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Anesthesia for noncardiac surgery in patients with ischemic heart disease

Anesthesia for noncardiac surgery in patients with ischemic heart disease
Literature review current through: May 2024.
This topic last updated: Mar 13, 2024.

INTRODUCTION — Patients with ischemic heart disease are at increased risk for perioperative cardiovascular events such as myocardial infarction, heart failure, life-threatening arrhythmias, and mortality. Those with recent myocardial infarction or unstable angina are at a very high risk if they require urgent or emergency surgery.

This topic reviews the preanesthesia consultation, anesthetic care, and immediate postoperative management of patients with ischemic heart disease during elective or emergency noncardiac surgery. Anesthetic management during noncardiac surgery in patients with heart failure (ischemic and nonischemic) is discussed in a separate topic. (See "Intraoperative management for noncardiac surgery in patients with heart failure".)

Anesthetic management of patients requiring cardiac surgery for coronary revascularization is discussed separately. (See "Anesthesia for coronary artery bypass grafting surgery".)

Other topics discuss preoperative medical evaluation and management of patients with ischemic heart disease. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Management of cardiac risk for noncardiac surgery".)

PREANESTHESIA CONSULTATION — All surgical patients with ischemic heart disease are assessed for potential risk of myocardial injury during the perioperative period [1-3]. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Management of cardiac risk for noncardiac surgery".)

Identifying patients with increased cardiac risk — Risk of perioperative myocardial injury is related to individual patient factors, as well as the type of surgical procedure (table 1 and table 2 and table 3). Assessments of risk determine intra- and postoperative anesthetic management [3-5].

Patient-related factors:

Recent myocardial infarction or unstable angina – Patients with recent (<60 days) myocardial infarction (MI) or unstable angina are at a very high risk for major cardiovascular outcome [6]. Perioperative acute coronary syndrome (ACS) confers particularly high risk for mortality [7]. Evaluation and management are discussed in separate topics. (See "Management of cardiac risk for noncardiac surgery", section on 'For recent acute coronary syndrome including myocardial infarction' and "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Very high-risk patients'.)

Recent percutaneous coronary intervention – Patients with coronary artery stents undergoing noncardiac surgery are at a high risk for adverse cardiovascular outcome even when receiving perioperative antiplatelet therapy, and are also at a high risk for major bleeding events [8]. In an observational study of 62,528 surgical patients undergoing general anesthesia, 133 patients underwent emergency surgery within 24 hours of percutaneous coronary intervention (PCI); mortality in these patients at 180 postoperative days was 10 percent (13/133) [9]. Reinitiating dual antiplatelet inhibitors (DAPT) <48 hours after surgery was associated with risk of postoperative bleeding (odds ratio [OR] 4.51, 95% CI 1.56-13.0).

Decision-making regarding the perioperative continuation of DAPT is made on a case-by-case basis with the patient, primary care physician, cardiologist, anesthesiologist, and surgeon involved. Clear recommendations should be made regarding the timing of surgery (including considerations for delaying elective surgery), location of surgery (eg, a free-standing ambulatory surgery center versus an in-hospital setting [10]), and timing of administration of DAPT during the periprocedural period [11]. Details are discussed in a separate topic. (See "Noncardiac surgery after percutaneous coronary intervention", section on 'Our approach'.)

Furthermore, contingency plans for managing surgical site bleeding or perioperative major adverse cardiac events (MACE) such as coronary stent thrombosis are necessary. (See "Perioperative myocardial infarction or injury after noncardiac surgery", section on 'Acute treatment'.)

Older age In a multinational retrospective study of more than 1.3 million patients with intermediate- or high-risk noncardiac surgery, 0.68 percent were diagnosed with perioperative ACS with a short-term mortality of 19.3 percent [12]. The strongest association with ACS was age >85 years (adjusted OR 2.52, 95% CI 2.1-3.1). Mortality risk has been associated with peak troponin level in older patients undergoing hip fracture repair surgery, including short-term (before 28 days), intermediate-term (before 180 days), and long-term (before 365 days) postoperative mortality [13]. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Management of cardiac risk for noncardiac surgery".)

Procedure-related factors

High-risk surgical procedure – Classic surgical risk categories predicting MACE, defined as cardiac death or acute MI, were typically categorized as high (>5 percent), intermediate (1 to 5 percent), or low (<1 percent) risk (table 2) [14]. However, patient-dependent and procedure-dependent risk factors exist within these categories (table 3) [12,15]. Details are discussed in separate topics. (See "Preoperative evaluation for anesthesia for noncardiac surgery", section on 'Surgical risk' and "Perioperative myocardial infarction or injury after noncardiac surgery", section on 'Risk factors'.)

Urgent or emergency surgery – If possible, we obtain a preoperative consultation with a cardiologist before urgent or emergency surgery. Consultation with a hematologist is also useful for patients who are receiving antiplatelet drugs. (See "Management of cardiac risk for noncardiac surgery", section on 'For urgent or emergency surgery' and 'Managing perioperative medications' below.)

Assessing preoperative studies

Electrocardiogram A preoperative baseline resting 12-lead electrocardiogram (ECG) is obtained for all patients with symptoms of myocardial ischemia and for asymptomatic patients at high risk for myocardial injury (table 1), particularly if a high-risk surgical procedure is planned (table 2) [1,3]. A baseline ECG is useful for comparison when the postoperative ECG is abnormal. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Electrocardiogram for some patients'.)

Laboratory studies Preoperative screening is performed in patients with high cardiac risk (table 1) [16,17]. This includes a cardiac troponin (cTn) level obtained at baseline to facilitate postoperative surveillance with troponin levels, as discussed separately. (See "Perioperative myocardial infarction or injury after noncardiac surgery", section on 'High-risk patients'.)

Other criteria for ordering preoperative blood tests are the same for patients with ischemic heart disease as for other patients undergoing noncardiac surgery. It is reasonable to obtain a metabolic panel (sodium, potassium, chloride, carbon dioxide, glucose, blood urea nitrogen, creatinine) in patients with diabetes or renal insufficiency, and in those receiving chronic diuretic therapy.

Managing perioperative medications

Beta blockers

Continue prior beta blocker therapy – Patients with ischemic heart disease who are already taking beta blockers preoperatively should continue their regular dose, including the morning of surgery and throughout the perioperative period, to minimize tachycardia or ischemia [1,3,18-20].

Avoid routine initiation of prophylactic beta blocker therapy – Beta blockers are not initiated prophylactically in the preoperative period unless recommended by a consulting cardiologist based on strong indications [19]. Further discussion is available in another topic. (See "Management of cardiac risk for noncardiac surgery", section on 'Beta blockers'.)

Statins – Patients taking statins should continue this therapy throughout the perioperative period [21]. A consultant cardiologist may recommend initiation of statin therapy in previously untreated patients [1,3,18]. (See "Management of cardiac risk for noncardiac surgery", section on 'Statins'.)

Antiplatelet therapy – Patient-specific and procedure-specific recommendations to continue or discontinue chronically administered aspirin, other antiplatelet agents such as the platelet P2Y12 receptor blockers clopidogrel, prasugrel, ticagrelor, and ticlopidine, and nonsteroidal anti-inflammatory drugs (NSAIDs) are discussed in detail in separate topics. (See "Perioperative medication management", section on 'Medications affecting hemostasis' and "Management of cardiac risk for noncardiac surgery", section on 'Antiplatelet therapy'.)

Notably, platelets should not be administered on a prophylactic basis, although platelet transfusion may be necessary to treat excessive perioperative bleeding.

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers – We individualize the decision to continue or discontinue angiotensin-converting enzyme (ACE) inhibitors based on the indications for the drug, the patient's blood pressure, and the type of surgery and anesthesia planned. For most patients, we usually withhold these agents on the morning of surgery, particularly if large perioperative fluid shifts are anticipated. However, when the indication is for heart failure or poorly controlled hypertension, we often continue the medication to avoid further exacerbation of these conditions. In all patients with hemodynamic instability, hypovolemia, or acute elevation of creatinine, ACE inhibitors and angiotensin receptor blockers (ARBs) are withheld. Further discussion is available in other topics. (See "Perioperative medication management", section on 'ACE inhibitors and angiotensin II receptor blockers' and "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Medication management'.)

Sodium-glucose co-transporter 2 (SGLT2) inhibitors Other treatments for heart failure with reduced ejection fraction (HFrEF) include SGLT2 inhibitors (eg, empagliflozin, dapagliflozin, ertugliflozin, bexagliflozin) which are stopped three to four days before surgery to avoid postoperative euglycemic diabetic ketoacidosis. Further discussion is available in other topics:

(See "Perioperative medication management", section on 'Sodium-glucose cotransporter 2 inhibitors'.)

(See "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Medication management'.)

(See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Sodium-glucose co-transporter 2 inhibitors'.)

Other cardiovascular medications – Chronically administered clonidine is continued since rebound hypertension may occur with abrupt withdrawal. Transdermal administration may replace oral administration in patients who will not resume oral intake soon after surgery. (See "Management of cardiac risk for noncardiac surgery", section on 'Clonidine'.)

We continue most other chronically administered cardiovascular medications (eg, calcium channel blockers, digoxin) in the perioperative period. Specific details are discussed separately. (See "Perioperative medication management", section on 'Cardiovascular medications'.)

Managing implantable cardioverter defibrillators and pacemakers — Patients with ischemic heart disease or ischemic cardiomyopathy may have a single- or dual-chamber pacemaker, biventricular pacemaker, and/or an implantable cardioverter defibrillator device (ICD) [22]. Perioperative management of these devices is discussed separately. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

MONITORING AND HEMODYNAMIC MANAGEMENT — Perioperative goals in patients with ischemic heart disease are to detect, prevent, and treat myocardial ischemia to avoid myocardial injury [23].

Monitoring for myocardial ischemia — Although myocardial ischemia is possible without any changes in systemic hemodynamics, monitoring for imbalances in myocardial oxygen (O2) supply versus demand, as well as for development of ischemia, is continuous throughout the perioperative period.

Electrocardiography The electrocardiogram (ECG) is continuously monitored to detect ST-segment depression or elevation [1,24]. Computerized ST-segment trending of continuous ECG monitoring is superior to visual clinical interpretation to identify ST-segment changes, and multiple-lead monitoring is more sensitive than single-lead monitoring [25].

Intra-arterial catheter Invasive measurement of arterial blood pressure (BP) is employed when significant BP changes are anticipated during the surgical procedure (eg, rapid blood loss or large fluid shifts), particularly in patients with severe coronary artery disease, cardiomyopathy, or hemodynamic instability. If significant hemodynamic changes are anticipated during anesthetic induction, the intra-arterial catheter should be inserted prior to induction.

Direct arterial BP monitoring is superior to indirect monitoring techniques for early detection of intraoperative hypotension [26]. In addition, an intra-arterial catheter is useful to assess fluid responsiveness by examining variations in the intra-arterial pressure waveform that occur during respiration (figure 1), guide management of vasoactive drugs, and facilitate sampling of arterial blood for measurements of blood gases and other laboratory values. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Monitoring blood pressure' and "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Monitoring intravascular volume status'.)

Central venous catheter The decision to place a central venous catheter (CVC) is based on the anticipation of significant blood loss and/or large fluid shifts, as well as the likelihood of administration of continuous infusions of vasoactive drugs. Measurement of central venous pressure (CVP) may provide supplemental data regarding intravascular volume status, although CVP is a poor predictor of fluid responsiveness [27-29]. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

Pulmonary artery catheter – It is not necessary to place a pulmonary artery catheter (PAC) for monitoring for myocardial ischemia [1,3]. Intraoperative changes in pulmonary artery pressure (PAP) or pulmonary artery wedge pressure (PCWP) are poor predictors of myocardial ischemia compared with ECG or transesophageal echocardiographic (TEE) monitoring [30]. Furthermore, there appears to be no benefit and possible harm from perioperative PAC use in most patients undergoing either cardiac or noncardiac surgery [31-34].

In a few selected patients with ischemic heart disease and concomitant cardiovascular conditions that significantly affect hemodynamics (eg, severe cardiomyopathy or valvular lesions), a PAC is inserted to monitor PAP, cardiac output, and mixed venous Hgb saturation (SvO2) during the perioperative period. The decision is based upon both the severity of cardiovascular pathology, presence of other systemic diseases such as renal failure, and the risks of the planned surgical procedure (eg, the potential for significant fluid shifts and bleeding). (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults".)

Transesophageal echocardiography Continuous intraoperative TEE monitoring may be useful to detect new regional wall motion abnormalities (RWMAs; eg, hypokinesis, akinesis, or dyskinesis) in patients at high risk, particularly those undergoing major surgery [24]. RWMAs indicate specific territories of myocardium perfused by each of the major coronary arteries supplying the left ventricular (LV) (figure 2 and figure 3) [24]. Ischemic changes may be chronic (pre-existing) or may develop or worsen during the surgical procedure. (See "Intraoperative transesophageal echocardiography for noncardiac surgery".)

TEE monitoring has higher sensitivity for detecting myocardial ischemia than ECG or PAC monitoring [35]. However, there are no data demonstrating that TEE monitoring can decrease the incidence of adverse perioperative cardiovascular events [1,36,37].

Emergency use of intraoperative or perioperative TEE is indicated to determine the cause of any unexplained persistent or life-threatening circulatory instability ("rescue echo"). For example, TEE may identify hypovolemia (movie 1), ventricular dysfunction (movie 2), pericardial effusion or cardiac tamponade, valvular stenosis or regurgitation, pulmonary embolism, or left ventricular outflow tract obstruction [38]. (See "Intraoperative rescue transesophageal echocardiography (TEE)".)

As an alternative to TEE assessment in emergency situations, transthoracic focused cardiac ultrasound can be considered for assessment of most of these potentially life-threatening conditions [39]. (See "Overview of perioperative diagnostic uses of ultrasound", section on 'Focused transthoracic cardiac ultrasound (FOCUS)'.)

Prevention of ischemia — The dominant mechanism of acute coronary syndrome in the perioperative period is demand ischemia, rather than acute coronary or stent thrombosis [40,41]. Thus, it is important to control hemodynamics to optimize O2 supply and minimize demand, regardless of the surgical procedure or the anesthetic techniques and agents selected. The following hemodynamic and physiologic goals are key (table 4):

Maintain low to normal heart rate – Maintain low to normal heart rate (HR) at 50 to 80 beats/minute (bpm) because tachycardia compromises both O2 supply and demand. Myocardial O2 supply is affected by the duration of diastole because 70 to 80 percent of coronary blood flow occurs during diastole. Also, myocardial O2 demand more than doubles when HR doubles [42]. The relationship between HR and the duration of diastole is nonlinear (figure 4) [43,44].

Prevention and treatment of tachycardia depend on the likely cause, timing of intraoperative occurrence, and the patient's baseline condition. (See "Hemodynamic management during anesthesia in adults", section on 'Heart rate targets'.)

Maintain normal to high-normal blood pressure – Maintain BP within 20 percent of baseline. Typically, aim for a mean arterial BP 75 to 95 mmHg and/or diastolic BP 65 to 85 mmHg to maintain coronary perfusion pressure. Severe hypotension reduces myocardial O2 supply, while severe hypertension increases demand.

Avoid hypotension Prevention and prompt treatment of arterial hypotension is warranted to avoid supply-mediated ischemia [45,46]. (See "Hemodynamic management during anesthesia in adults", section on 'Hypotension: Prevention and treatment'.)

In one retrospective study of 955 patients undergoing major noncardiac surgery, intraoperative hypotension was defined as systolic BP <90 mmHg for ≥10 minutes, or for any duration in the postoperative period requiring intervention [47]. A composite outcome of myocardial infarction or death occurred within 30 days of surgery in 16.4 percent of patients with obstructive coronary artery disease (CAD) and hypotension, compared with 6.7 percent of patients with CAD but without hypotension, and only 2.7 percent of patients without CAD or hypotension.

Avoid hypertension – Also, prevent and promptly treat hypertension, which may cause demand-mediated ischemia by increasing systolic wall stress and left ventricular end-diastolic pressure (LVEDP) (table 4). The subendocardium is particularly vulnerable to ischemia because the compressive effect of increases in LVEDP becomes the limiting factor for subendocardial coronary blood flow. (See "Hemodynamic management during anesthesia in adults", section on 'Hypertension: Prevention and treatment'.)

In one study in 15,109 patients, a minimum intraoperative systolic BP <100 mmHg was associated with myocardial injury (odds ratio [OR] 1.21, 95% CI 1.05-1.39) and mortality (OR 1.81, 95% CI 1.39-2.37) [23]. Risk was most likely if low systolic BP <100 mmHg occurred with HR >100 bpm (OR 1.42, 1.15-1.76). However, high systolic BP values exceeding 160 mmHg were also associated with myocardial injury (OR 1.16, 95% CI 1.01-1.34) and myocardial infarction (MI) (OR 1.34, 95% CI 1.09-1.64), suggesting that both low and high BP extremes should be avoided [23].

Maintain normal left ventricular end-diastolic volume – Avoid LV distention caused by fluid overload, as this may increase systolic wall stress and myocardial O2 demand. Although CVP or PAP values are used as surrogates to estimate LV volume, these measurements have limitations [27,31,48]. (See 'Monitoring for myocardial ischemia' above.)

Maintain adequate arterial O2 content – Maintain normal to high peripheral oxygen saturation (SpO2) ≥95 percent and adequate Hgb levels (avoiding anemia <7 to 8 g/dL). (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells'.)

Maintain normothermia – Normothermia favors tissue release of O2. Avoid hypothermia during and after surgery. Adverse consequences of hypothermia include shivering, which increases myocardial O2 demand and may result in myocardial ischemia. Although less common, perioperative hyperthermia is also avoided. Adverse consequences of hyperthermia also include increased metabolic rate and increased myocardial O2 demand. Details regarding temperature management are discussed separately. (See "Perioperative temperature management".)

Treatment of ischemia — Intraoperative myocardial ischemia is typically diagnosed by observing characteristic ST-segment changes on the ECG, most commonly new horizontal or downsloping ST-segment depressions. If TEE monitoring is employed, new ventricular RWMAs indicate myocardial ischemia that should be treated. (See 'Monitoring for myocardial ischemia' above.)

The following interventions optimize myocardial O2 supply and minimize myocardial O2 demand in patients who develop intraoperative myocardial ischemia [45]:

Treat tachycardia

Treat sinus tachycardia Intraoperative tachycardia (or even HR >80 bpm) caused by pain or inadequate anesthesia is treated by administering a dose of an intravenous anesthetic (eg, propofol), analgesic (eg, opioid), increasing the inhalation anesthetic concentration, or administering additional local anesthetic through an epidural catheter. If these measures are not effective to decrease HR, an intravenous beta blocker (eg, esmolol, metoprolol, or labetalol) is administered, whether or not there is evidence of ischemia. (See "Arrhythmias during anesthesia", section on 'Sinus tachycardia'.)

Treat atrial fibrillation or flutter with rapid ventricular response – Atrial fibrillation (AF) is a common arrhythmia, particularly in patients with underlying heart disease. Perioperative causes that may lead to development of atrial fibrillation (eg, hypovolemia, hypotension, anemia, trauma, and pain which may increase sympathetic activity) should be sought and managed. Treatment of acute or chronic AF depends on the ventricular response and presence of hemodynamic instability. Details are included in the algorithm and in a separate topic (algorithm 1). (See "Arrhythmias during anesthesia", section on 'Atrial fibrillation' and "Arrhythmias during anesthesia", section on 'Atrial flutter'.)

Avoid severe bradycardia Notably, severe bradycardia (eg, heart rate <40 bpm) is also avoided, as this limits cardiac output. Management is discussed separately (table 5). (See "Arrhythmias during anesthesia", section on 'Bradyarrhythmias'.)

Treat hypertension – Similar to increased HR, increased BP caused by pain or inadequate anesthesia are treated by administering a dose of an intravenous anesthetic (eg, propofol), analgesic (eg, opioid), increasing the inhalation anesthetic concentration, or administering additional local anesthetic through an epidural catheter. (See "Hemodynamic management during anesthesia in adults", section on 'Hypertension: Prevention and treatment'.)

Administration of an intravenous beta blocker (eg, esmolol, metoprolol, or labetalol) and/or a vasodilating agent (eg, labetalol, nicardipine, or nitroglycerin) may also be necessary. If hypertension is associated with persistent myocardial ischemia, an intravenous nitroglycerin infusion is titrated (at 10 to 200 mcg/minute; 0.1 to 3 mcg/kg/minute) to control BP (table 6). An intra-arterial catheter for continuous BP monitoring is desirable during titration of a continuous infusion of nitroglycerin.

Nitroglycerin causes coronary arterial vasodilation of the large epicardial conductance vessels and decreases LV preload due to venodilation. These benefits must be weighed against the risk of hypotension and the potential for reflex tachycardia. The additive vasodilatory effects of certain anesthetic agents and nitroglycerin may lead to significant hypotension and worsening myocardial ischemia. In patients without LV heart failure, addition of a phenylephrine infusion (at 10 to 200 mcg/minute; 0.1 to 2 mcg/kg/minute) may be useful to maintain adequate BP and prevent ischemia (table 7) [49-51]. (See "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents'.)

Prophylactic intravenous nitroglycerin is not administered, as it is not effective in reducing myocardial ischemia in patients undergoing noncardiac surgery [1,3]. Avoid transdermal nitroglycerin because absorption may be uneven. (See "Management of cardiac risk for noncardiac surgery", section on 'Nitrate therapy'.)

Treat hypotension – Decreases in BP (eg, mean arterial BP <75 mmHg or diastolic BP <65 mmHg) may be initially managed by reducing excessive anesthetic depth and/or administering intravenous fluid. (See "Hemodynamic management during anesthesia in adults", section on 'Hypotension: Prevention and treatment'.)

Detection of hypovolemia is often possible using TEE (movie 1), or by observing variations in the intra-arterial pressure waveform that occur during respiration to gauge fluid responsiveness. Details are discussed in a separate topic (figure 1). (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)

Significant hypotension is corrected by administering an alpha1 receptor agonist (eg, phenylephrine 40 to 100 mcg) and/or a direct/indirect sympathomimetic with beta and alpha agonist effects (eg, ephedrine 5 to 10 mg) as appropriate, with repeated doses if necessary. If hypotension persists, a continuous infusion of phenylephrine is administered (at 10 to 200 mcg/minute; 0.1 to 2 mcg/kg/minute). (See "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

Vasoplegia with severe or refractory hypotension due to low systemic vascular resistance (SVR) may be present in patients with septic shock or after prior administration of angiotensin-converting enzyme (ACE) inhibitors. Treatment is with a potent direct peripheral vasoconstrictor such as vasopressin or with the catecholamine norepinephrine. Vasopressin is also a good choice for treating systemic arterial hypotension in patients with pulmonary hypertension since it has a more selective systemic vasoconstricting effect than phenylephrine or norepinephrine, thereby sparing the pulmonary vasculature (table 7) [52]. Other agents may be employed to treat refractory hypotension if necessary (table 8). (See "Intraoperative use of vasoactive agents", section on 'Other agents to treat refractory vasoplegia'.)

Inotropic support may be needed for treatment of persistent hypotension caused by left or right ventricular dysfunction, which is best assessed with TEE monitoring (movie 2) (see "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Ventricular function'). Commonly employed agents include epinephrine, norepinephrine, or dopamine (at 5 to 20 mcg/kg/minute) (table 7). An intra-arterial catheter for continuous BP monitoring is necessary during titration of these potent inotropic and vasopressor infusions. (See "Intraoperative use of vasoactive agents", section on 'Adrenergic agents'.)

Treat low O2 saturation or anemia – Administer supplemental O2 to achieve normal to high SpO2 ≥95 percent and treat anemia to maintain adequate Hgb levels at ≥7 to 8 g/dL. In patients known to have acute coronary syndrome (ACS) or signs of myocardial or other organ ischemia, we typically use a higher Hgb threshold (<9 g/dL) to guide transfusion, particularly in the setting of ongoing bleeding during major surgery. Further discussion is available in a separate topic. (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells'.)

Treat hypothermia – Warm fluids and blood prior to administration. Blankets and forced-air devices should be used to avoid hypothermia and for active warming as necessary, while also avoiding hyperthermia. (See "Perioperative temperature management", section on 'Intraoperative hypothermia'.)

Treat arrhythmias - Arrhythmias are not uncommon in patients with ischemic heart disease. Treatment of the underlying cause of an arrhythmia is critical (eg, electrolyte disturbances, acute myocardial ischemia, adverse effect of an inotrope). Intraoperative management of specific cardiac arrhythmias is discussed separately. (See "Arrhythmias during anesthesia".)

ANESTHETIC MANAGEMENT

Premedication — Some cardiac surgical patients benefit from premedication with small incremental doses of a short-acting intravenous (IV) benzodiazepine anxiolytic (eg, midazolam 1 to 2 mg) and/or opioid (eg, fentanyl 50 mcg) to prevent tachycardia due to pain or anxiety, particularly during placement of intravascular catheters.

Selection of anesthetic technique — The choice of anesthetic technique is primarily guided by the requirements for the procedure, patient comorbidities, and preferences of the patient, surgeon, and anesthesiologist.

General anesthesia (GA) is necessary for many surgical procedures. Also, GA is typically selected if the patient has a strong preference due to reluctance to be awake or for patients with significant anxiety, inability to cooperate or communicate, neurocognitive dysfunction, or inability to lie supine comfortably (eg, congestive heart failure or severe chronic obstructive pulmonary disease). In addition, GA may be selected for patients who are not candidates for a neuraxial technique due to recent administration of anticoagulant medications or dual antiplatelet therapy. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

For appropriate surgical procedures (eg, lower extremity procedures), a neuraxial or regional anesthetic technique instead of or in addition to GA is often selected for patients undergoing these procedures, including those with ischemic heart disease [53]. Benefits (and risks) of neuraxial and regional anesthesia are discussed in other topics. (See "Overview of neuraxial anesthesia", section on 'General versus neuraxial anesthesia' and "Approach to the management of acute pain in adults", section on 'Regional anesthesia techniques'.)

For major open abdominal or thoracic surgery, a neuraxial anesthetic technique (eg, thoracic epidural analgesia [TEA], paravertebral block [PVB]) is often selected to supplement GA. Benefits include reduced doses of general anesthetic drugs, which may avoid their hypotensive effects, and superior postoperative analgesia compared with systemic opioids, as discussed in separate topics:

(See "Anesthesia for open abdominal aortic surgery".)

(See "Anesthesia for open pulmonary resection", section on 'Post-thoracotomy pain management'.)

In addition to providing superior postoperative analgesia compared with systemic opioids, a TEA may benefit patients with ischemic heart disease by improving myocardial oxygen balance with reduced heart rate (HR) due to cardiac sympathetic blockade and reduced preload and afterload (table 4) [54]. However, TEA has protean hemodynamic effects, including attenuation of normal cardiac reflexes and reduction in right ventricular contractility, which may not be beneficial in some individuals [54]. Although TEA has been successfully employed to treat refractory angina, it is not certain that clinical symptom relief is due to improved myocardial perfusion or placebo effect [55].

Support for selecting a neuraxial technique in addition to GA for major open abdominal or thoracic surgery comes from a meta-analysis of eight trials (1580 patients) in which participants were randomly assigned to regional anesthesia added to GA or GA alone [53]. The trials included in the meta-analysis enrolled participants of any age undergoing any type of surgical procedure; they were not limited to patients with underlying ischemic heart disease. Patients in the regional anesthesia group had lower rates of myocardial infarction at 30 days (4 versus 6 percent); however, the difference was not statistically significant (relative risk [RR] 0.69, 95% CI 0.44-1.09). Mortality rates at 30 days were similar in both groups (3.9 versus 3.8 percent).

Local anesthesia with monitored anesthesia care — Key issues during monitored anesthesia care (MAC) are to avoid tachycardia and hypertension caused by pain and/or anxiety to avoid hemodynamic changes that increase myocardial oxygen (O2) demand and/or decrease myocardial O2 supply (see 'Prevention of ischemia' above). Small doses of short-acting agents are typically administered to provide analgesia, anxiolysis, and/or sedation. These agents and other details are discussed separately. (See "Monitored anesthesia care in adults", section on 'Drugs used for sedation and analgesia for monitored anesthesia care'.)

Neuraxial anesthesia — The goal of neuraxial anesthesia is to produce adequate anesthesia during the intraoperative period and/or analgesia in the postoperative period without inducing hypotension that will compromise myocardial O2 balance.

Neuraxial anesthesia can decrease cardiac preload due to sympathetic blockade, with resultant hypotension. This is more likely to occur in patients with intravascular volume depletion or in those with heart failure and diastolic dysfunction who are dependent upon adequate preload. In these patients, we employ a modified neuraxial anesthetic technique (eg, a low-dose combined spinal-epidural with or without intrathecal opioids, a slowly titrated epidural or continuous spinal anesthetic). During onset of the block, fluid is judiciously administered to prevent hypotension. However, we avoid overhydration and/or rapid administration of large fluid boluses in patients with symptomatic heart failure. Reduced volumes of crystalloid and slower administration are appropriate (eg, administration in 250 mL increments as needed, with monitoring of the patient's hemodynamic and clinical response to each increment).

A vasopressor is often necessary to restore blood pressure (BP) to near-baseline levels. Significant hypotension is rapidly corrected by administering an alpha1 receptor agonist (eg, phenylephrine 40 to 100 mcg) and/or a direct/indirect sympathomimetic with beta and alpha agonist effects (eg, ephedrine 5 to 10 mg), with repeated doses as needed. (See 'Treatment of ischemia' above.)

Further details regarding neuraxial anesthetic techniques are available in a separate topic. (See "Overview of neuraxial anesthesia".)

General anesthesia

Induction — For induction and tracheal intubation, a reasonable approach is induction with a short-acting hypnotic (eg, low dose of propofol [approximately 1 mg/kg] or etomidate) combined with a small dose of an opioid (eg, fentanyl 1 to 2 mcg/kg) and lidocaine 50 to 100 mg to blunt the sympathetic response to laryngoscopy and intubation (see "General anesthesia: Intravenous induction agents"), as well as a neuromuscular blocking agent (NMBA).

Advantages and disadvantages of specific sedative-hypnotic induction agents include:

PropofolPropofol is the most commonly used IV induction agent. Propofol and most other anesthetic induction agents decrease systemic BP by attenuating sympathetic tone (ie, decreasing systemic vascular resistance [SVR]), increasing venous pooling (reducing venous return), and/or direct depression of myocardial contractility. To minimize hypotension, the initial propofol induction dose is reduced to approximately 1 mg/kg, and bolus injections may be administered in divided doses in older patients and others susceptible to developing hypotension (eg, patients with intravascular volume depletion and patients with diastolic dysfunction who are dependent upon adequate preload) [56,57]. Also, small doses of an alpha1 receptor agonist (eg, phenylephrine 40 to 100 mcg) can be administered prophylactically or following propofol induction to avoid or minimize hypotension. If tachycardia or hypertension owing to inadequate anesthesia develops, this can be rapidly treated with additional anesthetic agents or esmolol. (See "General anesthesia: Intravenous induction agents", section on 'Propofol' and "Anesthesia for the older adult", section on 'Intravenous anesthetic and adjuvant agents'.)

EtomidateEtomidate is an alternative induction agent that may be selected for patients with known severe cardiomyopathy, cardiogenic shock, or hemodynamic instability because it has minimal hemodynamic side effects [56]. Concerns with etomidate include transient inhibition of cortisol biosynthesis in critically ill patients [58]. However, the preponderance of evidence suggests that etomidate is not harmful if used as a single dose to induce anesthesia. (See "General anesthesia: Intravenous induction agents", section on 'Etomidate' and "Induction agents for rapid sequence intubation in adults for emergency medicine and critical care", section on 'Etomidate'.)

Ketamine – We avoid ketamine in most patients with ischemic heart disease because administration typically causes significant increases in HR, mean BP, and plasma epinephrine levels due to centrally mediated sympathetic nervous system stimulation. The increased HR is particularly undesirable. However, for patients with ischemic heart disease and coexisting cardiomyopathy with low ejection fraction <30 percent, a low-normal dose of ketamine (eg, 1 mg/kg) may be selected to prevent any decrease in SVR and coronary perfusion pressure. (See 'Prevention of ischemia' above and "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

Maintenance — Maintenance of GA may be with a volatile anesthetic agent (eg, sevoflurane, isoflurane, desflurane), a total intravenous anesthetic (TIVA) technique, or a combination of volatile and IV agents [1,3]. (See "Maintenance of general anesthesia: Overview".)

Limited data compare inhalation versus IV anesthetic techniques during noncardiac surgery [59,60]. The benefits of volatile inhalation anesthesia in cardiac surgery are discussed separately. (See "Anesthesia for cardiac surgery: General principles", section on 'Maintenance techniques'.)

Nitrous oxide (N2O) may be used to supplement TIVA or as part of an inhalation anesthetic technique. N2O causes mild myocardial depression, sympathetic nervous system stimulation, and increased pulmonary vascular resistance. In a large, randomized trial of 7112 patients undergoing major non-cardiac surgery, 3569 patients received N2O, while 3509 patients received none [61]. The primary composite outcome of death or cardiovascular complications (non-fatal myocardial infarction [MI], stroke, pulmonary embolisms, or cardiac arrest) was similar in each group. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Nitrous oxide'.)

Emergence — During emergence, sympathetic stimulation caused by excitement and pain, as well as by stimulation of airway reflexes during tracheal extubation, may result in tachycardia, hypertension, and myocardial ischemia. These hemodynamic changes are controlled by optimizing analgesia prior to emergence (eg, by administering a systemic opioid or a dose of local anesthetic via an existing epidural catheter), or with bolus doses of an IV beta blocker (eg, esmolol, labetalol, metoprolol) or vasodilating agent (eg, labetalol, nicardipine, nitroglycerin) as needed to treat these responses during and immediately after emergence and extubation.

POSTOPERATIVE MANAGEMENT

Monitoring for myocardial injury — Most perioperative myocardial injury occurs during the postoperative period [1]. For patients with high-risk ischemic heart disease (table 1), reasonable precautions include continuous multi-lead electrocardiography (ECG) monitoring in the post-anesthesia care unit (PACU) and subsequently in an intensive care unit (ICU) or stepdown unit so that evidence of ischemia can be detected [5]. Tachycardia, hypotension, and hypertension are avoided and promptly treated [2,62,63].

In addition, all patients with symptoms or ECG changes suggestive of myocardial ischemia or infarction (MI), as well as asymptomatic patients with high cardiac risk, should be monitored for myocardial injury with cardiac troponin (cTn) measurements and 12-lead ECGs (table 1 and algorithm 2) [5,64,65]. The 2021 American Heart Association scientific statement on the diagnosis and management of patients with myocardial injury after noncardiac surgery states that hospitalized "high-risk individuals having noncardiac surgery should have serial cTn measurements during the first 48 to 72 hours postoperatively" [5]. Although increased troponin levels indicate increased risk, controversy regarding appropriate subsequent interventions remains [66]. Detailed discussion is available in a separate topic. (See "Perioperative myocardial infarction or injury after noncardiac surgery".)

Managing pain — Effective postoperative pain management is important to avoid stress responses with adverse hemodynamics and hypercoagulable states [1]. Agents and techniques for managing acute postoperative pain are discussed separately. (See "Approach to the management of acute pain in adults".)

Notably, nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors are avoided in patients with myocardial ischemia as these agents carry a boxed warning regarding cardiovascular risk [3]. (See "NSAIDs: Adverse cardiovascular effects".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Perioperative cardiovascular evaluation and management".)

SUMMARY AND RECOMMENDATIONS

Preanesthetic consultation

Evaluation – Patients with ischemic heart disease (IHD) have increased risk for perioperative myocardial injury and life-threatening arrhythmias after noncardiac surgery, particularly after recent myocardial infarction (MI) or percutaneous coronary intervention, and during certain high-risk or emergency surgical procedures (table 1 and table 2 and table 3). Baseline resting 12-lead electrocardiogram (ECG) and cardiac troponin (cTn) level are obtained. (See 'Identifying patients with increased cardiac risk' above and 'Assessing preoperative studies' above.)

Medication management – Chronically administered beta blockers, statins, clonidine, calcium channel blockers, and digoxin are continued in the perioperative period. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may be held on the morning of surgery if large perioperative fluid shifts are anticipated. Administration of aspirin and other antiplatelet agents in the preoperative period depends upon specific patient and surgical factors. (See 'Managing perioperative medications' above and "Perioperative medication management".)

Monitoring for myocardial ischemia (see 'Monitoring for myocardial ischemia' above):

Continuous ECG monitoring, ideally with computerized ST-segment analysis

Intra-arterial catheterization for early detection of intraoperative hypotension when significant BP changes are expected, to assess fluid responsiveness (figure 1), guide management of vasoactive drugs, and facilitate measurements of blood gases

Central venous catheterization (CVC) when significant blood loss, large fluid shifts, or the need to administer vasoactive drugs is likely

Transesophageal echocardiography (TEE) to detect regional wall motion abnormalities (RWMAs) indicating myocardial ischemia (figure 2 and figure 3), ventricular dysfunction (movie 2), hypovolemia (movie 1), or other causes of hemodynamic instability

It is not necessary to place a pulmonary artery catheter since intraoperative changes in pulmonary artery pressure or pulmonary artery wedge pressure are poor predictors of myocardial ischemia

Goals during intraoperative management – Optimize myocardial oxygen (O2) supply and minimize O2 demand by maintaining the following parameters (table 4) (see 'Prevention of ischemia' above and 'Treatment of ischemia' above):

Low to normal heart rate (HR) of 50 to 80 beats/minute (bpm), with treatment of tachycardia and other arrhythmias

Normal to high blood pressure (BP) within 20 percent of baseline (typically a mean arterial BP 75 to 95 mmHg and/or diastolic BP 65 to 95 mmHg)

Normal left ventricular end-diastolic volume (LVEDV) with avoidance of fluid overload

Normal to high peripheral oxygen saturation (SpO2) ≥95 percent and adequate Hgb levels (avoiding anemia <7 to 8 g/dL).

Normothermia with avoidance of hypo- or hyperthermia

Anesthetic choices – The choice of anesthetic technique is guided primarily by the requirements for the procedure, patient comorbidities, and preferences of the patient, surgeon, and anesthesiologist. For appropriate surgical procedures (eg, lower extremity procedures), a neuraxial or regional anesthetic technique instead of or in addition to general anesthesia (GA) is often selected for any patient. For those undergoing major open abdominal or thoracic surgery, a neuraxial technique (eg, thoracic epidural analgesia [TEA], paravertebral block [PVB]) is often selected in addition to GA to provide superior postoperative analgesia compared with systemic opioids. TEA may also benefit patients with IHD by improving myocardial oxygen balance with reduced HR due to cardiac sympathetic blockade and reduced preload and afterload. (See 'Selection of anesthetic technique' above.)

Local anesthesia with monitored anesthesia care – Typically, small doses of short-acting agents are administered to provide analgesia, anxiolysis, and/or sedation to avoid tachycardia and hypertension caused by pain and/or anxiety. (See 'Local anesthesia with monitored anesthesia care' above.)

Neuraxial anesthesia – During onset of a neuraxial block, crystalloid is administered in 250 mL increments to prevent hypotension. Immediate correction of hypotension by administering boluses of a vasopressor agent (eg, phenylephrine 40 to 100 mcg and/or ephedrine 5 to 10 mg) is often necessary. (See 'Neuraxial anesthesia' above.)

General anesthesia

-Induction – A reasonable approach is induction with a short-acting hypnotic (eg, low dose of propofol or etomidate) combined with a moderate dose of an adjuvant agent such as an opioid and/or lidocaine to blunt the sympathetic response to laryngoscopy and intubation. (See 'Induction' above and "General anesthesia: Intravenous induction agents".)

-Maintenance A volatile anesthetic agent (eg, sevoflurane, isoflurane, desflurane), a total intravenous anesthetic (TIVA) technique, or a combination of these agents with or without nitrous oxide (N2O) may be selected. (See 'Maintenance' above.)

-Emergence Tachycardia and hypertension during emergence from anesthesia are prevented or controlled by optimizing analgesia (eg, with systemic opioid or local anesthetic administered via an existing epidural catheter). Intravenous (IV) beta blockers (eg, esmolol, labetalol, metoprolol) or vasodilating agents (eg, labetalol, nitroglycerin, nicardipine) are administered if necessary. (See 'Emergence' above.)

Postoperative management

Monitoring and managing myocardial ischemia Tachycardia, hypotension, and hypertension are avoided or promptly treated. In patients with symptoms or ECG changes suggestive of ischemia or MI, as well as asymptomatic patients with high cardiac risk (table 1 and algorithm 2), serial cTn measurements are obtained. (See 'Monitoring for myocardial injury' above.)

Managing pain Agents and techniques for management of acute postoperative pain are discussed separately. (See "Approach to the management of acute pain in adults".)

Nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors are avoided. (See "NSAIDs: Adverse cardiovascular effects".)

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Topic 90616 Version 47.0

References

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