Intraoperative management for noncardiac surgery in patients with heart failure

INTRODUCTION — Heart failure (HF) is a common clinical syndrome with symptoms (such as dyspnea, fatigue, or edema) caused by impaired ability of one or both ventricles to pump at a normal pressure due to a structural or functional cardiac disorder. This definition includes patients with American College of Cardiology/American Heart Association (ACC/AHA) stages C and D HF [1] (table 1) (see "Determining the etiology and severity of heart failure or cardiomyopathy", section on 'Definition'). HF is a significant risk factor for major adverse cardiac events with surgery (table 2 and figure 1). Patients with chronic HF or at risk for HF may experience acute HF in the perioperative period [2-7].

This topic will discuss intraoperative management of patients with chronic or acute HF during elective, urgent, or emergency surgery. Related perioperative management issues in heart failure patients are discussed in separate topics:

●Preoperative evaluation, assessment of risk and postoperative management for patients with HF. (See "Perioperative management of heart failure in patients undergoing noncardiac surgery".)

●Diagnosis of HF. (See "Heart failure: Clinical manifestations and diagnosis in adults".)

Related anesthetic management issues are discussed in separate topics:

●(See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure".)

●(See "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease".)

●(See "Anesthesia for noncardiac surgery in patients with ischemic heart disease".)

GENERAL CONSIDERATIONS — HF patients are at increased risk for acute HF, hypotension, hypertension, and arrhythmias during surgery. Causes of these hemodynamic aberrations include the stress response to surgery, alterations in intravascular volume (eg, blood loss and other fluid shifts), and effects of anesthetic agents and other medications [8,9]. This stress response involves release of catecholamines, hormones, and inflammatory mediators. These cause an increase in metabolic demand that must be met by an adequate increase in oxygen delivery, typically achieved by an increase in cardiac output (CO; determined by heart rate [HR], preload, afterload, and contractility) and adequate perfusion pressure.

Intraoperative management of these hemodynamic aberrations includes:

●Control of HR and rhythm

●Fluid replacement and diuretics

●Vasopressor and vasodilator drugs

●Administration of positive and negative inotropic drugs

MONITORING — Selection of monitoring modalities in patients with ventricular dysfunction is based on patient-specific and surgery-specific factors. The likelihood of substantial fluid shifts (from blood loss and nonhemorrhagic sources such as open body cavities and wounds) and other causes of hemodynamic instability are considered in selection of noninvasive and invasive monitors for a planned surgical procedure. (See "Intraoperative fluid management", section on 'Monitoring intravascular volume status'.)

Electrocardiography — All patients with HF (or at elevated risk for HF) have continuous electrocardiography monitoring to detect arrhythmias and/or myocardial ischemia. In patients with known or suspected coronary artery disease, computerized ST-segment trending is superior to visual clinical interpretation for identification of ST-segment changes. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Monitoring for myocardial ischemia'.)

Intra-arterial catheter — An intra-arterial catheter is typically inserted in patients with pre-existing severe ventricular dysfunction, severe valve disease, or hemodynamic instability (ideally prior to induction of anesthesia), as well as in those undergoing surgical procedures that are likely to cause rapid blood loss or large fluid shifts. When present, an intra-arterial catheter allows:

●Continuous monitoring of arterial blood pressure (BP), with prompt detection and treatment of hemodynamic perturbations.

●Evaluation of respirophasic variation in the arterial pressure waveform (figure 2). (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness' and "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Cardiac output'.)

●Use of a noninvasive device for cardiac output (CO) monitoring. (See "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Cardiac output'.)

●Access for frequent arterial blood gas measurements when necessary.

Central venous catheter — The decision to place a central venous catheter (CVC) is based on the likelihood of need for infusion of vasoactive drugs or administration of large volumes of intravenous (IV) fluid or blood products, or anticipated challenges in obtaining reliable intravascular access. Measurements of central venous pressure (CVP) poorly predict volume responsiveness in most patients, but do provide supplemental data to monitor trends in intravascular volume status, and may identify new-onset or worsening tricuspid regurgitation in patients with right-sided HF [10-15]. (See "Intraoperative fluid management", section on 'Traditional static parameters' and "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Monitoring'.)

Pulmonary artery catheter — Pulmonary artery catheter (PAC) monitoring is not routinely recommended for patients with cardiovascular disease, even those with elevated risk [16-19]. Evidence suggests no benefit and possible harm from PAC use in most patients undergoing either cardiac or noncardiac surgery [19-24]. The decision to insert a PAC to monitor CVP, pulmonary artery pressure (PAP), and CO should be based on patient factors (typically, conditions significantly affecting hemodynamics [eg, acute HF, shock, or severe valve disease] that cannot be corrected before surgery), surgical procedure (including expectation of associated fluid shifts), and practice setting (particularly experience with PAC monitoring to minimize potential risk for harmful incorrect interpretation of data) [16]. Details are discussed in other topics. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults" and "Intraoperative management of shock in adults", section on 'Pulmonary artery catheter'.)

Echocardiography — Transesophageal echocardiography (TEE) is useful to guide fluid management and vasoactive therapy during major surgical procedures, as it allows evaluation of left and right ventricle chamber size, global and regional systolic and diastolic ventricular function (including identification of new regional wall motion abnormalities suggestive of ischemia), valvular regurgitation, and estimation of pulmonary artery pressure. Intraoperative changes can be rapidly detected with TEE monitoring. (See "Intraoperative transesophageal echocardiography for noncardiac surgery".)

Emergency use of TEE is indicated to determine the cause of acute decompensation (eg, due to severe right or left ventricular dysfunction, pulmonary embolism, or hypovolemia) [16,25]. For such emergency situations, transthoracic echocardiography is also increasingly used in the operating room by the anesthesiologist or cardiology consultant [26,27]. (See "Intraoperative rescue transesophageal echocardiography (TEE)" and "Overview of perioperative uses of ultrasound", section on 'Transthoracic echocardiography'.)

ANESTHETIC CONSIDERATIONS — The process of choosing anesthetic technique for patients with HF is similar to that for other patients and is primarily guided by the requirements of the surgical procedure and the patient's preferences [16]. When either regional anesthesia or general anesthesia is surgically appropriate, the individualized risks and benefits and each technique are weighed. (See "Overview of anesthesia".)

Management of neuraxial anesthesia — For patients with HF, management of neuraxial anesthesia may be modified to avoid inducing hypotension. Neuraxial anesthesia causes sympathetic blockade which causes vasodilation and decreased cardiac preload resulting in hypotension. Hypotension is more likely to occur in patients with conditions associated with high sensitivity to preload including those with diastolic dysfunction. Although titrated volume administration in increments of 250 mL may be helpful in restoring blood pressure (BP), fluid overload should be avoided to avoid postoperative sequelae (eg, pulmonary edema). Thus, if hypotension develops without evidence of significant hypovolemia, administration of an alpha₁ receptor agonists (eg, phenylephrine) or direct/indirect sympathomimetic (eg, ephedrine) is appropriate, rather than rapid or significant volume loading [28]. (See "Overview of neuraxial anesthesia".)

Modified neuraxial anesthetic techniques are a reasonable option (eg, a low-dose combined spinal-epidural with or without intrathecal opioids, or a very slowly titrated epidural anesthetic), particularly for HF patients susceptible to hypotension (eg, recently decompensated HF).

Management of general anesthesia — For patients with HF, appropriate selection and dosing of general anesthetic agents is necessary to achieve the goals of inducing and maintaining an unconscious state without adverse hemodynamic effects such as hypotension. (See "Induction of general anesthesia: Overview" and "Maintenance of general anesthesia: Overview".)

Induction — When tracheal intubation is planned, a reasonable approach to intravenous anesthetic induction is use of a short-acting hypnotic (eg, etomidate 0.15 to 0.3 mg/kg, ketamine 1 to 2 mg/kg, or a reduced dose of propofol 1 to 2 mg/kg), together with a moderate dose of an opioid (eg, fentanyl, 1 to 2 mcg/kg) and/or lidocaine 50 to 100 mg to blunt the tachycardic response to laryngoscopy and intubation, as well as a muscle relaxant with rapid onset. Anesthetic induction in patients unable to lie supine due to orthopnea may be accomplished with elevation of the back of the operating room table.

The choice of short-acting hypnotic is based on patient-specific factors:

●Etomidate – In HF patients with hemodynamic instability, etomidate is useful since it has minimal hemodynamic side effects [29]. Although etomidate transiently inhibits cortisol biosynthesis, the preponderance of evidence suggests that this is not harmful in most clinical settings and does not preclude its use. (See "General anesthesia: Intravenous induction agents", section on 'Etomidate'.)

●Ketamine – Administration of ketamine usually results in significant increases in BP, heart rate (HR), and plasma epinephrine levels due to centrally mediated sympathetic nervous system stimulation. These effects are generally tolerated in patients with HF, including those with severely depressed ventricular function. However, in patients with ischemic heart disease, the tachycardic effect of ketamine is generally undesirable. Some clinicians select a combination of induction agents in patients with ischemic heart disease and left ventricular systolic dysfunction, 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. Notably, the stimulatory effect of ketamine depends upon the presence of adequate sympathetic reserve. In patients who have maximally activated their sympathetic response (eg, hemorrhage or cardiogenic shock), ketamine may decrease BP due to its mild direct myocardial depressant effect. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia' and "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

●Propofol – If propofol is used for induction, lower doses should be used (eg, 1 to 2 mg/kg) with slower administration of bolus injections [30]. Larger bolus doses of propofol may result in profound hypotension by decreasing systemic vascular resistance (SVR) due to inhibition of sympathetic vasoconstriction, decreasing preload, and direct depression of myocardial contractility. Hypotension is particularly likely in patients receiving angiotensin converting enzyme inhibitors or angiotensin receptor blockers. (See "General anesthesia: Intravenous induction agents", section on 'Propofol' and "Perioperative medication management", section on 'ACE inhibitors and angiotensin II receptor blockers'.)

Patients with acute decompensated HF who arrive in the operating room already intubated and sedated may not need any intravenous (IV) induction agent, although low doses of opioids, sedatives, or a volatile anesthetic agent will be necessary to maintain anesthesia during the surgical procedure.

Maintenance — General anesthesia may be maintained with either inhalation anesthetic agents or a total intravenous anesthetic (TIVA) technique, or with a combination of volatile and intravenous agents [16]. However only limited data comparing anesthetic techniques for noncardiac surgery are available. The benefits of inhalation anesthesia in cardiac surgery are discussed separately. (See "Management of cardiopulmonary bypass", section on 'Anesthetic agents'.)

Notably, lower than usual doses of volatile agents are used in patients with HF since these agents are mild myocardial depressants. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Cardiovascular effects'.)

HEMODYNAMIC MANAGEMENT

General approach — Hemodynamic management for patients with HF involves fluid management, limiting use of drugs with hemodynamically adverse effects, and selective use of intravenous (IV) vasodilators, inodilators, inotropes, and vasopressors, as indicated. Maintenance of hemodynamic stability during the perioperative period is important to avoid perioperative complications such as acute heart failure or worsening renal function [31-33]. Management of intraoperative acute HF is the same as for acute HF in other settings. (See "Treatment of acute decompensated heart failure: General considerations" and "Treatment of acute decompensated heart failure: Specific therapies" and "Treatment of acute decompensated heart failure in acute coronary syndromes".)

As for patients without HF undergoing noncardiac surgery, we generally target an intraoperative blood pressure (BP) within a narrow range around the patient's preoperative baseline BP to minimize the risk of end-organ hypoperfusion [34] (see "Hemodynamic management during anesthesia in adults", section on 'Blood pressure targets'):

●For patients with hypertension (baseline systolic BP ≥130 mmHg or diastolic BP ≥80 mmHg) including patients with HF with preserved ejection fraction (HFpEF), we target a BP of 80 to 110 percent of baseline and a systolic BP <160 mmHg.

●For patients who are normotensive (baseline systolic BP 95 to 129 mmHg and diastolic BP 50 to 79), we target a BP of 90 to 110 percent of baseline, and a mean arterial pressure (MAP) of 65 to 95 mmHg.

●For patients who are hypotensive (systolic BP <95 mmHg or diastolic BP<50 mmHg), we target a BP of 100 to 120 percent of baseline with target MAP of ≥60 mmHg. For patients with HF with reduced ejection fraction (HFrEF) with baseline systolic BP of <95 mmHg, we target an MAP of 60 to 80 mmHg as these patients may not tolerate higher afterload.

Approaches to the initial management of intraoperative hypotension, subsequent management of presumed left heart failure or dysfunction, and subsequent management of presumed right heart failure/dysfunction are presented in the algorithms (algorithm 1A-C).

Management of fluids and blood products

●Maintenance of euvolemia – For patients with HF, intraoperative fluid therapy is adjusted to maintain adequate preload to support cardiac output (CO) and tissue perfusion while avoiding detrimental elevations in filling pressures. Maintenance of euvolemia is particularly important for HF patients given the risk of perioperative worsening of renal function [31]. Prior to surgery, patients may have either intravascular volume overload due to their underlying disease or, conversely, they may have volume depletion due to diuretic administration. (See "Intraoperative fluid management", section on 'Hypovolemia' and "Intraoperative fluid management", section on 'Hypervolemia'.)

During surgery, fluid shifts and/or bleeding may significantly decrease preload necessitating fluid administration. However, care should be taken to limit volume expansion when hypotension is not the result of decreased preload. For example, anesthesia-induced vasodilation causing temporary hypotension should not be treated with excessive fluid administration; rather, administration of alpha₁ receptor agonists (eg, phenylephrine) or direct/indirect sympathomimetics (eg, ephedrine) would be appropriate. Fluid responsiveness (ie, increase in stroke volume following IV fluid administration) (figure 2) is estimated using standard hemodynamic measurements (eg, noninvasive BP and heart rate [HR]), qualitative visual assessment of left ventricular cavity size using transesophageal echocardiography (TEE) (movie 1), and in selected cases, one or more invasive monitors of dynamic hemodynamic parameters. Details describing methods and limitations of monitoring intravascular volume status are available in a separate topic. (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness' and "Intraoperative fluid management", section on 'Monitoring intravascular volume status' and 'Monitoring' above.)

For relatively brief minimally or moderately invasive surgery with planned early postoperative ambulation, a smaller fluid volume (eg, less than 1 L) is generally appropriate for HF patients, rather than the 1 to 2 L that is typically administered to patients without HF during such procedures. For major invasive surgical procedures, we typically employ a restrictive, zero-balance approach that minimizes fluid administration, or a goal-directed approach with fluid administration often in combination with vasopressor/inotropic support to achieve a pre-specified hemodynamic goal. (See "Intraoperative fluid management", section on 'Choosing a fluid management strategy'.)

Red blood cells (RBCs) are used to replace intraoperative blood loss when a transfusion threshold is met, as discussed separately. Transfusion of RBCs is appropriate for HF patients with borderline hemoglobin levels (<8 g/dL) who have ongoing bleeding, coagulopathy, or evidence of inadequate perfusion of vital organs. (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells'.)

When infusions of significant volumes of blood or other fluids are necessary, the risk of volume overload is managed by adjusting the rate of infusion and use of diuretics as needed (see "Use of diuretics in patients with heart failure"). Warming of blood and/or fluids prior to administration assists in maintaining normothermia to avoid the increased oxygen consumption associated with shivering

●Choice of fluids – We typically select a balanced electrolyte crystalloid solution for routine perioperative fluid administration to maintain normovolemia (see "Intraoperative fluid management", section on 'Choosing fluid: Crystalloid, colloid, or blood'). A continuous infusion of crystalloid may be supplemented with administration of smaller than usual (1 to 2 mL/kg) crystalloid boluses, as needed.

Use of vasoactive and inotropic agents — Vasodilator, vasopressor, and inotropic agents are used intraoperatively in selected clinical settings (algorithm 1A-C). Inotropes with vasodilatory activity are known as inodilators. If an infusion of an inotropic or vasoactive agent is necessary, an intra-arterial catheter is inserted to continuously monitor BP during titration (table 3 and table 4). (See 'Intra-arterial catheter' above and "Treatment of acute decompensated heart failure: Specific therapies".)

●Vasodilator and inodilator agents – Vasodilators (table 3) and inotrope/vasodilators (inodilators) (table 4) are used in selected patients with acute decompensated HF to reduce elevated filling pressures and/or left ventricular afterload. Indications include (see "Treatment of acute decompensated heart failure: Specific therapies", section on 'Vasodilator therapy' and "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'):

•Severe hypertension is generally treated with balanced vasodilator therapy (eg, nitroprusside).

•Severe fluid overload causing pulmonary edema is generally treated with a venodilator (eg, nitroglycerin) as an adjunct to diuretic therapy.

•Low CO despite adequate preload may be treated with an inodilator or a vasodilator (if tolerated) but may require an inotrope with vasopressor activity as a temporizing measure to treat hypotension.

●Vasopressors – Vasopressor therapy is used as a temporizing measure to preserve systemic BP in patients with marked hypotension or evidence of end-organ hypoperfusion, despite the potential for vasopressor-induced increases in afterload to decrease CO. When a vasopressor is required, it is reasonable to initially administer IV boluses of small doses of ephedrine, epinephrine, norepinephrine, or phenylephrine to maintain systemic BP while a vasopressor continuous infusion is prepared. Subsequently, a continuous infusion of a vasopressor such as dopamine, norepinephrine, vasopressin (listed in increasing order of potency) may be administered (table 4). (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Vasopressor therapy' and "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

●Inotropic agents – For patients with HFrEF with severe left ventricular systolic dysfunction and low CO syndrome (with hypotension or evidence of end-organ hypoperfusion) despite adequate preload, administration of an inotrope (an inodilator or in some cases, an inotrope with vasopressor activity (table 4) may increase CO by increasing contractility and heart rate (HR). However, the anesthesiologist will have only indirect indicators of CO (such as HR, systemic BP, and echocardiographic indicators and measures of stroke volume) unless this is being directly monitored during the surgical procedure using a pulmonary artery catheter or other CO monitoring device. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults", section on 'Calculation of cardiac output' and "Novel tools for hemodynamic monitoring in critically ill patients with shock", section on 'Cardiac output'.)

Inotropic agents are generally not indicated in patients with normal or near normal left ventricular ejection fraction (LVEF). (See 'Cardiomyopathy-specific considerations' below.)

Options for continuous infusion of an inotropic agent in HF patients include milrinone and dobutamine (table 4) (see "Treatment of acute decompensated heart failure: Specific therapies", section on 'Inotropic agents' and "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'):

•Milrinone is often selected because it is a nonadrenergic agent with inotropic and vasodilatory actions, with a lower incidence of dysrhythmias than dobutamine. Milrinone may be particularly efficacious in HF patients who are at risk for beta-receptor down-regulation. However, its vasodilatory properties limit its use in hypotensive patients.

•Dobutamine is an inotrope with inotropic and chronotropic activity, as well as some degree of vasodilation, predominantly by beta₁ adrenergic effects. The net effect is usually increased CO, with decreased systemic vascular resistance (SVR), with or without a small reduction in BP. Due to its chronotropic effect, dobutamine may be preferred when an increase in HR is desired. However, dysrhythmias may occur due to the beta₁ adrenergic effect.

Cardiomyopathy-specific considerations — Hemodynamic management differs for patients with different types of cardiomyopathy.

●HFrEF – The above discussion of inotrope use applies to selected patients with HFrEF.

●HFpEF – In contrast, for patients with HFpEF and for other causes of HF in which the left ventricular ejection fraction is normal or near normal, including restrictive cardiomyopathy and most patients with hypertrophic cardiomyopathy, inotropes are generally not indicated, and may cause further hemodynamic instability. Since both preload and HR determine CO, significant reduction of blood volume or filling pressures, bradycardia or tachycardia, and atrial arrhythmias such as atrial fibrillation or atrial flutter may not be well tolerated [18]. (See "Treatment and prognosis of heart failure with preserved ejection fraction" and "Restrictive cardiomyopathies", section on 'Treatment' and "Hypertrophic cardiomyopathy: Management of patients without outflow tract obstruction".)

●Hypertrophic cardiomyopathy – Specific considerations apply for hypertrophic cardiomyopathy. In clinical settings in which the systemic vascular resistance is decreased (eg, with vasodilator therapy), intravascular volume is low, or there is another cause for reduced preload the degree of dynamic left ventricular outflow obstruction may increase and decrease CO and BP. Thus, volume depletion should be avoided. Inotropic agents increase dynamic obstruction and should be avoided.

●Cardiac amyloidosis – Cardiac amyloidosis is increasingly recognized as an underdiagnosed cause of heart failure, especially in older adult males with HFpEF. Cardiac amyloid deposits are associated with severely reduced inotropic myocardial reserve and increased left and right ventricular filling pressures at rest during exercise. Anesthetic agents with negative inotropic actions should be avoided even in patients with a preserved LV ejection fraction [35]. (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery".)

●Right heart failure – Hemodynamic management of right ventricular failure is discussed in a separate topic. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Hemodynamic management'.)

Mechanical circulatory support devices — As use of mechanical circulatory support devices (such as left ventricular assist devices [LVADs]) or extracorporeal membrane oxygenation (ECMO) for advanced HF has increased, more patients with these devices are undergoing noncardiac surgery. In specialized units, patients with LVADs can safely undergo noncardiac surgery [36]. It is recommended that patients with LVADs who are scheduled for noncardiac surgery be managed perioperatively by a center experienced with implantation and follow-up [17]. Details are discussed in separate topics:

●(See "Anesthesia for noncardiac surgery in adults with a durable ventricular assist device".)

●(See "Short-term left ventricular mechanical circulatory support: Use of echocardiography during initiation and management".)

●(See "Extracorporeal life support in adults: Management of venoarterial extracorporeal membrane oxygenation (V-A ECMO)".)

MANAGEMENT OF ARRHYTHMIAS — Arrhythmias are common in patients with HF. In patients with acute decompensated HF, external defibrillation/pacing pads should be placed, since defibrillation, cardioversion, or pacing may become necessary. Intraoperative management of some key arrhythmias is summarized below. Management of specific cardiac arrhythmias is the same as in other settings as discussed in individual topic reviews, as noted. Perioperative management of implantable cardioverter defibrillators and pacemakers is discussed elsewhere [37,38]. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

●Ventricular arrhythmias – Ventricular fibrillation or pulseless ventricular tachycardia is life threatening, requiring immediate cardioversion or defibrillation. If the arrhythmia recurs after conversion, antiarrhythmic therapy, particularly amiodarone, may be effective. Management of unstable and stable patients with sustained VT is discussed separately. (See "Advanced cardiac life support (ACLS) in adults", section on 'Pulseless ventricular tachycardia and ventricular fibrillation' and "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis".)

●Atrial fibrillation – Atrial fibrillation (AF) is common in patients with HF. Short-term management of hemodynamically stable patients with AF generally focuses on control of the ventricular rate. (See "The management of atrial fibrillation in patients with heart failure".)

•For patients with HF with reduced ejection fraction (HFrEF), rate control agents include intravenous (IV) digoxin and IV amiodarone.

•For patients with HF with preserved ejection fraction (HFpEF), rate control agents include IV diltiazem or IV beta blocker (eg, esmolol).

Management of patients with hemodynamic instability or evidence of myocardial ischemia associated with AF is discussed separately. (See "The management of atrial fibrillation in patients with heart failure", section on 'Acute heart failure management'.)

●Bradycardia - Bradycardia resulting in signs and symptoms of inadequate perfusion (eg, hypotension, altered mental status) is usually treated with atropine, while simultaneous preparations are made for temporary pacing (transcutaneous or transvenous and/or a chronotropic agent [eg, dopamine, isoproterenol, epinephrine (table 4)]). However, administration of atropine or chronotropic agent may cause tachycardia, which is undesirable for patients with myocardial ischemia. (See "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia' and "Sinus bradycardia", section on 'Evaluation' and "Temporary cardiac pacing".)

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: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

●General considerations – Patients with heart failure (HF) undergoing noncardiac surgery are at risk for complications including acute decompensated HF, hypertension, hypotension, arrhythmias, and death (figure 1 and table 2). Causes of these hemodynamic aberrations include the stress response to surgery, alterations in intravascular volume (eg, blood loss and other fluid shifts), and effects of anesthetic agents and other medications. (See 'General considerations' above.)

●Monitoring – Selection of monitoring modalities is based on patient-specific and surgery-specific factors that include the likelihood of substantial fluid shifts, blood loss, or other causes of hemodynamic instability. (See 'Monitoring' above.)

●Neuraxial anesthesia – Management of neuraxial anesthesia may be modified to avoid inducing hypotension or excessive volume administration (eg, use of a low-dose combined spinal-epidural with or without intrathecal opioids, or a very slowly titrated epidural anesthetic). (See 'Management of neuraxial anesthesia' above.)

●General anesthesia – Appropriate selection and dosing of general anesthetic agents is necessary to achieve the goals of inducing and maintaining an unconscious state without adverse hemodynamic effects such as hypotension.

•Induction – When tracheal intubation is planned, a reasonable approach to intravenous anesthetic induction is use of a short-acting hypnotic administered together with a moderate dose of an opioid (eg, fentanyl) and/or lidocaine to blunt the tachycardic response to laryngoscopy and intubation, as well as a muscle relaxant with rapid onset. (See 'Induction' above.)

•Maintenance – General anesthesia may be maintained with inhalation anesthetic agents or a total intravenous anesthetic (TIVA) technique, or with combinations of inhalation and intravenous agents. Notably, lower than usual doses of volatile agents are used in patients with HF since these agents are myocardial depressants. (See 'Maintenance' above.)

●Fluid management – Perioperative fluid therapy is adjusted to maintain adequate preload to support cardiac output (CO) and tissue perfusion while avoiding detrimental elevations in filling pressures. Care should be taken to limit volume expansion when decreased preload is not the cause of hypotension; rather, administration of an alpha₁ receptor agonist (eg, phenylephrine) or a direct/indirect sympathomimetic (eg, ephedrine) would be appropriate. (See 'General approach' above.)

●Hemodynamic management – Hemodynamic management for patients with HF involves careful fluid management, limiting use of drugs with hemodynamically adverse side effects, and selective use of intravenous vasodilators, inodilators, inotropes, and vasopressors if indicated. Management of intraoperative acute HF is the same as for acute HF in other settings (see 'Use of vasoactive and inotropic agents' above):

•Use of vasoactive agents - Intraoperative use of vasoactive agents is indicated in selected clinical settings :

-Hypertension – Severe hypertension is treated with vasodilator therapy, preferably a balanced vasodilator (eg, nitroprusside) (table 3). Also, severe fluid overload causing pulmonary edema is treated with a vasodilator as an adjunct to diuretic therapy, preferably one with prominent venodilator activity (eg, nitroglycerin). (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Vasodilator therapy'.)

-Hypotension – Initial management of intraoperative hypotension and subsequent management of presumed left and/or right heart failure or dysfunction are presented in the algorithms (algorithm 1A-C). Vasopressor therapy is used to treat hypotension as a temporizing measure to preserve systemic blood pressure (BP) in patients with marked hypotension or evidence of end-organ hypoperfusion (table 4). (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Vasopressor therapy'.)

•Use of inotropic agents – Severe left ventricular systolic dysfunction with low CO syndrome (with hypotension or evidence of end-organ hypoperfusion) despite adequate preload is treated with an inotrope (eg, milrinone, dobutamine) (table 4). (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Inotropic agents'.)

•Cardiomyopathy-specific considerations – Hemodynamic management differs for patients with different types of cardiomyopathies. Patients with HF with normal or near normal ejection fraction (including patients with heart failure with preserved ejection fraction [HFpEF], restrictive cardiomyopathy or hypertrophic cardiomyopathy) are generally not treated with inotropes. (See 'Cardiomyopathy-specific considerations' above.)

●Management of arrhythmias – Arrhythmias are common in patients with HF. In patients with acute decompensated HF, external defibrillation/pacing pads should be placed, since defibrillation, cardioversion, or pacing may become necessary. (See 'Management of arrhythmias' above.)