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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: Aug 2023.
This topic last updated: Feb 14, 2022.

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

This topic will review the preanesthesia consultation, anesthetic care, and immediate postoperative management of patients with ischemic heart disease having elective, urgent, or emergency noncardiac surgery. Anesthetic management of patients with ischemic and nonischemic heart failure is discussed in detail separately (see "Intraoperative management for noncardiac surgery in patients with heart failure"). Preoperative medical evaluation and management of patients with known or suspected ischemic heart disease is addressed elsewhere. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Management of cardiac risk for noncardiac surgery".)

PREANESTHESIA CONSULTATION

Evaluation and management of high cardiac risk — 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".)

Risk of perioperative myocardial injury is related to individual patient factors as well as the type of surgical procedure [4,5]. Mortality risk was associated with peak troponin level in older patients with myocardial injury after hip fracture repair surgery, including short-term (before 28 days), intermediate-term (before 180 days), and long-term (before 365 days) postoperative mortality [6]. Postoperative acute coronary syndrome (ACS) confers particularly high risk for mortality [7]. 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 postoperative ACS with a short-term mortality of 19.3 percent [8]. Further discussion is available in other topics (table 1 and algorithm 1). (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Management of cardiac risk for noncardiac surgery".)

Special considerations guide perioperative management for the following subgroups of patients with ischemic heart disease:

Recent myocardial infarction or unstable angina – Patients with recent (<60 days) myocardial infarction (MI) or unstable angina are at very high risk for major cardiovascular outcome. 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 high risk for adverse cardiovascular outcome even when receiving perioperative antiplatelet therapy, and are also at high risk for major bleeding events [9]. 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) [10]. Reinitiating dual anti-platelet inhibitors (DAPT) <48 hours after surgery was associated with risk of postoperative bleeding (odds ratio [OR] 4.51, 95% CI 1.56-13.0). (See "Noncardiac surgery after percutaneous coronary intervention", section on 'Our approach'.)

Urgent or emergency surgery – If urgent or emergency surgery is necessary in a patient with ischemic heart disease, preoperative consultation with a cardiologist is useful in decision-making regarding management strategies. (See "Management of cardiac risk for noncardiac surgery", section on 'For urgent or emergency surgery'.)

If urgent or emergency surgery is performed after recent administration of antiplatelet drugs, platelet transfusion may be necessary to treat excessive bleeding. However, platelets should not be administered on a prophylactic basis. (See "Inherited platelet function disorders (IPFDs)", section on 'Platelet transfusion'.)

High-risk surgical procedure – Classic surgical risk categories predicting major adverse cardiovascular events, 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) [11]. However, patient-dependent and procedure-dependent risk factors exist within these categories (table 3) [8,12]. (See "Preoperative evaluation for anesthesia for noncardiac surgery", section on 'Surgical risk' and "Perioperative myocardial infarction or injury after noncardiac surgery", section on 'Predictors'.)

Preoperative medication management

Beta blockers – 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, in order to minimize tachycardia or ischemia [1,2,13,14]. In a large retrospective study, perioperative withdrawal of beta blockers was associated with increased risk for mortality within 48 hours after noncardiac surgery (odds ratio [OR] 3.61, 95% CI 1.75-7.35), albeit with a reduced need for vasopressor infusion in the early postoperative period and a lower likelihood of prolonged stay in the post-anesthesia care unit (3829 cases withdrawn from beta blocker therapy versus 15,316 cases with therapy continued) [15]. In another large study, 1924 patients who resumed beta blockers by the end of the first postoperative day after noncardiac surgery had a lower incidence of atrial fibrillation compared with 973 propensity-matched patients who had not resumed their beta blockers by that time (4.9 versus 7 percent; OR 0.69, 95% CI 0.50-0.95) [16]. However, beta blockers are not initiated prophylactically in the preoperative period unless recommended by a consulting cardiologist based on strong indications as this practice has been associated with increased risk of non-fatal stroke [14]. 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. A consultant cardiologist may recommend initiation of statin therapy in previously untreated patients [1,2,13]. (See "Management of cardiac risk for noncardiac surgery", section on 'Statins'.)

Aspirin – The decision to stop aspirin before non-cardiac surgery must balance the risk for coronary thrombosis versus the risk for surgical bleeding. Although risk of perioperative bleeding is small in patients taking aspirin for primary or secondary prevention of cardiovascular disease, the dose can be held for five to seven days before noncardiac surgery in most cases [17,18]. (See "Management of cardiac risk for noncardiac surgery", section on 'Antiplatelet therapy'.)

Notably, the approach to continuing perioperative antiplatelet administration differs in certain circumstances:

Patient-specific circumstances:

-Secondary prevention of cardiac events during noncardiac cardiovascular surgery such as carotid or peripheral vascular surgery. (See "Carotid endarterectomy", section on 'Antiplatelet therapy' and "Management of chronic limb-threatening ischemia".)

-Need for dual anti-platelet therapy (aspirin plus a P2Y12 receptor blocker, such as clopidogrel, prasugrel, or ticagrelor) after PCI. If a patient has received a bare metal stent (BMS) or drug eluting stent (DES) and must undergo noncardiac surgery necessitating discontinuation of the P2Y12 inhibitor, aspirin should be continued if possible [1]. (see "Noncardiac surgery after percutaneous coronary intervention", section on 'Our approach')

Procedure-specific circumstances – Consultation should be obtained with the surgeon/proceduralist, cardiologist, and/or neurologist about thrombosis versus bleeding risk. For selected procedures, discontinuation of antiplatelet medications is usually appropriate (eg, intracranial or spine surgery, cosmetic procedures, transurethral resection of the prostate [TURP]), with the details of timing typically determined using institutional or other guidelines as well as consultation with the surgeon and the prescribing clinician. These management decisions are discussed in a separate topic. (See "Perioperative medication management", section on 'Medications affecting hemostasis'.)

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers – Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are typically continued in the perioperative period, particularly for patients with coexisting heart failure [1,2,19]. Since these agents may cause perioperative hypotension, some clinicians administer the evening dose of an ACE inhibitor or ARB on the day before surgery but hold the morning dose on the day of surgery, particularly if large perioperative fluid shifts are anticipated [13,20,21]. ACE inhibitors and ARBs are always held in patients with hemodynamic instability, hypovolemia, or acute elevation of creatinine. Further discussion is available in another topic. (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'.)

Clonidine – Clonidine is continued if it has been chronically administered, 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'.)

Other cardiovascular medications – 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'.)

Laboratory — Preoperative screening is performed in patients with high cardiac risk (table 1); this includes a cardiac troponin level obtained at baseline, as discussed separately. (See "Perioperative myocardial infarction or injury after noncardiac surgery", section on 'Troponin'.)

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 receiving diuretic therapy chronically and in those with renal insufficiency.

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) [1,2]. 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'.)

Management of 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 ICDs and pacemakers is discussed elsewhere [23,24]. (See "Pacing system malfunction: Evaluation and management", section on 'Electromagnetic interference' and "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

ANESTHETIC GOALS — Anesthetic goals in patients with ischemic heart disease are prevention, detection, and treatment of myocardial ischemia to avoid myocardial injury [25].

Prevention of ischemia — The dominant mechanism of acute coronary syndrome in the perioperative period is demand ischemia, rather than acute coronary or stent thrombosis [26,27]. 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):

Low to normal heart rate – Maintain low to normal heart rate (HR; eg, 50 to 80 beats/minute [bpm]) [28]. Tachycardia compromises both oxygen (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 [29]. The relationship between HR and the duration of diastole is nonlinear (figure 1) [30,31].

In a large multicenter observational study of more than 16,000 noncardiac surgical patients, 7 percent sustained myocardial injury, while 2.8 percent had a myocardial infarction (MI), and 2.0 percent died within 30 days of surgery [25]. Intraoperative tachycardia with a HR >100 bpm was associated with myocardial injury (odds ratio [OR] 1.27, 95% CI 1.07-1.50) and MI (OR 1.34, 95% CI 1.05-1.70), as well as mortality (OR 2.65, 95% CI 2.06-3.41). A higher risk was noted if the duration of tachycardia exceeded 30 minutes (OR 2.22, 95% CI 1.71-2.88). Conversely, a slow HR <55 bpm was associated with reduced risk (OR 0.70, 95% CI 0.59-0.82), MI (OR 0.75, 95% CI 0.58-0.97), or mortality (OR 0.58, 95% CI 0.41-0.81) [25]. The investigators also noted a trend toward decreasing likelihood of myocardial injury with increasing duration of slow recorded HR <55 bpm.

Normal to high-normal blood pressure – Maintain blood pressure (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.

Prompt treatment of arterial hypotension is warranted to avoid supply-mediated ischemia [32,33]. 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 [34]. 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.

However, hypertension 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.

A minimum intraoperative systolic BP <100 mmHg was associated with myocardial injury (OR 1.21, 95% CI 1.05-1.39) and mortality (OR 1.81, 95% CI 1.39-2.37) in the large study cited above [25]. 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 MI (OR 1.34, 95% CI 1.09-1.64), suggesting that both low and high BP extremes should be avoided [25].

Normal left ventricular end-diastolic volume – Avoid left ventricular (LV) distention caused by fluid overload, as this may increase systolic wall stress and myocardial O2 demand. Although central venous pressure or pulmonary artery pressures are used as surrogates to estimate LV volume, these measurements have limitations [35-37]. (See 'Monitoring for myocardial ischemia' below.)

Adequate arterial O2 content – Maintain normal to high hemoglobin (Hgb) O2 saturation and maintain adequate Hgb levels. (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells'.)

Normothermia – Avoid hypothermia during and after surgery. Normothermia favors tissue release of O2. Adverse consequences of hypothermia include shivering, which increases myocardial O2 demand and may result in myocardial ischemia.

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

Cardiovascular monitoring in patients with ischemic heart disease includes the following [38,39]:

Electrocardiography – All patients have continuous electrocardiography (ECG) monitoring to detect myocardial ischemia and/or arrhythmias.

Computerized ST-segment trending is superior to visual clinical interpretation in the identification of ST-segment changes [40-43], and multiple-lead monitoring is more sensitive than single-lead monitoring. Although ECG is a relatively insensitive method for intraoperative detection of myocardial ischemia [38,44], leads II and V5 detected 80 percent of all episodes detected by a 12-lead ECG in one study [44], while another study suggested that lead V4 may be even more sensitive [45].

Despite limitations in sensitivity of ECG monitoring, intraoperative and postoperative ST-segment changes are associated with cardiac morbidity and mortality after noncardiac surgery in patients at high risk for myocardial ischemia [1,39].

Intra-arterial catheter Invasive measurement of arterial BP is employed when significant BP changes are anticipated during the surgical procedure and rapid detection is vital. These conditions apply to patients with severe coronary artery disease, cardiomyopathy, or hemodynamic instability, as well as to patients with chronic coronary syndrome, also referred to as stable ischemic heart disease, who are undergoing a major procedure that is likely to cause rapid blood loss or large fluid shifts. Direct arterial BP monitoring is superior to indirect monitoring techniques for the early detection of intraoperative hypotension [46,47]. Ideally, the intra-arterial catheter is inserted prior to induction of anesthesia.

In addition, an intra-arterial catheter is useful to guide management of vasoactive drugs and facilitate sampling of arterial blood for measurements of blood gases and other laboratory values throughout the perioperative period.

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 [36,48,49]. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

Pulmonary artery catheter – We do not recommend inserting a pulmonary artery catheter (PAC) for detection of myocardial ischemia [1,2]. Intraoperative changes in pulmonary artery or pulmonary artery wedge pressures are poor predictors of myocardial ischemia compared with ECG or transesophageal echocardiographic monitoring [50]. Furthermore, there appears to be no benefit and possible harm from perioperative PAC use in most patients undergoing either cardiac or noncardiac surgery [37,51-53].

In a few selected patients with severe cardiovascular conditions significantly affecting hemodynamics, PAC insertion may be reasonable to monitor pulmonary artery pressure, cardiac output, and mixed venous Hgb saturation (SvO2). The decision is based upon both the significance of the cardiovascular condition (eg, severe cardiomyopathy or valvular lesions), the 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 transesophageal echocardiography (TEE) monitoring may be useful to detect new regional wall motion abnormalities in patients at high risk, particularly those undergoing major surgery [38]. TEE monitoring has higher sensitivity for detecting myocardial ischemia than ECG or PAC monitoring [54-58]. However, there are no data demonstrating that TEE monitoring can decrease the incidence of adverse perioperative cardiovascular events [1,59,60]. (See "Intraoperative transesophageal echocardiography for noncardiac surgery".)

Emergency use of intraoperative or perioperative TEE is indicated to determine the cause of any unexplained persistent or life-threatening circulatory instability ("rescue echo") [61]. TEE may identify hypovolemia, left and/or right ventricular dysfunction, pericardial effusion or cardiac tamponade, valvular stenosis or regurgitation, pulmonary embolism, or left ventricular outflow tract obstruction [61]. (See "Intraoperative rescue transesophageal echocardiography (TEE)".) As an alternative to TEE assessment, transthoracic focused cardiac ultrasound can be considered for assessment of most of these potentially life threatening conditions [62]. (See "Overview of perioperative uses of ultrasound", section on 'Point-of care ultrasound (POCUS)' and "Overview of perioperative uses of ultrasound", section on 'Transthoracic echocardiography'.)

Treatment of ischemia — The decision to treat intraoperative myocardial ischemia is typically based on observing characteristic ST-segment changes on the ECG, most commonly new horizontal or downsloping ST-segment depressions. In addition, new ventricular regional wall motion abnormalities identified with echocardiography should be considered to indicate myocardial ischemia that should be treated. In such patients, treatment of tachycardia is usually the first step. If ischemic ECG or echocardiographic changes persist, administration of nitroglycerin is often effective. It is reasonable to use the combination of nitroglycerin and phenylephrine, the latter titrated to maintain normal arterial BP [63,64].

The following interventions optimize myocardial O2 supply and minimize myocardial O2 demand in patients who develop intraoperative myocardial ischemia [32]:

Treat tachycardia – Intraoperative tachycardia (or even heart rate [HR] exceeding 80 bpm) caused by pain or inadequate anesthesia is treated by administering a dose of an intravenous anesthetic (eg, propofol) or an opiate, or by deepening an inhaled general anesthetic. If an epidural catheter is in place, an additional dose of local anesthetic can be provided to deepen anesthesia. If these measures are not effective in decreasing HR, an intravenous beta blocker (eg, esmolol, metoprolol, or labetalol) is administered, whether or not there is evidence of ischemia.

Treat hypertension – Increases in BP caused by pain or inadequate anesthesia are treated by administering a dose of an intravenous anesthetic (eg, propofol) or an opiate, by deepening general anesthesia with an inhaled anesthetic, or by administering additional local anesthetic through an epidural catheter. 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. (See "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents'.)

For hypertensive patients who develop persistent myocardial ischemia during the intraoperative period, an intravenous nitroglycerin infusion is titrated (at 10 to 200 mcg/minute; 0.1 to 3 mcg/kg/minute) to control BP (table 5). Nitroglycerin causes coronary arterial vasodilation of the large epicardial conductance vessels and decreases left ventricular (LV) preload due to venodilation. These benefits must be weighed against the risk of hypotension and the potential for tachycardia. The additive vasodilatory effects of certain anesthetic agents and nitroglycerin may lead to significant hypotension and worsening myocardial ischemia. Thus, addition of a phenylephrine infusion (at 10 to 200 mcg/minute; 0.1 to 2 mcg/kg/minute) may be necessary to maintain adequate BP (table 6). An intra-arterial catheter for continuous BP monitoring is desirable during titration of a continuous infusion of nitroglycerin.

Prophylactic intravenous nitroglycerin is not administered, as it is not effective in reducing myocardial ischemia in patients undergoing noncardiac surgery [1,2,65]. 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 giving intravenous fluid (see "Intraoperative fluid management"). 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).

Vasoplegia (ie, severe or refractory hypotension with low systemic vascular resistance [SVR]) due to factors such as prior administration of angiotensin-converting enzyme (ACE) inhibitors or septic shock is treated 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 6) [66]. Other agents may be employed to treat refractory hypotension if necessary (table 7). (See "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

Inotropic support may be needed for treatment of persistent hypotension caused by left or right ventricular dysfunction. Commonly employed agents include epinephrine, norepinephrine, or dopamine (at 5 to 20 mcg/kg/minute) (table 6). An intra-arterial catheter for continuous BP monitoring is necessary during titration of potent inotropic and vasopressor infusions.

Treat low O2 saturation or anemia – Administer supplemental O2 to achieve a Hgb O2 saturation ≥95 percent and treat anemia to maintain adequate Hgb levels at ≥7 to 8 g/dL. We typically use a higher Hgb threshold (<9 g/dL) to guide transfusion in patients known to have acute coronary syndrome or signs of myocardial or other organ ischemia, particularly with ongoing bleeding during high-risk noncardiac surgery. Detailed discussion is available in a separate topic.

Prevent and treat hypothermia – Warm fluids and blood prior to administration. Blankets and forced-air devices should be used for active warming and avoidance of hypothermia.

MANAGEMENT OF ANESTHESIA

Premedication — Regardless of the anesthetic technique that is selected, pain or anxiety causing tachycardia and hypertension in the preoperative period is treated (see 'Prevention of ischemia' above). If the patient is in a monitored setting, midazolam 1 to 2 mg is often used shortly before (within 30 to 60 minutes) or during induction of general anesthesia as an adjunct to alleviate anxiety. However, since midazolam may cause mild decreases in systemic blood pressure (BP) and cardiac output [67], the dose is reduced or eliminated in hypovolemic patients and in older adult patients. Similarly, small doses of an opioid (eg, fentanyl 25 to 50 mcg) may be administered to treat preoperative pain in a monitored setting, with care to avoid respiratory depression. (See "Anesthesia for the older adult", section on 'Selection and dosing of anesthetic agents'.)

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

For major open abdominal or thoracic surgery, a neuraxial technique in addition to general anesthesia is preferred, unless contraindicated or refused by the patient. In patients undergoing open abdominal aortic surgery, a 2016 systematic review showed that addition of epidural analgesia to general anesthesia reduced risk of postoperative myocardial infarction (MI) as well as respiratory failure, and provided superior pain relief compared with systemic opioid-based analgesia, but there was no difference in mortality (1498 patients; 15 trials) [68]. In patients undergoing any type of surgery (minor as well as major procedures), a 2014 overview of nine systematic reviews of randomized controlled clinical trials summarized outcomes with use of neuraxial analgesia (with or without general anesthesia) compared with general anesthesia alone [69]. Use of neuraxial blockade alone reduced risk of postoperative pneumonia and 30-day mortality compared with general anesthesia alone, but there was no reduction in risk for MI.

Use of neuraxial anesthetic techniques may provide superior postoperative analgesia compared with systemic opioids. Thoracic epidural anesthesia (TEA) may improve myocardial oxygen balance by reducing heart rate due to cardiac sympathetic blockade, as well as by reducing preload and afterload (table 4) [70]. 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 [70]. 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 [71].

We do not place neuraxial needles or catheters in patients currently receiving anticoagulant drugs or antiplatelet therapy (other than aspirin alone) because of increased risk for spinal epidural hematoma (SEH). Neuraxial needle or catheter placement may be employed in patients who will subsequently require intraoperative anticoagulation with intravenous heparin (eg, AAA surgery). There is extensive experience with the safe use of therapeutic intraoperative unfractionated heparin in patients with epidural catheters when the heparin was given at least one hour after needle or catheter insertion into the neuraxial space [72]. Subsequent removal of a neuraxial catheter, usually in the postoperative period, should occur only after restoration of normal coagulation status for several hours. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

Further discussion regarding choice of anesthetic and analgesic techniques is available in separate topics:

(See "Approach to the management of acute pain in adults", section on 'Creating a plan for analgesia'.)

(See "Anesthesia for open abdominal aortic surgery", section on 'Postoperative pain management'.)

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

Local anesthesia with monitored anesthesia care — For patients with ischemic heart disease receiving monitored anesthesia care (MAC), key issues are avoidance of tachycardia and hypertension caused by pain and/or anxiety, because these hemodynamic changes increase myocardial oxygen demand and/or decrease myocardial oxygen supply (see 'Prevention of ischemia' above). Thus, small doses of short-acting agents (eg, midazolam, opioids, propofol) are administered to provide analgesia, anxiolysis, and/or sedation. Detection of hypotension or hypoventilation with resultant hypoxemia and hypercarbia with adverse effects on pulmonary artery pressure is particularly important.

Neuraxial anesthesia — The goal of neuraxial anesthesia in appropriate candidates (eg, those who are not receiving antiplatelet and anticoagulant medications and who consent to the procedure) is to produce adequate anesthesia during the intraoperative period and/or analgesia in the postoperative period without inducing hypotension that will compromise myocardial oxygen 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, or a slowly titrated epidural 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 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.)

General anesthesia

Induction — The goal of general anesthetic induction is to produce unconsciousness, amnesia, analgesia, muscle relaxation, and attenuation of the hemodynamic responses to intubation and surgical stimulation, while at the same time avoiding hemodynamic changes that would lead to myocardial oxygen imbalance and ischemia. (See 'Prevention of ischemia' above.)

When tracheal intubation is planned, a reasonable approach is induction with a short-acting hypnotic (eg, low dose of propofol [approximately 1 mg/kg]) 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"). If tachycardia develops, this can be rapidly treated with esmolol. Also, a muscle relaxant is administered to facilitate laryngoscopy.

Propofol is the most commonly used intravenous induction agent. In contrast to etomidate, propofol and most other anesthetic induction agents decrease systemic blood pressure (BP) by some combination of attenuated sympathetic tone (ie, decreased systemic vascular resistance [SVR]), increased venous pooling (reducing venous return), and/or direct depression of myocardial contractility. Thus, in order to minimize hypotension, the initial propofol induction dose is reduced to approximately 1 mg/kg or less, 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) [73,74]. Small doses of an alpha1 receptor agonist (eg, phenylephrine 40 to 100 mcg) can be given prophylactically or, if hypotension develops, following propofol induction. (See "General anesthesia: Intravenous induction agents", section on 'Propofol' and "Anesthesia for the older adult", section on 'Intravenous anesthetic and adjuvant agents'.)

Because it has minimal hemodynamic side effects, etomidate is an alternative anesthetic induction agent for patients with known severe cardiomyopathy, cardiogenic shock, or hemodynamic instability [73]. A possible concern with the use of etomidate is that it inhibits the biosynthesis of cortisol, an effect that lasts <24 hours following a single dose [75-80] (see "Causes of primary adrenal insufficiency (Addison disease)", section on 'Adverse effect of medications'). The clinical significance of this finding is uncertain [75,79,81]. (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'.)

We typically avoid ketamine in patients with ischemic heart disease because administration usually results in significant increases in heart rate, mean arterial pressure, and plasma epinephrine levels due to centrally mediated sympathetic nervous system stimulation. The increased heart rate, in particular, is undesirable. Some clinicians select a combination of induction agents in patients with ischemic heart disease and coexisting cardiomyopathy, with administration of ketamine 30 to 60 mg and a low dose of propofol 20 to 30 mg to produce unconsciousness while maintaining coronary perfusion, and esmolol 20 to 40 mg is coadministered to prevent tachycardia. (See 'Prevention of ischemia' above and "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

When a non-depolarizing neuromuscular blocking agent is chosen, anesthetic depth is maintained or deepened with a potent inhaled anesthetic (eg, sevoflurane or isoflurane) while waiting the few minutes for adequate muscle paralysis to perform tracheal intubation.

Maintenance — General anesthesia may be maintained with a volatile anesthetic agent, a total intravenous anesthetic (TIVA) technique, or most typically with a combination of volatile and intravenous agents [1,2,65]. For example, if a volatile anesthetic (eg, sevoflurane, isoflurane, or desflurane) is selected as the primary agent, doses of an opioid and/or other intravenous (IV) adjuvant agents (eg, propofol, neuromuscular blocking agent [NMBA]) are typically administered to supplement and reduce the total required dose of the inhalation agent, since a predominant effect of volatile anesthetics is dose-dependent vasodilation with resultant decreases in SVR and BP. Only limited data comparing anesthetic techniques for noncardiac surgery are available [82,83]. The benefits of volatile inhalation anesthesia in cardiac surgery are discussed separately. (See "Management of cardiopulmonary bypass", section on 'Anesthetic agents'.)

In the large, randomized ENIGMA-II trial, 7112 patients undergoing major non-cardiac surgery were randomized to receive nitrous oxide (3569 patients) or none (3509 patients). The primary outcome of composite death and cardiovascular complications (non-fatal MI, stroke, pulmonary embolisms, or cardiac arrest) did not differ between the groups [84]. (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 stimulation of airway reflexes during tracheal extubation, increase the potential for tachycardia and hypertension. This may lead to myocardial ischemia. These hemodynamic changes are controlled by optimizing analgesia prior to emergence (eg, by administering a systemic opioid or doses of local anesthetic via an existing epidural catheter) and/or by administering bolus doses of intravenous beta blockers (eg, esmolol, labetalol, or metoprolol) and/or vasodilating agents (eg, labetalol, nicardipine, or nitroglycerin) during and immediately after emergence and extubation.

Management of arrhythmias — Arrhythmias are not uncommon in patients with ischemic heart disease. Management of specific cardiac arrhythmias is the same as in other settings and is discussed in detail separately (see "Advanced cardiac life support (ACLS) in adults", section on 'Management of specific arrhythmias'). Potential reversible causes are investigated (eg, electrolyte abnormalities, acid-base disturbances, hypoxemia, direct cardiac irritation from a central venous catheter, myocardial ischemia). Intraoperative management of serious arrhythmias is summarized below:

Ventricular fibrillation – Ventricular fibrillation or ventricular tachycardia is life-threatening and requires immediate defibrillation or cardioversion. If the arrhythmia recurs, antiarrhythmic therapy, particularly amiodarone, may be effective. (See "Advanced cardiac life support (ACLS) in adults", section on 'Pulseless ventricular tachycardia and ventricular fibrillation'.)

Atrial fibrillation – Atrial fibrillation is a common arrhythmia, particularly in patients with underlying heart disease. In patients who are hemodynamically unstable (eg, myocardial ischemia, hypotension, pulmonary edema) due to atrial fibrillation with a rapid ventricular response, treatment options include intravenous rate control medications and/or cardioversion. Administration of rapidly acting drugs such as esmolol, diltiazem, or amiodarone may control ventricular rate. However, if the atrial fibrillation is associated with hypotension or evidence of cardiogenic shock, or it is clearly the cause of pulmonary edema, immediate cardioversion to restore sinus rhythm may be necessary. (See "Atrial fibrillation: Cardioversion" and "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy" and "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy", section on 'Determining urgency'.)

Decisions regarding long-term anticoagulation are made in consultation with the cardiologist in the early postoperative period, after the patient has been stabilized. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation".)

Bradycardia – Severe bradycardia (eg, heart rate <40 beats/minute [bpm]) may result in signs and symptoms of inadequate perfusion (eg, hypotension, altered mental status) and is usually treated with glycopyrrolate, atropine, or ephedrine, while preparations are made for transcutaneous pacing and/or a potent chronotropic agent (eg, epinephrine) (see "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia'). Administration of atropine, ephedrine, or epinephrine may cause tachycardia, which is undesirable in the setting of myocardial ischemia, but may be further managed following treatment of severe bradycardia.

Control of glucose — We maintain perioperative glucose <180 mg/dL (<10 mmol/L) in patients with ischemic heart disease and take care to avoid hypoglycemic episodes. Although hyperglycemia is associated with an approximately two- to fourfold increased risk of a myocardial ischemic event in vascular and other noncardiac surgery [85,86], hypoglycemia is also detrimental. A trial in critically ill patients showed that attempts to tightly control serum glucose (81 to 108 mg/dL [4.5 to 6.0 mmol/L]) are associated with more hypoglycemic episodes and higher mortality compared with more liberal glucose management (<180 mg/dL [<10 mmol/L]) [87]. (See "Glycemic control in critically ill adult and pediatric patients".)

POSTOPERATIVE MANAGEMENT

Monitoring for myocardial injury — Most perioperative myocardial injury occurs during the postoperative period [1]. For patients with ischemic heart disease at high cardiac risk (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 or promptly treated [3,88,89]. In addition, all patients with symptoms or ECG changes suggestive of ischemia or myocardial infarction (MI), as well as asymptomatic patients with high cardiac risk, should be monitored for myocardial injury with troponin measurements and 12-lead ECGs (table 1 and algorithm 2) [5,90,91]. 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 indicated increased risk, controversy regarding appropriate subsequent interventions remains [92]. These recommendations are discussed in detail separately.

Management of pain — Effective postoperative pain management is important to avoid stress, adverse hemodynamics, and hypercoagulable states [1]. For cooperative patients without contraindications undergoing major abdominal or thoracic surgery with a large incision, we suggest an epidural for postoperative analgesia. Alternatively, subarachnoid administration of a longer-acting opiate (eg, morphine or hydromorphone) may be administered to provide 12 to 24 hours of postoperative analgesia. However, nonselective nonsteroidal antiinflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors are avoided in patients with myocardial ischemia; these agents carry a boxed warning regarding cardiovascular risk [2] (see "NSAIDs: Adverse cardiovascular effects"). Other agents and techniques for management of postoperative pain are discussed separately. (See "Approach to the management of acute pain in adults".)

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 have increased risk for perioperative myocardial injury after noncardiac surgery, particularly after recent myocardial infarction (MI) or percutaneous coronary intervention (PCI), and during urgent or emergency surgery or certain high-risk surgical procedures (table 1 and algorithm 1). Screening for myocardial injury is performed in patients with high cardiac risk (table 1), particularly if a high-risk surgical procedure is planned (table 2 and table 3). This includes preoperative baseline cardiac troponin level and resting 12-lead electrocardiogram (ECG). (See 'Evaluation and management of high cardiac risk' above and 'Laboratory' above and 'Electrocardiogram' above.)

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

Anesthetic goals – Optimizing myocardial oxygen (O2) supply and minimizing demand are the primary anesthetic goals (see 'Prevention of ischemia' above):

Low to normal heart rate (eg, 50 to 80 beats/minute [bpm])

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) and avoidance of fluid overload

Normal to high hemoglobin saturation, normothermia, and treatment of severe anemia (ie, hemoglobin level <7 to 8 g/dL)

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

Continuous ECG monitoring, ideally with computerized ST-segment analysis .

Intra-arterial catheterization when moment-to-moment BP changes are anticipated and/or to guide management of vasoactive drugs

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

Perioperative transesophageal echocardiography (TEE) to determine the cause of unexplained persistent or life-threatening circulatory instability ("rescue echo")

We recommend against pulmonary artery catheter (PAC) catheterization for monitoring for ischemia (Grade 1B).

Treatment of ischemia (see 'Treatment of ischemia' above):

Treat tachycardia and/or hypertension caused by pain or light anesthesia by administering an opioid, deepening general anesthesia, or re-administering local anesthesia via an epidural. An intravenous (IV) beta blocker (eg, esmolol, metoprolol, labetalol) may be necessary to restore heart rate (HR) and/or BP to baseline levels, or a vasodilating agent (eg, nicardipine or nitroglycerin) may be necessary to control BP.

Treat hypotension (ie, mean BP <75 mmHg or diastolic BP <65 mmHg) by reducing excessive anesthetic depth and administering intravenous fluid and boluses of a vasopressor (eg, phenylephrine and/or ephedrine).

Persistent hypotension is treated with a titrated continuous infusion of phenylephrine or an inotropic agent if left or right ventricular dysfunction is suspected.

Correct hypoxemia (ie, hemoglobin saturation <95 percent) and severe anemia (ie, hemoglobin level <7 to 8 g/dL).

Prevent and treat hypothermia by warming fluids prior to administration and using blankets and forced-air devices.

Persistent myocardial ischemia associated with hypertension is treated with an IV nitroglycerin infusion and consideration of cardiology consultation.

Anesthetic choices – The choice of anesthetic technique should be guided primarily by the requirements for the procedure, patient comorbidities, and preferences of the patient, surgeon, and anesthesiologist. For perioperative pain control in patients undergoing major open abdominal or thoracic surgery, we suggest a neuraxial technique in addition to general anesthesia when appropriate (Grade 2C). (See 'Selection of anesthetic technique' above and 'Management of pain' above.)

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

General anesthesia

-Induction - The goal of general anesthetic induction is to attenuate hemodynamic responses to tracheal intubation (eg, tachycardia and hypertension) without causing hemodynamic changes that would lead to myocardial ischemia. A reasonable approach is induction with a short-acting hypnotic (eg, etomidate or a low dose of propofol) 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. Also, a muscle relaxant is administered to facilitate laryngoscopy. (See 'Induction' above and "General anesthesia: Intravenous induction agents".)

-Maintenance - Use of a volatile inhalational agent (eg, sevoflurane, isoflurane, or desflurane) as the primary technique or administration of total IV anesthesia (TIVA) are both reasonable choices. Nitrous oxide is also a reasonable choice (See 'Maintenance' above.)

-Emergence - Prevent or control tachycardia and hypertension during emergence from anesthesia by optimizing analgesia prior to emergence (eg, with IV opioid or doses of local anesthetic via an existing epidural catheter), and administer IV beta blockers (eg, esmolol, labetalol, or metoprolol) or vasodilating agents (eg, nicardipine or nitroglycerin) if necessary. . (See 'Emergence' above.)

Postoperative management – Postoperative screening for myocardial injury is employed in all patients with symptoms or ECG changes suggestive of ischemia or MI, as well as asymptomatic patients with high cardiac risk (table 1). This includes continuous ECG monitoring in the post-anesthesia care unit and subsequently in an intensive care unit or stepdown unit, as well as serial troponin measurements and 12-lead ECGs.

  1. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014; 130:2215.
  2. Kristensen SD, Knuuti J. New ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management. Eur Heart J 2014; 35:2344.
  3. Ruetzler K, Khanna AK, Sessler DI. Myocardial Injury After Noncardiac Surgery: Preoperative, Intraoperative, and Postoperative Aspects, Implications, and Directions. Anesth Analg 2020; 131:173.
  4. Eagle KA, McKay RE. Pre-Operative Risk Prediction: Will Better Tools Produce Better Outcomes? J Am Coll Cardiol 2019; 73:3079.
  5. Ruetzler K, Smilowitz NR, Berger JS, et al. Diagnosis and Management of Patients With Myocardial Injury After Noncardiac Surgery: A Scientific Statement From the American Heart Association. Circulation 2021; 144:e287.
  6. Vacheron CH, Hentzen J, Fauvernier M, et al. Association Between Short-, Intermediate-, and Long-term Mortality and Myocardial Injury After Noncardiac Surgery After Hip Fracture Surgery: A Retrospective Cohort. Anesth Analg 2021; 133:915.
  7. Tabit CE, Nathan S. Management of perioperative acute coronary syndromes by mechanism: a practical approach. Int Anesthesiol Clin 2021; 59:61.
  8. Mazzarello S, McIsaac DI, Beattie WS, et al. Risk Factors for Failure to Rescue in Myocardial Infarction after Noncardiac Surgery: A Cohort Study. Anesthesiology 2020; 133:96.
  9. Rodriguez A, Guilera N, Mases A, et al. Management of antiplatelet therapy in patients with coronary stents undergoing noncardiac surgery: association with adverse events. Br J Anaesth 2018; 120:67.
  10. Irie H, Kawai K, Otake T, et al. Outcomes of patients on dual antiplatelet therapy post-coronary stenting following emergency noncardiac surgery. Acta Anaesthesiol Scand 2019; 63:982.
  11. Kristensen SD, Knuuti J, Saraste A, et al. 2014 ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J 2014; 35:2383.
  12. Liu JB, Liu Y, Cohen ME, et al. Defining the Intrinsic Cardiac Risks of Operations to Improve Preoperative Cardiac Risk Assessments. Anesthesiology 2018; 128:283.
  13. Lomivorotov VV, Efremov SM, Abubakirov MN, et al. Perioperative Management of Cardiovascular Medications. J Cardiothorac Vasc Anesth 2018; 32:2289.
  14. Oprea AD, Lombard FW, Kertai MD. Perioperative β-Adrenergic Blockade in Noncardiac and Cardiac Surgery: A Clinical Update. J Cardiothorac Vasc Anesth 2019; 33:817.
  15. Kertai MD, Cooter M, Pollard RJ, et al. Is Compliance With Surgical Care Improvement Project Cardiac (SCIP-Card-2) Measures for Perioperative β-Blockers Associated With Reduced Incidence of Mortality and Cardiovascular-Related Critical Quality Indicators After Noncardiac Surgery? Anesth Analg 2018; 126:1829.
  16. Khanna AK, Naylor DF Jr, Naylor AJ, et al. Early Resumption of β Blockers Is Associated with Decreased Atrial Fibrillation after Noncardiothoracic and Nonvascular Surgery: A Cohort Analysis. Anesthesiology 2018; 129:1101.
  17. Devereaux PJ, Mrkobrada M, Sessler DI, et al. Aspirin in patients undergoing noncardiac surgery. N Engl J Med 2014; 370:1494.
  18. Columbo JA, Lambour AJ, Sundling RA, et al. A Meta-analysis of the Impact of Aspirin, Clopidogrel, and Dual Antiplatelet Therapy on Bleeding Complications in Noncardiac Surgery. Ann Surg 2018; 267:1.
  19. Zou Z, Yuan HB, Yang B, et al. Perioperative angiotensin-converting enzyme inhibitors or angiotensin II type 1 receptor blockers for preventing mortality and morbidity in adults. Cochrane Database Syst Rev 2016; :CD009210.
  20. London MJ. Preoperative Administration of Angiotensin-converting Enzyme Inhibitors or Angiotensin II Receptor Blockers: Do We Have Enough "VISION" to Stop It? Anesthesiology 2017; 126:1.
  21. Roshanov PS, Rochwerg B, Patel A, et al. Withholding versus Continuing Angiotensin-converting Enzyme Inhibitors or Angiotensin II Receptor Blockers before Noncardiac Surgery: An Analysis of the Vascular events In noncardiac Surgery patIents cOhort evaluatioN Prospective Cohort. Anesthesiology 2017; 126:16.
  22. WRITING COMMITTEE MEMBERS, Yancy CW, Jessup M, 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. Circulation 2013; 128:e240.
  23. American Society of Anesthesiologists. Practice advisory for the perioperative management of patients with cardiac implantable electronic devices: pacemakers and implantable cardioverter-defibrillators: an updated report by the american society of anesthesiologists task force on perioperative management of patients with cardiac implantable electronic devices. Anesthesiology 2011; 114:247.
  24. Crossley GH, Poole JE, Rozner MA, et al. The Heart Rhythm Society (HRS)/American Society of Anesthesiologists (ASA) Expert Consensus Statement on the perioperative management of patients with implantable defibrillators, pacemakers and arrhythmia monitors: facilities and patient management this document was developed as a joint project with the American Society of Anesthesiologists (ASA), and in collaboration with the American Heart Association (AHA), and the Society of Thoracic Surgeons (STS). Heart Rhythm 2011; 8:1114.
  25. Abbott TEF, Pearse RM, Archbold RA, et al. A Prospective International Multicentre Cohort Study of Intraoperative Heart Rate and Systolic Blood Pressure and Myocardial Injury After Noncardiac Surgery: Results of the VISION Study. Anesth Analg 2018; 126:1936.
  26. Helwani MA, Amin A, Lavigne P, et al. Etiology of Acute Coronary Syndrome after Noncardiac Surgery. Anesthesiology 2018; 128:1084.
  27. Smit M, Coetzee AR, Lochner A. The Pathophysiology of Myocardial Ischemia and Perioperative Myocardial Infarction. J Cardiothorac Vasc Anesth 2020; 34:2501.
  28. Andrews TC, Fenton T, Toyosaki N, et al. Subsets of ambulatory myocardial ischemia based on heart rate activity. Circadian distribution and response to anti-ischemic medication. The Angina and Silent Ischemia Study Group (ASIS). Circulation 1993; 88:92.
  29. Boerth RC, Covell JW, Pool PE, Ross J Jr. Increased myocardial oxygen consumption and contractile state associated with increased heart rate in dogs. Circ Res 1969; 24:725.
  30. Boudoulas H, Rittgers SE, Lewis RP, et al. Changes in diastolic time with various pharmacologic agents: implication for myocardial perfusion. Circulation 1979; 60:164.
  31. Chung CS, Karamanoglu M, Kovács SJ. Duration of diastole and its phases as a function of heart rate during supine bicycle exercise. Am J Physiol Heart Circ Physiol 2004; 287:H2003.
  32. Alkhatib CK, Rego-Cherian L, Cotter EK. Management of suspected intraoperative myocardial ischemia. Int Anesthesiol Clin 2021; 59:53.
  33. Wijnberge M, Schenk J, Bulle E, et al. Association of intraoperative hypotension with postoperative morbidity and mortality: systematic review and meta-analysis. BJS Open 2021; 5.
  34. Roshanov PS, Sheth T, Duceppe E, et al. Relationship between Perioperative Hypotension and Perioperative Cardiovascular Events in Patients with Coronary Artery Disease Undergoing Major Noncardiac Surgery. Anesthesiology 2019; 130:756.
  35. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest 2008; 134:172.
  36. Mark JB. Central venous pressure monitoring: clinical insights beyond the numbers. J Cardiothorac Vasc Anesth 1991; 5:163.
  37. Barone JE, Tucker JB, Rassias D, Corvo PR. Routine perioperative pulmonary artery catheterization has no effect on rate of complications in vascular surgery: a meta-analysis. Am Surg 2001; 67:674.
  38. Mark JB. Multimodal detection of perioperative myocardial ischemia. Tex Heart Inst J 2005; 32:461.
  39. González LS, Izquierdo DA, Davidovich RM. Definition and diagnosis of intraoperative myocardial ischemia. Int Anesthesiol Clin 2021; 59:45.
  40. Ellis JE, Shah MN, Briller JE, et al. A comparison of methods for the detection of myocardial ischemia during noncardiac surgery: automated ST-segment analysis systems, electrocardiography, and transesophageal echocardiography. Anesth Analg 1992; 75:764.
  41. Leung JM, Voskanian A, Bellows WH, Pastor D. Automated electrocardiograph ST segment trending monitors: accuracy in detecting myocardial ischemia. Anesth Analg 1998; 87:4.
  42. Slogoff S, Keats AS, David Y, Igo SR. Incidence of perioperative myocardial ischemia detected by different electrocardiographic systems. Anesthesiology 1990; 73:1074.
  43. Maile MD, Engoren MC, Tremper KK, et al. Variability of Automated Intraoperative ST Segment Values Predicts Postoperative Troponin Elevation. Anesth Analg 2016; 122:608.
  44. London MJ, Hollenberg M, Wong MG, et al. Intraoperative myocardial ischemia: localization by continuous 12-lead electrocardiography. Anesthesiology 1988; 69:232.
  45. Landesberg G, Mosseri M, Wolf Y, et al. Perioperative myocardial ischemia and infarction: identification by continuous 12-lead electrocardiogram with online ST-segment monitoring. Anesthesiology 2002; 96:264.
  46. Cockings JG, Webb RK, Klepper ID, et al. The Australian Incident Monitoring Study. Blood pressure monitoring--applications and limitations: an analysis of 2000 incident reports. Anaesth Intensive Care 1993; 21:565.
  47. Naylor AJ, Sessler DI, Maheshwari K, et al. Arterial Catheters for Early Detection and Treatment of Hypotension During Major Noncardiac Surgery: A Randomized Trial. Anesth Analg 2020; 131:1540.
  48. Marik PE, Cavallazzi R. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense. Crit Care Med 2013; 41:1774.
  49. Bentzer P, Griesdale DE, Boyd J, et al. Will This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? JAMA 2016; 316:1298.
  50. van Daele ME, Sutherland GR, Mitchell MM, et al. Do changes in pulmonary capillary wedge pressure adequately reflect myocardial ischemia during anesthesia? A correlative preoperative hemodynamic, electrocardiographic, and transesophageal echocardiographic study. Circulation 1990; 81:865.
  51. Sandham JD, Hull RD, Brant RF, et al. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med 2003; 348:5.
  52. Polanczyk CA, Rohde LE, Goldman L, et al. Right heart catheterization and cardiac complications in patients undergoing noncardiac surgery: an observational study. JAMA 2001; 286:309.
  53. Rajaram SS, Desai NK, Kalra A, et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Syst Rev 2013; :CD003408.
  54. Task Force for Preoperative Cardiac Risk Assessment and Perioperative Cardiac Management in Non-cardiac Surgery, European Society of Cardiology (ESC), Poldermans D, et al. Guidelines for pre-operative cardiac risk assessment and perioperative cardiac management in non-cardiac surgery. Eur Heart J 2009; 30:2769.
  55. Smith JS, Cahalan MK, Benefiel DJ, et al. Intraoperative detection of myocardial ischemia in high-risk patients: electrocardiography versus two-dimensional transesophageal echocardiography. Circulation 1985; 72:1015.
  56. Clements FM, de Bruijn NP. Perioperative evaluation of regional wall motion by transesophageal two-dimensional echocardiography. Anesth Analg 1987; 66:249.
  57. Kato M, Nakashima Y, Levine J, et al. Does transesophageal echocardiography improve postoperative outcome in patients undergoing coronary artery bypass surgery? J Cardiothorac Vasc Anesth 1993; 7:285.
  58. Gewertz BL, Kremser PC, Zarins CK, et al. Transesophageal echocardiographic monitoring of myocardial ischemia during vascular surgery. J Vasc Surg 1987; 5:607.
  59. Eisenberg MJ, London MJ, Leung JM, et al. Monitoring for myocardial ischemia during noncardiac surgery. A technology assessment of transesophageal echocardiography and 12-lead electrocardiography. The Study of Perioperative Ischemia Research Group. JAMA 1992; 268:210.
  60. London MJ, Tubau JF, Wong MG, et al. The "natural history" of segmental wall motion abnormalities in patients undergoing noncardiac surgery. S.P.I. Research Group. Anesthesiology 1990; 73:644.
  61. American Society of Anesthesiologists and Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Practice guidelines for perioperative transesophageal echocardiography. An updated report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology 2010; 112:1084.
  62. Ramsingh D, Bronshteyn YS, Haskins S, Zimmerman J. Perioperative Point-of-Care Ultrasound: From Concept to Application. Anesthesiology 2020; 132:908.
  63. Borer JS, Redwood DR, Levitt B, et al. Reduction in myocardial ischemia with nitroglycerin or nitroglycerin plus phenylephrine administered during acute myocardial infarction. N Engl J Med 1975; 293:1008.
  64. Hood WB Jr. Editorial: "Dynamite pills" in the coronary care unit? N Engl J Med 1975; 293:1040.
  65. Fleisher LA, Fleischmann 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; 64:e77.
  66. Augoustides JG, Savino JS. Vasopressin: the perioperative gift that keeps on giving. Anesthesiology 2014; 121:914.
  67. Reves JG, Fragen RJ, Vinik HR, Greenblatt DJ. Midazolam: pharmacology and uses. Anesthesiology 1985; 62:310.
  68. Guay J, Kopp S. Epidural pain relief versus systemic opioid-based pain relief for abdominal aortic surgery. Cochrane Database Syst Rev 2016; :CD005059.
  69. Guay J, Choi P, Suresh S, et al. Neuraxial blockade for the prevention of postoperative mortality and major morbidity: an overview of Cochrane systematic reviews. Cochrane Database Syst Rev 2014; :CD010108.
  70. Wink J, Veering BT, Aarts LPHJ, Wouters PF. Effects of Thoracic Epidural Anesthesia on Neuronal Cardiac Regulation and Cardiac Function. Anesthesiology 2019; 130:472.
  71. Gonon A, Richter A, Cederholm I, et al. Effects of thoracic epidural analgesia on exercise-induced myocardial ischaemia in refractory angina pectoris. Acta Anaesthesiol Scand 2019; 63:515.
  72. Liu SS, Mulroy MF. Neuraxial anesthesia and analgesia in the presence of standard heparin. Reg Anesth Pain Med 1998; 23:157.
  73. Das S, Forrest K, Howell S. General anaesthesia in elderly patients with cardiovascular disorders: choice of anaesthetic agent. Drugs Aging 2010; 27:265.
  74. Rivera R, Antognini JF. Perioperative drug therapy in elderly patients. Anesthesiology 2009; 110:1176.
  75. Chan CM, Mitchell AL, Shorr AF. Etomidate is associated with mortality and adrenal insufficiency in sepsis: a meta-analysis*. Crit Care Med 2012; 40:2945.
  76. Lundy JB, Slane ML, Frizzi JD. Acute adrenal insufficiency after a single dose of etomidate. J Intensive Care Med 2007; 22:111.
  77. Jabre P, Combes X, Lapostolle F, et al. Etomidate versus ketamine for rapid sequence intubation in acutely ill patients: a multicentre randomised controlled trial. Lancet 2009; 374:293.
  78. Schenarts CL, Burton JH, Riker RR. Adrenocortical dysfunction following etomidate induction in emergency department patients. Acad Emerg Med 2001; 8:1.
  79. Bruder EA, Ball IM, Ridi S, et al. Single induction dose of etomidate versus other induction agents for endotracheal intubation in critically ill patients. Cochrane Database Syst Rev 2015; 1:CD010225.
  80. Absalom A, Pledger D, Kong A. Adrenocortical function in critically ill patients 24 h after a single dose of etomidate. Anaesthesia 1999; 54:861.
  81. Komatsu R, You J, Mascha EJ, et al. Anesthetic induction with etomidate, rather than propofol, is associated with increased 30-day mortality and cardiovascular morbidity after noncardiac surgery. Anesth Analg 2013; 117:1329.
  82. Lindholm EE, Aune E, Norén CB, et al. The anesthesia in abdominal aortic surgery (ABSENT) study: a prospective, randomized, controlled trial comparing troponin T release with fentanyl-sevoflurane and propofol-remifentanil anesthesia in major vascular surgery. Anesthesiology 2013; 119:802.
  83. Zaugg M, Lucchinetti E. Sevoflurane--compared with propofol-based anesthesia reduces the need for inotropic support in patients undergoing abdominal aortic aneurysm repair: evidence of cardioprotection by volatile anesthetics in noncardiac surgery. Anesthesiology 2014; 120:1289.
  84. Myles PS, Leslie K, Chan MT, et al. The safety of addition of nitrous oxide to general anaesthesia in at-risk patients having major non-cardiac surgery (ENIGMA-II): a randomised, single-blind trial. Lancet 2014; 384:1446.
  85. Feringa HH, Vidakovic R, Karagiannis SE, et al. Impaired glucose regulation, elevated glycated haemoglobin and cardiac ischaemic events in vascular surgery patients. Diabet Med 2008; 25:314.
  86. Noordzij PG, Boersma E, Schreiner F, et al. Increased preoperative glucose levels are associated with perioperative mortality in patients undergoing noncardiac, nonvascular surgery. Eur J Endocrinol 2007; 156:137.
  87. NICE-SUGAR Study Investigators, Finfer S, Chittock DR, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009; 360:1283.
  88. Sigmund AE, Fang Y, Chin M, et al. Postoperative Tachycardia: Clinically Meaningful or Benign Consequence of Orthopedic Surgery? Mayo Clin Proc 2017; 92:98.
  89. Liem VGB, Hoeks SE, Mol KHJM, et al. Postoperative Hypotension after Noncardiac Surgery and the Association with Myocardial Injury. Anesthesiology 2020; 133:510.
  90. Sharma V, Sessler DI, Hausenloy DJ. The role of routine postoperative troponin measurement in the diagnosis and management of myocardial injury after non-cardiac surgery. Anaesthesia 2021; 76:11.
  91. Wijeysundera DN. Perioperative troponin screening and detection of myocardial injury. Int Anesthesiol Clin 2021; 59:1.
  92. Buse GL, Matot I. Pro-Con Debate: Cardiac Troponin Measurement as Part of Routine Follow-up of Myocardial Damage Following Noncardiac Surgery. Anesth Analg 2022; 134:257.
Topic 90616 Version 43.0

References

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