Perioperative arrhythmias

INTRODUCTION — 

Perioperative tachyarrhythmias (heart rate [HR] >100 beats per minute [bpm]) and bradyarrhythmias (HR <60 bpm) are common and vary depending on type of procedure and patient’s underlying co-morbidities [1,2]. While most intraoperative arrhythmias are transient and clinically insignificant, some indicate underlying pathology that warrants prompt treatment (eg, myocardial ischemia, electrolyte abnormalities), and some have 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. Additional details are available in the following related topics:

●Advanced cardiac life support (ACLS) for life-threatening arrhythmias

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

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

●Management of specific arrhythmias

•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 "Acquired third-degree (complete) atrioventricular block".)

Identification and management of arrhythmias detected on a preoperative electrocardiogram are discussed separately. (See "The preoperative ECG: Evaluation and implications for management in adults".)

POTENTIAL CONTRIBUTING FACTORS — 

Factors likely to contribute to the development of perioperative arrhythmias may be identified in the preoperative period or may be recognized and managed during the intraoperative period.

Medication effects

Heart rate — The effects of certain chronically or acutely administered medications may directly or indirectly cause changes in heart rate (HR).

●Medications that cause sinus bradycardia – As discussed below, certain medications may cause bradycardia during surgery or other invasive procedures. (See 'Causes of sinus bradycardia' below.)

●Medications that cause sinus tachycardia – Medications can cause tachycardia via direct effects (eg, beta-1 agonists increase HR) or indirectly (eg, anesthetic agents may cause hypotension which may trigger reflex tachycardia). (See 'Hypotension or anemia' below.)

●Tachycardia due to beta blocker withdrawal – Supraventricular tachycardias (SVTs) caused by beta blocker withdrawal is discussed below. (See 'Causes' below.)

QT interval prolongation — Some agents that are commonly administered in the perioperative period may prolong the QT interval (eg, methadone, droperidol, and ondansetron) (table 1). These agents should be avoided in patients with a history of prolonged QT interval since they may increase risk for the malignant ventricular arrhythmia torsades de pointes (TdP) (waveform 1). Other causes and potentiators of long QT syndrome are listed in the table (table 2). (See 'Polymorphic ventricular tachycardia (torsades de pointes)' below and "The preoperative ECG: Evaluation and implications for management in adults", section on 'QT prolongation'.)

Although many anesthetic agents (eg, opioids, dexmedetomidine, midazolam, etomidate, ketamine, volatile anesthetic agents) may cause slight prolongation of the QT interval (>440 ms), these are unlikely to cause TdP [3-11].

Local anesthetic systemic toxicity (LAST) — Clinical manifestations, prevention and management of LAST are discussed in detail separately (table 3). (See "Local anesthetic systemic toxicity".)

LAST should be suspected whenever physiologic changes, including arrhythmias, occur shortly after administration of a local anesthetic (eg, for regional anesthetic block). Cardiovascular signs usually occur simultaneously with or shortly after central nervous system (CNS) symptoms (such as agitation or altered responsiveness). Typically, tachycardia and hypertension occur, although bradycardia and hypotension have also been described as the first changes. Cardiovascular toxicity can lead to ventricular arrhythmias and/or asystole.

Patient-specific factors — A variety of acute and chronic conditions are causes of atrial and/or ventricular arrhythmias. These conditions are treated in the preoperative period when possible, with continuing management during the intraoperative period as needed.

Preexisting ECG abnormalities — Preoperative electrocardiograms (ECGs) are examined when available to identify preexisting arrhythmias and other findings associated with risk for development of intraoperative arrhythmia (eg, corrected QT interval [QTc] prolongation) (table 4), as discussed separately. (See "The preoperative ECG: Evaluation and implications for management in adults".)

Electrolyte abnormalities

Potassium disorders

●Hypokalemia – When hypokalemia is identified, its cause(s) and concurrent abnormalities (particularly hypomagnesemia) should be identified and treated. (See "Clinical manifestations and treatment of hypokalemia in adults" and "Evaluation of the adult patient with hypokalemia".)

Hypokalemia causes characteristic changes on the ECG such as ST segment depression, decreased T wave amplitude, and increased U wave amplitude (waveform 2), as well as prolongation of the QT interval. However, there is considerable interpatient variability in the serum potassium concentration associated with ECG changes and arrhythmias. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Cardiac arrhythmias and ECG abnormalities'.)

Although there are no definitive values of hypokalemia mandating cancellation of elective surgery, potassium <2.5 mmol/L can cause increased risk of arrhythmias including premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular (AV) block, and ventricular tachycardia (VT) and ventricular fibrillation (VF).

We generally administer potassium repletion when levels are <3.5 mmol/L. Patients undergoing surgery may be treated with 20 mEq of potassium in an intravenous (IV) saline solution administered over one hour through a central line. Alternatively, when given through a peripheral IV, the infusion should be infused over two hours to reduce risk of phlebitis.

The above IV doses do not take into account ongoing potassium losses. For patients with ongoing gastrointestinal or renal losses, potassium repletion must be increased to account for these losses. Some patients with renal potassium wasting may require treatment with a potassium-sparing diuretic. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Estimation of the potassium deficit'.)

Patients with severe perioperative hypokalemia (<3.0 mEq/L) or symptomatic hypokalemia (including arrhythmias) require more prompt IV potassium repletion and monitoring, as discussed separately. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Severe or symptomatic hypokalemia'.)

More cautious potassium repletion is warranted for patients with hypokalemia caused by potassium redistribution into cells, since there is a risk of rebound hyperkalemia, as discussed separately. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Treatment' and "Hypokalemic periodic paralysis" and "Thyrotoxic periodic paralysis".)

In prospective observational studies, serum potassium levels <3.5 mmol/L predicted serious perioperative arrhythmias and postoperative atrial fibrillation (AF) and atrial flutter in patients undergoing cardiac surgery [12], and hypokalemic patients undergoing noncardiac surgery experienced a higher frequency of major adverse cardiovascular events [13].

●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, VT and VF [14]. While patients with hyperkalemia may have peaked T waves (waveform 3), 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.

Preoperative management for patients with or without end-stage renal disease (ESRD) depends on the severity of hyperkalemia, as well as on whether the proposed procedure is elective or urgent. Details regarding management of perioperative hyperkalemia are noted in the algorithm and the table (algorithm 1 and table 5). Notably, succinylcholine should be avoided if potassium ≥5.5 mEq/L.

Many patients with preoperative hyperkalemia have ESRD. Further discussion of management for patients with ESRD is available in a separate topic. (See "Anesthesia for dialysis patients", section on 'Management of hyperkalemia'.)

Magnesium disorders

●Hypomagnesemia – Hypomagnesemia widens the QRS complex and increases the risk of TdP, sustained AF, frequent atrial or ventricular ectopic beats, and other ventricular arrhythmias [15]. Hypomagnesemia commonly occurs concurrently with hypokalemia and should be treated. Correction of hypomagnesemia may be required to correct hypokalemia. Clinical manifestations and treatment are discussed further separately. (See "Hypomagnesemia: Clinical manifestations of magnesium depletion", section on 'Cardiovascular manifestations' and "Hypomagnesemia: Evaluation and treatment".)

●Hypermagnesemia – Hypermagnesemia (>4 mEq/L) may cause conduction defects, bradycardia, and hypotension as well as neurologic impairment (eg, paralysis, somnolence, coma). In patients with normal or near normal kidney function, symptoms typically resolve with cessation of magnesium therapy (eg, IV magnesium infusion for treatment of eclampsia or preeclampsia). In patients with moderate kidney impairment, isotonic IV fluids plus a loop diuretic (eg, furosemide) are administered, in addition to discontinuing any magnesium therapy. Dialysis may be required in patients with severe kidney impairment. (See "Hypermagnesemia: Causes, symptoms, and treatment", section on 'Cardiovascular effects' and "Hypermagnesemia: Causes, symptoms, and treatment", section on 'Treatment'.)

Calcium disorders

●Hypocalcemia – Hypocalcemia prolongs the QT interval (waveform 4), but has less potential to trigger TdP compared with hypokalemia or hypomagnesemia; it infrequently causes heart block or ventricular dysrhythmias. Clinical manifestations of severe acute or symptomatic hypocalcemia are treated by administering IV calcium, as well as by treating concurrent hypomagnesemia, as 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 ECG. Although moderate hypercalcemia has no clinically important effects on cardiac conduction or the prevalence of supraventricular or ventricular arrhythmias, severe hypercalcemia may lead to various cardiac arrhythmias and ST-segment elevation that mimic myocardial infarction. Treatment is administration of IV saline, diuresis, calcitonin, and bisphosphonate, 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 the development of arrhythmias. Management of these disorders is discussed separately. (See "Mechanical ventilation during anesthesia in adults" and "Intraoperative advanced cardiac life support (ACLS)", section on 'Treat the etiology of the cardiac arrest'.)

Hypotension or anemia — Reflex responses to hypovolemia, vasodilation, low cardiac output, or anemia typically result in sinus tachycardia that is often associated with hypotension and may lead to development of other arrhythmias, as discussed below.

●Intraoperative management of hypovolemia is with administration of appropriate types and volumes of fluid, as discussed in detail separately. (See "Intraoperative fluid management".)

●Intraoperative management of vasodilation or low cardiac output is discussed separately. (See "Intraoperative use of vasoactive agents".)

●Prevention and management of perioperative anemia is discussed separately. (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Treatment of anemia and iron deficiency'.)

Heart disease — Heart disease (ischemic or nonischemic) is commonly associated with atrial and ventricular arrhythmias (eg, atrial fibrillation and ventricular tachycardia). (See 'Tachyarrhythmias' below.)

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 cardiomyopathy and/or heart failure are at risk for arrhythmias. Some will have a pacemaker for physiologic pacing (cardiac resynchronization therapy or conduction system pacing) or an implantable cardioverter defibrillator. Perioperative management of these devices is discussed separately. (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 cardiac and thoracic surgical procedures performed near the heart (eg, pulmonary resection or esophageal surgery), contact with cardiac or pulmonary venous structures may cause atrial or ventricular arrhythmias. Management of arrhythmias during cardiac surgery is 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 or pulmonary artery catheter [16]. When the guidewire or catheter enters the right atrium, premature atrial contractions, AF, or other SVTs may occur (see 'Supraventricular tachycardia' below). Upon entry into the right ventricle, right BBB [17] (see 'Conduction system disease' below), premature ventricular contractions (PVCs), or VT may occur (see 'Types of ventricular arrhythmia' 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) may cause atrial and/or ventricular arrhythmias via a similar mechanism.

●Electroconvulsive therapy – Anesthesia for electroconvulsive therapy (ECT) is associated with various arrhythmias. Bradycardia with hypotension, and in some cases asystole, is most common at the first ECT treatment. Premedication with an anticholinergic agent, either glycopyrrolate 0.2 mg IV or atropine 0.4 mg IV, is often used to prevent vagally-mediated bradycardia. Details are available in a separate topic. (See "Anesthesia for electroconvulsive therapy", section on 'Anticholinergic prophylaxis'.)

●Vagal reflexes causing bradycardia – Surgical manipulation may precipitate vagal reflexes that cause bradycardia. If HR does not increase when the surgical stimulus is temporarily stopped, an anticholinergic agent is administered. (See 'Pharmacologic treatment' below.)

Examples of vagal reflex responses to surgical manipulation include:

•Eye surgery – 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. (See "Anesthesia for elective eye surgery", section on 'Oculocardiac reflex manifestations'.)

•Abdominal surgery – During laparoscopic (or open) abdominal surgery, peritoneal stretching may cause a parasympathetically mediated bradycardia, which should resolve promptly when the surgeon ceases the inciting manipulation. (See "Anesthesia for laparoscopic and abdominal robotic surgery in adults", section on 'Cardiovascular changes'.)

•Carotid surgery – 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. (See "Anesthesia for carotid endarterectomy and carotid stenting", section on 'Hemodynamic management during CEA' and "Anesthesia for carotid endarterectomy and carotid stenting", section on 'Hemodynamic management during CAS or TCAR'.)

Neuraxial anesthesia with a high block — Neuraxial anesthesia with a high T1 to T4 anesthetic level may cause sinus bradycardia and hypotension [18-21]. Bradycardia caused by blockade of the cardiac accelerator fibers is treated with beta-adrenergic agonists such as ephedrine 5 to 10 mg or epinephrine 10 to 20 mcg, although atropine may also be administered. If bradycardia persists, an epinephrine infusion may be initiated (table 6). 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. This response has been termed the Bezold-Jarisch reflex, vasovagal syncope, or neurocardiogenic syncope [22]. 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) [20-22]. 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.

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. In addition, much of the other electronic equipment in the operating room may generate a range of ECG artifacts, which are not eliminated by selection of “monitor” or “filter” modes [23].

Of note, pacemaker stimulus outputs (ie, pacing spikes) are small-amplitude high-frequency signals that may be attenuated and not reliably detected on ECG monitors and recordings, particularly when the ECG “monitor” or “filter” selections are enabled. In some cases, pacing spikes may be seen in some leads, but not others. Selection of the least filtered “diagnostic” bandpass mode for ECG monitoring will most closely mirror standard 12-lead ECGs and help identify pacing spikes. In addition, ECG monitors include a "pacing mode" selection that improves detection of paced rhythms by highlighting the pacing spikes.

Stable waveforms from the pulse oximeter, capnometer, intra-arterial catheter, and/or central venous catheter are helpful to distinguish artifact from a true arrhythmia. Pulse oximeter and intra-arterial catheter waveforms are also helpful in identifying failure of pacemaker capture (pacemaker spikes not followed by P or QRS complexes with corresponding lack of arterial pulsations). (See "Basic patient monitoring during anesthesia", section on 'Sources of ECG artifact'.)

BRADYARRHYTHMIAS — 

Bradycardia is defined as a heart rate (HR) <60 beats per minute (bpm).

Sinus bradycardia — Sinus bradycardia with normal atrial and ventricular depolarization is the most common bradyarrhythmia during anesthesia and surgery (waveform 5).

Causes of sinus bradycardia — Intraoperative causes of sinus bradycardia include :

●Medications – Whether administered chronically or acutely in the operating room, medications that increase risk for sinus bradycardia include:

•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. Patients with ischemic heart disease or heart failure are often taking these agents chronically; thus, it is important to note baseline HR. Perioperative management recommendations for these patients include [24] (see "Management of cardiac risk for noncardiac surgery", section on 'Beta blockers'):

-For those on chronic beta blocker therapy, these agents are generally continued during the perioperative period.

-For those without an indication for long-term beta blocker therapy, prophylactic beta blockers are not routinely started in the immediate preoperative period given evidence of risk of harm.

-In those with an indication for long term beta blocker therapy who have not yet started such treatment, the timing of initiation (prior to or following the planned procedure) is individualized.

Also, beta blockers such as esmolol, metoprolol, or labetalol are commonly administered during the intraoperative period to treat myocardial ischemia, tachycardia, or hypertension. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Treatment of ischemia'.)

If sinus bradycardia is associated with hypotension caused by a beta blocker or calcium channel blocker overdose, then administration of the agent is discontinued. Further treatment, if necessary, is with administration of intravenous (IV) glucagon together with other interventions (table 7 and table 8) [25]. (See "Beta blocker poisoning", section on 'Management' and "Calcium channel blocker poisoning", section on 'Management' and "Sinus bradycardia", section on 'Management'.)

•Anticholinesterase agents – Sinus bradycardia may be caused by the muscarinic effects of an acetylcholinesterase inhibitor (eg, neostigmine) when such agents are used to reverse effects of nondepolarizing neuromuscular blocking agents (NMBA) near the end of surgery. The patient should always receive an appropriate dose of anticholinergic agent together with the selected acetylcholinesterase inhibitor. Dosing is discussed in a separate topic. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Anticholinesterases'.)

Underdosing the anticholinergic agent (relative to the acetylcholinesterase inhibitor agent) may lead to severe bradycardia. If this is suspected, repeated doses of glycopyrrolate 0.2 mg or atropine 0.4 mg are appropriate.

•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 [26-29]. Precautions include slow administration of sugammadex with continuous electrocardiographic monitoring. Particular caution is necessary when sugammadex is administered to a patient concurrently receiving other medications known to slow the HR. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Sugammadex'.)

•Opioids – Severe sinus bradycardia may occur when a large bolus dose of an opioid agent (eg, fentanyl, remifentanil, sufentanil) is administered [30-33].

•Dexmedetomidine – The selective alpha₂ agonist anesthetic agent dexmedetomidine can cause hypotension and/or bradycardia due to its sympatholytic effects. (See "Maintenance of general anesthesia", section on 'Dexmedetomidine'.)

•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 6). This effect tends to be transient; however, hemodynamically significant bradycardia may be treated with an anticholinergic agent.

●Vagal reflexes – Surgical manipulation may precipitate vagal reflexes that cause bradycardia. (See 'Procedure-specific factors' above.)

Myocardial ischemia is one of the causes of vagal stimulation that may cause bradycardia (table 9). (See "Sinus bradycardia", section on 'Etiology'.)

●Neuraxial anesthesia with a high block – Neuraxial anesthesia with a high T1 to T4 anesthetic level may cause hypotension and sinus bradycardia due to blockade of the cardiac accelerator fibers [18-21]. (See 'Neuraxial anesthesia with a high block' above.)

Treatment for sinus bradycardia — Mild or transient sinus bradycardia with HR 40 to 60 bpm in a normotensive and otherwise stable patient does not usually require treatment, although the cause should be sought and treated if appropriate. (See 'Causes of sinus bradycardia' above.)

In addition to managing the underlying etiology, severe sinus bradycardia with HR <40 bpm (and also higher heart rates when associated with hypotension) is treated with pharmacologic agents and occasionally with temporary pacing (table 10).

Pharmacologic treatment — Sinus bradycardia is treated pharmacologically with an 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.)

If bradycardia is associated with persistent 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 of ephedrine have been administered (eg, epinephrine, dopamine, dobutamine). For persistent severe bradycardia, continuous infusion of a positive chronotropic agent is typically initiated (table 6). (See "Intraoperative use of vasoactive agents", section on 'Vasopressor and positive inotropic agents'.)

●Hemodynamic stability – For patients who remain normotensive and otherwise 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, to avoid undesirable tachycardia, particularly in those with ischemic heart disease. A reasonable alternative is the administration of small incremental doses of atropine 0.2 mg.

●Special considerations – Certain circumstances require specific approaches to bradycardia with or without hemodynamic stability:

•Management of beta blocker overdose, including use of glucagon, is discussed separately (table 7). (See "Beta blocker poisoning", section on 'Management'.)

•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 'Conduction system disease' below and 'Temporary pacing options' below.)

•Patients with a transplanted heart have functional denervation; thus, anticholinergic drugs will not be effective. A direct-acting positive chronotropic agent such as isoproterenol or epinephrine should be used instead. Although re-innervation may occur over time, this should not be assumed. Thus, direct-acting agents are preferred. (See "Anesthesia for heart transplantation", section on 'Denervation of the transplanted heart' and "Heart transplantation in adults: Arrhythmias".)

●Neuraxial anesthesia with a high block – Bradycardia caused by blockade of the cardiac accelerator fibers is treated with beta-adrenergic agonists such as ephedrine 5 to 10 mg or epinephrine 10 to 20 mcg. Atropine may also be administered. For severe or persistent bradycardia, epinephrine is administered as described above (table 6). (See 'Neuraxial anesthesia with a high block' above.)

Temporary pacing options — Occasionally, temporary pacing may be necessary for a patient with recurrent or severe bradycardia with hemodynamic instability. Temporary pacing is rarely indicated in a hemodynamically stable patient with an HR of 40 to 60 bpm. Capture should be confirmed by comparing the paced rate with the pulse rates detected by pulse oximetry and/or intra-arterial catheter waveforms. (See "Temporary cardiac pacing".)

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. Given the potential instability of capture and patient discomfort associated with this type of pacing, transcutaneous pacing is generally a temporizing measure until temporary transvenous pacing is implemented or a permanent pacemaker is inserted. (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.

The following concerns have been noted for transcutaneous pacing:

•Successful capture and pacing are not achieved in all patients. Pacing capture may be difficult to achieve in a patient with severe obesity or when appropriate pad placement is not possible. Examples include patients undergoing thoracic surgery, placement in the lateral or prone position, and those with extensive burns or excessive hair.

•Capture may be interrupted by movement or inconsistent adhesion of the pacing pads. Since the large stimulus artifact may be inaccurately interpreted on the monitor as capture, continuous confirmation of the pulse rate is required.

•For patients who are awake or only mildly sedated, transcutaneous pacing may be painful. (See "Temporary cardiac pacing", section on 'Transcutaneous'.)

●Transvenous pacing – Intraoperative transvenous pacing is generally the temporary pacing method of choice if transcutaneous pacing fails to reliably capture, is not feasible (eg, due to the location of the surgical procedure), or is likely to be disrupted. Transvenous pacing requires insertion of an introducer sheath in a central vessel, most commonly the right internal jugular vein. In some cases, 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. Also, presence of a mechanical prosthetic tricuspid valve is a contraindication for transvenous pacing. (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 when the pacing lead contacts the right ventricle. Correct placement requires expertise in both transvenous wire insertion and pacing technology; thus, cardiology consultation may be required. Ideally, fluoroscopy is used with direct visualization of the pacing lead during insertion to ensure optimal placement within the right ventricle. If intraoperative fluoroscopy is not possible, transesophageal echocardiography examination or a postoperative radiograph is necessary to check correct final positioning of the pacing lead. (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 on a pacing PAC are typically less stable than those of a dedicated transvenous pacing wire since they only abut the endocardium and are not otherwise affixed. 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).

●Epicardial pacing wires – This method of temporary pacing is used for patients undergoing cardiac surgery, as discussed separately. (See "Temporary cardiac pacing", section on 'Epicardial'.)

Conduction system disease — Patients receiving anesthesia may have pre-existing and/or new onset conduction delays including AV block, left bundle branch block (BBB) (waveform 6), right BBB (waveform 7), or fascicular block (waveform 8 and waveform 9).

Causes of conduction system disease — New onset of perioperative conduction abnormalities typically occurs in the setting of intrinsic cardiac disease, perioperative ischemia, electrolyte abnormalities, excessive vagal tone, or prior surgical or transcatheter aortic valve replacement. (See "The preoperative ECG: Evaluation and implications for management in adults", section on 'Bundle branch blocks and fascicular blocks (hemiblocks)'.)

Transient right BBB occasionally occurs during insertion of a PAC and may progress to complete heart block in a patient with a pre-existing left BBB. For this reason, transcutaneous pacing pads should be positioned before PAC insertion for a patient with left BBB [34,35].

Management of AV block — AV block is classified as first, second, or third degree:

●First-degree AV block – This occurs when there is delayed but intact conduction from the atria to the ventricles (waveform 10) and does not require treatment. (See "First-degree atrioventricular block".)

●Second-degree AV block – This 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 11)); or prolonged PR intervals with occasional dropped ventricular beats (Mobitz Type II (waveform 12)). Second-degree AV block occurring in the perioperative setting may require intervention (pharmacologic or pacing depending upon presentation) if bradycardia causes symptoms or hemodynamic compromise (algorithm 3 and algorithm 4). (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)" and "Second-degree atrioventricular block: Mobitz type II".)

●Third-degree AV block – With third-degree (complete) AV block, no atrial impulses conduct to the ventricles so P waves are discordant with QRS waves (ie, there is AV dissociation) (waveform 13 and waveform 14). Pacing is typically required for patients with hemodynamic instability (algorithm 5). Patients with third-degree AV block who are hemodynamically stable do not require urgent therapy but should be continuously monitored with transcutaneous pacing pads in place, since the intrinsic ventricular rhythm is usually very slow (approximately 30 to 40 bpm) and may progress to symptomatic bradycardia (algorithm 5). (See "Acquired third-degree (complete) atrioventricular block".)

●Asystole – Patients who develop severe intraoperative bradycardia are at risk for progression to asystole which requires immediate initiation of advanced cardiac life support (ACLS) (algorithm 6). (See "Advanced cardiac life support (ACLS) in adults", section on 'Asystole and pulseless electrical activity'.)

AV DISSOCIATION

Definition and causes of AV dissociation — Atrioventricular (AV) dissociation is defined as independent activation of the atria and ventricles [36]. AV dissociation may be observed during both tachyarrhythmias and bradyarrhythmias. Causes of AV dissociation include complete (third-degree) AV block as well as conditions in which the ventricles are activated by stimuli from the AV junction or ventricle (including junctional or ventricular escape, accelerated rhythm, or tachycardia) without atrial capture [36,37]. While some causes of AV dissociation such as complete heart block and sustained ventricular tachycardia require intervention, other causes such as isorhythmic AV dissociation are relatively benign and often self-limited. (See 'Causes of conduction system disease' above and 'Types of ventricular arrhythmia' below.)

Isorhythmic AV dissociation — Isorhythmic AV dissociation most commonly occurs during sinus rhythm with a competing junctional escape rhythm at a similar rate. The electrocardiogram (ECG) may show variation in the P-P interval and one or more QRS complexes without a preceding P wave, which may be misinterpreted as AV block or atrial fibrillation (waveform 15). Because AV conduction is intact during the competing rhythm, AV conduction may result in periodic ventricular capture or fusion beats.

Isorhythmic AV dissociation occurs commonly in anesthetized patients, particularly those receiving volatile inhaled anesthetics [38-40]. This dysrhythmia is generally benign and self-limited, causing no or mild hypotension; and it usually requires no treatment unless the patient is dependent on AV synchrony for adequate ventricular filling (eg, due to diastolic dysfunction). If necessary, small doses of a vasopressor may be administered (table 6).

TACHYARRHYTHMIAS

Categories — Tachyarrhythmias (rhythms with heart rate [HR] >100 beats per minute [bpm]) are categorized into narrow and wide QRS complex tachycardias and regular or irregular rhythms (algorithm 7).

●Narrow QRS complex tachycardias (QRS <120 ms) – These are nearly always supraventricular tachyarrhythmias (SVTs), which arise from the sinus node, atria, atrioventricular (AV) node, His bundle, or a combination of these sites. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)

●Wide QRS complex tachycardias (QRS ≥120 ms) – These include ventricular tachycardia (VT); they also include SVTs with bundle branch block (BBB), aberrant conduction, or antegrade conduction via an accessory pathway). (See "Wide QRS complex tachycardias: Approach to the diagnosis".)

General approach to management — Management of tachyarrhythmias involves addressing underlying causes [41], and possible additional interventions based upon the type of arrhythmia and the patient’s hemodynamic status. A general approach to tachyarrhythmias is described in the algorithm (algorithm 8), although management is tailored to the specific type of arrhythmia. (See "Overview of the acute management of tachyarrhythmias".)

Causes — Intraoperative causes of sinus tachycardia and other tachyarrhythmias include:

●Sympathetic stimulation due to surgical stimuli – The most common cause of intraoperative sinus tachycardia and associated hypertension is inadequate anesthesia resulting in sympathetic stimulation in response to pain or other noxious stimuli, or anxiety in an awake patient. Sympathetic activity triggers catecholamine release, increased HR, and arrhythmogenicity. Examples include sympathetic responses to laryngoscopy and endotracheal intubation during induction of anesthesia, responses to incision and surgical manipulation, 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, administering an analgesic agent for painful stimuli, or administering a sedative agent for anxiety. Opioid analgesic agents or the anesthetic agent dexmedetomidine are particularly likely to slow a rapid HR. (See "Hemodynamic management during anesthesia in adults", section on 'Adjustment of anesthetic depth'.)

●Hypotension or anemia – Reflex responses to anemia or causes of hypotension (eg, hypovolemia or vasodilation) cause sinus tachycardia. However, patients with these causes of sinus tachycardia may or may not have overt hypotension. Prompt treatment is indicated before hypotension develops or worsens. (See 'Heart rate' above and 'Hypotension or anemia' above.)

•Hypovolemia – Hypovolemia is treated with volume repletion and addressing causes (eg, acute blood loss). (See "Hemodynamic management during anesthesia in adults", section on 'Fluid administration' and "Hemodynamic management during anesthesia in adults", section on 'Trendelenburg positioning'.)

•Vasodilation or refractory hypotension – When hypotension is caused by vasodilation or does not immediately respond to treatment of the apparent cause, vasopressor agents are administered. Inotropic agents are used as a temporizing measure if the likely cause of hypotension is impaired left ventricular and/or right ventricular systolic function. (See "Intraoperative use of vasoactive agents" and "Use of vasopressors and inotropes".)

•Anemia – Intraoperative management of anemia is discussed separately. (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Intraoperative strategies'.)

•Effects of anesthetic agents – Anesthetic agents may cause or exacerbate hypotension and compensatory sinus tachycardia, particularly if anesthetic depth is excessive.

●Beta blocker withdrawal – Acute beta blocker withdrawal (eg, omission of one or more doses of a chronically administered beta blocker) in the perioperative period is a common cause of sinus tachycardia and other SVTs. For this reason, beta blocker withdrawal may increase risk for myocardial ischemia or infarction. (See "Major side effects of beta blockers", section on 'Beta blocker withdrawal'.)

●Other causes – Other perioperative causes of tachycardia requiring prompt intervention include hypoxemia, hypercarbia, fever, sepsis, or malignant hyperthermia.

SUPRAVENTRICULAR TACHYCARDIA — 

Supraventricular tachyarrhythmias (SVTs) usually have a narrow QRS complex (<120 milliseconds), although some have a wide QRS complex (≥120 milliseconds) (algorithm 9).

Sinus tachycardia — Sinus tachycardia is the most common SVT during anesthesia and surgery.

●Treatment of cause – The first step in managing sinus tachycardia is to identify and treat the cause (eg, light anesthesia or hypovolemia). (See 'Causes' above.)

Such treatment is often sufficient to resolve the tachycardia, particularly if it is mild with heart rate (HR) 100 to 120 beats per minute (bpm). Intravenous (IV) beta blocker therapy is administered when tachycardia is likely due to beta blocker withdrawal.

●Beta blocker therapy – If tachycardia does not resolve after appropriate and adequate interventions to address the cause (eg, treatment of hypovolemia), then pharmacologic treatment may be indicated. Even mild tachycardia may be associated with clinically significant deterioration in patients with ischemic heart disease due to shortening of the diastolic time period for coronary blood flow to the left ventricle (LV) and increased myocardial oxygen demand may cause exacerbation of ischemia (figure 2 and table 11). In patients with severe aortic or mitral stenosis, tachycardia may cause clinical deterioration by diminishing time for LV filling. In many cases, a short-acting IV beta blocker such as esmolol in 20 to 50 mg bolus doses administered every two to three minutes is appropriate to decrease HR to 80 to 100 bpm.

Nonselective beta blockers are avoided in patients with asthma or chronic obstructive lung disease (COPD) (table 12). (See "Management of the patient with COPD and heart disease", section on 'Beta-2 agonists' and "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents' and 'Conduction system disease' above.)

Beta blocker therapy is avoided in patients with acute decompensated heart failure with reduced ejection fraction, or those with markedly impaired atrioventricular (AV) conduction or sinus node dysfunction. (See "Treatment of acute decompensated heart failure: General considerations", section on 'Treatment goals for acute versus chronic HF' and 'Causes of sinus bradycardia' above and "Intraoperative use of vasoactive agents", section on 'Beta blockers'.)

In contrast, for patients with preserved ejection fraction who develop hypotension caused by dynamic LV outflow tract obstruction during sinus tachycardia, treatment may include a beta blocker to reduce HR and contractility, administered with a vasoconstrictor such as phenylephrine to increase afterload, and appropriate volume administration to restore preload. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Management of hypotensive patients'.)

Persistent or recurrent tachycardia – If sinus tachycardia persists after administration of a cumulative dose of 200 mg of esmolol, alternative causes of tachycardia should be sought and addressed.

If initial beta blocker administration was effective and appropriate, but recurrent tachycardia occurs, options include:

●Esmolol infusion – Continuous infusion of esmolol (eg, 50 to 300 mcg/minute) is appropriate during the intraoperative period. However, another beta blocker is typically 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 boluses – Administration of a longer-acting beta blocker 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. Administration of a longer-acting agent is often timed near the end of surgery during preparation for emergence and extubation. Since metoprolol is a beta-1 selective beta blocker (table 12), it is preferred to labetalol and other nonselective beta blockers for patients with asthma or COPD. Beta blocker therapy should be titrated in small doses in patients with depressed LV or right ventricle (RV) ejection fraction or hyperadrenergic states such as cocaine or methamphetamine overdose. (See "Intraoperative use of vasoactive agents", section on 'Antihypertensive agents'.)

Atrial fibrillation or flutter — Atrial fibrillation (AF) is a common arrhythmia characterized by rapid low amplitude continuously varying small atrial waves (f waves) with generally an irregular ventricular response (waveform 16 and waveform 17). AF may occur intermittently or persistently in patients with a variety of cardiac and pulmonary abnormalities and is more common during or after certain types of surgery (eg, cardiac or thoracic procedures). (See 'Procedure-specific factors' above.)

Atrial flutter is a much less common rapid regular atrial rhythm (typical atrial rate of 300 beats per minute and a ventricular rate of 150 beats per minute) (waveform 18) that occurs in many of the same settings as AF (waveform 18 and waveform 19) and is managed similarly. (See "The electrocardiogram in atrial fibrillation" and "Electrocardiographic and electrophysiologic features of atrial flutter".)

During the perioperative period, new onset of AF or atrial flutter may occur suddenly or be recurrent, and the ventricular response rate for AF or atrial flutter will often be fast [42-44]. Perioperative causes for these changes should be sought and treated [45].

Treatment of acute or chronic AF with a rapid ventricular response is based on the patient’s symptoms and signs, hemodynamic stability, rate of ventricular response, presence/absence of preexcitation (activation via an accessory pathway), and likelihood of atrial thrombus. A HR >150 bpm is usually associated with hypotension, while a HR <120 bpm may be well tolerated. Patients with AF duration ≥48 hours are at risk for atrial thrombi which may embolize during or following cardioversion.

●Hemodynamic instability with AF and rapid ventricular response (≥120 bpm) – For patients with new-onset AF who are hemodynamically unstable (eg, hypotension, myocardial ischemia, pulmonary edema) with a rapid ventricular response, the decisions regarding timing of cardioversion are based on the patient’s symptoms and signs, whether atrial fibrillation is judged to be the cause of hemodynamic instability, and the likelihood of atrial thrombus (which is related to the duration of AF without therapeutic anticoagulation and other risk factors such as prior thromboembolism, heart failure, and diabetes mellitus). Emergency cardioversion is indicated if the patient has hemodynamic compromise (eg, hypotension or pulmonary edema) or angina caused by AF with a rapid ventricular response. (See "Atrial fibrillation: Cardioversion" and "Basic principles and technique of external electrical cardioversion and defibrillation".)

For patients at risk for atrial thrombus who do not require emergency cardioversion but may benefit from urgent cardioversion, transesophageal echocardiography (TEE) is helpful for identifying atrial thrombus which would influence the timing of cardioversion. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation" and "Atrial fibrillation: Cardioversion" and "Basic principles and technique of external electrical cardioversion and defibrillation".)

●Hemodynamic stability with AF and rapid ventricular response (≥120 bpm) – For patients who are hemodynamically stable during AF with a rapid ventricular response, treatment with an agent for rate control is usually appropriate (see 'Agents for rate control' below), rather than treatment with immediate synchronized cardioversion. Therapeutic anticoagulation is initiated as soon as possible after the surgical procedure has been completed since patients with 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 and a ventricular response <120 bpm are often hemodynamically stable. An agent for rate control can be administered. (See 'Agents for rate control' below and "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy".)

If hemodynamic instability is present with a HR <120 bpm, other causes for hypotension should be sought and addressed.

Multifocal atrial tachycardia — Multifocal atrial tachycardia (MAT) originates from two or more foci in the atrium. The rhythm is irregular and P waves have two or more differing morphologies (waveform 20). MAT is less common than AF and can be difficult to distinguish from AF. MAT is usually associated with an underlying significant cardiopulmonary disease (eg, chronic obstructive pulmonary disease, heart failure), and may be evident on the preoperative electrocardiogram (ECG). (See "Multifocal atrial tachycardia" and "The preoperative ECG: Evaluation and implications for management in adults", section on 'Multifocal atrial tachycardia (MAT)'.)

MAT typically does not cause symptoms or hemodynamic compromise. However, if it causes myocardial ischemia, heart failure, or impaired perfusion, then treatment with a beta blocker or calcium channel blocker may be necessary to control the rapid HR (table 13). (See "Multifocal atrial tachycardia".)

Atrioventricular nodal reentrant tachycardia (AVNRT) — AVNRT is a paroxysmal SVT due to existence of dual pathway and reentry circuit within the AV node (waveform 21 and waveform 22). Tachycardia may be triggered by increases in adrenergic tone. Management of AVNRT is summarized in the algorithm (algorithm 10). (See "Atrioventricular nodal reentrant tachycardia".)

Atrioventricular reentrant tachycardia (AVRT) — AVRT is a reentrant tachycardia with a circuit comprised of two pathways, the normal AV conduction system and an AV accessory pathway, linked by common proximal (atrial) and distal (ventricular) tissue.

Orthodromic and antidromic types — The type of AVRT impacts its electrocardiographic morphology and management (see "The preoperative ECG: Evaluation and implications for management in adults", section on 'Atrioventricular reentrant tachycardia (AVRT)' and "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations", section on 'Supraventricular tachycardia'):

Patients with hemodynamically unstable AVRT (orthodromic or antidromic) are treated with urgent cardioversion, as discussed separately. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Unstable patients'.)

●Orthodromic AVRT – The reentrant impulse passes through the AV node in the antegrade direction from atrium to ventricle and the accessory pathway in the retrograde direction. Thus, the QRS complex is usually narrow, but may be wide in a patient with aberrant conduction or pre-existing bundle branch block (BBB). Patients with hemodynamically stable orthodromic AVRT are treated with an AV nodal blocking agent (adenosine, verapamil, beta blocker), as discussed below and separately. (See 'Agents for rate control' below and "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Orthodromic AVRT (regular, narrow QRS complex)'.)

●Antidromic AVRT – The reentrant impulse conducts through the accessory pathway in the antegrade direction from atrium to ventricle and the AV node (or occasionally another accessory pathway) in the retrograde direction. Thus, the QRS complex is wide (maximally pre-excited). Management is discussed below and separately (table 14). (See 'Agents for rate control' below and "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Antidromic AVRT (regular, wide QRS complex)'.)

Wolff-Parkinson-White (WPW) syndrome — WPW syndrome is present in a subset of patients with an accessory pathway. WPW syndrome is characterized by WPW pattern (ventricular pre-excitation during sinus rhythm due to early ventricular activation through an accessory pathway) plus SVT involving the accessory pathway. Ventricular pre-excitation manifests on the ECG as a short PR interval and widened QRS complex, with slowly conducted "delta waves" at the beginning of the QRS complex (waveform 23). (See "The preoperative ECG: Evaluation and implications for management in adults", section on 'Atrioventricular reentrant tachycardia (AVRT)' and "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Electrocardiographic findings'.)

Patients with WPW syndrome may develop orthodromic AVRT, antidromic AVRT, or AF (which may conduct via the accessory pathway). AF with rapid antegrade conduction via the accessory pathway poses a risk of degenerating to ventricular fibrillation (VF). While such degeneration is rare, some medications, primarily AV nodal blockers (eg, verapamil, adenosine, digoxin) are associated with an increased risk for VF in patients who have AF and pre-excitation because these agents promote preferential conduction via the accessory pathway. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Arrhythmias associated with WPW'.)

In any patient with known WPW syndrome, it is critically important to consult the cardiology service preoperatively to ascertain whether the patient is at risk for AF with rapid antegrade conduction via the accessory pathway and 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]). This allows selection of the correct initial pharmacologic therapy in the event of an intraoperative tachyarrhythmia (table 14) [46].

Agents for rate control — The selection of agents for rate control in hemodynamically stable patients with AF, AVNRT, or AVRT is based on the clinical setting:

●For patients without heart failure with reduced ejection fraction (HFrEF) and without pre-excitation – A beta blocker (eg, bolus doses of esmolol 10 to 25 mg or metoprolol 1 to 5 mg) or calcium channel blocker (eg, verapamil or diltiazem) may be administered to decrease HR to ≤80 bpm, provided that blood pressure (BP) is adequate (table 13).

●For patients with HFrEF, but without pre-excitation – IV digoxin or IV amiodarone may be used to decrease the HR (table 13). While amiodarone is usually more effective than digoxin, it poses a risk of inducing cardioversion (with potential risk of thromboembolism in patients with AF who may have an atrial thrombus). (See "Atrial fibrillation and heart failure: Management".)

●For most patients with suspected antidromic AVRT (wide QRS), the treatment of choice is procainamide (algorithm 11 and table 14).

●For most patients with AF with pre-excitation, the first line therapy is IV ibutilide or IV procainamide (algorithm 11 and table 14).

Ventricular paced rhythms — In the setting of an 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 ventricular tachycardia (VT) on the ECG, particularly if the rate is rapid (waveform 24). 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 programmer'.)

WIDE COMPLEX TACHYARRHYTHMIAS

Initial management and evaluation — Most wide complex tachycardias (WCTs; defined as QRS complex width ≥120 milliseconds and heart rate [HR] >100 beats per minute [bpm]) are of ventricular origin; however, origin may be difficult to immediately ascertain. Possible causes should be immediately investigated and treated, 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) [47]. (See 'Potential contributing factors' above and "Intraoperative advanced cardiac life support (ACLS)", section on 'Causes of intraoperative cardiopulmonary arrest'.)

Initial management of a WCT depends on whether the patient is hemodynamically stable and has a pulse. Hemodynamic instability may occur with any WCT regardless of etiology but is more likely if the diagnosis is ventricular tachycardia (VT) rather than a supraventricular tachycardia (SVT). (See 'Monomorphic ventricular tachycardia' below.)

A continuous rhythm strip should be obtained during any intervention that is intended to slow or terminate the WCT. Even if successfully treated, expert cardiology consultation is recommended as soon as possible for any patient who develops a WCT. (See "Wide QRS complex tachycardias: Approach to management", section on 'Vagal maneuvers' and "Wide QRS complex tachycardias: Approach to management", section on 'Pharmacologic interventions'.)

●Unstable patients with WCT

•WCT with no pulse – Patients who are pulseless or unresponsive due to hemodynamic compromise are immediately treated according to the standard Advanced cardiac life support (ACLS) algorithm including emergency asynchronous cardioversion/defibrillation (algorithm 6).

•WCT with a pulse and instability – Patients with a pulse and instability (hypotension, ischemic chest discomfort, acute heart failure, or signs of shock such as acutely altered mental status) are promptly treated with emergency synchronized cardioversion to prevent further clinical deterioration and cardiac arrest (algorithm 8). (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'.)

●Stable patients with WCT – For hemodynamically stable patients with WCT, additional time may be spent attempting to determine the diagnosis, and pharmacologic treatments may be appropriate (algorithm 8). A full 12-lead electrocardiogram (ECG) may be useful to distinguish VT from SVT (algorithm 12). Features consistent with VT include atrioventricular (AV) dissociation, concordance (waveform 25), and fusion/capture beats. 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 [47,48].

When the diagnosis of a WCT is uncertain, it is treated as VT. (See "Wide QRS complex tachycardias: Approach to the diagnosis" and "Wide QRS complex tachycardias: Approach to management".)

Types of ventricular arrhythmia

Monomorphic ventricular tachycardia — VT typically presents with hypotension with or without a pulse. A regular rhythm with a widened QRS complex may be monomorphic VT (waveform 26) or ventricular flutter (waveform 27). (See "Wide QRS complex tachycardias: Approach to the diagnosis".)

Acute management is discussed above. (See 'Initial management and evaluation' above.)

Polymorphic ventricular tachycardia (torsades de pointes) — Polymorphic VT is an unstable rhythm with continuously varying QRS complex morphology in any ECG lead. Polymorphic VT occurring in an individual with prolonged QT interval in sinus rhythm is torsades de pointes (TdP) (waveform 28). The approach to management is based upon whether there is hemodynamic stability and whether there is hemodynamic instability as summarized in the algorithms (algorithm 13 and algorithm 6) and discussed separately. Cardiology consultation is obtained as soon as possible. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management", section on 'Patients with acute TdP' and "Overview of the acute management of tachyarrhythmias", section on 'Polymorphic ventricular tachycardia'.)

Ventricular fibrillation — Ventricular fibrillation (VF; (waveform 29)) requires immediate treatment with defibrillation and ACLS, with repeated shocks as indicated (algorithm 6). During 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'.)

Other ventricular arrhythmias

Premature ventricular contractions — Premature ventricular contractions (PVCs) are common in the general population, even in patients without cardiac disease (waveform 30). 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 (see 'Heart disease' above and 'Electrolyte abnormalities' above). These conditions should be suspected as contributing factors and treated if confirmed. (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 31).

Similar to patients with PVCs, electrolyte abnormalities and myocardial ischemia should be suspected and treated as needed. (See 'Premature ventricular contractions' above.)

We continue electrocardiographic monitoring during the intraoperative and postoperative periods to monitor for sustained VT or VF. Further management is discussed separately. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".)

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 selected patients including those:

●With ECG evidence of myocardial ischemia. (See "Perioperative myocardial infarction or injury after noncardiac surgery".)

●With a persistent or clinically significant arrhythmia (eg, new onset atrial fibrillation [AF], second or third degree atrioventricular [AV] block, ventricular tachycardia [VT]).

●Requiring continuous infusion of an antiarrhythmic agent, temporary pacing, cardioversion, or defibrillation during the perioperative 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 require perioperative 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

●Risk factors for perioperative arrhythmias

•Medications – A number of drugs alter the heart rate (HR) (see 'Heart rate' above) or prolong the QT interval (table 1) which may increase risk for torsades de pointes (TdP) (waveform 1) (see 'QT interval prolongation' above). Local anesthetic systemic toxicity also causes arrhythmias, as discussed separately. (See "Local anesthetic systemic toxicity".)

•Patient-specific factors – These include:

-Preexisting arrhythmias and other preoperative electrocardiogram (ECG) abnormalities (table 4). (See "The preoperative ECG: Evaluation and implications for management in adults".)

-Electrolyte disorders such as hyperkalemia (algorithm 1 and table 5 and waveform 3), hypokalemia (waveform 2), hypocalcemia (waveform 4), hypercalcemia, and magnesium disorders may require urgent management. (See 'Electrolyte abnormalities' above.)

-Metabolic disorders, respiratory disorders, hypovolemia, vasodilation, low cardiac output, or anemia. (See 'Metabolic and respiratory abnormalities' above and 'Hypotension or anemia' above.)

-Myocardial ischemia, infarction, or heart failure. (See 'Heart disease' above.)

•Procedure-specific factors – Arrhythmias are more likely during intrathoracic procedures, intravascular interventions, electroconvulsive therapy (ECT), or procedures that precipitate vagal reflexes causing bradycardia and/or vasodilation. (See 'Procedure-specific factors' above.)

•Neuraxial anesthesia with T1 to T4 anesthetic level – (See 'Neuraxial anesthesia with a high block' above.)

●Intraoperative diagnosis – The ECG is continuously monitored to detect abnormalities and distinguish artifacts. (See 'Intraoperative diagnosis' above.)

●Bradyarrhythmias

•Sinus bradycardia – Sinus bradycardia with HR <60 beats per minute (bpm) is common (waveform 5). (See 'Sinus bradycardia' above.)

For hemodynamic instability with HR <40 bpm, intravenous (IV) atropine is administered (0.5 mg), with further treatment as outlined in the algorithm and in a separate topic (algorithm 2) (see "Sinus bradycardia"). Occasionally, temporary pacing (eg, transcutaneous or transvenous) may be required. (See 'Temporary pacing options' above.)

For a hemodynamically stable patient with HR <40 bpm, we suggest IV glycopyrrolate (Grade 2C), administered in 0.2 mg increments (up to 1 mg). A reasonable alternative is administration of small incremental doses of atropine 0.2 mg. (See 'Pharmacologic treatment' above.)

•Conduction system disease – Management of atrioventricular (AV) block is discussed in separate topics:

-First-degree AV block (waveform 10) does not require treatment. (See "First-degree atrioventricular block".)

-Second-degree AV block (Mobitz Type I [Wenckebach] (waveform 11) or Mobitz Type II (waveform 12)) may require pharmacologic or pacing intervention if bradycardia causes symptoms or hemodynamic compromise, as noted in the algorithms and in separate topics (algorithm 3 and algorithm 4). (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)" and "Second-degree atrioventricular block: Mobitz type II".)

-Third-degree AV block (waveform 13 and waveform 14) with hemodynamic instability typically requires pacing, as noted in the algorithm and in a separate topic (algorithm 5). (See "Acquired third-degree (complete) atrioventricular block".)

●AV dissociation – AV dissociation is defined as independent activation of the atria and ventricles. While some causes of AV dissociation such as complete heart block and sustained ventricular tachycardia require intervention, other causes such as isorhythmic AV dissociation are relatively benign and often self-limited. (See 'AV dissociation' above.)

●Tachyarrhythmias – Tachyarrhythmias (rhythms with HR >100 bpm) are categorized into narrow QRS complex tachycardias (QRS <120 ms) and wide QRS complex tachycardias (QRS ≥120 ms), and regular or irregular rhythms (algorithm 7). (See 'Categories' above.)

•Narrow QRS complex tachycardias (QRS <120 ms) – These are nearly always supraventricular tachyarrhythmias (SVTs) which arise from the sinus node, atria, AV node, His bundle, or a combination of these sites. (See 'Supraventricular tachycardia' above and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)

•Wide QRS complex tachycardias (QRS >120 ms) – These include ventricular tachycardia (VT); they also include SVTs with bundle branch block (BBB), aberrant conduction, or antegrade conduction via an accessory pathway. (See 'Wide complex tachyarrhythmias' above and "Wide QRS complex tachycardias: Approach to the diagnosis".)

Management involves addressing underlying causes and additional interventions depending on the type of arrhythmia and hemodynamic status, as outlined above and discussed in separate topics (algorithm 8). (See 'General approach to management' above and 'Supraventricular tachycardia' above and 'Wide complex tachyarrhythmias' above.)