The preoperative ECG: Evaluation and implications for management in adults

INTRODUCTION — 

An electrocardiogram (ECG) is a key component of the evaluation of selected patients prior to noncardiac surgery. (See 'Indications and rationale' below.)

This topic reviews our approach to the management of patients with abnormalities noted on their preoperative ECG. Decisions regarding additional testing, interventions, postponement of the surgical procedure, or selection of anesthetic agents or modification of anesthesia techniques may be impacted by specific abnormal ECG findings (table 1).

Other implications of specific ECG abnormalities are reviewed in various other UpToDate topics.

The principles of ECG analysis are reviewed in a separate topic (waveform 1). (See "ECG tutorial: Basic principles of ECG analysis".)

GENERAL CONSIDERATIONS

Indications and rationale — A preoperative ECG is obtained in selected patients to identify potential cardiac issues that might require further evaluation or might alter management, including the timing of an elective surgical procedure and/or anesthetic management (selection of agents or techniques) [1]. The preoperative ECG is also useful for comparison if ECG abnormalities are noted intraoperatively or on postoperative ECGs. Indications for preoperative ECG are discussed separately. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Electrocardiogram for some patients'.)

Interpretation — In many cases, one or more recent ECGs with interpretation by computer algorithms will be available for review at the time of the preanesthetic consultation, ideally with review and interpretation by an expert reader. In any patient with an indication for a preoperative ECG, at least one 12-lead ECG should be reviewed and interpreted by an expert reader.

The anesthesiologist should be familiar with ECG analysis since certain abnormalities may warrant further evaluation or alterations in management including potential postponement of an elective surgical procedure.

A summary of common ECG findings and the level of concern they raise is provided in the table (table 1).

Key considerations — The following factors influence evaluation and response to preoperative ECG abnormalities:

●Is the abnormality new or old? An attempt should be made to compare the current ECG with one or more prior ECGs. Most chronic ECG abnormalities do not routinely warrant additional testing or intervention. Many patients have nonspecific ECG abnormalities that reflect prior history of heart disease, but do not necessarily predict increased perioperative risk, particularly for low-risk surgical procedures (table 2).

●Does the patient have a history of cardiovascular disease?

●Does the patient have active cardiovascular symptoms (such as angina or dyspnea)?

●What is the individualized risk of the surgical procedure? This is based on:

•The surgical procedure (table 2)

•The urgency of the surgery (emergency/urgent or elective)

•Patient characteristics and risk factors

For patients at risk for adverse cardiovascular outcomes, surgical risk may be estimated using a combination of the revised cardiac risk index (RCRI) (table 3) and the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) calculator. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Using risk assessment tools' and "Evaluation of cardiac risk prior to noncardiac surgery".)

P WAVE ABNORMALITIES — 

The P wave represents atrial depolarization.

Marked left or right atrial abnormality reflects atrial enlargement or intra-atrial block and is generally one of a constellation of clinical findings of an underlying condition, often already noted or suggested by the patient's history and physical examination, as discussed separately. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "ECG tutorial: Chamber enlargement and hypertrophy", section on 'Left atrial abnormality/enlargement' and "ECG tutorial: Chamber enlargement and hypertrophy", section on 'Right atrial abnormality/enlargement'.)

●Left atrial abnormality/enlargement is associated with hypertension, valvular heart disease (mitral or aortic), and left ventricular diastolic and/or systolic dysfunction.

●Right atrial abnormality/enlargement is associated with pulmonary hypertension and tricuspid valve disease.

Q WAVES — 

Possibly pathologic Q waves should be distinguished from normal findings. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Significance of Q waves' and "Pathogenesis and diagnosis of Q waves on the electrocardiogram".)

●Pathologic-appearing Q waves (in the absence of left ventricular hypertrophy or left bundle branch block) [2]:

•Any Q wave in leads V2-V3 that is >0.02 s or a QS complex in leads V2-V3.

•Q wave ≥0.03 s and ≥1 mm deep or QS complex in leads I, II, aVL, aVF or V4-V6 in any two leads of a contiguous lead grouping (I, aVL; V1-V6; II, III, aVF).

•R wave >0.04 s in V1-V2 and R/S >1 with a concordant positive T wave in absence of conduction defect.

Of note, pathologic Q or QS waves occur not only with myocardial infarction (MI) but also with multiple other conditions, including left ventricular hypertrophy, left bundle branch block, left anterior fascicular block (hemiblock), right ventricular hypertrophy, stress (takotsubo) cardiomyopathy, Wolf-Parkinson-White pre-excitation, cardiomyopathy, cardiac amyloidosis, myocarditis, acute cor pulmonale, and hyperkalemia [2].

ECG diagnosis of MI in patients with bundle branch block (BBB) or a paced rhythm is discussed separately. (See "Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm".)

When pathologic Q waves are identified, clinical evaluation includes determining if the Q waves are pathologic, their acuity, and their cause. However, postponement of surgery is generally unnecessary if chronic pathologic Q waves are identified in an asymptomatic patient.

●Normal Q waves [2]:

•A QS complex in lead V1 is a common normal variant.

•A Q wave <0.03 s and <25 percent of the R wave amplitude in lead III is likely normal if the frontal QRS axis is between -30 and 0°.

•A Q wave may also be normal in aVL if the frontal QRS axis is between 60 and 90°.

•Septal Q waves are small, nonpathological Q waves <0.03 s and <25 percent of the R-wave amplitude in leads I, aVL, aVF, and V4-V6. These physiologic Q waves are caused by normal initial septal depolarization, directed from left to right and anteriorly.

QRS COMPLEX ABNORMALITIES — 

The QRS complex represents ventricular depolarization. (See "ECG tutorial: Basic principles of ECG analysis", section on 'QRS complex' and "ECG tutorial: Basic principles of ECG analysis", section on 'Step 3: Analyze the QRS morphology'.)

QRS axis deviation — The presence of chronic left (more negative than -30°) or right axis (more positive than +90° to +100°) deviation usually has no specific implications for anesthetic management. However, chronic QRS axis deviation might indicate important underlying conditions such as ventricular hypertrophy. (See "ECG tutorial: Chamber enlargement and hypertrophy".)

An acute (newly identified) major change in QRS axis may be a sign of an acute cardiopulmonary condition (eg, pulmonary embolus). Lead misplacement should be excluded and investigation of potential causes is warranted (table 1).

Bundle branch blocks and fascicular blocks (hemiblocks)

Criteria — Bundle branch blocks (BBBs) are defined by prolonged QRS duration >120 milliseconds and distinct patterns of QRS morphology (waveform 2 and waveform 3 and waveform 4 and waveform 5) [3,4]. (See "ECG tutorial: Intraventricular block".)

A left anterior fascicular block, or hemiblock, is characterized by left axis deviation >-45° up to -90°, together with a qR pattern in lead I and rS patterns in leads II, III, and AVF (waveform 6).

A left posterior fascicular block, or hemiblock, is characterized by a pathologic right axis, >+90° (usually ˃100°) up to 180°, in concert with relatively small R and deep S waves in leads I and aVL, and small Q and tall R waves in leads III and aVF (waveform 7). Left posterior fascicular block is almost always seen with right BBB (waveform 8).

Other causes of right axis deviation such as normal variants (especially in young adults), right ventricular overload syndromes, and lateral wall myocardial infarction (MI) should be excluded.

New or acute BBB or fascicular block (hemiblock) — Appearance of a new or acute BBB warrants review of clinical history and investigation of potential causes. Similar to BBB, the presence of new or acute fascicular block (hemiblock) merits further evaluation and consultation. (See "Left bundle branch block", section on 'Etiology' and "Right bundle branch block", section on 'Etiology' and "Left anterior fascicular block", section on 'Etiology' and "Left posterior fascicular block", section on 'Etiology'.)

●Functional BBB – In some cases, new onset of a left or right BBB or a fascicular block (hemiblock) may be "rate related" and temporary, occurring at a fast heart rate (HR) when the bundle refractory period exceeds that of the R-R interval.

●Acute cardiopulmonary pathology – Acute causes of BBB include myocardial ischemia, myocardial infarction, endocarditis with abscess formation, or myocarditis. Right BBB develops in some patients with pulmonary embolus. (See "Conduction abnormalities after myocardial infarction" and "Clinical presentation and diagnostic evaluation of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Electro- or echocardiography'.)

Chronic BBB or fascicular block (hemiblock) — The presence of chronic BBB, especially left BBB, is most commonly associated with slowly progressive structural heart disease that affects the conduction system (eg, ischemic heart disease, hypertension, valvular heart disease, cardiomyopathies). An RBBB may also occur in patients with chronic pulmonary hypertension.

Postponement of surgery for further evaluation is not necessary in an asymptomatic patient with chronic left or right BBB. Although chronic BBBs have been associated with postoperative myocardial infarction (MI), their presence on a preoperative ECG does not improve risk prediction after high-risk surgery compared with simply noting a history of ischemic heart disease [5]. Similarly, presence of a chronic fascicular block (hemiblock) would not require further modification of the anesthetic plan.

Low-grade versus high-grade atrioventricular (AV) block — Slow atrioventricular (AV) nodal conduction due to AV block is usually caused by increased vagal tone or degenerative or inflammatory disease of the conduction system. AV block is classified as first, second, or third degree.

Low-grade AV block — Surgery is generally not delayed for evaluation or treatment of patients with first-degree AV block (prolonged PR interval) or second-degree Mobitz I AV block. (See 'First-degree AV block (prolonged PR interval)' below and 'Mobitz Type I (Wenckebach) second-degree AV block' below.)

First-degree AV block (prolonged PR interval) — First-degree AV block occurs when there is delayed but intact conduction from atria to ventricles, hallmarked by a prolonged PR interval >200 milliseconds (waveform 9). (See "First-degree atrioventricular block".)

Although surgery is not delayed for isolated first-degree AV block, severe symptomatic bradycardia may occur due to vagal reflexes, or techniques or agents that increase vagal tone and exacerbate the delay in AV nodal conduction in patients with first-degree AV block, similar to patients with sinus bradycardia. (See 'Sinus bradycardia' below.)

Also, vagolytic agents such as atropine, and chronotropic agents such as ephedrine should be immediately available to treat severe bradycardia. (See "Perioperative arrhythmias", section on 'Sinus bradycardia'.)

Mobitz Type I (Wenckebach) second-degree AV block — Second-degree AV block occurs when there is intermittent conduction from the atria to the ventricles. Block is classified as Mobitz Type I or II.

In Mobitz Type I second-degree AV block (Wenckebach), there is typically progressive decrement in AV conduction with prolongation of the PR interval until a single ventricular beat is dropped (waveform 10). In atypical cases, the PR interval is similar for conducted beats except for a shorter PR interval after the non-conducted P wave. Mobitz type I AV block is a benign condition with low risk of progression to complete heart block. Causes include disease of the conduction system (eg, associated with myocardial ischemia or infarction or myocarditis), enhanced vagal tone [6], or use of AV nodal blocking drugs. (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)".)

A few simple precautions during anesthetic management are warranted in patients with Mobitz Type I (Wenckebach) second-degree AV block. As with patients with first-degree AV block, precautions regarding techniques or agents that may increase vagal tone are prudent to avoid further delay in AV nodal conduction. Furthermore, vagolytic agents such as atropine and chronotropic agents such as ephedrine should be immediately available to treat severe bradycardia. (See 'Sinus bradycardia' below and "Perioperative arrhythmias", section on 'Sinus bradycardia'.)

High-grade AV block — Elective surgery is generally postponed in a patient with second-degree Mobitz II or third-degree AV block. If urgent or emergency surgery is necessary, temporary pacing should be initiated as soon as possible since complete heart block may develop, resulting in a slow intrinsic ventricular escape rhythm. Since any rhythm originating in the more distal conduction system at or below the bundle of His is not as sensitive to vagal activity, the ventricular escape rhythm may not be responsive to atropine.

Mobitz Type II second-degree AV block — In Mobitz Type II second-degree AV block, the atrial impulses intermittently fail to conduct to the ventricles, and the ECG shows intermittently dropped ventricular beats (waveform 11 and waveform 12). Usually, this is two-to-one block. QRS complexes are often wide or show a pattern of BBB reflecting disease in the distal conduction system. (See "Second-degree atrioventricular block: Mobitz type II".)

Patients with Mobitz Type II second-degree AV block are at increased risk for progression to complete heart block and symptomatic bradycardia.

●Elective surgery – Elective procedures are postponed and cardiology evaluation should be obtained.

●Urgent surgery – Vagal maneuvers and anesthetic, and other agents that increase vagal tone should be avoided since vagal stimuli may exaggerate the AV conduction delay leading to symptomatic bradycardia [6]. Although atropine is the typical first line of therapy for treatment of bradycardia, responsiveness may be poor due to the infranodal location of the block (algorithm 1). In such patients, positive chronotropic agents are administered (eg, epinephrine, dopamine, dobutamine, isoproterenol) in an attempt to increase HR (table 4). In some cases, temporary pacing may be necessary to alleviate bradycardia and maintain hemodynamic stability. This is achieved by intravenous insertion of temporary transvenous pacing wires during the preoperative or early intraoperative period of an emergency procedure, or by use of other temporary pacing options such as transcutaneous, transesophageal, or pulmonary artery catheter pacing modalities. These options are discussed in more detail separately. (See "Temporary cardiac pacing" and "Perioperative arrhythmias", section on 'Temporary pacing options'.)

Third-degree AV block — Third-degree AV block (ie, complete heart block) occurs when atrial impulses do not conduct to the ventricles so that P waves are dissociated from QRS complexes (waveform 13). This occurs due to advanced disease of the conduction system. Patients with third-degree AV block typically present with symptomatic bradycardia. Causes of similar ECG findings, such as isorhythmic AV dissociation (waveform 14), should be excluded. (See "Acquired third-degree (complete) atrioventricular block".)

A cardiologist is immediately consulted, and elective surgery is postponed, similar to management of patients with Mobitz II second-degree AV block. If urgent or emergency surgery is necessary, temporary pacing should be initiated as soon as possible since the intrinsic ventricular rhythm is likely to be very slow (approximately 30 to 40 beats/minute [bpm]), and responsiveness to atropine will likely be poor. (See "Temporary cardiac pacing" and "Perioperative arrhythmias", section on 'Temporary pacing options'.)

ST SEGMENT ABNORMALITIES

ST segment depression — The ST segment is usually isoelectric (ie, at the baseline when compared with the T-P segment) and has a slight upward concavity (waveform 15). (See "ECG tutorial: Basic principles of ECG analysis", section on 'ST segment' and "ECG tutorial: Basic principles of ECG analysis", section on 'Step 7: ST segment-T wave'.)

Chronic ST segment depression — Chronic and nonspecific ST segment depressions are seen in a variety of cardiac conditions, as discussed separately. These do not significantly affect anesthetic management. (See "ECG tutorial: ST- and T-wave changes", section on 'ST-T-wave changes associated with specific disease states'.)

Acute ST segment depression in multiple leads — ST segment depression is defined as a horizontal or down-sloping ST segment that is depressed ≥0.05 mm below the baseline, measured at 0.08 seconds after the J point, in two contiguous leads (waveform 16).

New ST segment depression, particularly if horizontal or downsloping, is a nonspecific sign of myocardial ischemia or subendocardial injury and warrants consultation with the cardiology service (table 5), as well as possible postponement of elective surgery. (See "ECG tutorial: ST- and T-wave changes", section on 'Myocardial ischemia, injury, and infarction' and "ECG tutorial: Myocardial ischemia and infarction", section on 'ST-segment depression'.)

ST segment elevation — ST segment elevation may be a normal variant (waveform 17) or may represent an evolving myocardial infarction (MI), acute pericarditis (table 6), stress cardiomyopathy, or various other pathologies (table 7), as discussed in separate topics:

●(See "ECG tutorial: ST- and T-wave changes".)

●(See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

●(See "Diagnosis of acute myocardial infarction".)

●(See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Electrocardiogram'.)

●(See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Electrocardiogram'.)

The J point is the junction between the end of the QRS and the beginning of the ST segment (figure 1). In patients having an acute MI, the J point is initially elevated, while the ST segment has a concave configuration that typically becomes convex or rounded upward as the MI evolves (waveform 18).

Acute ST segment elevation

●Acute ST elevation MI (STEMI) – ST segment elevation in two or more consecutive leads is the hallmark of acute ST elevation myocardial infarction (STEMI) (waveform 18) and (waveform 19 and waveform 20 and waveform 21 and waveform 22 and waveform 23). Notably, the ST segment with acute MI may be concave, plateaued, or convex. Details are discussed in separate topics. (See "ECG tutorial: Myocardial ischemia and infarction" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

Acute MI is a consideration in any patient presenting with ST segment elevation, particularly if associated with chest discomfort or other possible symptoms of MI. Elective surgery is cancelled and the cardiology service is consulted. (See "Overview of the acute management of ST-elevation myocardial infarction".)

●Acute pericarditis – ECG changes in acute pericarditis (figure 2) differ from those in acute STEMI in several ways, as noted in the table (table 6). New ECG changes consistent with acute pericarditis merit further evaluation and treatment. Elective surgery should be postponed until resolution of symptoms. Urgent/emergency surgery can proceed once presence of significant pericardial effusion is excluded. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Electrocardiogram'.)

Early repolarization (J point elevation) — Early repolarization (also known as J point elevation) is identified when there is J point elevation of ≥0.1 mV in two adjacent leads with either a slurred or notched morphology (waveform 17 and waveform 24). Early repolarization is a relatively common ECG finding that usually has no clinical implications for anesthetic care. However, a small minority of patients with an early repolarization pattern present with sudden cardiac arrest due to idiopathic ventricular fibrillation.

Previous ECGs, if available, are valuable to determine whether J point elevation is chronic or new. The following clinical features distinguish acute ST elevation MI from early repolarization: symptoms and signs of MI, ST elevation, and accompanying ECG changes develop and evolve with MI and are accompanied by reciprocal ST depressions. (See "Early repolarization" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Early repolarization'.)

T WAVE ABNORMALITIES — 

A normal T wave is broad, has a slow upstroke, and rapid downstroke (see "ECG tutorial: Basic principles of ECG analysis", section on 'T wave'). T wave abnormalities that warrant further investigation include:

Chronic T wave changes

●Chronic T wave inversions – T wave inversions that are known to be chronic do not typically warrant further investigation prior to anesthesia. (See "ECG tutorial: ST- and T-wave changes", section on 'ST-T-wave changes associated with specific disease states'.)

●Chronic peaked T waves – Chronic causes of tall, peaked T waves include left bundle branch block (BBB) or chronic left ventricular hypertrophy. (See 'Chronic BBB or fascicular block (hemiblock)' above.)

Acute T wave changes

●Acute changes in T wave direction and amplitude – Acute dynamic changes may signify acute myocardial ischemia (MI) warranting consultation with the cardiology service and possible postponement of elective surgery (table 5). (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Abnormal T waves' and "ECG tutorial: Myocardial ischemia and infarction", section on 'T-wave changes'.)

●Acute peaked T waves – Tall peaked T waves with a narrow base (ie, "tented") may be an early sign of hyperkalemia (figure 3), although ECG changes vary considerably in hyperkalemic patients [7]. In addition, hyperacute prominent (usually broad) T waves may be seen during the early phases of an acute MI with or without ST elevation. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and "ECG tutorial: Myocardial ischemia and infarction".)

Chronic tall, peaked T waves may be observed in the following settings: normal variant early repolarization, left BBB, or left ventricular hypertrophy (in right precordial leads with a QS or rS morphology).

Elective surgery is postponed until potassium and/or troponin levels are measured if either hyperkalemia or acute MI is suspected. Also, the cardiology service is consulted if acute MI is suspected (table 5). (See "ECG tutorial: ST- and T-wave changes", section on 'Tall T waves' and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Abnormal T waves'.)

QT PROLONGATION — 

The QT interval is typically corrected for heart rate (HR) to determine the QTc interval. A prolonged QTc is ≥470 milliseconds for men (460-469 is considered borderline) and ≥480 milliseconds for women (where 460-479 is considered borderline). A QTc >500 milliseconds is considered highly abnormal for both men and women. However, a relative prolongation in a given individual within the normal or borderline range may also be clinically relevant. (See "ECG tutorial: Basic principles of ECG analysis", section on 'QT interval'.)

Potential development of a life-threatening polymorphic ventricular arrhythmia (torsades de pointes [TdP]) is a concern in patients with significant acquired or congenital QTc prolongation (see "Perioperative arrhythmias", section on 'Polymorphic ventricular tachycardia (torsades de pointes)') [8]. For this reason, if a prolonged QTc interval is noted on the preoperative ECG, the preanesthetic consultation should include inquiries about history of syncope and family history of sudden death, as well as review of all medications, and attention to serum potassium and magnesium levels.

●Elective surgery – There are numerous causes of QTc prolongation. Most of these are acquired due to effects of certain medications or electrolyte abnormalities (table 8 and table 9). (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

•Acquired long QT – For patients with significant new QTc interval prolongation that may be corrected by discontinuation of culprit medications (table 8), or by correction of an electrolyte abnormality, elective surgical procedures should be postponed. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)

•Congenital long QT – Patients with newly discovered congenital long QT syndromes who have not previously been evaluated by a cardiologist should have a consultation before surgery. (See "Congenital long QT syndrome: Treatment", section on 'Treatment'.)

●Urgent or emergency surgery – For patients with QTc prolongation who require urgent or emergency surgery, the following precautions are necessary:

•Avoid certain pharmacologic agents – To reduce risk of development of TdP, we avoid certain commonly used perioperative medications that might further prolong the QTc interval including the antiemetic agents droperidol, haloperidol, and ondansetron, and the opioid methadone (table 8) [8-12]. Also, volatile anesthetic agents (eg, sevoflurane, desflurane, isoflurane) are used cautiously as these are associated with QT prolongation [8,13]. Propofol has the least effect on QT interval and can be safely used as an induction agent or as a component of a total intravenous anesthesia (TIVA) technique [14]. Details are discussed in separate topics:

-(See "Perioperative arrhythmias", section on 'QT interval prolongation'.)

-(See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Ventricular arrhythmias'.)

-(See "Acquired long QT syndrome: Definitions, pathophysiology, and causes", section on 'Drugs that prolong the QT interval'.)

•Avoid sympathetic stimulation – Since TdP can be triggered by catecholamines, sympathetic stimulation is avoided or minimized throughout the perioperative period [15,16]. Beta adrenergic blocking agents may be protective and should be continued if chronically administered. Beta blockers may also be used to treat tachycardia, hypertension, or presumed myocardial ischemia (MI) during the perioperative period [17]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease".)

•Correct electrolyte abnormities and respiratory alkalosis – Electrolyte abnormalities that predispose to TdP are corrected (eg, hypokalemia, hypomagnesemia, hypocalcemia). Intraoperative hyperventilation is avoided because acute respiratory alkalosis may lead to hypokalemia and hypocalcemia. (See "Perioperative arrhythmias", section on 'Polymorphic ventricular tachycardia (torsades de pointes)' and "Acquired long QT syndrome: Definitions, pathophysiology, and causes", section on 'Metabolic abnormalities'.)

BRADYARRHYTHMIAS

Sinus bradycardia — Sinus bradycardia is identified by normal P waves (positive in lead II and negative in lead aVR) at a heart rate (HR) <60 beats/minute (bpm).

Sinus bradycardia occurs in a variety of physiologic and disease states. It is a normal condition in well-conditioned athletes. It may also be caused by temporary increases in vagal tone, use of negative chronotropic drugs (eg, beta blockers, calcium channel blockers), sinus node dysfunction, or hyperkalemia.

In the vast majority of patients, sinus bradycardia itself does not directly cause symptoms. The patient should be queried about the presence or absence of symptoms and examined for any evidence of hemodynamic compromise as a result of the bradycardia (algorithm 2).

●Asymptomatic patients with sinus bradycardia and stable hemodynamics may generally proceed with the planned procedure.

However, it is prudent to plan anesthetic management to avoid worsening sinus bradycardia. Exacerbation may be caused by vagal reflexes (during laryngoscopy and endotracheal intubation or during gastrointestinal or laparoscopic procedures), neuraxial anesthesia with a high (T1 to T4) anesthetic level, and by certain intravenous (IV) agents that increase vagal tone (eg, negative chronotropic agents, opioids, vasoconstrictors, sugammadex, or anticholinesterase agents coadministered with an inadequate dose of an anticholinergic agent). (See "Perioperative arrhythmias", section on 'Procedure-specific factors' and "Perioperative arrhythmias", section on 'Neuraxial anesthesia with a high block' and "Perioperative arrhythmias", section on 'Causes of sinus bradycardia'.)

Also, vagolytic agents such as atropine and chronotropic agents such as ephedrine should be immediately available to treat severe bradycardia. (See "Perioperative arrhythmias", section on 'Sinus bradycardia'.)

●For patients with bradycardia with symptoms or other evidence of hemodynamic instability, further evaluation is warranted and elective surgery is cancelled. (See "Sinus bradycardia", section on 'Differential diagnosis' and "Sinus bradycardia", section on 'Further evaluation'.)

Management of bradycardia with hemodynamic compromise is described separately (algorithm 2). (See "Sinus bradycardia", section on 'Management'.)

Sinus arrhythmia — Physiologic (respiratory) sinus arrhythmia appears as periodic narrowing and widening of the RR intervals (waveform 25). It is caused by rhythmic changes in vagal tone that occur during the respiratory cycle, with increases in heart rate during inspiration, and slowing of the HR during expiration that may transiently result in bradycardic rate <50 bpm. This is a normal phenomenon with no implications for anesthetic care. (See "Normal sinus rhythm and sinus arrhythmia", section on 'Sinus arrhythmia'.)

Atrioventricular block with bradycardia — The differential diagnosis of bradycardia includes causes other than sinus bradycardia such as second- or third-degree atrioventricular (AV) block, junctional escape rhythm, or ventricular escape rhythm (table 10). Management of patients with preoperative high-grade AV block causing symptomatic bradycardia is discussed above. (See 'Low-grade versus high-grade atrioventricular (AV) block' above.)

PACED RHYTHMS — 

A key finding that should be identified on the preoperative electrocardiogram is the presence of a paced rhythm.

●Atrial pacing is identified by the presence of a pacing stimulus (spike) followed by a P wave (waveform 26). (See "ECG tutorial: Pacemakers", section on 'Atrial pacing only'.)

●Ventricular pacing is identified by the presence of a pacing stimulus followed by a QRS complex. When the right ventricle (RV) is paced, the QRS complex is generally wide with left bundle branch block morphology (waveform 27). With cardiac physiologic pacing (which includes cardiac resynchronization therapy as well as conduction system pacing), the QRS may be narrow and QRS morphology varies. (See "ECG tutorial: Pacemakers".)

●Many patients have AV sequential pacing (waveform 28). (See "ECG tutorial: Pacemakers", section on 'Dual-chamber atrioventricular sequential pacing'.)

Perioperative management of patients with a pacemaker or implantable cardioverter defibrillator is discussed separately. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

SUPRAVENTRICULAR TACHYARRHYTHMIAS

General presentation and approach — Tachycardia generally refers to any rhythm with heart rate (HR) >100 beats/minute (bpm). Supraventricular tachyarrhythmias (SVTs) usually have a narrow QRS complex (<120 milliseconds) and may be paroxysmal or sustained. However, a supraventricular tachyarrhythmia may be associated with a wide QRS as discussed below. (See 'Differential diagnosis of WCT' below and "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias".)

Underlying causes of any preoperative SVT should be identified and corrected prior to elective surgery (algorithm 3) [18]. In the preoperative setting, adrenergic stimulation due to causes such as hypovolemia, anxiety, or beta blocker withdrawal is a common cause of supraventricular tachyarrhythmias that may manifest as sinus tachycardia or other SVTs.

In most instances, termination of the SVT or achievement of ventricular rate control results in resolution of associated symptoms. However, elective surgery should be postponed and a cardiology consultation should be obtained for patients with symptoms related to tachycardia or when there is difficulty achieving rate control. (See "Overview of the acute management of tachyarrhythmias", section on 'Narrow QRS complex tachyarrhythmias'.)

Sinus tachycardia — Sinus tachycardia is associated with P waves that are almost always positive or initially positive in lead II (waveform 29).

Preoperative mild to moderate sinus tachycardia typically occurs at a HR of 100 to 125 bpm. In most cases, preoperative sinus tachycardia on the ECG does not warrant delay in surgery, unless required for timely treatment of the cause of the tachycardia.

Typical causes of sinus tachycardia that should be identified and treated as appropriate include adrenergic stimulation resulting from anxiety, inadequate analgesia, or as a reflex response to hypovolemia or anemia (eg, due to blood loss). Other possible preoperative causes include withdrawal from chronically administered medications that control HR, substance use (eg, cocaine), fever, sepsis, myocardial ischemia, hypoxemia, or hypercarbia. Thus, determining the etiology of sinus tachycardia should be part of an overall patient assessment. (See "Sinus tachycardia: Evaluation and management".)

SVT with regular rhythm

Atrioventricular nodal reentrant tachycardia — Atrioventricular nodal reentrant tachycardia (AVNRT) is a paroxysmal SVT due to existence of a dual pathway substrate, allowing a re-entrant circuit within the atrioventricular (AV) node (waveform 30 and waveform 31). Tachycardia may be triggered by increases in adrenergic tone. A past history of palpitations is often elicited. (See "Atrioventricular nodal reentrant tachycardia".)

Vagal maneuvers may be attempted or intravenous (IV) adenosine or a calcium channel blocker (eg, diltiazem or verapamil) or IV beta blocker (eg, esmolol or metoprolol) may be administered to transiently delay conduction through the AV node and terminate AVNRT (table 11).

Electrical cardioversion is reserved for patients who are hemodynamically unstable and those with AVNRT that persists despite vagal maneuvers and AV nodal blocking medications (algorithm 4 and algorithm 5). (See "Cardioversion for specific arrhythmias".)

Patients with successfully treated AVNRT can generally proceed with planned surgery.

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.

●Types of AVRT – AVRT may be orthodromic or antidromic:

•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).

•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).

•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 32 and waveform 33). Most patients with WPW pattern are asymptomatic and do not have WPW syndrome. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Electrocardiographic findings'.)

Patients with WPW syndrome may develop reentrant supraventricular arrhythmias, particularly if adrenergic stimulation leads to facilitated conduction through the accessory pathway with rapid conduction of the supraventricular rhythm. Atrial fibrillation (AF) occurs in a minority of patients with WPW syndrome. Patients with AF with rapid ventricular response via conduction over one or more accessory pathways are at risk for degeneration into ventricular fibrillation. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Arrhythmias associated with WPW'.)

●Management – In patients with known AVRT or WPW pre-excitation syndrome, the anesthesiologist should consult the cardiologist who has been caring for the patient.

Anesthetic planning to minimize risk of tachyarrhythmias includes avoiding marked increases in sympathetic stimulation (eg, during laryngoscopy and endotracheal intubation, surgical incision, or emergence from anesthesia). Also, any IV agents that may promote tachycardia due to sympathomimetic activity (eg, ketamine, ephedrine, epinephrine) or vagolytic activity (eg, atropine, glycopyrrolate) are administered cautiously (ie, in small incremental doses) [19]. Furthermore, techniques such as a high spinal block or IV agents that increase vagal tone (eg, succinylcholine, neostigmine) are employed cautiously, as these may transiently block AV nodal conduction and promote conduction of impulses down the accessory pathway [19,20].

Preoperative review of the medical records and/or consultation with a cardiologist is necessary to choose the correct initial pharmacologic therapy should an intraoperative tachyarrhythmia occur, as discussed separately. AV blocking medications are contraindicated in patients with pre-excitation AF. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome".)

Focal atrial tachycardia (AT) — Focal atrial tachycardia (AT) is a regular atrial rhythm with a HR >100 bpm that originates outside of the sinus node, typically with a change in P wave axis or morphology (waveform 34). This arrhythmia can mimic sinus tachycardia especially when the origin is close to the sinoatrial node. Focal AT may occur in patients with chronic structural heart disease in response to adrenergic stimulation or elevated left or right atrial pressures. However, it can also be associated with acute events, such as acute changes in preload or afterload, myocardial ischemia, hypoxia, or hypokalemia. (See "Focal atrial tachycardia".)

Treatment should focus on identifying and correcting the underlying etiology and establishing rate control. Elective surgery is postponed if adequate rate or rhythm control is not achieved, or if hemodynamic instability develops. Hemodynamically stable patients who require urgent surgery are treated with a beta blocker or nondihydropyridine calcium channel blocker (ie, diltiazem or verapamil) to slow the ventricular response and/or terminate the arrhythmia. The cardiology service is consulted for decisions regarding additional treatment options such as electrical cardioversion, administration of additional rate-controlling agents, or antiarrhythmic medications. (See "Focal atrial tachycardia", section on 'Treatment'.)

SVT with irregular rhythm

Premature atrial complexes (beats) — Premature atrial complexes (PACs) (waveform 35 and waveform 36) are usually benign and commonly occur in patients with a normal heart, particularly in those with increased sympathetic tone due to anxiety, chronic smoking, or alcohol use. PACs also occur in patients with cardiopulmonary diseases such as chronic obstructive pulmonary disease, ischemic heart disease, cardiomyopathy, or valvular heart disease. Frequent PACs may be a forerunner of atrial fibrillation or other supraventricular tachycardias. Planned surgery and anesthetic care are not altered by isolated PACs. (See "Supraventricular premature beats".)

Multifocal atrial tachycardia (MAT) — Multifocal atrial tachycardia (MAT) originates from two or more foci in the atrium. The rhythm is irregular and P waves have three or more differing morphologies. (waveform 37). (See "Multifocal atrial tachycardia".)

MAT is an uncommon arrhythmia that is usually associated with significant cardiopulmonary disease (eg, chronic obstructive pulmonary disease, chronic heart failure).

Most episodes of MAT do not cause symptoms or hemodynamic compromise. Treatment is aimed at underlying disorders such as poor oxygenation, acid-base disturbances, hypokalemia, or hypomagnesemia. In hemodynamically stable patients with symptomatic MAT, the HR can usually be appropriately reduced with premedication (eg, anxiolytic or analgesic agent) and/or administration of verapamil or a beta blocker (if not contraindicated). Elective surgery is not typically postponed.

Atrial fibrillation or atrial flutter

●Atrial fibrillation or atrial flutter – Atrial fibrillation or flutter are common arrhythmias that occur in patients with a variety of cardiac and pulmonary abnormalities (waveform 38 and waveform 39 and waveform 40 and waveform 41 and waveform 42). (See "The electrocardiogram in atrial fibrillation" and "Electrocardiographic and electrophysiologic features of atrial flutter".)

•New onset of atrial fibrillation or flutter – New onset of atrial fibrillation or flutter warrants postponement of elective surgery for evaluation and management by the cardiology service including optimization of rate and rhythm control and planning anticoagulant therapy, as discussed in separate topics [21,22]. (See "Atrial fibrillation in patients undergoing noncardiac surgery", section on 'Preoperative atrial fibrillation' and "Perioperative arrhythmias", section on 'Atrial fibrillation or flutter'.)

Management of new onset atrial fibrillation or flutter in patients requiring emergency or urgent surgery also includes rate or rhythm control. Typically, rate control is chosen in this setting unless cardioversion is deemed necessary due to hemodynamic instability. Anticoagulant therapy is typically deferred until after surgery. Details regarding management are discussed separately. (See "Atrial fibrillation in patients undergoing noncardiac surgery", section on 'Emergency surgery'.)

•Paroxysmal, long-standing or permanent atrial fibrillation – For patients with a history of paroxysmal, persistent, long-standing, or permanent atrial fibrillation or flutter [22], sympathetic stimulation should be avoided to avoid triggering a rapid ventricular response.

VENTRICULAR ARRHYTHMIAS

Premature ventricular complexes — Premature ventricular complexes (PVCs; contractions) (waveform 43) are common in the general population. Isolated PVCs are usually clinically insignificant, particularly in otherwise healthy patients without cardiac disease, and have no specific implications for anesthetic management. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation".)

Frequent PVCs may be associated with electrolyte abnormalities, sleep apnea, and a variety of cardiac conditions (table 12). Electrolyte abnormalities should be sought and corrected. Since frequency of PVCs may increase with release of catecholamines, sympathetic stimulation due to pain, anxiety, or inadequate anesthetic depth should be avoided or minimized.

Ventricular tachycardia (VT) — Nonsustained ventricular tachycardia (NSVT) is diagnosed when three or more consecutive PVCs occur at a rate >100 beats/minute (bpm) lasting <30 seconds (waveform 44). Sustained VT is defined as VT lasting ≥30 seconds or causing hemodynamic collapse in <30 seconds.

Similar to PVCs, NSVT can occur in a variety of acute and chronic conditions. Acute onset or increased frequency of PVCs appearing as couplets, triplets, or runs of NSVT may indicate myocardial “irritability” triggered or exacerbated by factors such as hypoxia, myocardial ischemia, volume overload, sympathetic stimulation, or electrolyte abnormalities. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".)

Prompt evaluation and treatment is generally warranted for patients with VT, even those who are hemodynamically stable because hemodynamic instability may develop without warning. Consultation with a cardiologist and postponement of elective surgery is necessary in patients with new onset frequent NSVT, or sustained VT. Continuous ECG monitoring is initiated while the underlying abnormality is sought and corrected. However, in some cases (eg, a patient with known NSVT with reduced left ventricular ejection fraction and history of implantable cardioverter-defibrillator placement), further assessment may be unnecessary after a period of continuous ECG monitoring and/or consultation with a cardiologist.

Differential diagnosis of WCT — Most wide complex tachycardias (WCTs) with QRS complexes ≥120 milliseconds and heart rate (HR) >100 bpm are ventricular tachycardia. (See 'Ventricular tachycardia (VT)' above.)

However, the differential diagnosis for WCTs includes SVT with wide QRS due to bundle branch block (BBB) (at baseline or due to rate-related aberrancy), pre-excitation, or ventricular pacing (algorithm 3). (See "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations", section on 'Supraventricular tachycardia' and "Wide QRS complex tachycardias: Approach to the diagnosis".)

For patients presenting with a WCT of underdetermined cause discovered on the preoperative ECG, elective surgery is usually postponed pending timely evaluation and management with expert cardiology consultation, even if the patient is hemodynamically stable. (See "Wide QRS complex tachycardias: Approach to management".)

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: Supraventricular arrhythmias" and "Society guideline links: Ventricular arrhythmias".)

SUMMARY AND RECOMMENDATIONS

●Rationale – A preoperative electrocardiogram (ECG) is obtained in selected patients to identify potential cardiac issues that might require further evaluation or might alter management, including the timing of an elective surgical procedure and/or anesthetic management (selection of agents or techniques). The preoperative ECG is also useful for comparison if ECG abnormalities are noted intraoperatively or on a postoperative ECG. (See 'Indications and rationale' above.)

●Interpretation – In patients with an indication for a preoperative ECG, at least one 12-lead ECG should be reviewed and interpreted by an expert reader. The anesthesiologist should be familiar with ECG analysis since certain abnormalities may warrant further evaluation with possible delay of the surgical procedure, or have implications for selection of anesthetic agents or techniques. (See 'Interpretation' above.)

●Key considerations – The evaluation and response to preoperative ECG abnormalities (table 1) are influenced by the following factors:

•Is the abnormality new or old?

•Does the patient have a history of cardiovascular disease?

•Does the patient have cardiovascular symptoms?

•What is the individualized risk of the surgical procedure?

●Approach to ECG findings – A summary of common ECG findings and the level of concern they raise is provided in the following sections and in the table (table 1):

•P wave abnormality – This is generally one manifestation of a constellation of clinical findings suggestive of cardiovascular disease, often previously diagnosed. (See 'P wave abnormalities' above.)

•Q waves – When pathologic Q waves are identified, clinical evaluation includes determining if the Q waves are pathologic, their acuity and their cause. Postponement of surgery is generally unnecessary if chronic pathologic Q waves are identified in an asymptomatic patient. (See 'Q waves' above.)

•QRS complex abnormalities – These include QRS axis deviation, bundle branch block, and atrioventricular (AV) block. (See 'QRS complex abnormalities' above.)

-Acute QRS axis deviation or new bundle branch block – Either of these conditions is an indication for clinical evaluation to determine the cause.

-High grade AV block – Elective surgery is generally postponed in a patient with second-degree Mobitz II or third-degree AV block. If urgent or emergency surgery is necessary, temporary pacing should be initiated as soon as possible since complete heart block may develop, resulting in a slow intrinsic ventricular escape rhythm.

•ST segment abnormalities – Evaluation of ST segment depression or elevation includes determining its acuity and cause. Acute ST depression in multiple leads suggestive of myocardial ischemia or acute ST elevation suggestive of acute myocardial infarction is an indication for cardiac consultation and possible postponement of elective surgery. (See 'ST segment abnormalities' above.)

•T wave abnormalities – Acute peaked T waves may be caused by hyperkalemia or acute myocardial infarction and thus warrant prompt evaluation. (See 'T wave abnormalities' above.)

•QT prolongation – New diagnosis of prolongation of the QT interval corrected for heart rate (QTc) is an indication for evaluation and management of the cause, which may involve postponing elective surgery. (See 'QT prolongation' above.)

•Bradyarrhythmias – The approach to major bradyarrhythmias is based upon the severity, cause, symptoms, and hemodynamic status (algorithm 1 and algorithm 2). (See 'Bradyarrhythmias' above.)

•Tachyarrhythmias – While supraventricular tachyarrhythmias are typically narrow complex tachycardias and ventricular arrhythmias are typically wide complex tachycardias, wide complex tachycardias may be supraventricular or ventricular (algorithm 3 and algorithm 5) (See 'Differential diagnosis of WCT' above.)

-Atrial tachyarrhythmias – The approach to these arrhythmias is based upon the cause, symptoms, and hemodynamic status. (See 'Supraventricular tachyarrhythmias' above.)

-Ventricular tachycardia – Prompt evaluation and treatment is generally warranted for patients with VT, even those who are hemodynamically stable because hemodynamic instability may develop without warning. Consultation with a cardiologist and postponement of elective surgery is necessary in patients with new onset frequent NSVT, or sustained VT. (See 'Ventricular tachycardia (VT)' above.)