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Arrhythmias during anesthesia

Arrhythmias during anesthesia
Literature review current through: Aug 2023.
This topic last updated: Apr 18, 2022.

INTRODUCTION — Intraoperative tachyarrhythmias (heart rate [HR] >100 beats per minute [bpm]) and bradyarrhythmias (HR <60 bpm) are common; nearly 11 percent of patients experience abnormal HR or rhythm during general anesthesia [1,2]. While most intraoperative arrhythmias are transient and clinically insignificant, some indicate underlying pathology (eg, myocardial ischemia, electrolyte abnormalities), and some are due to a procedure-specific or medication-specific etiology. Occasionally an arrhythmia causes intraoperative hemodynamic instability.

This topic reviews common etiologies, recognition, and acute management of intraoperative cardiac arrhythmias. Other topics address life-threatening arrhythmias that require advanced cardiac life support (ACLS) in the perioperative or other settings:

ACLS

(See "Intraoperative advanced cardiac life support (ACLS)".)

(See "Advanced cardiac life support (ACLS) in adults".)

Further treatment of specific arrhythmias is discussed in additional topics:

Tachyarrhythmias

(See "Sinus tachycardia: Evaluation and management".)

(See "Overview of the acute management of tachyarrhythmias".)

Bradyarrhythmias

(See "Sinus bradycardia".)

(See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)".)

(See "Second-degree atrioventricular block: Mobitz type II".)

(See "Third-degree (complete) atrioventricular block".)

POTENTIAL CONTRIBUTING FACTORS — Factors likely to contribute to development of arrhythmias may be identified in the preoperative period, or recognized and managed during the intraoperative period.

Preexisting electrocardiographic (ECG) abnormalities — Preoperative electrocardiograms (ECGs) are examined when available, and may identify preexisting arrhythmias (eg, atrial fibrillation [AF], premature ventricular contractions [PVCs]) or other abnormal findings that predispose the patient to development of an intraoperative arrhythmia (eg, QTc prolongation, bundle branch block [BBB], Wolff-Parkinson-White [WPW] pattern). A detailed discussion of preoperative ECG evaluation is available in a separate topic. (See "The preoperative ECG: Evaluation and implications for anesthetic management".)

Medication effects

Medications that increase risk for bradycardia — Certain chronically or acutely administered medications may cause severe bradycardia:

Negative chronotropic agents – Beta blockers or other negative chronotropic agents (eg, calcium channel blockers, digoxin, amiodarone) are the most common cause of drug-induced sinus bradycardia. In a 2019 meta-analysis in noncardiac surgical patients, those receiving beta blockers administered in the perioperative period to prevent surgery-related complications had a higher incidence of clinically significant bradycardia defined as a heart rate (HR) <60 bpm and/or requiring treatment (risk ratio [RR] 2.49, 95% CI 1.74-3.56; 490 studies, 12,239 participants) compared with patients who had none [3]. In that meta-analysis, patients receiving beta blockers also had a higher incidence of hypotension (RR 1.40, 95% CI 1.29-1.51; 49 studies, 12,304 participants).

Patients with ischemic heart disease are often taking these medications chronically, or they may have been administered during the perioperative period. Baseline (admission) HR is noted, and bradycardia is treated only if it is severe (eg, HR <40 beats per minute [bpm]) or associated with evidence of poor systemic perfusion or hemodynamic instability, as noted below. (See 'Pharmacologic treatment of bradycardia' below.)

Anticholinesterase agents – Sinus bradycardia may be caused by the muscarinic effects of an acetylcholinesterase inhibitor (eg, neostigmine or edrophonium) when such agents are used to reverse effects of nondepolarizing neuromuscular blocking agents (NMBA) near the end of surgery. The patient should receive an adequate dose of anticholinergic agent (eg, glycopyrrolate or atropine) when the acetylcholinesterase inhibitor is administered. Underdosing an anticholinergic agent (relative to the acetylcholinesterase inhibitor agent) may lead to severe bradycardia. When this is suspected, repeated doses of glycopyrrolate 0.2 mg or atropine 0.4 mg are appropriate. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Anticholinesterases'.)

Sugammadex – Severe sinus bradycardia and asystole have been reported after administration of sugammadex for reversal of steroidal NMBA such as rocuronium. Although this adverse effect of sugammadex is rare, it is potentially life-threatening [4,5]. Particular caution is necessary when sugammadex is given to a patient concurrently receiving medications that may slow the HR (see above). Precautions include slow administration of sugammadex with continuous electrocardiographic monitoring, as well as ensuring immediate availability of atropine and positive chronotropic agents (see below). (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Sugammadex' and 'Pharmacologic treatment of bradycardia' below.)

Opioids – Severe sinus bradycardia may occur when a large bolus dose of an opioid agent (eg, fentanyl, remifentanil, sufentanil) is administered [6-9]. Treatment with small doses of a beta-adrenergic agonist (eg, ephedrine 5 to 10 mg) and/or an anticholinergic agent (eg, glycopyrrolate in 0.2 mg increments up to 1 mg or small incremental doses of atropine 0.2 mg) will typically restore adequate HR.

Vasoconstrictors – The carotid baroreceptor reflex response to hypertension may be triggered by administration of a large dose of a vasoconstrictor such as phenylephrine and result in sinus bradycardia (table 1). This effect tends to be transient, however hemodynamically significant bradycardia may be treated with an anticholinergic agent such as glycopyrrolate.

Medications that may prolong the QT interval — Certain agents that are commonly administered in the perioperative period may prolong the QT interval (eg, methadone, droperidol, ondansetron (table 2)) and increase risk for Torsades de pointes (TdP), a malignant ventricular arrhythmia (see 'Polymorphic ventricular tachycardia (torsades de pointes)' below). Thus, such agents are avoided in patients with a history of prolonged QT interval. (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Ventricular arrhythmias'.)

Although many anesthetic agents (eg, opioids, dexmedetomidine, midazolam, etomidate, ketamine, volatile anesthetic agents) may cause mild prolongation of the QT interval (>440 ms), these are unlikely to cause TdP (table 3) [10-18]. Other causes and potentiators of long QT syndrome are listed in the table (table 4).

Patient-specific factors — Both atrial and ventricular arrhythmias are more likely to occur under certain abnormal physiologic conditions (table 5). These conditions are treated in the preoperative period when possible, with continuing management during the intraoperative period when indicated.

Electrolyte abnormalities

Potassium

Hypokalemia – Although there are no definitive values of hypokalemia where elective surgery must be cancelled, potassium <2.5 mmol/L can lead to QT prolongation and increased risk of arrhythmia. Potassium repletion is considered when levels are less than 3.5 mmol/L, typically with 20 mEq over one hour through a central line, or over two hours through a peripheral intravenous (IV) line due to risk of phlebitis.

Hypokalemia is associated with a variety of arrhythmias including premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular (AV) block, and ventricular tachycardia (VT) or ventricular fibrillation (VF). Serum potassium levels <3.5 mmol/L predicted serious perioperative arrhythmias and postoperative AF and atrial flutter, and hypokalemic patients undergoing noncardiac surgery experienced a higher frequency of major adverse cardiovascular events compared with controls [19,20]. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Cardiac arrhythmias and ECG abnormalities'.)

Hypokalemia often produces characteristic changes on the ECG such as ST segment depression, decreased T wave amplitude, and increased U wave amplitude occurring at the end of the T wave (waveform 1), as well as prolongation of the QT interval. However, these changes are not seen in all patients, and there is considerable interpatient variability in the serum potassium concentration associated with progression of either ECG changes or arrhythmias.

Hyperkalemia – Hyperkalemia can lead to a variety of conduction abnormalities (eg, left bundle branch block [BBB], right BBB, bifascicular block, advanced AV block), as well as sinus bradycardia, sinus arrest, asystole, or VT or VF [21]. Although patients with hyperkalemia may have peaked T waves (waveform 2), there is neither an orderly progression of ECG abnormalities seen in individual patients as the potassium rises, nor does the absence of ECG changes preclude life-threatening cardiac arrhythmias associated with hyperkalemia.

Many patients with preoperative hyperkalemia have end-stage renal disease (ESRD). Preoperative management for patients with or without ESRD depends on the severity of hyperkalemia, as well as on whether the proposed procedure is elective or urgent. Notably, succinylcholine should be avoided if potassium ≥5.5 mEq/L. Details regarding management of perioperative hyperkalemic patients are discussed in a separate topic (algorithm 1 and table 6). (See "Anesthesia for dialysis patients", section on 'Management of hyperkalemia'.)

Magnesium

Hypomagnesemia – Hypomagnesemia widens the QRS complex and increases the risk of torsades de pointes (TdP), sustained AF, frequent atrial or ventricular ectopic beats, and other ventricular arrhythmias [22]. Clinical manifestations and treatment are discussed separately. (See "Hypomagnesemia: Clinical manifestations of magnesium depletion", section on 'Cardiovascular' and "Hypomagnesemia: Evaluation and treatment".)

Hypermagnesemia – Hypermagnesemia (>4 mEq/L) may cause conduction defects, bradycardia, and hypotension. Symptoms typically resolve with cessation of magnesium therapy (eg, IV magnesium infusion for treatment of eclampsia or preeclampsia). In patients with renal insufficiency, isotonic IV fluids plus a loop diuretic (eg, furosemide) are administered, in addition to discontinuing any magnesium therapy. Postoperative dialysis is occasionally necessary. (See "Hypermagnesemia: Causes, symptoms, and treatment", section on 'Cardiovascular effects' and "Hypermagnesemia: Causes, symptoms, and treatment", section on 'Treatment'.)

Calcium

Hypocalcemia – Hypocalcemia prolongs the QT interval (waveform 3), but has less potential to trigger TdP compared with hypokalemia or hypomagnesemia. Clinical manifestations and treatment of severe acute or symptomatic hypocalcemia by administering IV calcium, as well as treatment of concurrent hypomagnesemia, are discussed separately. (See "Clinical manifestations of hypocalcemia", section on 'Cardiovascular' and "Treatment of hypocalcemia", section on 'Severe symptomatic and/or acute hypocalcemia'.)

Hypercalcemia – Acute hypercalcemia shortens the myocardial action potential, as reflected in a shortened QT interval on the electrocardiogram (ECG). Although moderate hypercalcemia has no clinically important effects on cardiac conduction or the prevalence of supraventricular or ventricular arrhythmias, various cardiac arrhythmias and ST-segment elevation mimicking myocardial infarction have been described with severe hypercalcemia. Treatment is with saline hydration, as described separately. (See "Clinical manifestations of hypercalcemia" and "Treatment of hypercalcemia", section on 'Volume expansion with isotonic saline'.)

Metabolic and respiratory abnormalities — Hypoxemia, hypocarbia or hypercarbia, and acid-base disturbances are contributing factors for arrhythmias. When possible, such abnormalities are corrected. (See "Intraoperative advanced cardiac life support (ACLS)", section on 'Treat the etiology of the cardiac arrest'.)

Intravascular volume depletion — Anemia or dehydration typically results in sinus tachycardia and may lead to development of other arrhythmias.

Myocardial ischemia or failure — Myocardial ischemia or infarction may be associated with atrial or ventricular arrhythmias including supraventricular tachycardia (SVT), conduction defect, or ectopic ventricular activity. Prevention and management of perioperative myocardial ischemia is reviewed separately. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia' and "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Treatment of ischemia'.)

Patients with moderate or severe right or left ventricular heart failure often have a history of arrhythmias, and may have a biventricular pacemaker for cardiac resynchronization therapy and/or implantable cardioverter defibrillator for antitachycardia therapy. Perioperative management of these devices is discussed elsewhere. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

Procedure-specific factors — Both atrial and ventricular arrhythmias are more likely during certain types of surgical procedures or other interventions.

Intrathoracic procedures — During thoracic surgical procedures performed near the heart (eg, pulmonary or esophageal surgery), contact with cardiac or pulmonary venous structures may cause atrial or ventricular arrhythmias. Prevention and management of arrhythmias that commonly occur during cardiac surgery are discussed separately. (See "Management of cardiopulmonary bypass", section on 'Arrhythmias' and "Intraoperative problems after cardiopulmonary bypass", section on 'Arrhythmias'.)

Intravascular interventions — Transient atrial or ventricular arrhythmias commonly occur during insertion of a central venous catheter or pulmonary artery catheter [23]. When the guidewire or catheter enters the right atrium, premature atrial contractions, AF, or other SVTs may occur (see 'Other narrow QRS complex atrial tachyarrhythmias' below). Upon entry into the right ventricle, right BBB [24] (see 'Bundle branch blocks' below), PVCs, or VT may occur (see 'Ventricular arrhythmias' below). For this reason, the ECG is continuously monitored during insertion of such catheters.

Other intravascular interventions performed by surgeons or other interventionalists (eg, cardiac catheterization, endovascular revascularization) often cause atrial and/or ventricular arrhythmias.

Electroconvulsive therapy — Anesthesia for electroconvulsive therapy (ECT) is associated with various arrhythmias. (See "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Anesthesia technique'.)

Administration of local anesthetics — Local anesthetic systemic toxicity (LAST) should be suspected whenever physiologic changes, including arrhythmias, occur shortly after administration of a local anesthetic (eg, for a peripheral nerve block). Cardiovascular signs usually occur simultaneously with or shortly after central nervous system symptoms. Typically, tachycardia and hypertension occur, although bradycardia and hypotension have also been described as the first changes. Cardiovascular toxicity can progress to ventricular arrhythmias and/or asystole.

Prevention and management of LAST are discussed in detail separately (table 7). (See "Local anesthetic systemic toxicity".)

INTRAOPERATIVE DIAGNOSIS

Standard electrocardiography — The electrocardiogram (ECG) is continuously monitored for all patients receiving anesthetic agents for sedation, regional anesthesia, or general anesthesia. For those with risk factors for myocardial ischemia, both leads II and V5 are typically used. (See "Basic patient monitoring during anesthesia", section on 'Electrocardiogram' and "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Monitoring for myocardial ischemia'.)

If a tachyarrhythmia or bradyarrhythmia develops that cannot be readily diagnosed, all available leads are displayed on the intraoperative monitor and a 12-lead ECG is obtained as soon as feasible.

Recognition of artifacts — Notably, artifact due to electrocautery or pacing spikes can mimic ventricular tachycardia (VT) or ventricular fibrillation (VF). Ventricular-paced rhythms can also mimic VT (see 'Ventricular paced rhythms' below). Operating room ECG monitors have filtering capability to minimize artifact when set in "monitor" or "filter" mode rather than "diagnostic" mode. However, pacemaker stimulus outputs (ie, pacing spikes) are small-amplitude high-frequency signals that may be attenuated and are not reliably detected. In some cases, detection in the monitor or filter mode is possible in some of the leads, but not in all leads. As a result, most ECG monitors include a "pacing mode" selection that improves detection of paced rhythms by highlighting the pacing spikes.

Stable waveforms from the pulse oximeter, intra-arterial catheter, and/or central venous catheter are helpful to distinguish artifact from a true arrhythmia. (See "Basic patient monitoring during anesthesia", section on 'Sources of ECG artifact'.)

BRADYARRHYTHMIAS — Management of bradyarrhythmias with a heart rate (HR) <60 beats per minute (bpm) depends upon whether the patient is hemodynamically stable or unstable (table 8).

Sinus bradycardia — Sinus bradycardia with a slow HR <60 bpm but with normal atrial and ventricular depolarization is the most common bradyarrhythmia during anesthesia and surgery (waveform 4). Sinus bradycardia due to a variety of conditions such as chronic use of negative chronotropic medications (eg, beta blockers, calcium channel blockers), temporary increases in vagal tone, athletic conditioning, or intrinsic sinus node dysfunction may also occur in other nonsurgical settings.

Mild sinus bradycardia (ie, HR 40 to 60 bpm) in a hemodynamically stable patient does not usually require pharmacologic treatment, although the cause may require treatment. (See 'Causes of sinus bradycardia' below.)

Treatment of severe sinus bradycardia associated with hemodynamic instability includes pharmacologic and temporary pacing options. (See 'Pharmacologic treatment of bradycardia' below and 'Temporary pacing options' below.)

Causes of sinus bradycardia — Unique intraoperative causes of sinus bradycardia include:

Vagal reflexes – Surgical manipulation may precipitate vagal reflexes that cause bradycardia. Examples include:

During eye surgery, the oculocardiac reflex may occur when traction of the extraocular muscles activates a parasympathetic response via the ophthalmic branch of the trigeminal nerve, causing severe bradycardia and even asystole.

During open or laparoscopic abdominal surgery, peritoneal stretching may cause a parasympathetically mediated bradycardia. The surgeon should immediately cease manipulation when these vagal reflexes occur.

During carotid endarterectomy, removal of carotid plaque may cause stimulation of the carotid sinus nerve resulting in reflex bradycardia and hypotension. Pretreatment with glycopyrrolate or local infiltration of lidocaine around the nerve and carotid sinus may prevent this reflex.  

If HR does not increase when the surgical stimulus is temporarily stopped, an anticholinergic agent is administered. (See 'Pharmacologic treatment of bradycardia' below.)

Neuraxial anesthesia – Neuraxial anesthesia with a high T1 to T4 anesthetic level may cause sinus bradycardia and hypotension [25-28]. Optimal treatment of bradycardia caused by blockade of the cardiac accelerator fibers is with beta-adrenergic agonists such as ephedrine 5 to 10 mg or epinephrine 10 to 20 mcg, although atropine may be administered. If bradycardia persists, an epinephrine infusion may be initiated (table 1). Any epidural infusions should be temporarily discontinued.

Notably, severe bradycardia or asystole associated with hypotension may occur suddenly in an otherwise healthy individual during the course of spinal anesthesia. Immediate treatment with incrementally increased doses of epinephrine is necessary to avoid cardiac arrest (eg, initial bolus of 10 to 20 mcg, then 100 mcg, then a larger bolus dose of 0.5 to 1.0 mg if there is minimal response) [27-29]. This phenomenon is called vasovagal syncope or neurocardiogenic syncope and is also known as the Bezold-Jarisch reflex. Onset of severe bradycardia or asystole is often unanticipated since there is often a delay of 30 minutes or more between administration of the spinal anesthetic and occurrence of such severe cardiovascular depression.

Medications – Chronically and acutely administered medications that increase risk for sinus bradycardia are discussed above. (See 'Medications that increase risk for bradycardia' above.)

Pharmacologic treatment of bradycardia — Sinus bradycardia is treated pharmacologically with an intravenous (IV) anticholinergic agent if it is severe with HR <40 bpm, associated with transient episodes of asystole, or if there are signs of inadequate systemic perfusion (eg, electrocardiographic evidence of ischemia) or overt hemodynamic instability.

Hemodynamic instability – For hemodynamically unstable patients with sinus bradycardia, IV atropine 0.5 mg is administered, and may be repeated every three to five minutes up to a total of 3 mg (algorithm 2). In rare cases, temporary pacing may be necessary. (See 'Temporary pacing options' below.)

Hemodynamic stability – For patients who remain hemodynamically stable during severe sinus bradycardia (ie, <40 bpm), we typically administer IV glycopyrrolate in 0.2 mg increments (up to 1 mg) rather than atropine, in order to avoid undesirable tachycardia, particularly in those with ischemic heart disease. A reasonable alternative is administration of small incremental doses of atropine 0.2 mg.

If bradycardia is associated with hypotension, treatment may include administration of ephedrine 10 to 20 mg. Since tachyphylaxis to ephedrine may occur, another chronotropic agent is typically substituted after 50 to 60 mg have been administered (eg, epinephrine, dopamine, dobutamine). For persistent severe bradycardia, continuous infusion of a positive chronotropic agent is typically initiated (table 1). (See "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

A special circumstance is the patient with a transplanted heart. Due to functional denervation, normal responses to anticholinergic drugs will not typically be effective; instead, a positive chronotropic agent such as isoproterenol (or possibly epinephrine) is selected. (See "Anesthesia for heart transplantation", section on 'Denervation of the transplanted heart' and "Heart transplantation in adults: Arrhythmias".)

Notably, neither glycopyrrolate nor atropine is likely to work for bradycardia caused by conduction delays originating below the atrioventricular (AV) node; treatment is described below. (See 'Bundle branch blocks' below and 'Temporary pacing options' below.)

Temporary pacing options — In patients who have recurrent or severe bradycardia with hemodynamic instability, temporary pacing may be necessary (see "Temporary cardiac pacing"). (Temporary pacing is rarely indicated in a hemodynamically stable patient with a HR of 40 to 60 bpm.)

Temporary pacing options during the perioperative period include:

Transcutaneous pacing – Transcutaneous pacing is usually the most rapid way to correct bradycardia in the perioperative setting. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator", section on 'Placement of transcutaneous pacing/defibrillator pads'.)

Transcutaneous pads should be placed to the right of the sternum immediately below the clavicle and at the left ventricular apex, usually at the fifth or sixth intercostal space in the midaxillary line, although anterior-posterior pad positioning is an alternative for selected surgical procedures (figure 1). The pacing mode of an external defibrillator with pacing capability is activated, and the pacing current is increased up to 65 to 100 milliamperes until a stable HR is achieved. Appropriate pacing capture of the myocardium typically results in increased cardiac output and stabilization of hemodynamics. Notably, for patients who are awake or only mildly sedated, transcutaneous pacing may be painful. (See "Temporary cardiac pacing", section on 'Transcutaneous'.)

Pacing capture may be difficult to achieve in a morbidly obese patient or when appropriate pad placement is not possible (eg, thoracic surgery, lateral or prone position, extensive burns, excessive hair).

Transvenous pacing – Intraoperative transvenous pacing may be used if transcutaneous pacing fails to reliably capture the myocardium or is not feasible (eg, due to the location of the surgical procedure). Transvenous pacing requires insertion of an introducer sheath in a central vessel, most commonly the right internal jugular vein. This may be impractical once a surgical case is underway, depending on the type of surgery, prior positioning of the patient, and configuration of the sterile surgical drapes. (See "Temporary cardiac pacing", section on 'Transvenous'.)

Insertion of the pacing lead requires continuous electrocardiographic (ECG) monitoring due to a high risk for inducing arrhythmias. Correct placement requires expertise in both transvenous wire insertion and pacing technology; thus, cardiology consultation may be required. Ideally, use of fluoroscopy with direct visualization of the pacing lead during insertion will ensure optimal placement within the right ventricle. If intraoperative fluoroscopy is not possible, a postoperative radiograph is necessary to check correct positioning. Notably, a contraindication for transvenous pacing is presence of a mechanical prosthetic tricuspid valve. (See "Temporary cardiac pacing", section on 'Procedural aspects of temporary transvenous pacing'.)

Pacing pulmonary artery catheters – Specialized pulmonary artery catheters (PACs) with pacing capability can be used with an external pacemaker. Anesthesiologists are typically familiar with positioning a pacing PAC by employing pressure waveform analysis during insertion. Catheter position can be confirmed with intraoperative transesophageal echocardiography (TEE) and/or a postoperative radiograph. However, the leads within a pacing PAC are typically less stable than those of a dedicated transvenous pacing wire. Other disadvantages of a pacing PAC are similar to those for a transvenous pacing lead (eg, challenges with placement of an introducer sheath in a central vein, contraindication with a mechanical tricuspid valve).

Other bradyarrhythmias

Sinus node dysfunction — Sinus node dysfunction is characterized by a sluggish or absent sinoatrial (SA) nodal pacemaker and/or depressed escape pacemakers in the presence or absence of atrioventricular (AV) nodal conduction disturbances. The patient's HR responses to physiologic demands may be abnormal, and profound sinus bradycardia, sinus pauses, sinus arrest, or nodal exit block may occur.

Intraoperative management involves addressing the underlying etiology (eg, drug toxicity from excess calcium channel blockers, beta blockers, or digoxin, or myocardial ischemia). For patients who are hemodynamically unstable, atropine may be administered, followed by chronotropic agents such as isoproterenol, epinephrine, dopamine, or dobutamine for continued HR support. For patients who are acutely unstable and in danger of arrest, temporary pacing should be initiated [30]. (See "Sinus node dysfunction: Clinical manifestations, diagnosis, and evaluation" and "Sinus node dysfunction: Treatment", section on 'Introduction'.)

Bundle branch blocks — Either a left bundle branch block (BBB) (waveform 5), right BBB (waveform 6), or fascicular block (waveform 7 and waveform 8) can occur during anesthesia. New onset of such blocks usually indicates either intrinsic cardiac disease or myocardial ischemia, which should be rapidly addressed.

Transient right BBB occasionally occurs during insertion of a PAC, which may lead to complete heart block in a patient with a preexisting left BBB. For this reason, transcutaneous pacing pads should be positioned before PAC insertion for a patient with left BBB.

Further treatment of patients with BBB is discussed in separate topics:

(See "Left bundle branch block".)

(See "Right bundle branch block".)

(See "Left anterior fascicular block".)

(See "Left posterior fascicular block".)

First, second, or third degree AV block — New onset of perioperative AV block typically occurs in the setting of intrinsic cardiac disease, perioperative ischemia, electrolyte abnormalities, excessive vagal tone, or prior surgical or transcatheter aortic valve replacement. AV block is classified as first, second, or third degree:

First degree AV block occurs when there is delayed but intact conduction from the atria to the ventricles (waveform 9), and does not require treatment. (See "First-degree atrioventricular block".)

Second degree AV block occurs when there is intermittent conduction from the atria to the ventricles, with either progressive prolongation of the PR interval until there is a dropped ventricular beat (Mobitz Type I [Wenckebach] (waveform 10)); or prolonged PR intervals with occasional dropped ventricular beats (Mobitz Type II (waveform 11)). Second degree AV block occurring in the perioperative setting may require pacing if bradycardia is severe or causes hemodynamic compromise.

Third degree AV block occurs when atrial impulses do not conduct to the ventricles so that P waves are discordant with QRS waves (waveform 12 and waveform 13 and waveform 14). Pacing is typically required since the intrinsic ventricular rhythm is usually very slow (approximately 30 to 40 bpm). (See "Third-degree (complete) atrioventricular block".)

Asystole — Patients who develop severe intraoperative bradycardia are at risk for progression to asystole or pulseless electrical activity requiring immediate initiation of advanced cardiac life support (ACLS) (algorithm 3). (See "Advanced cardiac life support (ACLS) in adults", section on 'Asystole and pulseless electrical activity'.)

ATRIAL TACHYARRHYTHMIAS — Atrial tachyarrhythmias with a heart rate (HR) >100 beats per minute (bpm) are classified as having either a narrow QRS complex (QRS duration of <120 ms) or a wide QRS complex (QRS duration >120 ms). (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Approach to the diagnosis".)

Sinus tachycardia — Sinus tachycardia has a narrow QRS complex and is the most common atrial tachyarrhythmia during anesthesia and surgery. For most patients with mild sinus tachycardia at 100 to 120 bpm, prompt treatment of the underlying cause is adequate. (See 'Causes of sinus tachycardia' below.)

Appropriate treatment of sinus tachycardia requires careful consideration of the most likely cause in order to avoid adverse effects due to inappropriate treatment. For example, administration of beta blockers to a hypovolemic patient may lead to severe hypotension. Another example is a patient who has tachycardia due to sympathetic stimulation, in whom excessive fluid administration may lead to hypervolemia and pulmonary edema.

Causes of sinus tachycardia

Sympathetic stimulation – The cause of intraoperative sinus tachycardia accompanied by hypertension is usually sympathetic stimulation in response to pain or other noxious stimuli. Examples include sympathetic responses to laryngoscopy and endotracheal intubation during induction of anesthesia, responses to incision and surgical manipulation during the maintenance phase of anesthesia, or pain and stimulation of airway reflexes during emergence and extubation. Tachycardia due to sympathetic stimulation is treated by increasing doses of intravenous (IV) and/or inhalation anesthetic agents to deepen anesthesia and/or by administering an analgesic agent, similar to treatment of intraoperative hypertension. (See "Hemodynamic management during anesthesia in adults", section on 'Adjustment of anesthetic depth'.)

Hypovolemia or anemia – Reflex responses to hypovolemia or anemia cause tachycardia, which is often associated with hypotension. Treatment is administration of appropriate types and volumes of fluid, as discussed in detail separately. (See "Intraoperative fluid management".)

Other causes – Other causes of intraoperative sinus tachycardia include hypoxemia, hypercarbia, fever, sepsis, or malignant hyperthermia. These etiologies should be identified and treated.

Pharmacologic treatment of tachycardia — Intraoperative sinus tachycardia is usually treated with a short-acting IV beta blocker to decrease HR to <80 bpm if HR is >120 bpm, or at a lower HR if the patient has ischemic heart disease or severe aortic or mitral stenosis. Even short episodes of tachycardia may be associated with significant myocardial ischemia in susceptible patients due to shortening of the diastolic time period for coronary blood flow to the left ventricle (LV) and increased myocardial oxygen demand (figure 2 and table 9). Time for LV filling is also diminished with even mild tachycardia. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia' and "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease", section on 'Aortic stenosis' and "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease", section on 'Mitral stenosis'.)

Typically, bolus doses of esmolol 20 to 50 mg are administered every two to three minutes. Administration of a cumulative dose of 200 mg should prompt a search for alternative causes of tachycardia.

Beta blockers should be avoided in patients with significant hypovolemia or acute hemorrhage causing anemia [31,32], and in those with decompensated heart failure, as noted above. Also, patients with acute or severe bronchospastic lung disease and those with a markedly impaired conduction system (eg, sinus node dysfunction) should not receive beta blockers. (See "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents'.)

For recurrent tachycardia, options include:

If beta blocker administration is effective and appropriate, options for treatment of recurrent tachycardia include (see "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents'):

Esmolol infusion – Esmolol may be administered as a continuous infusion (eg, 50 to 300 mcg/minute). However, infusion of esmolol is usually avoided or another beta blocker is substituted in the immediate postoperative period, since administration of any vasoactive infusion necessitates discharge from the post-anesthesia care unit (PACU) to a monitored setting.

Metoprolol or labetalol – Longer-acting beta blockers such as small bolus doses of metoprolol 1 to 5 mg or labetalol 5 to 10 mg are reasonable alternatives to esmolol if intravascular volume status is adequate. Such longer-acting agents are often administered near the end of surgery during preparation for emergence and extubation. Since labetalol is a nonselective beta blocker, it should be titrated in small doses in patients with asthma, chronic obstructive lung disease, heart failure, or hyperadrenergic states such as cocaine or methamphetamine overdose.

Deepening anesthesia – Adjuvant agents such as opioids or dexmedetomidine are particularly likely to slow a rapid HR. (See "Maintenance of general anesthesia: Overview", section on 'Analgesic component: Opioid agents' and "Maintenance of general anesthesia: Overview", section on 'Dexmedetomidine'.)

Other narrow QRS complex atrial tachyarrhythmias — Acute management of other supraventricular tachycardias (SVTs) with a narrow QRS complex depends on whether the patient is hemodynamically stable (algorithm 4). Often, an SVT that is not sinus tachycardia can be terminated with vagal maneuvers or IV pharmacologic therapy (table 10). For hemodynamically unstable patients or those with SVT that persists after administration of pharmacologic therapy, electrical cardioversion is attempted if sinus tachycardia has been ruled out [33]. (See "Overview of the acute management of tachyarrhythmias" and "Cardioversion for specific arrhythmias".)

Atrial fibrillation — Atrial fibrillation (AF) may occur with sudden onset during or shortly after surgery, or may be chronic (waveform 15) [34,35] (see "The electrocardiogram in atrial fibrillation"). Perioperative causes that may lead to development of atrial fibrillation should be sought and treated. These include hypovolemia, hypotension, anemia, trauma, and pain, which may increase sympathetic activity, catecholamine release, HR, and arrhythmogenicity [36].

Treatment of acute or chronic AF with a rapid ventricular response depends on hemodynamic stability (algorithm 4). A HR >150 bpm is usually associated with hypotension, while a HR <120 bpm may be well tolerated.

Hemodynamic instability with AF and rapid ventricular response (≥120 bpm) – Patients with new-onset AF who are hemodynamically unstable (eg, hypotension, myocardial ischemia, pulmonary edema) should undergo immediate synchronized cardioversion (figure 1). (See "Atrial fibrillation: Cardioversion" and "Basic principles and technique of external electrical cardioversion and defibrillation".)

Hemodynamic stability with AF and rapid ventricular response (≥120 bpm) – Patients with known prior or controlled AF who are hemodynamically stable during AF with a rapid ventricular response may be treated with a beta blocker or a calcium channel blocker for attempted control of HR, rather than with immediate cardioversion. This is often the best option, as patients with chronic AF are at risk for the development of thrombi in the left atrial appendage that may embolize during or after cardioversion. (See "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy".)

AF with nonrapid ventricular response (<120 bpm) – Patients with AF with a ventricular response <120 bpm are often hemodynamically stable. Those at risk for developing ischemia or hemodynamic instability require pharmacologic control of the ventricular rate (table 10). (See "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy".)

A beta blocker (eg, bolus doses of esmolol 10 to 25 mg or metoprolol 1 to 5 mg) may be administered to decrease HR to ≤80 bpm, provided that BP is adequate.

Administration of a calcium channel blocker (eg, verapamil or diltiazem) is a reasonable alternative [37,38]. Since both beta blockers and calcium channel blockers have negative inotropic effects, small incremental doses should be employed, and these agents should be avoided in patients with left ventricular systolic failure.

Amiodarone is commonly used to maintain sinus rhythm after cardioversion and is sometimes selected to slow the ventricular rate in patients who remain in AF.

Notably, in a 2019 meta-analysis, a lower incidence of atrial fibrillation or flutter was found in patients receiving beta blockers administered in the perioperative period to prevent noncardiac surgery-related complications (risk ratio [RR] 0.41, 95% CI 0.21-0.79; nine studies, 9080 participants), although the risk of bradycardia and/or hypotension was increased, compared with patients who did not receive beta blockers [3] (see 'Medications that increase risk for bradycardia' above). Furthermore, in a 2018 retrospective study of more than surgical patients receiving chronic beta blocker therapy, early resumption of beta blockers on postoperative day one was associated with decreased risk of postoperative atrial fibrillation after noncardiac surgery [39]. Patients receiving amiodarone or statins may also have a lower incidence of perioperative atrial fibrillation compared with controls [40]. However, neither beta blockers nor other pharmacologic agents are used routinely for prophylaxis of atrial arrhythmias.

Atrial flutter — Atrial flutter typically presents with a rapid ventricular rate (approximately 150 bpm) (waveform 16) (see "Electrocardiographic and electrophysiologic features of atrial flutter"). Intraoperative treatment depends on whether the patient is hemodynamically stable and is similar to that for AF. (See 'Atrial fibrillation' above.)

Atrioventricular nodal reentrant tachycardia — Atrioventricular (AV) nodal reentrant tachycardia (AVNRT) is a paroxysmal SVT due to a reentry circuit around the AV node (waveform 17 and waveform 18). Cardioversion should be attempted in a hemodynamically unstable patient who does not respond immediately to vagal maneuvers (such as carotid sinus massage and the Valsalva maneuver) and/or pharmacologic treatment with adenosine or a calcium channel blocker (table 10). (See "Atrioventricular nodal reentrant tachycardia".)

Multifocal atrial tachycardia — Multifocal atrial tachycardia (MAT) is an uncommon arrhythmia that is usually associated with an underlying disorder such as severe pulmonary disease, pulmonary hypertension, coronary artery disease, valvular heart disease, hypomagnesemia, or theophylline use. MAT commonly presents with at least three distinct P wave morphologies on ECG, with a rapid, irregular atrial rate of >100 bpm (waveform 19). It can be difficult to distinguish MAT from AF. Definitive treatment of MAT relies on addressing the underlying disorder, however in the setting of severe hemodynamic instability antiarrhythmic medications to achieve rate control may be used (eg, beta blockers or calcium channel blockers (table 10)). (See "Multifocal atrial tachycardia".)

Wide QRS complex atrial tachyarrhythmias — Wide QRS complex atrial tachyarrhythmias are most often due to aberrant conduction or preexcitation, and more rarely due to medication effect (eg, antiarrhythmics such as amiodarone) or electrolyte disorders (eg, hyperkalemia). SVT with aberrant conduction is monomorphic with a very regular RR interval. A trial of vagal maneuvers and/or adenosine can provide both diagnostic information and may be therapeutic if the wide complex tachycardia resolves. A continuous rhythm strip should be obtained during any intervention that is intended to slow or terminate the SVT.

Acute management of wide complex tachycardia depends on whether the patient is hemodynamically stable. Hemodynamic instability may occur with any wide complex tachycardia regardless of etiology, but is more likely if the diagnosis is ventricular tachycardia (VT) rather than an SVT.

Hemodynamic instability with wide QRS complex SVT – Prompt treatment with electrical cardioversion is necessary to prevent further clinical deterioration or sudden cardiac arrest in a hemodynamically unstable patient. (See "Advanced cardiac life support (ACLS) in adults", section on 'Regular wide complex' and "Advanced cardiac life support (ACLS) in adults", section on 'Irregular wide complex'.)

Hemodynamic stability with wide QRS complex SVT – In a stable patient with wide QRS complex SVT known to be supraventricular in origin, management is similar to that for narrow QRS complex SVTs. Expert cardiology consultation is recommended as soon as possible. (See "Wide QRS complex tachycardias: Approach to management", section on 'Vagal maneuvers' and "Wide QRS complex tachycardias: Approach to management", section on 'Pharmacologic interventions'.)

For hemodynamically stable patients, additional time may be spent attempting to determine the diagnosis. If the initial diagnosis of wide complex tachycardia was made from a single-lead rhythm strip, a full 12-lead ECG may be useful to rule out VT (see 'Monomorphic ventricular tachycardia' below), in that the presence of AV dissociation and/or a QRS width ≥0.16 seconds is diagnostic of VT [41]. However, in approximately 10 percent of patients with wide complex tachycardia, a definitive diagnosis of SVT versus VT is difficult to establish. Thus, expert cardiology consultation is obtained as soon as possible [33,42]. (See "Wide QRS complex tachycardias: Approach to the diagnosis".)

Wolff-Parkinson-White syndrome — Patients with Wolff-Parkinson-White (WPW) syndrome have an AV reciprocating tachycardia (AVRT) due to a macroreentrant circuit that can degenerate into AF (waveform 20). During the preoperative consultation for patients with this diagnosis, it is critically important to determine whether the AVRT is orthodromic (with antegrade conduction occurring via the AV node and retrograde conduction via an accessory pathway) or antidromic (with antegrade conduction occurring via the accessory pathway and retrograde conduction via the AV node [or sometimes via a second accessory pathway]) in order to select the correct initial pharmacologic therapy in the event of an intraoperative tachyarrhythmia. Ideally, preoperative consultation includes input from an electrophysiology cardiologist in any patient with known or suspected WPW syndrome. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Acute treatment of symptomatic arrhythmias'.)

Hemodynamic instability – For hemodynamically unstable patients with known or suspected WPW, treatment is immediate synchronized cardioversion, similar to treatment of SVT due to other etiologies (algorithm 4).

SVT with hemodynamic stability – For a hemodynamically stable patient, intraoperative management depends on whether conduction is orthodromic or antidromic. However, since it is often difficult to determine if a wide QRS complex tachyarrhythmia has antidromic or orthodromic conduction (and whether it is definitely of supraventricular origin rather than VT), we typically treat stable patients with wide complex tachyarrhythmia with IV procainamide in an effort to terminate the tachycardia, or at least slow the ventricular response while awaiting expert cardiology consultation. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Antidromic AVRT'.)

Patients with orthodromic AVRT may have either a narrow or wide QRS complex. If the complex is narrow or the patient is known to have orthodromic AVRT, initial treatment is one or more vagal maneuvers. If vagal maneuvers are ineffective, adenosine or verapamil may be administered (table 10). (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Orthodromic AVRT'.)

Patients with antidromic AVRT always have a wide QRS complex tachycardia [43]. Standard AV nodal blocking agents should never be administered (eg, beta blockers, non-dihydropyridine calcium channel blockers [verapamil and diltiazem], amiodarone, adenosine, digoxin) if the QRS complex is wide, because blocking the AV node may result in faster conduction of atrial impulses to the ventricle via the accessory pathway, with consequent increase in ventricular rate, exacerbation of hemodynamic instability, and potential for degeneration of the rhythm into lethal VT or ventricular fibrillation (VF) [44].

VENTRICULAR ARRHYTHMIAS — Ventricular rhythms have a wide QRS complex (>120 ms). Possible causes should be investigated and treated immediately, with particular attention to the "H's (ie, hypoxia, hypovolemia, acidosis [hydrogen ion], hypo- or hyperkalemia, hypothermia) and T's" (ie, tension pneumothorax, cardiac tamponade, toxins, pulmonary or coronary thrombosis) [33]. (See 'Potential contributing factors' above and "Intraoperative advanced cardiac life support (ACLS)", section on 'Causes of intraoperative cardiopulmonary arrest'.)

Ventricular fibrillation — Ventricular fibrillation (VF) requires immediate treatment with defibrillation and advanced cardiac life support (ACLS), with repeated shocks as indicated (algorithm 3 and waveform 21). During cardiopulmonary resuscitation (CPR), intravenous (IV) epinephrine 1 mg every three to five minutes is administered, as well as amiodarone 300 mg for the first dose and 150 mg for the second and third doses. (See "Advanced cardiac life support (ACLS) in adults", section on 'Pulseless ventricular tachycardia and ventricular fibrillation' and "Intraoperative advanced cardiac life support (ACLS)", section on 'Initial resuscitation'.)

Monomorphic ventricular tachycardia — Ventricular tachycardia (VT) or flutter typically presents with hypotension with or without a pulse. A regular rhythm with a widened QRS complex may be monomorphic VT (waveform 22) or ventricular flutter (waveform 23). (See "Wide QRS complex tachycardias: Approach to the diagnosis".)

Pulseless ventricular tachycardia – VT with a diminished pulse visible with intra-arterial monitoring requires immediate synchronized cardioversion and ACLS, while patients with no visible or palpable pulse require defibrillation and ACLS (algorithm 3 and algorithm 4). (See "Advanced cardiac life support (ACLS) in adults", section on 'Regular wide complex'.)

Ventricular tachycardia with a pulse – VT with a pulse may be treated with synchronized cardioversion (algorithm 4).

If necessary, myocardial perfusion is augmented with infusion of a vasoconstrictor such as phenylephrine, vasopressin, or norepinephrine (table 1) . Epinephrine is generally avoided due to possible exacerbation of myocardial ischemia, but if selected, the infusion should be titrated to effect to avoid tachycardia. Once blood pressure is adequate, amiodarone or lidocaine may be administered to reduce the frequency of VT. (See "Wide QRS complex tachycardias: Approach to management".)

Polymorphic ventricular tachycardia (torsades de pointes) — Torsades de pointes (TdP) is an irregular polymorphic VT (waveform 24).

Hemodynamic instability – Prompt defibrillation and ACLS is indicated for TdP causing pulselessness, but synchronized cardioversion may be attempted if a diminished pulse is visible with intra-arterial monitoring (algorithm 3 and algorithm 4). (See "Advanced cardiac life support (ACLS) in adults", section on 'Irregular wide complex'.)

Hemodynamic stability – For a hemodynamically stable patient having recurrent episodes of TdP, first-line therapy in the perioperative period is administration of magnesium sulfate 2 grams as a slow IV bolus. Temporary transvenous overdrive pacing (atrial or ventricular) at approximately 100 beats per minute (bpm) is generally reserved for patients with TdP associated with long QT syndrome if there is no response to IV magnesium.

Cardiology consultation is obtained as soon as possible, similar to management of other wide QRS complex tachycardias. Further details are discussed separately. (See "Overview of the acute management of tachyarrhythmias", section on 'Polymorphic ventricular tachycardia'.)

Other ventricular arrhythmias

Premature ventricular contractions — Premature ventricular contractions (PVCs) are common in the general population, even in patients without cardiac disease (waveform 25). Isolated PVCs are usually clinically insignificant, particularly if they occur in a healthy surgical patient due to increased sympathetic stimulation. Frequent PVCs may be a sign of myocardial ischemia or electrolyte abnormalities. These conditions should be suspected as contributing factors and treated if confirmed, particularly in patients with cardiovascular comorbidities (eg, hypertension, ischemic heart disease, systolic or diastolic heart failure, hypertrophic cardiomyopathy). (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation".)

Nonsustained ventricular tachycardia — Nonsustained VT is diagnosed when three or more consecutive ventricular beats are noted on the ECG, at a rate >120 bpm but lasting <30 seconds (waveform 26).

For hemodynamically stable patients with nonsustained VT who have a heart rate (HR) >100 bpm but no compromise of cardiac function, a beta blocker or calcium channel blocker may be administered to reduce the ventricular rate (table 10). Amiodarone or class IB antiarrhythmic agents (eg, lidocaine) may also be effective to maintain sinus rhythm. Similar to patients with PVCs, electrolyte abnormalities and myocardial ischemia should be suspected and treated. We continue electrocardiographic monitoring during the intraoperative and postoperative periods since degeneration into a nonperfusing rhythm (eg, VT or VF) may occur. Further management is discussed separately. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".)

Ventricular paced rhythms — In the setting of a supraventricular tachycardia (SVT) in a patient with a pacemaker, the pacemaker may "track" the atrial rate and pace the ventricle with the same rate. This may appear similar to VT on the electrocardiogram (ECG), particularly if the rate is rapid (waveform 27). It is also possible for a pacemaker to cause retrograde conduction that passes from the ventricle to the atrium, and then conducts again to the ventricle, resulting in an endless loop tachycardia with a wide QRS complex.

To achieve a normal ventricular rate, it may be necessary to reset the pacemaker to an asynchronous mode (at a lower rate) with a magnet or a programming machine. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator", section on 'Magnet application' and "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator", section on 'Reprogramming with a programming machine'.)

POSTOPERATIVE MANAGEMENT — The electrocardiogram (ECG) is continuously monitored in the post-anesthesia care unit (PACU) in all patients, but this is especially important for those who developed an arrhythmia during anesthesia and surgery.

A cardiology consultation should be obtained for patients with evidence of myocardial ischemia (see "Perioperative myocardial infarction or injury after noncardiac surgery"), as well as those who developed a persistent or clinically significant arrhythmia (eg, new onset atrial fibrillation [AF], second or third degree atrioventricular [AV] block, ventricular tachycardia [VT]) or required pharmacologic or other treatment (eg, infusion of an antiarrhythmic agent, pacing, cardioversion) during the intraoperative period.

Patients who had self-limited arrhythmias such as sinus tachycardia, sinus bradycardia, first degree AV block, or premature ventricular contractions (PVCs) usually do not need a postoperative cardiology consultation, particularly if they did not require treatment for hemodynamic instability. In most of these cases, inciting causes are easily corrected and have often resolved by the time the patient arrives in the PACU.

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: Arrhythmias in adults" and "Society guideline links: Basic and advanced cardiac life support in adults".)

SUMMARY AND RECOMMENDATIONS

Contributing factors – Factors contributing to development of arrhythmias may include (see 'Potential contributing factors' above):

Preexisting abnormalities – Preexisting arrhythmias or other abnormal findings on the electrocardiogram (ECG).(See 'Preexisting electrocardiographic (ECG) abnormalities' above.)

Medication effects – Certain medications that increase risk for bradycardia or prolong the QT interval. (See 'Medication effects' above.)

Patient-specific factors:

-Electrolyte abnormalities (See 'Electrolyte abnormalities' above.)

-Hypoxemia, hypocarbia or hypercarbia, acid-base disturbances (See 'Metabolic and respiratory abnormalities' above.)

-Intravascular volume depletion (See 'Intravascular volume depletion' above.)

-Myocardial ischemia or failure (See 'Myocardial ischemia or failure' above.)

Procedure-specific factors:

-Intrathoracic procedures (See 'Intrathoracic procedures' above.)

-Intravascular interventions (See 'Intravascular interventions' above.)

-Electroconvulsive therapy (ECT) (See 'Electroconvulsive therapy' above.)

-Local anesthetic systemic toxicity (LAST) (table 7) (See 'Administration of local anesthetics' above.)

Diagnosis – If a perioperative arrhythmia cannot be readily diagnosed, all available leads are displayed on the monitor, and a 12-lead ECG is obtained. Notably, artifact due to electrocautery or pacing spikes can mimic ventricular tachycardia (VT) or ventricular fibrillation (VF). Stable waveforms from the pulse oximeter, intra-arterial catheter, and/or central venous catheter may be helpful to distinguish artifact from a true arrhythmia. (See 'Intraoperative diagnosis' above.)

Management of bradyarrhythmias – Bradyarrhythmias with heart rate (HR) <60 bpm include (table 8) (see 'Bradyarrhythmias' above):

Sinus bradycardia

-Mild sinus bradycardia – Bradycardia with HR 40 to 60 bpm with normal atrial and ventricular depolarization in a hemodynamically stable patient does not usually require pharmacologic treatment. Causes are sought and treated. (See 'Causes of sinus bradycardia' above.)

-Severe sinus bradycardia – Bradycardia with HR <40 bpm is treated with intravenous (IV) anticholinesterase agents (eg, atropine 0.5 mg for hemodynamically unstable patients, with repeated doses every three to five minutes up to a total of 3 mg (algorithm 2), or IV glycopyrrolate 0.2 mg for hemodynamically stable patients, with repeated doses up to 1 mg). Further treatment of associated hypotension may include ephedrine 10 to 20 mg as bolus doses, or a continuous infusion of a positive chronotropic agent (eg, epinephrine, dopamine, dobutamine (table 1)). (See 'Pharmacologic treatment of bradycardia' above.)

-In some cases, a temporary pacing option may be necessary (eg, transcutaneous, transvenous, transesophageal, or pulmonary artery catheter with pacing capabilities). (See 'Temporary pacing options' above.)

Atrioventricular (AV) block – First degree AV block does not require treatment. Second degree AV block may require pacing if bradycardia is severe or causes hemodynamic compromise. Third degree AV block usually requires pacing due to a very slow HR (ie, 30 to 40 bpm). (See 'First, second, or third degree AV block' above.):

Supraventricular tachyarrhythmias (SVTs) – SVTs with a narrow QRS complex (QRS duration <120 ms) include (see 'Atrial tachyarrhythmias' above):

Sinus tachycardia – For sinus tachycardia with HR 100 to 120 beats per minute [bpm]), prompt treatment of the underlying cause (eg, inadequate anesthesia and/or analgesia, hypovolemia, anemia) is usually adequate. For patients with HR >120 bpm or ischemic heart disease, an IV beta blocker is typically administered to decrease HR to <80 bpm. (See 'Sinus tachycardia' above.)

Other narrow QRS complex SVTs – Treatment depends on whether the patient is hemodynamically stable (algorithm 4). Ventricular rate >150 bpm is usually associated with hypotension, while a ventricular rate <120 bpm may be well tolerated. (See 'Other narrow QRS complex atrial tachyarrhythmias' above.)

-Atrial fibrillation or flutter (see 'Atrial fibrillation' above and 'Atrial flutter' above):

For hemodynamically unstable patients with new-onset atrial fibrillation (AF) or flutter, treatment is immediate synchronized cardioversion (figure 1).

For hemodynamically stable patients with preexisting AF who develop a rapid ventricular response or those with HR <120 bpm, IV beta blockers (eg, esmolol, metoprolol) or calcium channel blockers (eg, verapamil, diltiazem) may control HR (table 10), rather than employing immediate cardioversion (with exposure to risk for atrial thrombus embolization).

-AV nodal reentrant tachycardia (AVNRT) – For hemodynamically unstable patients who do not respond immediately to vagal maneuvers (such as carotid sinus massage and the Valsalva maneuver) and/or pharmacologic treatment with adenosine or a calcium channel blocker (table 10), cardioversion should be attempted. (See 'Atrioventricular nodal reentrant tachycardia' above.)

-Multifocal atrial tachycardia (MAT) – For a rapid ventricular response, pharmacologic agents are administered to achieve rate control (eg, IV beta blockers or calcium channel blockers (table 10)). (See 'Multifocal atrial tachycardia' above.)

SVTs with a wide QRS complex – SVTs with QRS duration >120 ms include (see 'Wide QRS complex atrial tachyarrhythmias' above):

SVT with aberrant conduction – Monomorphic wide complex SVT often responds to a trial of vagal maneuvers and/or adenosine. Further management is similar to that for narrow QRS complex SVTs in a stable patient with a SVT known to be supraventricular in origin (algorithm 4). (See 'Wide QRS complex atrial tachyarrhythmias' above.)

Wolff-Parkinson-White (WPW) syndrome:

-For hemodynamically unstable patients with known or suspected WPW syndrome, we typically treat with IV procainamide to terminate the tachycardia or slow the ventricular response, particularly if it is difficult to determine whether conduction is orthodromic (ie, through the AV node) or antidromic (ie, via an accessory pathway), or whether the arrhythmia might actually be VT rather than SVT.

-For hemodynamically stable patients with suspected WPW syndrome, standard AV nodal blocking agents (ie, beta blockers, calcium channel blockers, amiodarone, adenosine, digoxin) should NOT be administered unless it is known that conduction is orthodromic. Risks for blocking the AV node in a patient with antidromic conduction include faster conduction of atrial impulses to the ventricle with increased ventricular rate, hemodynamic instability, or rhythm degeneration into VT or VF. (See 'Wolff-Parkinson-White syndrome' above.)

Ventricular rhythms (see 'Ventricular arrhythmias' above):

Pulseless VF or VT (see 'Ventricular fibrillation' above and 'Monomorphic ventricular tachycardia' above):

-VF or VT with no visible or palpable pulse is treated with immediate defibrillation and advanced cardiac life support (ACLS), with repeated shocks as indicated (algorithm 3).

-VT with a pulse, even if diminished, may be treated with synchronized cardioversion (algorithm 4).

Torsades de pointes (TdP) (see 'Polymorphic ventricular tachycardia (torsades de pointes)' above):

-For TdP without a pulse, prompt defibrillation and ACLS are indicated (waveform 24 and algorithm 3).

-For a hemodynamically unstable patient with a diminished pulse (eg, visible with intra-arterial monitoring), synchronized cardioversion may be attempted (waveform 24 and algorithm 3 and algorithm 4).

-For a hemodynamically stable patient with recurrent intraoperative episodes of TdP, first-line therapy is administration of magnesium sulfate 2 g as a slow IV bolus. Temporary transvenous overdrive pacing (atrial or ventricular) at approximately 100 bpm is generally reserved for patients with TdP associated with long QT syndrome.

Other ventricular arrhythmias – Frequent premature ventricular contractions (PVCs), nonsustained VT, monomorphic VT, and ventricular paced rhythms are not immediately life-threatening. (See 'Other ventricular arrhythmias' above.)

Postoperative management – In the post-anesthesia care unit (PACU), the ECG is continuously monitored and a cardiology consultation is obtained for patients with persistent or clinically significant arrhythmia (eg, new onset of AF, second or third degree AV block, VT), suspected myocardial ischemia, or if intraoperative pharmacologic or other treatment (eg, infusion of an antiarrhythmic agent, pacing, cardioversion) was necessary. (See 'Postoperative management' above.)

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Topic 94357 Version 31.0

References

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