Arrhythmias during anesthesia

Authors: Emily Methangkool, MD, Aman Mahajan, MD, PhD, MBA

Section Editor: Jonathan B Mark, MD
Deputy Editor: Nancy A Nussmeier, MD, FAHA

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.

Literature review current through: Jun 2022. | 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
"Hemodynamic management during anesthesia in adults", 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
"Hemodynamic management during anesthesia in adults", 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 "Hemodynamic
management during anesthesia in adults", 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 atrial fibrillation:
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 atrial fibrillation: 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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