one preoperative reading, but requires confirmation by a history of consistently elevated measurements. Although preoperative anxiety or pain may produce some degree of hypertension in normal patients, patients with a history of hypertension generally exhibit greater preoperative elevations in blood pressure.
Epidemiological studies demonstrate a direct and continuous correlation between both diastolic and systolic blood pressures and mortality rates. The definition of systemic hypertension is arbitrary: a consistently elevated diastolic blood pressure greater than 90 mm Hg or a systolic pressure greater than 140 mm Hg. A common classification scheme is listed in Table 21–3. Prehypertension is said to exist when the diastolic pressure is 80–89 mm Hg or the systolic pressure is 120–139 mm Hg. Whether patients with borderline hypertension are at some increased risk for cardiovascular complications remains unclear. Accelerated or severe hypertension is defined as a recent, sustained, and progressive increase in blood pressure, usually with diastolic blood pressures in excess of 110 to 119 mm Hg. Kidney dysfunction is often present in such patients. A hypertensive urgency reflects blood pressure elevation of >180/120 mm Hg without signs of organ injury (eg, hypertensive encephalopathy, heart failure). A hypertensive emergency is characterized by severe hypertension (>180/120 mm Hg) often associated with papilledema, encephalopathy, or other organ injury.
TABLE 21–3Classification of blood pressure (adults). ||Download (.pdf) TABLE 21–3 Classification of blood pressure (adults).
|Category of Blood Pressure ||Systolic Pressure (mm Hg) ||Diastolic Pressure (mm Hg) |
|Normal ||<120 ||<80 |
|Prehypertension ||120–139 ||80–89 |
|Hypertension || || |
| Mild ||140–159 ||90–99 |
| Moderate ||≥160 ||≥100 |
| Hypertensive Urgency/Emergency ||>180 ||>120 |
Hypertension can be either idiopathic (essential) or, less commonly, secondary to other medical conditions such as renal disease, renal artery stenosis, primary hyperaldosteronism, Cushing disease, acromegaly, pheochromocytoma, pregnancy, or estrogen therapy. Essential hypertension accounts for 80% to 95% of cases and may be associated with an abnormal baseline elevation of cardiac output, systemic vascular resistance (SVR), or both. An evolving pattern is commonly seen over the course of the disease, where cardiac output returns to (or remains) normal, but SVR becomes abnormally high. The chronic increase in cardiac afterload results in concentric left ventricular hypertrophy and altered diastolic function. Hypertension also alters cerebral autoregulation, such that normal cerebral blood flow is maintained in the face of high blood pressures; autoregulation limits may be in the range of mean blood pressures of 110 to 180 mm Hg.
The mechanisms responsible for the changes observed in hypertensive patients seem to involve vascular hypertrophy, hyperinsulinemia, abnormal increases in intracellular calcium, and increased intracellular sodium concentrations in vascular smooth muscle and renal tubular cells. Sympathetic nervous system overactivity and enhanced responses to sympathetic agonists are present in some patients. Hypertensive patients sometimes display an exaggerated response to vasopressors and vasodilators. Overactivity of the renin–angiotensin–aldosterone system seems to play an important role in patients with accelerated hypertension.
Effective drug therapy reduces the progression of hypertension and the incidence of stroke, congestive heart failure, coronary artery disease (CAD), and kidney damage. Effective treatment can also delay and sometimes reverse concomitant pathophysiological changes, such as left ventricular hypertrophy and altered cerebral autoregulation.
Some patients with mild hypertension require only single-drug therapy, which may consist of a thiazide diuretic, angiotensin-converting enzyme (ACE) inhibitor, angiotensin-receptor blocker (ARB), β-adrenergic blocker, or calcium channel blocker, although guidelines and outcome studies favor the first three options. Concomitant illnesses should guide drug selection. All patients with a prior MI should receive a β-adrenergic blocker and an ACE inhibitor (or ARB) to improve outcomes, irrespective of the presence of hypertension. In many patients, the “guideline-specified” agents will also be more than sufficient to control hypertension.
Patients with moderate to severe hypertension often require two or three drugs for control. The combination of a diuretic with a β-adrenergic blocker and an ACE inhibitor is often effective when single-drug therapy is not. As previously noted, ACE inhibitors (or ARBs) prolong survival in patients with congestive heart failure, left ventricular dysfunction, or a prior MI. Familiarity with the names, mechanisms of action, and side effects of commonly used antihypertensive agents is important for anesthesiologists (Table 21–4).
TABLE 21–4Summary of drugs used in hypertension.1 ||Download (.pdf) TABLE 21–4 Summary of drugs used in hypertension.1
|Subclass, Drug ||Mechanism of Action ||Effects ||Clinical Applications ||Pharmacokinetics, Toxicities, Interactions |
|Thiazides: hydrochlorothiazide, chlorthalidone ||Block Na/Cl transporter in renal distal convoluted tubule ||Reduce blood volume and poorly understood vascular effects ||Hypertension, mild heart failure || |
|Loop diuretics: furosemide ||Block Na/K/Cl transporter in renal loop of Henle ||Like thiazides; greater efficacy ||Severe hypertension, heart failure || |
|Spironolactone, eplerenone ||Block aldosterone receptor in renal collecting tubule || |
Increase Na and decrease K excretion
Poorly understood reduction in heart failure mortality
|Aldosteronism, heart failure, hypertension || |
|SYMPATHOPLEGICS, CENTRALLY ACTING |
|Clonidine, methyldopa ||Activate α2-adrenoceptors || |
Reduce central sympathetic outflow
Reduce norepinephrine release from noradrenergic nerve endings
Clonidine also used in withdrawal from abused drugs
Oral; clonidine also as patch
Toxicity: sedation; methyldopa hemolytic anemia
|SYMPATHETIC NERVE TERMINAL BLOCKERS |
|Reserpine ||Blocks vesicular amine transporter in noradrenergic nerves and depletes transmitter stores ||Reduces all sympathetic effects, especially cardiovascular, and reduces blood pressure ||Hypertension but rarely used || |
Oral; long duration (days)
Toxicity: Psychiatric depression, gastrointestinal disturbances
|Guanethidine ||Interferes with amine release and replaces norepinephrine in vesicles ||Same as reserpine ||Same as reserpine ||Severe orthostatic hypotension, sexual dysfunction |
|Selectively block α1-adrenoceptors || |
Prevent sympathetic vasoconstriction
Reduce prostatic smooth muscle tone
Benign prostatic hyperplasia
Toxicity: Orthostatic hypotension
|Block β1-receptors; carvedilol also blocks α-receptors; nebivolol also releases nitric oxide || |
Prevent sympathetic cardiac stimulation
Reduce renin secretion
|Hypertension, heart failure, coronary disease || |
Propranolol: Nonselective prototype β-blocker
Metoprolol and atenolol: Very widely used β1-selective blockers
|Nonselective block of L-type calcium channels || |
Reduce cardiac rate and output
Reduce vascular resistance
|Hypertension, angina, arrhythmias || |
|Nifedipine, amlodipine, other dihydropyridines ||Block vascular calcium channels > cardiac calcium channels ||Reduce vascular resistance ||Hypertension, angina || |
Causes nitric oxide release
Metabolite opens K channels in vascular smooth muscle
Reduces vascular resistance
Arterioles more sensitive than veins
Minoxidil also used to treat hair loss
Toxicity: Angina, tachycardia
Hydralazine: Lupus-like syndrome
|PARENTERAL AGENTS |
Releases nitric oxide
Activates D1 receptors
Opens K channels
|Powerful vasodilation ||Hypertensive emergencies || |
Parenteral; short duration
Toxicity: Excessive hypotension, shock
|ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS |
|Captopril, many others ||Inhibit angiotensin-converting enzyme || |
Reduce angiotensin II levels
Reduce vasoconstriction and aldosterone secretion
Hypertension, heart failure
Toxicity: Cough, angioedema, hyperkalemia, renal impairment
|ANGIOTENSIN RECEPTOR BLOCKERS (ARBs) |
|Losartan, many others ||Block AT1 angiotensin receptors ||Same as ACE inhibitors but no increase in bradykinin ||Hypertension, heart failure || |
Toxicity: Same as ACE inhibitors but less cough
|RENIN INHIBITOR |
|Aliskiren ||Inhibits enzyme activity of renin ||Reduces angiotensin I and II and aldosterone ||Hypertension || |
Toxicity: Hyperkalemia, renal impairment
A recurring question in anesthetic practice is the degree of preoperative hypertension that is acceptable for patients scheduled for elective surgery. Except for optimally controlled patients, most hypertensive patients present to the operating room with some degree of hypertension. Although data suggest that even moderate preoperative hypertension (diastolic pressure >90–110 mm Hg) is not clearly statistically associated with postoperative complications, other data indicate that the untreated or poorly controlled hypertensive patient is more apt to experience intraoperative episodes of myocardial ischemia, arrhythmias, or hemodynamic instability. Careful intraoperative adjustments in anesthetic depth and use of vasoactive drugs should reduce the incidence of postoperative complications referable to poor preoperative control of hypertension.
Although patients should ideally undergo elective surgery only when rendered normotensive, accomplishing this over the short term is not always feasible or even desirable because hypertensive patients have altered cerebral autoregulation. Excessive reductions in blood pressure can compromise cerebral perfusion. Moreover, the decision to delay or to proceed with surgery should be individualized, based on the severity of the preoperative blood pressure elevation; the likelihood of coexisting myocardial ischemia, ventricular dysfunction, or cerebrovascular or renal complications; and the nature and urgency of the procedure. With rare exceptions, antihypertensive drug therapy should be continued up to the time of surgery. Some clinicians withhold ACE inhibitors and ARBs on the morning of surgery because of their association with an increased incidence of intraoperative hypotension; however, withholding these agents increases the risk of marked perioperative hypertension and the need for parenteral antihypertensive agents. It also requires the surgical team to remember to restart the medication after surgery. The decision to delay elective surgical procedures in patients with sustained preoperative diastolic blood pressures higher than 110 mm Hg should be made when the perceived benefits of delayed surgery exceed the risks. Unfortunately, there are few appropriate studies to guide the decision-making.
The preoperative history should address the severity and duration of the hypertension, the drug therapy currently prescribed, and the presence or absence of hypertensive complications. Symptoms of myocardial ischemia, ventricular failure, impaired cerebral perfusion, or peripheral vascular disease should be elicited, as well as the patient’s record of compliance with the drug regimen. The patient should be questioned regarding chest pain, exercise tolerance, shortness of breath (particularly at night), dependent edema, postural lightheadedness, syncope, episodic visual disturbances or episodic neurological symptoms, and claudication. Adverse effects of current antihypertensive drug therapy (Table 21–5) should also be identified.
TABLE 21–5Adverse effects of long-term antihypertensive therapy. ||Download (.pdf) TABLE 21–5 Adverse effects of long-term antihypertensive therapy.
|Class ||Adverse Effects |
|Diuretics || |
|Thiazide ||Hypokalemia, hyponatremia, hyperglycemia, hyperuricemia, hypomagnesemia, hyperlipidemia, hypercalcemia |
|Loop ||Hypokalemia, hyperglycemia, hypocalcemia, hypomagnesemia, metabolic alkalosis |
|Potassium sparing ||Hyperkalemia |
|Sympatholytics || |
|β-Adrenergic blockers ||Bradycardia, conduction blockade, myocardial depression, enhanced bronchial tone, sedation, fatigue, depression |
|α-Adrenergic blockers ||Postural hypertension, tachycardia, fluid retention |
|Central α2-agonists ||Postural hypotension, sedation, dry mouth, depression, decreased anesthetic requirements, bradycardia, rebound hypertension, positive Coombs test and hemolytic anemia (methyldopa), hepatitis (methyldopa) |
|Ganglionic blockers ||Postural hypotension, diarrhea, fluid retention, depression (reserpine) |
|Vasodilators || |
|Calcium channels blockers ||Cardiac depression, bradycardia, conduction blockade (verapamil, diltiazem), peripheral edema (nifedipine), tachycardia (nifedipine), enhanced neuromuscular nondepolarizing blockade |
|ACE inhibitors1 ||Cough, angioedema, reflex tachycardia, fluid retention, renal dysfunction, hyperkalemia, bone marrow depression (captopril) |
|Angiotensin-receptor antagonists ||Hypotension, renal failure in bilateral renal artery stenosis, hyperkalemia |
|Direct vasodilators ||Reflex tachycardia, fluid retention, headache, systemic lupus erythematosus-like syndrome (hydralazine), pleural or pericardial effusion (minoxidil) |
Physical Examination & Laboratory Evaluation
Ophthalmoscopy is useful in hypertensive patients. Visible changes in the retinal vasculature usually parallel the severity and progression of arteriosclerosis and hypertensive damage in other organs. An S4 cardiac gallop is common in patients with LVH. Other physical findings, such as pulmonary rales and an S3 cardiac gallop, are late findings and indicate congestive heart failure. Blood pressure can be measured in both the supine and standing positions. Orthostatic changes may be due to volume depletion, excessive vasodilation, or sympatholytic drug therapy. Preoperative administration of a carbohydrate drink the night before and on the morning of surgery can promote hemodynamic stability after induction of anesthesia. Although asymptomatic carotid bruits are usually hemodynamically insignificant, they may be reflective of atherosclerotic vascular disease that may affect the coronary circulation. When a bruit is detected, further workup should be guided by the urgency of the scheduled surgery and the likelihood that further investigations, if diagnostic, would result in a change in therapy. Doppler studies of the carotid arteries can be used to define the extent of carotid disease.
The ECG is often normal, but in patients with a long history of hypertension, it may show evidence of ischemia, conduction abnormalities, an old infarction, or LVH or strain. A normal ECG does not exclude CAD or LVH. Similarly, a normal heart size on a chest radiograph does not exclude ventricular hypertrophy. Echocardiography is a sensitive test for LVH and can be used to evaluate ventricular systolic and diastolic functions in patients with symptoms of heart failure. Chest radiographs are rarely useful in an asymptomatic patient, but may show frank cardiomegaly or pulmonary vascular congestion.
Kidney function is typically evaluated by measurement of serum creatinine levels. Serum electrolyte levels (K) should be determined in patients taking diuretics or digoxin or those with kidney impairment. Mild to moderate hypokalemia (3–3.5 mEq/L) is often seen in patients taking diuretics, but does not have adverse outcome effects. Potassium replacement should be undertaken only in patients who are symptomatic or who are also taking digoxin. Hypomagnesemia is often present and may be a cause of perioperative arrhythmias. Hyperkalemia may be encountered in patients who are taking potassium-sparing diuretics or ACE inhibitors, particularly those with impaired renal function.
Mild to moderate preoperative hypertension often resolves following administration of an agent such as midazolam.
The anesthetic for a hypertensive patient should maintain an appropriately stable blood pressure range. Patients with borderline hypertension may be treated as normotensive patients. Those with long-standing or poorly controlled hypertension, however, have altered autoregulation of cerebral blood flow; higher than normal mean blood pressures may be required to maintain adequate cerebral blood flow. Hypertension, particularly in association with tachycardia, can precipitate or exacerbate myocardial ischemia, ventricular dysfunction, or both. Arterial blood pressure should generally be kept within 20% of preoperative levels.
Most hypertensive patients do not require special intraoperative monitors. Direct intraarterial pressure monitoring should be reserved for patients with wide swings in blood pressure and those undergoing major surgical procedures associated with rapid or marked changes in cardiac preload or afterload. Electrocardiographic monitoring should focus on detecting signs of ischemia. Urinary output should generally be monitored with an indwelling urinary catheter in patients with a preexisting kidney impairment who are undergoing procedures expected to last more than 2 h. Ventricular compliance (see Chapter 20) is typically reduced in patients with ventricular hypertrophy. Excessive intravenous fluid administration in patients with decreased ventricular compliance can also result in elevated pulmonary arterial pressures and pulmonary congestion.
Induction of anesthesia and endotracheal intubation are often associated with hemodynamic instability in hypertensive patients. Regardless of the level of preoperative blood pressure control, many patients with hypertension display an accentuated hypotensive response to induction of anesthesia, followed by an exaggerated hypertensive response to intubation. Many, if not most, antihypertensive agents and general anesthetics are vasodilators, cardiac depressants, or both. In addition, many hypertensive patients present for surgery in a volume-depleted state. Sympatholytic agents attenuate the normal protective circulatory reflexes, reducing sympathetic tone and unmasking vagal activity.
Hypertensive patients may exhibit severe hypertension during airway manipulation. One of several techniques may be used before intubation to attenuate the hypertensive response:
Deepening anesthesia with a potent volatile agent
Administering a bolus of an opioid (fentanyl, 2.5–5 mcg/kg; alfentanil, 15–25 mcg/kg; sufentanil, 0.5–1.0 mcg/kg; or remifentanil, 0.5–1 mcg/kg)
Administering lidocaine, 1.5 mg/kg intravenously, intratracheally, or topically in the airway
Achieving β-adrenergic blockade with esmolol, 0.3–1.5 mg/kg; metoprolol 1–5 mg; or labetalol, 5–20 mg
Choice of Anesthetic Agents
The superiority of any one agent or technique over another has not been established. Propofol, barbiturates, benzodiazepines, and etomidate are equally safe for inducing general anesthesia in most hypertensive patients. Ketamine by itself can precipitate marked hypertension; however, it is almost never used as a single agent. When administered with a small dose of another agent, such as a benzodiazepine or propofol, ketamine’s sympathetic stimulating properties can be blunted or eliminated.
Anesthesia may be safely maintained with volatile or intravenous agents. Regardless of the primary maintenance technique, addition of a volatile agent or intravenous vasodilator generally allows convenient intraoperative blood pressure control.
Should hypotension develop, a small dose of a direct-acting agent, such as phenylephrine (25–50 mcg), may be beneficial. Patients taking sympatholytics preoperatively may exhibit a decreased response to ephedrine. Vasopressin as a bolus or infusion can also be employed to restore vascular tone in the hypotensive patient.
Intraoperative hypertension not responding to an increase in anesthetic depth (particularly with a volatile agent) can be treated with a variety of parenteral agents (Table 21–6). Readily reversible causes—such as inadequate anesthetic depth, hypoxemia, or hypercapnia—should always be excluded before initiating antihypertensive therapy. Selection of a hypotensive agent depends on the severity, acuteness, and cause of hypertension; the baseline ventricular function; the heart rate; and the presence of bronchospastic pulmonary disease. β-Adrenergic blockade alone or as a supplement is a good choice for a patient with good ventricular function and an elevated heart rate, but is relatively contraindicated in a patient with reactive airway disease. Metoprolol, esmolol, or labetalol is often used intraoperatively. Nicardipine or clevidipine may be preferable to β-blockers for patients with bronchospastic disease. Nitroprusside remains the most rapid and effective agent for the intraoperative treatment of moderate to severe hypertension. Nitroglycerin may be less effective, but is also useful in treating or preventing myocardial ischemia. Fenoldopam, a dopaminergic agonist, is also a useful hypotensive agent; furthermore, it increases renal blood flow. Hydralazine provides sustained blood pressure control, but also has a delayed onset and can cause reflex tachycardia. Reflex tachycardia is not seen with labetalol because of its combined α- and β-adrenergic blockade.
TABLE 21–6Parenteral agents for the acute treatment of hypertension. ||Download (.pdf) TABLE 21–6 Parenteral agents for the acute treatment of hypertension.
Postoperative hypertension is common and should be anticipated in patients who have poorly controlled baseline blood pressure. Close blood pressure monitoring should be continued in both the postanesthesia care unit and the early postoperative period. Postoperatively, marked sustained elevations in blood pressure can contribute to the formation of wound hematomas and the disruption of vascular suture lines.
Hypertension in the recovery period is often multifactorial and enhanced by respiratory abnormalities, anxiety and pain, volume overload, bladder distention, or any combination of these. Contributing causes should be corrected and parenteral antihypertensive agents given if necessary. Intravenous labetalol is particularly useful in controlling hypertension and tachycardia, whereas vasodilators are useful in controlling blood pressure in the setting of a slow heart rate. When the patient resumes oral intake, preoperative antihypertensive medications should be restarted.
Myocardial ischemia results from a metabolic oxygen demand that exceeds the oxygen supply. Ischemia can therefore result from increased myocardial metabolic demand, reduced myocardial oxygen delivery, or a combination of both. Common causes include coronary arterial thrombosis or vasospasm; severe hypertension or tachycardia (particularly in the presence of ventricular hypertrophy); severe hypotension, hypoxemia, or anemia; and severe aortic stenosis or regurgitation.
By far, the most common cause of myocardial ischemia is atherosclerosis of the coronary arteries. CAD is responsible for about 25% of all deaths in Western societies and is a major cause of perioperative morbidity and mortality. The overall incidence of CAD in surgical patients is estimated to be between 5% and 10%. Major preoperative risk factors for CAD include hyperlipidemia, hypertension, diabetes, cigarette smoking, increasing age, male sex, and a positive family history. Other risk factors include obesity, a history of cerebrovascular or peripheral vascular disease, menopause, use of high-estrogen oral contraceptives by women who smoke, and a sedentary lifestyle.
CAD may be manifested by symptoms, characteristic electrocardiographic or echocardiographic findings, or biochemical evidence of myocardial necrosis (infarction); symptoms (usually angina) or characteristic echocardiographic or electrocardiographic findings of ischemia; or arrhythmias (including sudden death), symptoms (orthopnea, dyspnea on exertion), signs (rales, dependent edema, shock), or echocardiographic changes suggestive of ventricular dysfunction. An ambulatory patient presenting with risk factors for CAD and new symptoms would normally undergo some form of stress testing to confirm the suspected diagnosis.
Unstable angina is defined as (1) an abrupt increase in severity, frequency (more than three episodes per day), or duration of anginal attacks (crescendo angina); (2) angina at rest; or (3) new onset of angina (within the past 2 months) with severe or frequent episodes (more than three per day). Unstable angina may occur following MI or be precipitated by major surgery or by noncardiac medical conditions, including severe anemia, fever, infections, thyrotoxicosis, hypoxemia, and emotional distress in previously stable patients.
Unstable angina, particularly when it is associated with significant ST-segment changes at rest, usually reflects severe underlying coronary disease and may be followed by MI. Plaque disruption with platelet aggregates or thrombi and vasospasm are frequent pathological correlates. Critical stenosis in one or more major coronary arteries is present in more than 80% of patients with these symptoms. Patients with unstable angina require evaluation and treatment, which may include admission to a coronary care unit and some form of coronary intervention.
Anginal chest pains are most often substernal, exertional, radiating to the neck or arm, and relieved by rest or nitroglycerin. Variations are common, including epigastric, back, or neck pain, or transient shortness of breath from ventricular dysfunction (anginal equivalent). Nonexertional ischemia and silent (asymptomatic) ischemia are fairly common occurrences, particularly following surgery. Patients with diabetes have an increased incidence of silent ischemia.
Symptoms are generally absent until the atherosclerotic lesions cause 50% to 75% occlusion of the coronary circulation. When a stenotic segment reaches 70% occlusion, maximum compensatory dilation is usually present distally: blood flow may be adequate at rest, but inadequate with increased metabolic demand. An extensive collateral blood supply allows some patients to remain relatively asymptomatic despite severe disease. Coronary vasospasm is also a cause of transient transmural ischemia in some patients; most vasospastic episodes occur at preexisting stenotic lesions in epicardial vessels and may be precipitated by a variety of factors, including emotional upset and hyperventilation (Prinzmetal angina). Coronary spasm is more often observed in patients who have angina with varying levels of activity or emotional stress (variable-threshold); it is less common with classic exertional (fixed-threshold) angina.
The overall prognosis of patients with CAD is related to both the number and severity of coronary obstructions, as well as to the extent of ventricular dysfunction.
Treatment of Ischemic Heart Disease
The general approach in treating patients with ischemic heart disease is five-fold:
Correction of risk factors, with the hope of slowing disease progression
Modification of the patient’s lifestyle to reduce stress and improve exercise tolerance
Correction of complicating medical conditions that can exacerbate ischemia (ie, hypertension, anemia, hypoxemia, hyperthyroidism, fever, infection, or adverse drug effects)
Pharmacological manipulation of the myocardial oxygen supply–demand relationship
Correction of coronary lesions by percutaneous coronary intervention (angioplasty [with or without stenting] or atherectomy) or coronary artery bypass surgery
The most commonly used pharmacological agents for stable ischemic heart disease are nitrates, β-blockers, calcium channel blockers, and platelet inhibitors. Those drugs with circulatory effects are compared in Table 21–7.
TABLE 21–7Comparison of antianginal agents.1 ||Download (.pdf) TABLE 21–7 Comparison of antianginal agents.1
| || ||Calcium Channel Blockers || |
|Cardiac Parameter ||Nitrates ||Verapamil ||Nifedipine Nicardipine Nimodipine ||Diltiazem ||β-Blockers |
|Preload ||↓↓ ||— ||— ||— ||—/↑ |
|Afterload ||↓ ||↓ ||↓↓ ||↓ ||—/↓ |
|Contractility ||— ||↓↓ ||— ||↓ ||↓↓↓ |
|SA node automaticity ||↑/— ||↓↓ ||↑/— ||↓↓ ||↓↓↓ |
|AV conduction ||— ||↓↓↓ ||— ||↓↓ ||↓↓↓ |
A. Beta-Adrenergic Blocking Agents
These drugs are first-line agents for patients with stable ischemic heart disease. They decrease myocardial oxygen demand by reducing heart rate and contractility, and, in some cases, afterload (via their antihypertensive effect). In contrast to other agents, they increase survival in patients with impaired left ventricular function, they increase survival after MI, and they reduce the likelihood of a subsequent infarction. Optimal blockade results in a resting heart rate between 50 and 60 beats/min and prevents appreciable increases with exercise (<20 beats/min increase during exercise). Available agents differ in receptor selectivity, intrinsic sympathomimetic (partial agonist) activity, and membrane-stabilizing properties (Table 21–8). Membrane stabilization results in antiarrhythmic activity. Agents with intrinsic sympathomimetic properties are better tolerated by patients with mild to moderate ventricular dysfunction. Certain β-blockers (bisoprolol, carvedilol, and extended-duration metoprolol) improve survival in patients with chronic heart failure. Blockade of β2-adrenergic receptors also can mask hypoglycemic symptoms in patients with diabetes, delay metabolic recovery from hypoglycemia, and impair the handling of large potassium loads. Cardioselective (β1-receptor-specific) agents, although generally better tolerated than nonselective agents in patients with reactive airways, must still be used cautiously in such patients. The selectivity of cardioselective agents tends to be dose dependent. Patients on long-standing β-blocker therapy should have these agents continued perioperatively. Acute β-blocker withdrawal in the perioperative period places patients at a markedly increased risk of cardiac morbidity and mortality. β-Blocker therapy should be continued perioperatively in patients who take these agents chronically.
TABLE 21–8Comparison of β-adrenergic blocking agents.
B. Calcium Channel Blockers
These agents are chosen when a patient cannot take a β-blocker or when treatment with a β-blocker is insufficient. The effects and uses of the most commonly used calcium channel blockers are shown in Table 21–9. Calcium channel blockers reduce myocardial oxygen demand by decreasing cardiac afterload and augment myocardial oxygen supply via coronary vasodilation. Verapamil and diltiazem also reduce demand by slowing the heart rate.
TABLE 21–9Comparison of calcium channel blockers. ||Download (.pdf) TABLE 21–9 Comparison of calcium channel blockers.
| || || || ||Clinical Use |
|Agent ||Route ||Dosage1 ||Half-life ||Angina ||Hypertension ||Cerebral Vasospasm ||Supraventricular Tachycardia |
|Verapamil ||PO ||40–240 mg ||5 h ||+ ||+ || ||+ |
| ||IV ||5–15 mg ||5 h ||+ || || ||+ |
|Nifedipine ||PO ||30–180 mg ||2 h ||+ ||+ || || |
| ||SL ||10 mg ||2 h ||+ ||+ || || |
|Diltiazem ||PO ||30–60 mg ||4 h ||+ ||+ || ||+ |
| ||IV ||0.25–0.35 mg/kg ||4 h ||+ || || ||+ |
|Nicardipine ||PO ||60–120 mg ||2–4 h ||+ ||+ || || |
| ||IV ||0.25–0.5 mg/kg ||2–4 h ||+ ||+ || || |
|Nimodipine ||PO ||240 mg ||2 h || || ||+ || |
|Bepridil2 ||PO ||200–400 mg ||24 h ||+ ||+ || || |
|Isradipine ||PO ||2.5–5.0 mg ||8 h || ||+ || || |
|Felodipine ||PO ||5–20 mg ||9 h || ||+ || || |
|Amlodipine ||PO ||2.5–10 mg ||30–50 h ||+ ||+ || || |
Nifedipine’s potent effects on the systemic blood pressure may precipitate hypotension, reflex tachycardia, or both. Its tendency to decrease afterload generally offsets any negative inotropic effect. Long-acting verapamil, diltiazem, amlodipine, or felodipine are preferred. Nicardipine and clevidipine generally have the same effects as nifedipine but are shorter acting, and clevidipine is particularly useful as a vasodilator infusion. Nimodipine is primarily used in preventing cerebral vasospasm following subarachnoid hemorrhage.
All calcium channel blockers potentiate depolarizing and nondepolarizing neuromuscular blocking agents and the circulatory effects of volatile agents. Verapamil and diltiazem can potentiate depression of cardiac contractility and conduction in the atrioventricular (AV) node by volatile anesthetics. Nifedipine and similar agents can potentiate systemic vasodilation by volatile and intravenous agents.
Nitrates decrease venous and arteriolar tone, increase vascular capacitance, and reduce ventricular wall tension. These effects tend to reduce myocardial oxygen demand. Prominent venodilation makes nitrates excellent agents when congestive heart failure is also present.
Additionally, nitrates dilate the coronary arteries. Even minor degrees of dilation at stenotic sites may be sufficient to increase blood flow, because flow is directly related to the fourth power of the radius. Nitrate-induced coronary vasodilation preferentially increases subendocardial blood flow in ischemic areas. This favorable redistribution of coronary blood flow to ischemic areas may be dependent on the presence of collaterals in the coronary circulation.
Nitrates can be used for both the treatment of acute ischemia and prophylaxis against frequent anginal episodes.
Chronic aspirin therapy reduces coronary events in patients with CAD and prevents coronary and ischemic cerebral events in at-risk patients. Other platelet antagonists are generally also included in patients who have undergone percutaneous coronary stenting. Careful review of anticoagulant/antiplatelet medications is a mandatory element of preanesthetic assessment, especially if neuraxial anesthesia is being considered (see Chapter 45).
E. Other Agents and Other Treatments
ACE inhibitors prolong survival in patients with congestive heart failure or left ventricular dysfunction. Antiarrhythmic therapy in patients with complex ventricular ectopy who have significant CAD and left ventricular dysfunction should be guided by an electrophysiological study. Patients with inducible sustained ventricular tachycardia (VT) or ventricular fibrillation are candidates for an automatic internal cardioverter-defibrillator (ICD). Treatment of ventricular ectopy (with the exception of sustained VT) in patients with good ventricular function does not improve survival and may increase mortality. In contrast, ICDs have been shown to improve survival in patients with advanced cardiomyopathy (ejection fraction <30%), even in the absence of demonstrable arrhythmias.
Moderate to severe angina frequently requires combination therapy with two or more classes of agents. Patients with ventricular dysfunction may not tolerate the combined negative inotropic effect of a β-blocker and a calcium channel blocker together; an ACE inhibitor or ARB is better tolerated and seems to improve survival. Similarly, the additive effect of a β-blocker and a calcium channel blocker on the AV node may precipitate heart block in susceptible patients.
The importance of ischemic heart disease—particularly a history of MI—as a risk factor for perioperative morbidity and mortality is reviewed earlier in this chapter. Most studies confirm that perioperative outcome is related to disease severity, ventricular function, and the type of surgery to be undertaken. Patients with extensive (three-vessel or left main) CAD, a recent history of MI, or ventricular dysfunction are at greatest risk of cardiovascular complications. As previously mentioned, current guidelines recommend revascularization only when such treatment would be indicated irrespective of the patient’s need for surgery.
Chronic stable (mild to moderate) angina does not seem to increase perioperative risk substantially. Similarly, a history of prior coronary artery bypass surgery or coronary angioplasty alone does not seem to substantially increase perioperative risk. In some studies, maintenance of chronic β-receptor blockers in the perioperative period has been shown to reduce perioperative mortality and the incidence of postoperative cardiovascular complications; however, other studies have shown an increase in stroke and death following preoperative introduction of β-blockers to at-risk patients. Consequently, initiating therapy with β-blockers in at-risk patients who will undergo surgery is no longer recommended. Like β-blockers, statins should be continued perioperatively in patients so routinely treated, as acute perioperative withdrawal of statins is associated with adverse outcomes. The ACC/AHA recommendations are summarized in a set of useful guidelines that also provide guidance on the timing of surgery following percutaneous coronary interventions and the deployment of coronary stents (Table 21–10).
TABLE 21–10Summary of recommendations for perioperative therapy.1 ||Download (.pdf) TABLE 21–10 Summary of recommendations for perioperative therapy.1
|Recommendations ||COR2 ||LOE |
|Coronary revascularization before noncardiac surgery |
|Revascularization before noncardiac surgery is recommended when indicated by existing CPGs ||I ||C |
|Coronary revascularization is not recommended before noncardiac surgery exclusively to reduce perioperative cardiac events ||III: No Benefit ||B |
|Timing of elective noncardiac surgery in patients with previous PCI |
|Noncardiac surgery should be delayed after PCI ||I ||C: 14 d after balloon angioplasty |
| || ||B: 30 d after BMS implantation |
|Noncardiac surgery should optimally be delayed 365 d after DES implantation ||I ||B |
|A consensus decision as to the relative risks of discontinuation or continuation of antiplatelet therapy can be useful ||IIa ||C |
|Elective noncardiac surgery after DES implantation may be considered after 180 d ||IIb3 ||B |
|Elective noncardiac surgery should not be performed in patients in whom DAPT will need to be discontinued perioperatively within 30 d after BMS implantation or within 12 mo after DES implantation ||III: Harm ||B |
|Elective noncardiac surgery should not be performed within 14 d of balloon angioplasty in patients in whom aspirin will need to be discontinued perioperatively ||III: Harm ||C |
|Perioperative-β-blocker therapy |
|Continue-β-blockers in patients who are on β-blockers chronically ||I ||BSR4 |
|Guide management of β-blockers after surgery by clinical circumstances ||IIa ||BSR4 |
|In patients with intermediate- or high-risk preoperative tests, it may be reasonable to begin β-blockers ||IIb ||CSR4 |
|In patients with ≥3 RCRI factors, it may be reasonable to begin β-blockers before surgery ||IIb ||BSR4 |
|Initiating β-blockers in the perioperative setting as an approach to reduce perioperative risk is of uncertain benefit in those with a long-term indication but no other RCRI risk factors ||IIb ||BSR4 |
|It may be reasonable to begin perioperative β-blockers long enough in advance to assess safety and tolerability, preferably >1 d before surgery ||IIb ||BSR4 |
|β-blocker therapy should not be started on the day of surgery ||III: Harm ||BSR4 |
|Preoperative statin therapy |
|Continue statins in patients currently taking statins ||I ||B |
|Perioperative initiation of statin use is reasonable in patients undergoing vascular surgery ||IIa ||B |
|Perioperative initiation of statins may be considered in patients with a clinical risk factor who are undergoing elevated-risk procedures ||IIb ||C |
|α2-Agonists are not recommended for prevention of cardiac events ||III: No Benefit ||B |
|ACE inhibitors |
|Continuation of ACE inhibitors or ARBs is reasonable perioperatively ||IIa ||B |
|If ACE inhibitors or ARBs are held before surgery, it is reasonable to restart as soon as clinically feasible postoperatively ||IIa ||C |
|Antiplatelet agents |
|Continue DAPT in patients undergoing urgent noncardiac surgery during the first 4 to 6 wk after BMS or DES implantation, unless the risk of bleeding outweighs the benefit of stent thrombosis prevention ||I ||C |
|In patients with stents undergoing surgery that requires discontinuation P2Y12 inhibitors, continue aspirin and restart the P2Y12 platelet receptor-inhibitor as soon as possible after surgery ||I ||C |
|Management of perioperative antiplatelet therapy should be determined by consensus of treating clinicians and the patient ||I ||C |
|In patients undergoing nonemergency/nonurgent noncardiac surgery without prior coronary stenting, it may be reasonable to continue aspirin when the risk of increased cardiac events outweighs the risk of increased bleeding ||IIb ||B |
|Initiation or continuation of aspirin is not beneficial in patients undergoing elective noncardiac noncarotid surgery who have not had previous coronary stenting ||III: No Benefit ||B |
| || ||C: If risk of ischemic events outweighs risk of surgical bleeding |
|Perioperative management of patients with CIEDs |
|Patients with ICDs should be on a cardiac monitor continuously during the entire period of inactivation, and external defibrillation equipment should be available. Ensure that ICDs are reprogrammed to active therapy ||I ||C |
The most important symptoms to elicit include chest pain, dyspnea, poor exercise tolerance, syncope, or near syncope. The relationship between symptoms and activity level should be established. Activity should be described in terms of everyday tasks, such as walking or climbing stairs. Patients may be relatively asymptomatic despite severe CAD if they have a sedentary lifestyle. Patients with diabetes are particularly prone to silent ischemia. Easy fatigability or shortness of breath suggests impaired ventricular function.
A history of unstable angina or MI should include the time of its occurrence and whether it was complicated by arrhythmias, conduction disturbances, or heart failure. Arrhythmias and conduction abnormalities are more common in patients with previous infarction and in those with poor ventricular function. This latter group of patients will often have ICDs.
Physical Examination & Routine Laboratory Evaluation
Evaluation of patients with CAD is similar to that of patients with hypertension. Laboratory evaluation in patients who have a history compatible with recent unstable angina and are undergoing emergency procedures should include cardiac enzymes. Normal serum levels of troponins, creatine kinase (MB isoenzyme), and lactate dehydrogenase (type 1 isoenzyme) are useful in excluding MI.
The baseline ECG is normal in 25% to 50% of patients with CAD but no prior MI. Electrocardiographic evidence of ischemia often becomes apparent only during angina. The most common baseline abnormalities are nonspecific ST-segment and T-wave changes. Prior infarction may be manifested by Q waves or loss of R waves in the leads closest to the infarct. First-degree AV block, bundle-branch block, or hemiblock may be present. Persistent ST-segment elevation following MI may be indicative of a left ventricular aneurysm. A long rate-corrected QT interval (QTc > 0.44 s) may reflect the underlying ischemia, drug toxicity (usually class Ia antiarrhythmic agents, antidepressants, or phenothiazines), electrolyte abnormalities (hypokalemia or hypomagnesemia), autonomic dysfunction, mitral valve prolapse, or, less commonly, a congenital abnormality. Patients with a long QT interval are at risk of developing ventricular arrhythmias—particularly polymorphic VT (torsades de pointes), which can lead to ventricular fibrillation. The long QT interval reflects nonuniform prolongation of ventricular repolarization and predisposes patients to reentry phenomena. In contrast to polymorphic ventricular arrhythmias with a normal QT interval, which respond to conventional antiarrhythmics, polymorphic tachyarrhythmias with a long QT interval generally respond best to pacing or magnesium salts.
The chest radiograph can be used to exclude cardiomegaly or pulmonary vascular congestion secondary to ventricular dysfunction.
Continuous ambulatory electrocardiographic (Holter) monitoring is useful in evaluating arrhythmias, antiarrhythmic drug therapy, and severity and frequency of ischemic episodes. Silent (asymptomatic) ischemic episodes are frequently found in patients with CAD. Frequent ischemic episodes on preoperative Holter monitoring correlate well with intraoperative and postoperative ischemia. Holter monitoring showing no ischemic episodes has an excellent negative predictive value for postoperative cardiac complications.
B. Exercise Electrocardiography
The usefulness of this test without associated cardiac imaging is limited in patients with baseline ST-segment abnormalities and those who are unable to increase their heart rate (>85% of maximal predicted) because of fatigue, dyspnea, or drug therapy. Overall sensitivity is 65%, and specificity is 90%. Exercise testing is most sensitive (85%) in patients with three-vessel or left main CAD. Disease that is limited to the left circumflex artery may also be missed because ischemia in its distribution may not be evident on the standard surface ECG. A normal test does not necessarily exclude CAD, but suggests that severe disease is not likely. The degree of ST-segment depression, its severity and configuration, the time of onset in the test, and the time required for resolution are important findings. A myocardial ischemic response at low levels of exercise is associated with a significantly increased risk of perioperative complications and long-term cardiac events. Other significant findings include changes in blood pressure and the occurrence of arrhythmias. Exercise-induced ventricular ectopy frequently indicates severe CAD associated with ventricular dysfunction. The ischemia presumably leads to electrical instability in myocardial cells. Given that risk seems to be associated with the extent of potentially ischemic myocardium, testing often includes perfusion scans or echocardiographic assessments; however, in ambulatory patients, exercise ECG testing alone is useful because it estimates functional capacity and detects myocardial ischemia.
C. Myocardial Perfusions Scans and Other Imaging Techniques
Myocardial perfusion imaging using thallium-201 or technetium-99m is used in evaluating patients who cannot exercise (eg, peripheral vascular disease) or who have underlying ECG abnormalities that preclude interpretation during exercise (eg, left bundle-branch block). If the patient cannot exercise, images are obtained before and after injection of an intravenous coronary dilator (eg, dipyridamole or adenosine) to produce a hyperemic response similar to exercise. Myocardial perfusion studies following exercise or injection of dipyridamole or adenosine have a high sensitivity, but only fairly good specificity for CAD. They are best for detecting two- or three-vessel disease. These scans can locate and quantitate areas of ischemia or scarring and differentiate between the two. Perfusion defects that fill in on the redistribution phase represent ischemia, not previous infarction. The negative predictive value of a normal perfusion scan is approximately 99%.
Magnetic resonance imaging, positron emission tomography, and computed tomography scans are increasingly being used to define coronary artery anatomy and determine myocardial viability.
This technology provides information about both regional and global ventricular function and may be carried out at rest, following exercise, or with administration of dobutamine. Detectable regional wall motion abnormalities and the derived left ventricular ejection fraction correlate well with angiographic findings. Moreover, dobutamine stress echocardiography seems to be a reliable predictor of adverse cardiac complications in patients who cannot exercise. New or worsening wall motion abnormalities following dobutamine infusion are indicative of significant ischemia. Patients with an ejection fraction of less than 50% tend to have more severe disease and increased perioperative morbidity. Dobutamine stress echocardiography, however, may not be reliable in patients with left bundle-branch block because septal motion may be abnormal, even in the absence of left anterior descending CAD in some patients.
Coronary angiography remains the definitive way to evaluate CAD and is associated with a low complication rate (<1%). The location and severity of occlusions can be defined, and coronary vasospasm may also be observed on angiography. In evaluating fixed stenotic lesions, occlusions greater than 50% to 75% are generally considered significant. The severity of disease is often expressed according to the number of major coronary vessels affected (one-, two-, or three-vessel disease). Significant stenosis of the left main coronary artery is of great concern because disruption of flow in this vessel will have adverse effects on almost the entire left ventricle.
Ventriculography, measurement of the ejection fraction, and measurement of intracardiac pressures, also provide important information. Indicators of significant ventricular dysfunction include an ejection fraction less than 50%, a left ventricular end-diastolic pressure greater than 18 mm Hg, a cardiac index less than 2.2 L/min/m2, and marked or multiple wall motion abnormalities.
Allaying fear, anxiety, and pain preoperatively are desirable goals in patients with CAD. Satisfactory premedication minimizes sympathetic activation, which adversely affects the myocardial oxygen supply–demand balance. Overmedication is equally detrimental and should be avoided because it may result in hypoxemia, respiratory acidosis, and hypotension. Most clinicians now limit premedication to small doses of intravenous midazolam (or the equivalent) given immediately before invasive procedures or before transporting the patient to the operating theater.
Preoperative medications should generally be continued until the time of surgery. The sudden withdrawal of antianginal medication perioperatively—particularly β-blockers—can precipitate a sudden, rebound increase in ischemic episodes. Statins should also be continued in the perioperative period. Prophylactic administration of nitrates intravenously or transdermally to patients with CAD in the perioperative period provides no benefit to patients not previously on long-term nitrate therapy and without evidence of ongoing ischemia. Transdermal absorption of nitroglycerin may be erratic in the perioperative period.
The intraoperative period is regularly associated with factors and events that can adversely affect the myocardial oxygen demand–supply relationship. Activation of the sympathetic system plays a major role. Hypertension and enhanced contractility increase myocardial oxygen demand, whereas tachycardia increases demand and reduces supply. Although myocardial ischemia is commonly associated with tachycardia, ischemia can occur in the absence of any apparent hemodynamic derangement.
The overwhelming priority in managing patients with ischemic heart disease is maintaining a favorable myocardial supply–demand relationship. Autonomic-mediated increases in heart rate and blood pressure should be controlled with deeper planes of general anesthesia, adrenergic blockade, vasodilators, or a combination of these. Excessive reductions in coronary perfusion pressure or arterial oxygen content must be avoided. Higher diastolic pressures may be preferable in patients with high-grade coronary occlusions. Excessive increases—such as those caused by fluid overload—in left ventricular end-diastolic pressure should be avoided because they increase ventricular wall tension (afterload) and can reduce subendocardial perfusion (see Chapter 20). Transfusion carries its own risks and consequently there is no set transfusion trigger in patients with CAD; however, most clinicians are reluctant to have hemoglobin levels fall below 7 g/dL. Anemia can lead to tachycardia, worsening the balance between myocardial oxygen supply and demand. The ACC/AHA recommendations for the anesthetic management of the patient with CAD disease for noncardiac surgery are summarized in Table 21–11.
TABLE 21–11Summary of recommendations for anesthetic consideration and intraoperative management.1 ||Download (.pdf) TABLE 21–11 Summary of recommendations for anesthetic consideration and intraoperative management.1
|Recommendations ||COR2 ||LOE |
|Volatile general anesthesia versus total intravenous anesthesia |
|Use of either a volatile anesthetic agent or total intravenous anesthesia is reasonable for patients undergoing noncardiac surgery ||IIa ||A |
|Perioperative pain management |
|Neuraxial anesthesia for postoperative pain relief can be effective to reduce MI in patients undergoing abdominal aortic surgery ||IIa ||B |
|Preoperative epidural analgesia may be considered to decrease the incidence of preoperative cardiac events in patients with hip fracture ||IIb ||B |
|Prophylactic intraoperative nitroglycerin |
|Prophylactic intravenous nitroglycerin is not effective in reducing myocardial ischemia in patients undergoing noncardiac surgery ||III: No Benefit ||B |
|Intraoperative monitoring techniques |
|Emergency use of perioperative TEE in patients with hemodynamic instability is reasonable in patients undergoing noncardiac surgery if expertise is readily available ||IIa ||C |
|Routine use of intraoperative TEE during noncardiac surgery is not recommended ||III: No Benefit ||C |
|Maintenance of body temperature |
|Maintenance of normothermia may be reasonable to reduce perioperative cardiac events ||IIb ||B |
|Hemodynamic assist devices |
|Use of hemodynamic assist devices may be considered when urgent or emergency noncardiac surgery is required in the setting of acute severe cardiac dysfunction ||IIb ||C |
|Perioperative use of pulmonary artery catheters |
|Use of pulmonary artery catheterization may be considered when underlying medical conditions that significantly affect hemodynamics cannot be corrected before surgery ||IIb ||C |
|Routine use of pulmonary artery catheterization is not recommended ||III: No Benefit ||A |
Intraarterial pressure monitoring is reasonable in most patients with severe CAD and major or multiple cardiac risk factors who are undergoing any but the most minor procedures. Central venous (or rarely pulmonary artery) pressure can be monitored during prolonged or complicated procedures involving large fluid shifts or blood loss. Noninvasive methods of cardiac output determination and volume assessment have been previously discussed in this text and we recommend them. Transesophageal echocardiography (TEE) and transthoracic echocardiography (TTE) can provide valuable information, both qualitative and quantitative, on contractility and ventricular chamber size (preload) perioperatively.
Early ischemic changes are subtle and involve changes in T-wave morphology, including inversion, tenting, or both (Figure 21–2). More obvious ischemia may be seen in the form of progressive ST-segment depression. Down-sloping and horizontal ST depressions are of greater specificity for ischemia than is up-sloping depression. New ST-segment elevations are rare during noncardiac surgery and are indicative of severe ischemia, vasospasm, or infarction.
Electrocardiographic signs of ischemia. Patterns of ischemia and injury. (Data from Schamroth L. The 12 Lead Electrocardiogram. Oxford, UK: Blackwell; 1989.)
It should be noted that an isolated minor ST elevation in the mid-precordial leads (V3 and V4) can be a normal variant in young patients. Ischemia may also present as an unexplained intraoperative atrial or ventricular arrhythmia or the onset of a new conduction abnormality. The sensitivity of the ECG in detecting ischemia is related to the number of leads monitored. Studies suggest that the V5, V4, II, V2, and V3 leads (in decreasing sensitivity) are most useful. Ideally, at least two leads should be monitored simultaneously. Usually, lead II is monitored for inferior wall ischemia and arrhythmias, and V5 is monitored for anterior wall ischemia. When only one lead can be monitored, a modified V5 lead provides the greatest sensitivity.
The increasing number of individuals treated with drug-eluting stents can be problematic perioperatively, especially when antiplatelet therapy must be discontinued (eg, emergency spinal surgery). Such patients are at very increased risk of thrombosis and perioperative MI. Anesthesia providers should never for nonsurgical reasons (eg, desire to perform a spinal anesthetic) discontinue antiplatelet or antithrombotic agents perioperatively without first discussing the risks and benefits of the proposed anesthetic requiring suspension of antiplatelet therapy with the patient and his or her cardiologist. The ACC/AHA guidelines offer recommendations on the approach of bringing patients to surgery following percutaneous coronary interventions and the type of interventions suggested when subsequent surgery is expected (Figure 21–3).
Algorithm for antiplatelet management in patients with percutaneous coronary intervention (PCI) and noncardiac surgery. Colors correspond to the following classes of recommendations: class I, green; class IIa, yellow; class IIb, orange; class III, red. (*Assuming the patient is currently on dual antiplatelet therapy [DAPT].) ASA, acetylsalicylic acid; ASAP, as soon as possible; BMS, bare-metal stent; DES, drug-eluting stent; P2Y, adenosine diphosphate receptor antagonist. (Reproduced with permission from Fleisher LA, Fleischman KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol. 2014 Dec 9;64(22):e77-e137.)
B. Hemodynamic Monitoring
The most common hemodynamic abnormalities observed during ischemic episodes are hypertension and tachycardia. They are almost always a cause (rather than the result) of ischemia. Hypotension is a late and ominous manifestation of progressive ventricular dysfunction. TEE readily will demonstrate a dysfunctional ventricle and ventricular wall motion changes associated with myocardial ischemia. Ischemia is frequently, but not always, associated with an abrupt increase in pulmonary capillary wedge pressure; however, it is rare for pulmonary capillary wedge pressure to be measured during general anesthesia.
C. Transesophageal Echocardiography
TEE can be helpful in detecting global and regional cardiac dysfunction, as well as valvular function, in surgical patients. Moreover, detection of new regional wall motion abnormalities is a more sensitive and earlier indication of myocardial ischemia than the ECG. In animal studies in which coronary blood flow is gradually reduced, regional wall motion abnormalities develop before the ECG changes. Although the occurrence of new intraoperative abnormalities correlates with postoperative MIs in some studies, not all such abnormalities are necessarily ischemic. Both regional and global abnormalities can be caused by changes in heart rate, altered conduction, preload, afterload, or drug-induced changes in contractility. Decreased systolic wall thickening may be a more reliable index for ischemia than endocardial wall motion alone.
Arrhythmias, Pacemakers, and Internal Cardioverter-Defibrillator Management
Electrolyte disorders, heart structure defects, inflammation, myocardial ischemia, cardiomyopathies, and conduction abnormalities can all contribute to the development of perioperative arrhythmias and heart block. Consequently, anesthesia providers must be prepared to treat both chronic and new-onset cardiac rhythm abnormalities.
Supraventricular tachycardias (SVTs) can have hemodynamic consequences secondary to loss of AV synchrony and decreased diastolic filling time. Loss of the “P” wave on the ECG with a fast ventricular response is consistent with SVTs. Most SVTs occur secondary to a reentrant mechanism. Reentrant arrhythmias occur when conduction tissues in the heart depolarize or repolarize at varying rates. In this manner, a self-perpetuating loop of repolarization and depolarization can occur in the conduction pathways or AV node, or both. SVTs producing hemodynamic collapse are treated perioperatively with synchronized cardioversion. Adenosine can likewise be given to slow AV node conduction and potentially disrupt the reentrant loop. SVTs in patients without accessory conduction bundles (Wolff–Parkinson–White [WPW] syndrome) are treated with β-blockers and calcium channel blockers. In patients with known WPW, procainamide or ibutilide can be used to treat SVTs. Use of intravenous amiodarone, adenosine, digoxin, or non-dihydropyridine calcium channel antagonists is considered a class III recommendation by the AHA/ACC as these agents may harmfully increase the ventricular response in patients with preexcitation syndromes such as WPW. At times, SVTs manifest with a broad QRS complex and seem to be similar to VTs. Such rhythms, when they present, should be treated like VT, until proven otherwise.
Atrial fibrillation (AF) can complicate the perioperative period (Figure 21–4). Up to 35% of cardiac surgery patients develop postoperative AF.
Posterior view of principal electrophysiological mechanisms of atrial fibrillation. A: Focal activation. The initiating focus (indicated by the dot) often lies within the region of the pulmonary veins. The resulting wavelets represent fibrillatory conduction, as in multiple-wavelet reentry. B: Multiple-wavelet reentry. Wavelets (arrows) randomly reenter tissue previously activated by the same or another wavelet. The routes the wavelets travel vary. LA, left atrium; PV, pulmonary vein; ICV, inferior vena cava; SCV, superior vena cava; RA, right atrium. (Reproduced with permission from Konings KT, Kirchhof CJ, Smeets JR, et al. High-density mapping of electrically induced atrial fibrillation in humans. Circulation. 1994 Apr;89(4):1665-1680.)
The ACC/AHA guidelines recommend antithrombotic therapy in patients with long-standing AF to prevent thromboembolic ischemic stroke. Consequently, many patients with AF will present to the operating room on some form of antithrombotic therapy (eg, warfarin, direct thrombin, or factor Xa inhibitors). Patients may require discontinuation of oral anticoagulation therapy prior to invasive procedures. Bridging with heparin is often utilized in patients at high risk for thromboembolism (eg, patients with mechanical heart valves).
When AF develops perioperatively, rate control with β-blockers can often be instituted. Chemical cardioversion can be attempted with amiodarone or procainamide. Of note, if the duration of AF is greater than 48 hours, or unknown, ACC/AHA guidelines recommend anticoagulation for 3 weeks prior to, and 4 weeks following, either electrical or chemical cardioversion. Additionally, TEE can be performed to rule out the presence of left atrial or left atrial appendage thrombus.
Should AF develop postoperatively, ventricular rate response can be controlled with AV nodal blocking agents, unless contraindicated. Should AF result in hemodynamic instability, synchronized cardioversion should be attempted. Patients at high risk of AF following cardiac surgery can be treated with prophylactic amiodarone. Many centers routinely administer β-blockers or amiodarone to all patients undergoing coronary artery surgery to reduce the risk of new onset AF.
AF is most frequently associated with loss of atrial muscle and the development of fibrosis. Fibrosis may contribute to reentrant mechanisms of AF as depolarization/repolarization becomes nonhomogeneous. AF may also develop from a focal source often located in the pulmonary veins. In patients with an accessory bundle, AF can produce rapid ventricular responses and hemodynamic collapse. Drugs that slow conduction across the AV node (eg, digitalis, verapamil, diltiazem) do not slow conduction across the accessory pathway, potentially leading to hemodynamic collapse. The ACC/AHA guidelines likewise recommend caution in the use of β-blockers for AF in patients with preexcitation syndromes.
Ventricular arrhythmias have been the subject of much review by the AHA (Table 21–12). Ventricular premature contractions (VPCs) can appear perioperatively secondary to electrolyte abnormalities (hypokalemia, hypomagnesium, hypocalcemia), acidosis, ischemia, embolic phenomenon, mechanical irritation of the heart from central lines, cardiac manipulation, and drug effects. Correction of the underlying source of any arrhythmia should be addressed. Patients can likewise present with VPCs secondary to various cardiomyopathies.
TABLE 21–12Classification of ventricular arrhythmias.1 ||Download (.pdf) TABLE 21–12 Classification of ventricular arrhythmias.1
|Classification by Clinical Presentation |
|Hemodynamically stable ||Asymptomatic ||The absence of symptoms that could result from an arrhythmia. |
| ||Minimal symptoms, eg, palpitations || |
Patient reports palpitations felt in either the chest, throat, or neck as described by the following:
Heartbeat sensations that feel like pounding or racing
An unpleasant awareness of heartbeat
Feeling skipped beats or a pause
|Hemodynamically unstable ||Presyncope || |
Patient reports presyncope as described by the following:
|Syncope ||Sudden loss of consciousness with loss of postural tone, not related to anesthesia, with spontaneous recovery as reported by the patient or observer. Patient may experience syncope when supine. |
|Sudden cardiac death ||Death from an unexpected circulatory arrest, usually due to a cardiac arrhythmia occurring within an hour of the onset of symptoms. |
|Sudden cardiac arrest ||Death from an unexpected circulatory arrest, usually due to a cardiac arrhythmia occurring within an hour of the onset of symptoms, in whom medical intervention (eg, defibrillation) reverses the event. |
|Classification by Electrocardiography |
|Nonsustained VT2 || || |
Three or more beats in duration, terminating spontaneously in <30 s.
VT is a cardiac arrhythmia of three or more consecutive complexes in duration emanating from the ventricles at a rate of >100 bpm (cycle length <600 ms)
|Monomorphic ||Nonsustained VT with a single QRS morphology. |
|Polymorphic ||Nonsustained VT with a changing QRS morphology at cycle length between 600 and 180 ms. |
|Sustained VT || ||VT >30 s in duration and/or requiring termination due to hemodynamic compromise in <30 s. |
|Monomorphic ||Sustained VT with a stable single QRS morphology. |
|Polymorphic ||Sustained VT with a changing or multiform QRS morphology at cycle length between 600 and 180 ms. |
|Bundle-branch reentrant tachycardia || ||VT due to reentry involving the His-Purkinje system, usually with LBBB morphology; this usually occurs in the setting of cardiomyopathy. |
|Bidirectional VT || ||VT with a beat-to-beat alternans in the QRS frontal plane axis, often associated with digitalis toxicity. |
|Torsades de pointes || || |
Characterized by VT associated with a long QT or QTc, and electrocardiographically characterized by twisting of the peaks of the QRS complexes around the isoelectric line during the arrhythmia:
“Typical,” initiated following “short-long-short” coupling intervals.
Short coupled variant initiated by normal-short coupling.
|Ventricular flutter || ||A regular (cycle length variability ≤30 ms) ventricular arrhythmia approximately 300 bpm (cycle length 200 ms) with a monomorphic appearance; no isoelectric interval between successive QRS complexes. |
|Ventricular fibrillation || ||Rapid, usually more than 300 bpm/200 ms (cycle length ≤180 ms), grossly irregular ventricular rhythm with marked variability in QRS cycle length, morphology, and amplitude. |
|Classification by Disease Entity |
Chronic coronary heart disease
Congenital heart disease
Structurally normal hearts
Sudden infant death syndrome
The incidence of sudden cardiac death (SCD) is estimated at 1 to 2/1000 per year. Consequently, some patients will experience an unexpected death in the perioperative period. All anesthesia providers must be prepared to resuscitate and manage patients with ventricular arrhythmias, including ventricular tachycardia (VT) (nonsustained and sustained) and ventricular fibrillation.
Nonsustained VT is a short run of ventricular ectopy that lasts <30 s and spontaneously terminates, whereas sustained VT persists longer than 30 s. VT is either monomorphic or polymorphic, depending on the QRS complex. If the QRS complex morphology changes, it is designated as polymorphic VT. Torsades des pointes is a form of VT associated with a prolonged QT interval, producing a sine wave-like VT pattern on the ECG. Ventricular fibrillation requires immediate resuscitative efforts and defibrillation.
Patients presenting with ventricular ectopy and nonsustained runs of VT routinely undergo investigation prior to surgery; however, patients with such rhythm abnormalities may not be at greater risk for nonfatal MI or cardiac death perioperatively. Supraventricular and ventricular arrhythmias constitute active cardiac conditions that warrant evaluation and treatment prior to elective, noncardiac surgery. Electrophysiological studies are undertaken to determine the possibility for catheter-mediated ablation of VTs.
Should VT present perioperatively, cardioversion is recommended whenever hemodynamic compromise occurs. Otherwise, treatment with amiodarone or procainamide can be attempted. At all times, therapy should also be directed at identifying any causative sources of the arrhythmia. β-Blockers are useful in the treatment of VT, especially if ischemia is a suspected causative factor in the development of rhythm. The use of β-blockers following MI has reduced the incidence of post-MI ventricular fibrillation.
Torsades des pointes is associated with conditions that lengthen the QT interval. If the arrhythmia develops in association with pauses, pacing can be effective. Likewise, some patients may benefit from isoproterenol infusions, if they develop pause-dependent torsades des pointes. Magnesium sulfate may be useful in patients with long QT syndrome and episodes of torsades.
The development of perioperative ventricular fibrillation requires defibrillation and the use of resuscitation algorithms. Amiodarone can be used to stabilize the rhythm following successful defibrillation.
ICDs are recommended in patients with a history of survived SCD, decreased ventricular function following MI, and left ventricular ejection fractions less than 35%. Additionally, ICDs are used to treat potential sudden cardiac death in patients with dilated, hypertrophic, arrhythmogenic right ventricular and genetic cardiomyopathies. ICDs usually have a biventricular pacing function that improves the effectiveness of left ventricular contraction. Patients with heart failure frequently have a widened QRS complex greater than 120 ms. In such patients, ventricular systole is less efficient, as the lateral and septal left ventricular walls do not effectively contract because of the conduction delay. Cardiac resynchronization therapy has been shown to improve functional status in patients with heart failure.
Anesthetic management for the placement of ICDs and other electrophysiological procedures (eg, catheter ablation) depends on the patient’s underlying conditions. Many patients present with systolic and diastolic heart failure and depend on sympathetic tone to maintain blood pressure. Some patients tolerate ICD placement using deep sedation rather than general anesthesia. However, catheter-based electrophysiological studies can be quite time consuming, and patients can develop atelectasis and airway obstruction. Thus, general anesthesia is often used in the electrophysiology laboratory. Should the patient’s blood pressure suddenly decline during electrophysiologic studies, development of pericardial tamponade should be suspected. Emergent drainage of tamponade may be necessary.
Many patients present to surgery with ICDs in place. Published guidelines of the American Society of Anesthesiologists can provide assistance in the management of such patients. Management is a three-step process, as follows:
Preoperative. Identify the type of device and determine if it is used for antibradycardia functions. Consult with the patient’s cardiologist preoperatively as to the device’s function and use history.
Intraoperative. Determine what electromagnetic interference is likely to present intraoperatively and advise the use of bipolar electrocautery where possible. Assure the availability of temporary pacing and defibrillation equipment and apply pads as necessary. Patients who are pacemaker-dependent can be programmed to an asynchronous mode to mitigate electrical interference. Magnet application to ICDs may disable the antitachycardia function, but not convert to an asynchronous pacemaker. Consultation with the patient’s cardiologist and interrogation of the device is often necessary. Most patients will have a card on which the device model and manufacturer are provided. A telephone call to the device manufacturer can provide information about device performance and the best method for managing the device (eg, reprogramming or applying a magnet) prior to surgery. A large number of ICD models are in use; however, most suspend their antitachycardia function in response to a magnet.
Postoperative. The device must be interrogated to ensure that therapeutic functions have been restored. Patients should be continuously monitored until the antitachycardia functions of the device are restored and its function has been confirmed.
ICDs are particularly problematic intraoperatively when electrocautery is used because the device may (1) interpret cautery as ventricular fibrillation; (2) inhibit pacemaker function due to cautery artifact; (3) increase the pacing rate due to activation of a rate-responsive sensor; or (4) temporarily or permanently reset to a backup or reset mode. Use of bipolar cautery, placement of the grounding pad far from the ICD device, and limiting use of the cautery to only short bursts help to reduce the likelihood of problems, but will not eliminate them.
When there is greater risk of stray currents from the cautery, the ICD device should have the defibrillator function programmed off immediately before surgery and reprogrammed back on immediately afterward. External defibrillation pads should be applied and attached to a defibrillator machine intraoperatively. Careful monitoring of the arterial pulse with pulse oximetry or an arterial waveform is necessary to ensure that the pacemaker is not inhibited and that there is arterial perfusion during episodes of ECG artifact from surgical cautery.
An increasing number of patients present for surgery with either systolic or diastolic heart failure. Heart failure may be secondary to ischemia, valvular heart disease, infectious agents, or many forms of cardiomyopathy. Patients may experience heart failure symptoms with both a preserved and reduced ejection fractions. Most heart failure patients seek medical attention for complaints of dyspnea and fatigue. Heart failure develops over time, as symptoms worsen (Figure 21–5). Patients generally undergo echocardiography to diagnose structural heart defects, to detect signs of cardiac “remodeling,” to determine the left ventricular ejection fraction, and to assess the heart’s diastolic function. Laboratory evaluations of concentration of brain natriuretic peptide (BNP) are likewise obtained to distinguish heart failure from other causes of dyspnea. BNP is released from the heart, and its elevation is associated with impaired ventricular function.
Stages in the development of heart failure and recommended therapy by stage. ACEI, angiotensin-converting enzyme inhibitor; AF, atrial fibrillation; ARB, angiotensin-receptor blocker; CAD, coronary artery disease; CRT, cardiac resynchronization therapy; DM, diabetes mellitus; EF, ejection fraction; GDMT, guideline-directed medical therapy; HF, heart failure; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; HRQOL, health-related quality of life; HTN, hypertension; ICD, implantable cardioverter-defibrillator; LV, left ventricular; LVH, left ventricular hypertrophy; MCS, mechanical circulatory support; MI, myocardial infarction. (Reproduced with permission from Yancy C, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013 Oct 15;62(16):e147-e239.)
The body attempts to compensate for LV systolic failure through activation of the sympathetic and renin–angiotensin–aldosterone system. Consequently, patients experience salt retention, volume expansion, sympathetic stimulation, and vasoconstriction. The heart dilates to maintain stroke volume in spite of decreased contractility. Over time, compensatory mechanisms fail and contribute to the symptoms associated with heart failure (eg, dependent edema, tachycardia, decreased tissue perfusion). Patients with systolic heart failure are likely to present to surgery having been previously treated with diuretics, β-blockers, ACE inhibitors or ARBs, and possibly aldosterone antagonists. Electrolytes must be measured, as diuretics frequently lead to hypokalemia. ARB or ACE inhibitor use may contribute to hypotension in the surgical patient with heart failure. ACE inhibitors are rarely associated with angioedema requiring emergent airway management.
Myocardial relaxation is a dynamic, not passive, process. The heart with preserved diastolic function accommodates volume during diastole, with minimal increases in left ventricular end-diastolic pressure. Conversely, the heart with diastolic dysfunction relaxes poorly and produces increased left ventricular end-diastolic pressure. The increased left ventricular end-diastolic pressure is transmitted to the left atrium and pulmonary vasculature resulting in symptoms of congestion. Patients with any form of heart failure have increased risk of perioperative morbidity.
Hypertrophic cardiomyopathy (HCM) is an autosomal dominant trait that affects 1 in 500 adults. Many patients are unaware of the condition, and some will present with sudden cardiac death as the initial manifestation. Symptoms include dyspnea, exercise intolerance, palpitations, and chest pain. Clinically, HCM is detected by the murmur of dynamic left ventricular outflow tract (LVOT) obstruction in late systole. Symptomatic patients frequently have a thickened intraventricular septum of 20 to 30 mm. A variety of genetic variants have been identified as causative. The myocardium of the intraventricular septum is abnormal, and many patients can develop diastolic dysfunction without pronounced dynamic obstructive gradients. During systole, the anterior leaflet of the mitral valve abuts the intraventricular septum (Figure 21–6), producing obstruction and a late systolic murmur.
The midesophageal long axis view is shown. As a consequence of the hypertrophied interventricular septum, flow patterns within the heart are altered so that the anterior leaflet of the mitral valve is drawn during ventricular systole into the left ventricular outflow tract (LVOT), producing obstruction. This is known as systolic anterior motion of the mitral valve. (Reproduced with permission from Wasnick J, Hillel Z, Kramer D, et al. Cardiac Anesthesia & Transesophageal Echocardiography. New York, NY: McGraw-Hill Education; 2011.)
Perioperative management is aimed at minimizing the degree of LVOT obstruction. This is accomplished by maintaining adequate intravascular volume, avoiding vasodilatation, and reducing myocardial contractility through the use of β-blockers.