The preoperative ECG: Evaluation and implications for anesthetic management

INTRODUCTION — Prior to noncardiac surgery, an electrocardiogram (ECG) is obtained in all patients with known cardiovascular disease, significant arrhythmia, or significant structural heart disease unless the patient is undergoing low-risk surgery (surgery associated with less than 1 percent morbidity/mortality, such as ambulatory surgery) (table 1). The primary rationale for obtaining a preoperative ECG in stable patients comes from the utility of having a baseline ECG should a postoperative ECG be abnormal. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Initial evaluation'.)

This topic reviews our approach to the management of patients whose baseline ECG is abnormal. Abnormal ECG findings may or may not indicate additional testing, interventions, postponement of the surgical procedure, or selection of anesthetic agents or techniques.  

This topic will not discuss the pathophysiology of ECG abnormalities or their differential diagnosis. The reader is referred to relevant UpToDate topics in each of the sections below. Other aspects of perioperative evaluation and management of cardiac risk are discussed in separate topics:

●(See "Preoperative medical evaluation of the healthy adult patient", section on 'Electrocardiogram'.)

●(See "Management of cardiac risk for noncardiac surgery".)

INITIAL CONSIDERATIONS — The preoperative ECG should be evaluated for the presence of prominent Q waves or significant ST-segment deviation (which raises the possibility of myocardial ischemia or infarction), as well as chamber abnormality/hypertrophy, QTc prolongation, bundle branch block (BBB), or arrhythmias. In many cases, a recent ECG with interpretation by computer algorithms is available for review at the time of the presurgical anesthetic consultation. Such preoperative ECGs should also be reviewed and interpreted by an expert reader.

The normal ECG (waveform 1) is discussed elsewhere (see "ECG tutorial: Basic principles of ECG analysis"). Many patients have preoperative ECG abnormalities that are nonspecific and reflect prior history of heart disease, but do not necessarily predict increased perioperative risk, particularly during low-risk surgical procedures (table 1). Management of a preoperative ECG abnormality depends in part on the answers to the following questions:

●Is the abnormality new or old? An attempt should be made to compare the current ECG with one or more older ECGs. Many patients with chronically abnormal ECGs will require no additional testing or intervention.

●Does the patient have a history of cardiovascular disease?

●Does the patient have active cardiovascular symptoms?

●Is the planned procedure elective, semi-urgent, or urgent/emergency?

P WAVE ABNORMALITIES — Marked left or right atrial abnormality may signal an underlying condition such as cardiomyopathy, valvular heart disease, or pulmonary hypertension that merits consultation with patient's medical team or cardiologist.

QRS COMPLEX ABNORMALITIES — The QRS complex represents ventricular depolarization. (See "ECG tutorial: Basic principles of ECG analysis", section on 'QRS complex'.)

QRS axis deviation — The normal mean QRS electrical axis (in the frontal plane) is between -30 and +90° in adults (figure 1 and waveform 2). The presence of chronic left (more negative than -30°) or right axis (more positive than +90°) deviation usually has no specific implications for anesthetic management. QRS axis deviation might be important as it relates, for example, to ventricular hypertrophy or myocardial infarction (MI).

An acute (newly identified) major change in QRS axis may be a clue to new cardiac or pulmonary abnormality. For example, acute pulmonary embolism may lead to new right axis deviation. Investigation of potential causes is warranted, which may lead to postponement of elective surgery in some cases. (See "ECG tutorial: Basic principles of ECG analysis", section on 'Axis'.)

Ventricular hypertrophy — The ECG may be interpreted as showing left or right ventricular hypertrophy (LVH or RVH). (See "ECG tutorial: Chamber enlargement and hypertrophy", section on 'Left ventricular hypertrophy' and "Left ventricular hypertrophy: Clinical findings and ECG diagnosis" and "ECG tutorial: Chamber enlargement and hypertrophy", section on 'Right ventricular hypertrophy'.).

Acute LVH does not occur and acute RVH is uncommon. Right ventricular overload may be acute or subacute in patients with pulmonary thromboembolism or asthma.

Chronic RVH, while uncommon, is associated with many significant comorbid diseases, such as pulmonic stenosis or pulmonary hypertension syndromes. Such patients often need evaluation for cardiac or pulmonary risk prior to noncardiac surgery.

ECG evidence of LVH is always due to sustained pressure or volume load, usually of months to years duration, as with aortic stenosis or systemic hypertension. Such patients often have diastolic dysfunction and preload dependency, and are at risk for subendocardial ischemia, which is exacerbated by hypovolemia, low systemic vascular resistance, and/or tachycardia. The anesthetic plan should be designed to minimize these hemodynamic aberrations, as noted in topics addressing anesthetic management of patients with these cardiovascular diseases:

●(See "Anesthesia for patients with hypertension".)

●(See "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease", section on 'Aortic stenosis'.)

●(See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery".)

Bundle branch blocks and hemiblocks — Bundle branch blocks (BBBs) are defined by prolonged QRS duration >120 milliseconds and distinct patterns of QRS morphology (waveform 3 and waveform 4 and waveform 5 and waveform 6) [1,2]. (See "ECG tutorial: Intraventricular block" and "Left bundle branch block" and "Right bundle branch block".)

The presence of chronic left or right axis BBB reflects a history of cardiac disease (eg, ischemic heart disease, hypertension, valvular heart disease, cardiomyopathies). In asymptomatic patients with chronic left or right BBB, postponement of surgery for further evaluation is not necessary. Although chronic BBBs have been associated with postoperative 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 [3].

In patients with a chronic left BBB, perioperative insertion of a right heart catheter (eg, a pulmonary artery catheter) incurs significant risk of inducing complete heart block due to transient impairment of conduction in the right bundle (which courses in the subendocardium along the interventricular septum) [4,5]. For this reason, continuous ECG and hemodynamic monitoring is necessary, and the operator must ensure immediate availability of temporary transcutaneous or transvenous pacemaker system. (See "Right bundle branch block", section on 'Iatrogenic RBBB' and "Temporary cardiac pacing".)

Appearance of a new or acute BBB warrants investigation of potential causes. In some cases, new onset of a left or right BBB may be "rate related" and temporary, occurring at fast heart rates when the bundle refractory period exceeds that of the R-R interval. In other cases, acute onset of a BBB indicates acute prolongation of the refractory period as a result of a clinically significant new cardiac or pulmonary abnormality causing myocardial ischemia or strain. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Electrocardiography' and "Conduction abnormalities after myocardial infarction".)

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 7). A left posterior fascicular block, or hemiblock, is characterized by a pathologic right axis, >+90° up to 180°, together with small R and deep S waves in leads I and aVL, and small Q and tall R waves in leads III and aVF (waveform 8) (see "ECG tutorial: Intraventricular block"). Similar to BBB, presence of chronic hemiblocks would not require further modification of the anesthetic plan, while the presence of new or acute hemiblock merits further evaluation and consultation.

Q waves — There is no consensus regarding criteria for diagnosis of MI based on pathologic Q waves. Small Q waves are often seen in leads I, aVL, and V4-V6 as a result of initial septal depolarization and are considered normal. (See "ECG tutorial: Basic principles of ECG analysis", section on 'QRS complex' and "Pathogenesis and diagnosis of Q waves on the electrocardiogram" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Significance of Q waves'.)

However, initial Q waves that are deep (>1 mm), broad (>0.03 to 0.04 seconds), and present in two or more consecutive leads are a characteristic finding in patients with a prior MI, particularly when there are also associated T wave changes (typically T wave inversions) in the same leads. Postponement of surgery is unnecessary if these findings are chronic in an asymptomatic patient.

Wolff-Parkinson-White syndrome — In patients with known pre-excitation syndrome (ie, Wolff-Parkinson-White [WPW] syndrome), the anesthesiologist should consult the cardiologist who has been caring for the patient.

WPW occurs due to early ventricular activation through an accessory pathway [6,7]. This 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 9 and waveform 10). In some patients, diagnosis of WPW pattern is prompted by these incidental findings on a preoperative ECG. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Electrocardiographic findings'.)

Patients with WPW may develop supraventricular arrhythmias with rapid ventricular rates (see "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Arrhythmias associated with WPW'). Preoperative review of the medical records and/or consultation with an electrophysiology cardiologist is necessary in order to choose the correct initial pharmacologic therapy should an intraoperative tachyarrhythmia occurs, as discussed separately. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome".)

Anesthetic planning to avoid tachyarrhythmias includes minimizing risk of rapid ventricular responsiveness by avoiding marked increases in sympathetic stimulation (eg, during laryngoscopy and endotracheal intubation, surgical incision, or emergence from anesthesia). Also, any intravenous (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) [6]. Furthermore, techniques such as a high spinal block or IV agents that increase vagal tone (eg, succinylcholine, neostigmine) are employed cautiously, as these may promote conduction of impulses down the accessory pathway [6,7].

ST-SEGMENT ABNORMALITIES — The ST-segment is usually isoelectric (ie, at the baseline when compared with the T-P segment) and has a slight upward concavity (waveform 2). (See "ECG tutorial: Basic principles of ECG analysis", section on 'ST segment'.)

ST-segment elevation — ST-segment elevation may be a normal variant or represent an acute, evolving myocardial infarction (MI) or myopericarditis.

Tombstone-shaped (convex) ST segment elevation in two or more consecutive leads is the hallmark of acute ST-elevation myocardial infarction (STEMI) (waveform 11) and (waveform 12 and waveform 13 and waveform 14 and waveform 15 and waveform 16). (See "ECG tutorial: Myocardial ischemia and infarction" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and "ECG tutorial: ST and T wave changes".)

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

ECG changes in acute pericarditis (figure 2) differ from those in acute STEMI in several ways, as noted in the table (table 2). 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) — The J point is the junction between the end of the QRS and the beginning of the ST-segment (waveform 17). Early repolarization or "J-point elevation" is a relatively common benign QRS variant with no clinical implications for anesthetic care; this is often seen in young adults who have a thin chest wall. However, 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 11). The presence or absence of clinical signs and symptoms is the primary distinguishing feature between an evolving MI and benign J point elevation. Previous ECGs, if available, are valuable to determine whether J point elevation is chronic or new. (See "Early repolarization" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Early repolarization'.)

ST-segment depression — ST-segment depression is defined as a horizontal or down-sloping ST-segment that is depressed ≥0.05 mV below the baseline, measured at 0.08 seconds after the J point, in two contiguous leads (waveform 17).

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 often indicates myocardial ischemia or injury and warrants consultation with the cardiology service (table 3), as well as possible postponement of elective surgery. (See "ECG tutorial: Myocardial ischemia and infarction", section on 'ST-segment depression' and "ECG tutorial: ST and T wave changes", section on 'Myocardial ischemia, injury, and infarction'.)

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 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'.)

However, acute dynamic changes in T wave direction and amplitude may signify acute myocardial ischemia warranting consultation with the cardiology service and possible postponement of elective surgery (table 3). (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'.)

Tall peaked T waves — Tall peaked T waves with a narrow base are an early sign of hyperkalemia [8]. In addition, prominent (ie, "hyper-acute") T waves may be seen during the early phases of an acute MI. If acute MI is suspected, the cardiology service is immediately consulted (table 3). Elective surgery is postponed if either hyperkalemia or acute MI is suspected. (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'.)

Chronic, nonemergency causes of tall peaked T waves include left bundle branch block (BBB) or left ventricular hypertrophy. (See 'Bundle branch blocks and hemiblocks' above and "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery".)

QT INTERVAL PROLONGATION — The QT interval is normally <0.44 sec in men and <0.45 to 0.46 sec in women. It is typically corrected for heart rate (termed the QTc interval). This corresponds to a QTc of <470 milliseconds for men and <480 milliseconds for women. A QTc >500 milliseconds is considered highly abnormal for both men and women. (See "ECG tutorial: Basic principles of ECG analysis", section on 'QT interval'.)

There are numerous causes of QTc prolongation; most of these are acquired due to effects of certain medications or electrolyte abnormalities (table 4 and table 5) (see "Acquired long QT syndrome: Definitions, pathophysiology, and causes"). Patients with apparent newly discovered congenital long QT syndromes who have not previously been evaluated by cardiology should be referred. (See "Congenital long QT syndrome: Treatment", section on 'Treatment'.)

Potential development of a life-threatening ventricular arrhythmia (torsades de pointes [TdP]) is a major concern in patients with significant acquired or congenital QTc prolongation. For this reason, the preanesthetic assessment in a patient with QTc prolongation on the ECG should include inquiry about history of syncope and family history of sudden death as well as review of all medications. Elective surgical procedures should be postponed for patients with significant new QTc interval prolongation that may be corrected by discontinuation of culprit medications (table 4), or by correction of an electrolyte abnormality. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management", section on 'Patients with acute TdP'.)

Drugs commonly used in the perioperative period that might further prolong the QT interval are avoided in patients with prolonged QTc interval (table 4). These include the antiemetic agents droperidol, haloperidol, and ondansetron, and the opioid methadone. Also, volatile anesthetic agents (eg, sevoflurane, desflurane, isoflurane) are used cautiously as these are associated with QT prolongation. 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 (IV) anesthetic technique [9]. (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Ventricular arrhythmias' and "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

Since TdP can be triggered by catecholamines, sympathetic stimulation is avoided or minimized throughout the perioperative period [10,11]. Beta adrenergic blocking agents may have a protective role and should be continued if chronically administered, as well as used to treat perioperative episodes of tachycardia, hypertension, or presumed myocardial ischemia [12]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease".)

Since electrolyte abnormalities predispose to TdP, low serum concentrations of potassium, magnesium, or calcium should be avoided and/or treated throughout the perioperative period. Intraoperative hyperventilation is also avoided because acute respiratory alkalosis may lead to hypokalemia and hypocalcemia. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes", section on 'Metabolic abnormalities'.)

Other causes and potentiators of long QT syndrome are listed in the table (table 5).

ATRIAL PREMATURE BEATS (APBS) — Atrial premature beats (APBs) (waveform 18 and waveform 19) are usually benign and commonly occur in patients with normal hearts, particularly in patients with increased sympathetic tone due to smoking or alcohol. APBs also occur in patients with cardiopulmonary diseases such as chronic obstructive pulmonary disease, ischemic heart disease, cardiomyopathy, or valvular heart disease. (See "Supraventricular premature beats".)

Planned surgery and anesthetic care are not altered by this finding.

VENTRICULAR PREMATURE BEATS (VPBs) — Ventricular premature beats (VPBs) (waveform 20) are common in the general population. Isolated VPBs are usually clinically insignificant, particularly in otherwise healthy patients without cardiac disease. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation".)

Frequent VPBs may be associated with electrolyte abnormalities, myocardial ischemia, hypertension, left ventricular hypertrophy, heart failure, hypertrophic cardiomyopathy, myocarditis, or congenital heart disease. Since frequency of VPBs may increase with release of catecholamines (eg, pain, inadequate anesthetic depth), sympathetic stimulation should be avoided or minimized, and administration of a beta blocking agent may be useful. Electrolyte abnormalities should be sought and corrected.

Non-sustained ventricular tachycardia (NSVT) — Nonsustained ventricular tachycardia (NSVT) is diagnosed when three or more consecutive ventricular beats occur at a rate >120 beats per minute (bpm) lasting <30 seconds (waveform 21). (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management".)

Similar to VPBs, NSVT can occur in a variety of acute and chronic conditions. Occasional couplets or triplets are commonly seen and chronic in asymptomatic patients with cardiopulmonary conditions, such as left ventricular dysfunction with reduced ejection fraction (EF) or obstructive sleep apnea. Surgery is not typically postponed in such patients. However, management should be individualized after review of prior ECGs, if available. In patients with new onset or frequent NSVT, a period of continuous ECG monitoring and/or consultation with a cardiologist is warranted, whereas triplets in a patient with known reduced EF and history of implantable cardioverter-defibrillator placement may not require further assessment.

Acute onset or increased frequency of couplets or triplets, or runs of NSVT usually indicate myocardial irritability triggered or exacerbated by factors such as hypoxia, myocardial ischemia, volume overload, sympathetic stimulation, or electrolyte abnormalities. The cardiology service is consulted and surgery is postponed while the underlying abnormality is sought, particularly if frequent or sustained runs of NSVT are not quickly resolved.

SUSTAINED TACHYARRHYTHMIAS — Tachycardia generally refers to any rhythm with a heart rate (HR) >100 beats per minute (bpm). The origin of the arrhythmia may be the sinus node, atrium, atrioventricular node (or junctions), His bundle, or ventricle. These arrhythmias may be paroxysmal or sustained.

Supraventricular tachyarrhythmias — Supraventricular tachyarrhythmias (SVTs), which include sinus tachycardia, usually have a narrow QRS complex (<120 milliseconds). (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias".)

Underlying causes of a preoperative supraventricular tachyarrhythmia should be identified and treated prior to elective surgery (algorithm 1) [13]. Elevated preoperative HR ≥90 bpm was associated with increased risk of myocardial injury after major noncardiac surgery in a large retrospective study of more than 41,000 patients [14]. In most instances, termination of the SVT or achievement of ventricular rate control results in resolution of any symptoms. Referral to the cardiology service for further treatment depends on the cause and clinical consequences of the SVT, as explained below. (See "Overview of the acute management of tachyarrhythmias", section on 'Narrow QRS complex tachyarrhythmias'.)

SVTs with a regular rhythm include:

●Sinus tachycardia – Sinus tachycardia has normal P and QRS complexes (waveform 22). Preoperative mild to moderate sinus tachycardia (eg, a rate of 105 to 125 bpm) is usually due to 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 the HR, hypoxemia or hypercarbia, myocardial ischemia, fever, sepsis, or substance abuse (eg, cocaine). Thus, determining the etiology of sinus tachycardia should be part of an overall patient assessment. Surgery and anesthetic care are not typically altered if the cause can be identified and managed appropriately. (See "Sinus tachycardia: Evaluation and management".)

●Atrioventricular nodal reentrant tachycardia (AVNRT) – Atrioventricular nodal reentrant tachycardia (AVNRT) is a paroxysmal SVT due to a reentry circuit with separate electrical pathways within or proximal to the atrioventricular (AV) node (waveform 23 and waveform 24). Tachycardia can be triggered by increases in adrenergic tone. (See "Atrioventricular nodal reentrant tachycardia".)

Vagal maneuvers may be attempted or intravenous (IV) adenosine or a calcium channel blocker may be administered to transiently delay in conduction through the AV node and terminate AVNRT (table 6). Elective surgery is postponed in patients who do not rapidly convert to sinus rhythm with initial efforts.

●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 25). Focal AT may occur in patients with chronic structural heart disease in response to atrial stretch due to elevated left or right atrial pressures. However, focal AT 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. Hemodynamically stable patients whose surgery cannot be delayed 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. Elective surgery is postponed if adequate rate or rhythm control is not achieved or if hemodynamic instability develops. The cardiology service is consulted for decisions regarding additional treatment options such as electrical cardioversion, administration of additional rate-controlling medication, or chemical cardioversion with IV amiodarone. (See "Focal atrial tachycardia", section on 'Treatment'.)

SVTs with an irregular rhythm include:

●Atrial fibrillation or atrial flutter – Atrial fibrillation manifests as irregularly irregular beats and absent P waves (waveform 26 and waveform 27 and waveform 28). Atrial flutter typically presents with flutter waves appearing as saw tooth deflections with variable atrioventricular conduction (waveform 29). Atrial flutter with 2:1 AV conduction is a common presentation of atrial flutter, with regular-appearing narrow QRS tachycardia at a ventricular rate of approximately 150 bpm with low amplitude flutter waves superimposed on T waves (waveform 30). (See "The electrocardiogram in atrial fibrillation" and "Electrocardiographic and electrophysiologic features of atrial flutter".)

New onset of atrial fibrillation or flutter warrants postponement of elective surgery for evaluation and management by the cardiology service [15]. (See "Arrhythmias during anesthesia", section on 'Atrial fibrillation' and "Arrhythmias during anesthesia", section on 'Atrial flutter'.)

●Multifocal atrial tachycardia (MAT) – Multifocal atrial tachycardia (MAT) originates from two or more foci in the atrium. The P waves have two or more differing morphologies and the rhythm is irregular (waveform 31). (See "Multifocal atrial tachycardia".)

MAT is an uncommon arrhythmia that is usually associated with significant pulmonary disease. Patients with MAT are typically hemodynamically stable. The HR can be appropriately reduced with premedication (eg, anxiolytic or analgesic agent) and/or administration of a beta blocker. Elective surgery need not be postponed in such patients.

A rapid ventricular response may be associated with hypotension, particularly if the rapid HR causes myocardial ischemia. Elective surgery is postponed in patients who are symptomatic or if there is difficulty achieving rate control, and the cardiology service is consulted for further evaluation and management.

Wide complex tachyarrhythmias — In wide complex tachycardia (WCT), the QRS complexes are wide (ie, ≥120 milliseconds) and the HR is >100 bpm. Most WCTs are due to ventricular tachycardia, but the differential diagnosis includes a variety of SVTs. (See "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations", section on 'Supraventricular tachycardia' and "Wide QRS complex tachycardias: Approach to the diagnosis".)

Management of WCT depends on whether the impulse originates in the atria or the ventricles (algorithm 2). Most patients with WCT on the preoperative ECG should have surgery postponed until evaluation by cardiology. (See "Wide QRS complex tachycardias: Approach to management".)

BRADYARRHYTHMIAS

Sinus bradycardia — Sinus bradycardia has normal P and QRS complexes at a heart rate (HR) <50 to 60 beats per minute (bpm) (waveform 32) (see "Sinus bradycardia"). An extremely low preoperative HR (eg, <40 bpm) has been associated with development of myocardial injury after major noncardiac surgery [14].

Sinus bradycardia occurs in a variety of normal and abnormal conditions, including temporary increases in vagal tone, use of negative chronotropic drugs (eg, beta blockers, calcium channel blockers), or sinus node dysfunction. Asymptomatic patients with sinus bradycardia at a HR ≥45 bpm with stable hemodynamics may proceed with the planned procedure. However, it is prudent to plan anesthetic management to avoid worsening bradycardia. For example, bradycardia may be caused or exacerbated 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, opioids, negative chronotropic agents, vasoconstrictors, or anticholinesterase agents coadministered with an inadequate dose of an anticholinergic agent). Thus, vagolytic agents such as atropine and chronotropic agents such as ephedrine should be immediately available to treat severe bradycardia. (See "Arrhythmias during anesthesia", section on 'Sinus bradycardia'.)

Sinus arrhythmia — Sinus arrhythmia appears as periodic narrowing and widening of PP intervals on the ECG (waveform 33). It is caused by rhythmic changes in vagal tone that occur during the respiratory cycle, with slowing of the HR during expiration that may transiently result in a rate <60 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 — 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:

First degree AV block — First degree atrioventricular (AV) block occurs when there is delayed but intact conduction from atria to ventricles, hallmarked by a prolonged PR interval >200 milliseconds (waveform 34). (See "First-degree atrioventricular block".)

Surgery is not delayed for evaluation or treatment of patients with first degree AV block. Similar to patients with sinus bradycardia, 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. Thus, it is prudent to use caution when employing these agents or techniques, and to ensure immediate availability of vagolytic and chronotropic agents to treat severe bradycardia if necessary. (See 'Sinus bradycardia' above.)

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

●Mobitz Type I – With Mobitz Type I (Wenckebach) second degree AV block, there is progressive prolongation of the PR interval until a single ventricular beat is dropped (waveform 35). Patients with Type I second degree AV block may have disease of the conduction system, enhanced vagal tone, or may be receiving AV nodal blocking drugs. This is a benign condition with low risk of progression to complete heart block. (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)".)

However, intraoperative vagal stimuli or use of AV nodal blocking agents can exaggerate the conduction delay and lead to symptomatic bradycardia. As with first degree AV block, surgery is not delayed for evaluation or treatment of patients with Type I second degree AV block. However, precautions regarding causes of vagal reflexes and use of techniques or agents that may increase vagal tone are prudent to avoid further delay in AV nodal conduction, similar to precautions in patients with sinus bradycardia [16]. Vagolytic and chronotropic agents should be immediately available to treat severe bradycardia. (See 'Sinus bradycardia' above and 'First degree AV block' above.)

●Mobitz Type II – Patients with Mobitz Type II second degree AV block have intermittently dropped ventricular beats (waveform 36 and waveform 37), and are at increased risk for progression to symptomatic bradycardia and complete heart block. (See "Second-degree atrioventricular block: Mobitz type II".)

For patients with Mobitz Type II AV block, a cardiologist is consulted, and elective surgery is postponed.

If urgent or emergency surgery is necessary, 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 [16]. 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 3). In such patients, positive chronotropic agents are administered in an attempt to increase HR (eg, epinephrine, dopamine, dobutamine, isoproterenol) (table 7).

In some cases, temporary pacing may be necessary to alleviate bradycardia and maintain hemodynamic stability. Temporary transvenous pacing wires are inserted during the preoperative or early intraoperative period for an emergency procedure, if possible, or other temporary options are employed, such as transcutaneous, transesophageal, or pulmonary artery catheter pacing modalities. These options are discussed in more detail separately. (See "Temporary cardiac pacing" and "Arrhythmias during anesthesia", section on 'Temporary pacing options'.)

Third degree AV block — Third degree atrioventricular (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 38). This occurs due to advanced disease of conduction system. Patients with third degree AV block typically present with symptomatic bradycardia. (See "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 become very slow (approximately 30 to 40 bpm), and responsiveness to atropine will likely be poor. (See "Temporary cardiac pacing" and "Arrhythmias during anesthesia", section on 'Temporary pacing options'.)

RECOMMENDATIONS OF OTHERS — Our recommendations are in broad agreement with those made by in the 2014 American College of Cardiology/American Heart Association (ACC/AHA) and European Society of Cardiology/European Society of Anesthesiology (ESC/ESA) guidelines on noncardiac surgery [17-19].

SUMMARY AND RECOMMENDATIONS

●General considerations – The anesthesiologist should be familiar with analysis of an electrocardiogram (ECG), as certain abnormalities warrant further evaluation or management that may result in postponement of the surgical procedure, or have implications for selection of anesthetic agents or techniques. (See "ECG tutorial: Basic principles of ECG analysis".)

●Findings of potential concern – The following ECG findings or diagnoses warrant further evaluation and/or management, and may warrant delay of elective surgery in some cases:

•Acute axis deviation. (See 'QRS axis deviation' above.)

•New bundle branch block (BBB) (waveform 3 and waveform 4 and waveform 5 and waveform 6). (See 'Bundle branch blocks and hemiblocks' above.)

•Acute ST-segment elevation in acute ST-elevation myocardial infarction (STEMI) (waveform 11 and waveform 12 and waveform 13 and waveform 14 and waveform 15 and waveform 16), or acute pericarditis (table 2). (See 'ST-segment elevation' above.)

•Acute ST-segment depression in multiple leads often indicating myocardial ischemia or subendocardial injury. (See 'ST-segment depression' above.)

•Type II second degree atrioventricular (AV) block or third degree AV block (waveform 36 and waveform 37 and waveform 38). If urgent or emergency surgery is necessary, temporary pacing should be initiated as soon as possible since the intrinsic ventricular rhythm with complete heart block is likely to become very slow, and responsiveness to atropine is usually poor (algorithm 3). (See 'Third degree AV block' above and 'Second degree AV block' above.)

•Tall peaked T waves. (See 'Tall peaked T waves' above.)

•Certain narrow complex supraventricular tachyarrhythmias (SVTs) (waveform 26 and waveform 27 and waveform 28 and waveform 23 and waveform 24 and waveform 25). (See 'Supraventricular tachyarrhythmias' above.)

•Wide complex tachycardia (WCT) (algorithm 2), including acute onset of nonsustained ventricular tachycardia (waveform 21). (See 'Wide complex tachyarrhythmias' above.)

●Findings potentially affecting the anesthetic approach – It is usually not necessary to postpone surgery if the following ECG findings are present, although the anesthetic approach may change:

•Prolongation of the corrected QT (QTc) interval. For patients who require urgent or emergency surgery, drugs that might further prolong the QTc interval are avoided throughout the perioperative period (table 4). Additionally, sympathetic stimulation should be avoided or minimized, electrolyte abnormalities that predispose to torsades de pointes (TdP) corrected (eg, hypokalemia, hypomagnesemia, hypocalcemia), and perioperative respiratory alkalosis avoided. (See 'QT interval prolongation' above and "Arrhythmias during anesthesia", section on 'Polymorphic ventricular tachycardia (torsades de pointes)'.)

•Left ventricular hypertrophy (LVH) produces typical ECG changes in patients with chronic hypertension, aortic stenosis, or hypertrophic cardiomyopathy with left ventricular outflow tract obstruction. The anesthetic plan is designed to minimize hypovolemia, hypotension, and tachycardia in such patients. (See 'Ventricular hypertrophy' above.)

•Sinus bradycardia at a heart rate ≥45 bpm, first degree AV block, or Type I second degree AV block. Anesthetic management should avoid exacerbation of bradycardia due to vagal reflexes, a high spinal block, or agents that increase vagal tone (eg, opioids, negative chronotropic agents, vasoconstrictors, anticholinesterase agents coadministered with an inadequate dose of an anticholinergic vagolytic agent). Vagolytic (eg, atropine) and chronotropic (eg, ephedrine) agents should be immediately available to treat severe bradycardia. (See 'Sinus bradycardia' above and 'First degree AV block' above and 'Second degree AV block' above.)