Ventricular arrhythmias

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor: Cafer Zorkun, M.D., Ph.D. [2] Vishnu Vardhan Serla M.B.B.S. [3] Nehal Eid, M.D.[4]

## Overview

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Ventricular arrhythmias (VAs) are abnormal cardiac rhythms originating from the ventricles, encompassing a spectrum from benign premature ventricular complexes (PVCs) to life-threatening ventricular tachycardia (VT) and ventricular fibrillation (VF). VAs are the most common cause of sudden cardiac death (SCD), which accounts for approximately 50% of all cardiovascular deaths in the United States.[1] The 2017 AHA/ACC/HRS guideline and the 2022 ESC guideline provide the primary frameworks for the evaluation, risk stratification, and management of patients with VAs and for the prevention of SCD.[2]

## Historical Perspective

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The recognition of ventricular arrhythmias dates to the early days of electrocardiography. The development of the implantable cardioverter-defibrillator (ICD) by Michel Mirowski in the 1980s revolutionized the management of life-threatening VAs. Landmark trials including MADIT, MADIT-II, SCD-HeFT, and AVID established the role of ICDs in both primary and secondary prevention of SCD. The CAST trial in 1989 demonstrated that suppression of PVCs with class IC antiarrhythmic drugs (flecainide, encainide) paradoxically increased mortality in post-myocardial infarction patients, fundamentally changing the approach to pharmacologic management of VAs.

## Classification

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Ventricular arrhythmias are classified by morphology, duration, and clinical context:[3]

Type  | Definition

|

Premature ventricular complex (PVC) | A premature depolarization originating from the ventricles
Nonsustained VT (NSVT) | ≥3 consecutive ventricular beats at a rate >100 bpm lasting 30 seconds and not requiring termination due to hemodynamic compromise
Sustained VT | VT lasting ≥30 seconds or requiring termination due to hemodynamic compromise in 30 seconds
Monomorphic VT | Sustained VT with a stable single QRS morphology
Polymorphic VT | Sustained VT with a changing or multiform QRS morphology at cycle length between 600 and 180 ms
Torsades de pointes | Polymorphic VT associated with a prolonged QT or QTc, characterized by twisting of the QRS peaks around the isoelectric line
Bundle-branch re-entrant tachycardia | VT due to re-entry involving the His-Purkinje system, usually with LBBB morphology; typically occurs in the setting of cardiomyopathy
Bidirectional VT | VT with beat-to-beat alternation in the QRS frontal plane axis; often associated with digitalis toxicity or catecholaminergic polymorphic ventricular tachycardia ↗
Ventricular flutter | Regular ventricular arrhythmia at approximately 300 bpm with monomorphic appearance and no isoelectric interval between successive QRS complexes
Ventricular fibrillation | Rapid (usually >300 bpm), grossly irregular ventricular rhythm with marked variability in QRS cycle length, morphology, and amplitude
Electrical storm | ≥3 episodes of sustained VT, VF, or appropriate ICD shocks within 24 hours

## Pathophysiology

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The mechanisms underlying ventricular arrhythmias include:

Re-entry: The most common mechanism in structural heart disease. Scar tissue from prior myocardial infarction or fibrosis creates zones of slow conduction bordered by areas of functional or anatomic block, forming a re-entrant circuit. The border zone between viable and fibrotic tissue is the typical substrate for monomorphic VT in ischemic cardiomyopathy.[4]

Triggered activity: Caused by afterdepolarizations. Delayed afterdepolarizations (DADs) are the mechanism of outflow tract VT and digitalis-induced arrhythmias. Early afterdepolarizations (EADs) underlie torsades de pointes in the setting of QT prolongation.

Abnormal automaticity: Enhanced automaticity in ventricular tissue, particularly in ischemic or injured myocardium, or in Purkinje fibers.

Channelopathies: Genetic mutations affecting cardiac ion channels (e.g., long QT syndrome, Brugada syndrome ↗, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome) create spatial electrical heterogeneity that predisposes to VF.

## Causes

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### Structural Heart Disease:

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Coronary artery disease: The most common cause of VT and VF, accounting for 76–82% of clinically documented cases

Dilated cardiomyopathy

Hypertrophic cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

Cardiac sarcoidosis ↗

Myocarditis

Congenital heart disease (e.g., tetralogy of Fallot ↗)

Valvular heart disease (e.g., aortic stenosis, mitral valve prolapse)

Left ventricular noncompaction

### Inherited Channelopathies (Structurally Normal Heart):

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Long QT syndrome (LQTS)

Brugada syndrome

Catecholaminergic polymorphic ventricular tachycardia (CPVT)

Short QT syndrome (SQTS)

Early repolarization syndrome

Idiopathic VF

### Idiopathic VT (Structurally Normal Heart):[5]

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Outflow tract VT: Right ventricular outflow tract (RVOT) or left ventricular outflow tract (LVOT), including aortic sinus of Valsalva origin

Idiopathic left ventricular tachycardia: Left posterior fascicular (verapamil-sensitive), left anterior fascicular, or high septal fascicular VTach.

Papillary muscle VT

Mitral or tricuspid annular VT

### Reversible / Secondary Causes:

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Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia)

Myocardial ischemia or acute myocardial infarction Drug-induced (QT-prolonging medications, digitalis toxicity, sympathomimetics, class IC antiarrhythmics in structural heart disease)

Hypoxia

Acidosis

Thyroid disorders

Cocaine or other stimulant use

## Differentiating Ventricular Arrhythmias from Other Diseases

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The differential diagnosis of a wide QRS complex tachycardia includes:

Diagnosis  | Key Distinguishing Features

|

Ventricular tachycardia | AV dissociation, capture/fusion beats, concordance in precordial leads, QRS >140 ms (RBBB) or >160 ms (LBBB), northwest axis
Supraventricular tachycardia with aberrant conduction | Typical RBBB or LBBB morphology, preceding P waves, prior ECG showing bundle branch block
Supraventricular tachycardia with pre-excitation (Wolff-Parkinson-White syndrome)  | History of pre-excitation on baseline ECG, irregular rate (pre-excited atrial fibrillation)
Pacemaker-mediated tachycardia | Pacing spikes visible, device interrogation confirms diagnosis
Artifact | Baseline rhythm visible between artifact deflections, patient clinically stable

The Brugada algorithm is a widely used stepwise approach for differentiating VT from SVT with aberrancy, with reported sensitivity and specificity exceeding 95%.

## Epidemiology and Demographics

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SCD accounts for approximately 230,000 to 350,000 deaths per year in the United States. The estimated total annual burden of out-of-hospital cardiac arrest is approximately 356,500, with an additional 209,000 in-hospital cardiac arrests occurring annually.

Age: Risk of SCD in the general population beginning at age 35 is estimated at approximately 1 per 1,000 per year. In children, adolescents, and young adults, the annual risk is approximately 1 per 100,000.

Sex: SCD is more common in men than in women across all age groups.

Underlying substrate: Ischemic heart disease remains the most common substrate associated with SCD, although its relative contribution appears to be decreasing, with various forms of cardiomyopathy increasing.

PVCs: Found on longer-term monitoring in approximately 50% of all people with or without heart disease. Frequent PVCs (≥1 PVC on a 12-lead ECG or >30 PVCs per hour) are associated with increased cardiovascular risk and mortality.

## Risk Factors

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Reduced left ventricular ejection fraction (LVEF)

Prior myocardial infarction

Heart failure

Coronary artery disease

Family history of SCD

Inherited cardiomyopathy or channelopathy

Electrolyte abnormalities

QT-prolonging medications

Stimulant drug use

## Natural History, Complications, and Prognosis

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The prognosis of ventricular arrhythmias depends on the underlying substrate:

PVCs in structurally normal hearts: Generally benign prognosis. Very frequent PVCs (>10,000–20,000 per day) may cause PVC-induced cardiomyopathy, which is potentially reversible with PVC suppression. NSVT: In the absence of structural heart disease, prognosis is generally favorable. In patients with ischemic or nonischemic cardiomyopathy, NSVT is associated with increased risk of SCD.[6] Sustained VT/VF: Associated with high mortality without treatment. Electrical storm is associated with increased mortality. Out-of-hospital cardiac arrest: Overall survival rate is estimated at approximately 10%. Survival is better when the initial rhythm is shockable (VF or pulseless VT) compared with pulseless electrical activity or asystole. Idiopathic VT: Outflow tract VT and fascicular VT in structurally normal hearts carry an excellent prognosis.

### Management

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#### Patients Without Heart Disease

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In the absence of heart disease, PVCs are associated with little or no increased risk of developing a dangerous arrhythmia. In this situation, the risk-to-benefit ratio of antiarrhythmic drug therapy does not support routine treatment.[7] It is important to review medications, determine if stimulants are being used, and correct electrolyte abnormalities. If no underlying cause is found, the optimal approach is patient reassurance. Patients should be made aware of the potential dangers of antiarrhythmic drug therapy as determined in the Cardiac Arrhythmia Suppression Trials (CAST and CAST II).[8] [9]

CAST showed that the risk of dying increased, rather than decreased, with successful long-term suppression of premature ventricular complexes after myocardial infarction in older patients. At best, CAST II showed no impact on long-term survival from drug treatment that successfully suppressed premature ventricular complexes. If patients with multiple premature ventricular complexes have severe, disabling symptoms, beta blockers are the safest initial choice.Referral to a cardiologist is indicated if beta-blocker therapy is not effective. In this situation, the next agents to be tried would be class I antiarrhythmic drugs, such as flecainide (Tambocor) and amiodarone (Cordarone), although radiofrequency ablation of an ectopic focus may also be an appropriate treatment.

#### Patients with Structural Heart Disease

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The occurrence of premature ventricular complexes in patients with structural heart disease has been shown to significantly increase the risk of subsequent morbidity and mortality. Coronary heart disease, cardiomyopathy, and congestive heart failure are the major cardiac diseases associated with unfavorable outcomes in patients with premature ventricular complexes.

## Ventricular Tachycardia

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Ventricular tachycardia refers to a rhythm originating from a ventricular ectopic focus. ECG shows ≥3 consecutive ventricular complexes at >100 bpm with wide QRS (≥120 ms)with no associated P waves.

In patients with bundle branch block, Wolff-Parkinson-White syndrome, or aberrant conduction, supraventricular tachycardia can resemble ventricular tachycardia. Because of the morbidity and mortality associated with untreated ventricular tachycardia, any wide-complex tachycardia should be assumed to be ventricular tachycardia until proved otherwise. Physicians should keep in mind that patients with ventricular tachycardia can have minimal symptoms.

'''Sustained VT''': lasts >30 seconds or requires termination for hemodynamic compromise

'''Nonsustained VT (NSVT)''': ≥3 beats, self-terminates in 30 seconds

'''Monomorphic VT''': single stable QRS morphology; usually scar-related reentry

'''Polymorphic VT''': changing QRS morphology; think ischemia, channelopathy, or metabolic cause

'''Torsades de pointes''': polymorphic VT + prolonged QT interval

'''Electrical storm''': ≥3 sustained VT/VF episodes within 24 hours

### Management of Ventricular Tachycardia

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## Acute Management

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Unstable VT:

Immediate synchronized cardioversion (Class I); defibrillation if pulseless

IV amiodarone for VT persisting/recurring after shock (Class I)

150 mg over 10 min → 1 mg/min × 6 hr → 0.5 mg/min × 18 hr

IV beta-blocker for recurrent VT/VF storm post-MI (Class IIa)

Stable Monomorphic VT:

Synchronized cardioversion with sedation is appropriate at any point (Class I)

IV procainamide preferred over amiodarone for pharmacological termination (Class IIa; supported by PROCAMIO trial)

Loading: up to 50 mg/min IV, max ~1 g; maintenance 2–6 mg/min

Caution in severe HF, acute MI, advanced kidney disease

IV amiodarone or sotalol as alternatives (Class IIb)

IV lidocaine: less effective for stable VT; more useful for VF/polymorphic VT arrest

Do NOT Use:

IV verapamil/diltiazem for wide-complex tachycardia of unknown origin (Class III: Harm)

Prophylactic lidocaine or high-dose amiodarone in suspected acute MI (Class III: Harm)

Multiple concurrent antiarrhythmic drugs (proarrhythmic risk)

Electrical Storm:

ICD reprogramming + IV beta-blocker (preferably propranolol) + IV amiodarone

Sedation to reduce sympathetic drive (ESC Class I)

Catheter ablation for drug-refractory cases (AHA/ACC/HRS Class I)

Stellate ganglion block or cardiac sympathetic denervation for refractory storm

Mechanical circulatory support (e.g., VA-ECMO) as bridge if needed

Minimize catecholaminergic vasopressors/inotropes (proarrhythmic)

## Catheter Ablation – Key Evidence

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Class I indication: recurrent sustained monomorphic VT despite AAD therapy; incessant VT or electrical storm

VANISH2 (NEJM 2025): First-line ablation vs. AAD in post-MI VT (n=416) → ablation superior (HR 0.75; P=0.03) for composite of death, ICD shock, VT storm, or treated sustained VT over 4.3 years

VANISH (2016): Ablation vs. AAD escalation in drug-refractory VT → ablation superior (59.1% vs. 68.5% composite endpoint)

PARTITA (2022): Early ablation after first ICD shock → reduced death/HF hospitalization (HR 0.11; P=0.034); small trial, stopped early

SMASH-VT (2007): ICD + ablation vs. ICD alone → ICD therapy 12% vs. 33% at 2 years

Success rates: >80% for idiopathic VT; 56–77% for ischemic; 38–67% for nonischemic cardiomyopathy

## ICD Therapy

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Secondary prevention (Class I):

Survived SCA due to VT/VF or hemodynamically significant sustained VT, not due to reversible cause, with >1 year expected survival

Primary prevention (Class I):

Ischemic or nonischemic cardiomyopathy, LVEF ≤35%, NYHA II–III, on ≥3 months optimal medical therapy (≥40 days post-MI for ischemic)

Ischemic cardiomyopathy, LVEF ≤30%, NYHA I (≥40 days post-MI)

High-risk inherited cardiomyopathies/channelopathies per disease-specific criteria

Note: DANISH trial showed no overall survival benefit of primary prevention ICD in nonischemic cardiomyopathy, possibly due to improved HF therapy

## Chronic Medical Therapy

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Beta-blockers: recommended for all patients with structural heart disease and VT

Amiodarone or sotalol: for recurrent VT with significant symptoms/ICD shocks despite beta-blocker (Class I)

Amiodarone: more effective but high adverse effect burden (thyroid, lung, liver, neuropathy); may increase all-cause mortality in ICD recipients

Sotalol: better side-effect profile; avoid if LVEF 20%; adjust for renal function; monitor QTc

Mexiletine: add-on for breakthrough VT on amiodarone + beta-blocker

GDMT for HF: beta-blocker + ACEi/ARB/ARNI + MRA reduces SCD risk (Class I)

## Special Populations

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Pregnancy:

DC cardioversion safe at standard energy for unstable VT (HRS Class I)

Stable idiopathic VT: IV beta-blocker (RVOT VT) or IV verapamil (fascicular VT)

Stable VT: IV procainamide for acute therapy (HRS Class I)

Chronic suppression: beta-blockers preferred; flecainide, sotalol, or mexiletine if needed

Amiodarone: last resort (fetal hypothyroidism risk); minimize dose and duration

Channelopathies:

Long QT syndrome: beta-blockers ± left cardiac sympathetic denervation

Brugada syndrome: ICD for SCA survivors; quinidine or epicardial ablation for recurrent shocks

CPVT: nadolol preferred; add flecainide if refractory

Cardiac Sarcoidosis:

ICD Class I for sustained VT/SCA or LVEF ≤35%

ICD Class IIa for LVEF >35% with syncope, scar on MRI/FDG-PET, pacing indication, or inducible VT

## Prognosis

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Idiopathic VT: favorable prognosis, low SCD risk

Structural heart disease VT: >40% recurrence within 2 years; significant mortality risk

Dilated cardiomyopathy + VT: 38% death/transplant at 4 years; LVEF ≤32% + early recurrence → 55% 1-year mortality/transplant rate

Post-ablation predictors of mortality: high LV end-diastolic volume, atrial fibrillation, COPD, polymorphic VTs, periprocedural complications

## When to Refer to Electrophysiology

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Sustained VT or VF for ICD/ablation evaluation

Recurrent VT despite antiarrhythmic drugs

Electrical storm or incessant VT

Suspected channelopathy or familial cardiomyopathy

NSVT with structural heart disease for risk stratification

Unexplained syncope with structural heart disease or family history of SCD

Consider advanced HF referral if severely reduced EF with early VT recurrence post-ablation

## 2017 AHA/ACC/HRS[10] and 2022 ESC Guideline[11] Updates for Diagnostic Evaluation

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### Diagnostic Evaluation (2017 AHA/ACC/HRS)

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#### 12-Lead ECG and Exercise Testing (2017 AHA/ACC/HRS)

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Class I

1. In patients with sustained, hemodynamically stable, wide complex tachycardia, a 12-lead ECG during tachycardia should be obtained. (Level of Evidence: B-NR)
2. In patients with VA symptoms associated with exertion, suspected ischemic heart disease, or [[[catecholaminergic polymorphic ventricular tachycardia](https://www.openevidence.com/rare-disease/catecholaminergic-polymorphic-ventricular-tachycardia)]], exercise treadmill testing is useful to assess for exercise-induced VA. (Level of Evidence: B-NR)
3. In patients with suspected or documented VA, a 12-lead ECG should be obtained in sinus rhythm to look for evidence of heart disease. (Level of Evidence: B-NR)

Note: The 2017 AHA/ACC/HRS guideline states that data on the use of microvolt T-wave alternans (TWA) and the signal-averaged ECG (SAECG) are inconclusive, and as such these tests are not routinely used in clinical practice; the one exception is the potential use of SAECG in patients with arrhythmogenic right ventricular cardiomyopathy.

#### Ambulatory Electrocardiography (2017 AHA/ACC/HRS)

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Class I

1. Ambulatory electrocardiographic monitoring is useful to evaluate whether symptoms, including palpitations, presyncope, or syncope, are caused by VA. (Level of Evidence: B-NR)

A 24-hour continuous Holter monitor recording is appropriate when symptoms occur at least once a day or when quantitation of PVCs/NSVT is desired to assess possible VA-related depressed ventricular function. For sporadic symptoms, event or "looping" monitors are more appropriate because they can be activated over extended periods of time and increase diagnostic yield. Adhesive patch electrocardiographic monitors can record for weeks and allow for continuous short-term 1-lead monitoring and patient activation for symptoms. Importantly, when the suspicion of VA in a patient is high, outpatient ambulatory monitoring is inappropriate as prompt diagnosis and prevention of VA are warranted.

#### Implanted Cardiac Monitors (2017 AHA/ACC/HRS)

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Class IIa

1. In patients with sporadic symptoms (including syncope) suspected to be related to VA, implanted cardiac monitors can be useful. (Level of Evidence: B-R)

Implanted cardiac monitors provide continuous rhythm monitoring and stored recordings of electrograms based on patient activation or preset parameters, allowing a prolonged monitoring period of a few years. They are generally reserved for patients in whom other ambulatory monitoring is nonrevealing due to the infrequency of events. A 25% added yield in diagnosis has been described after an unrevealing external ambulatory monitor.

#### Noninvasive Cardiac Imaging (2017 AHA/ACC/HRS)

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Class I

1. In patients with known or suspected VA that may be associated with underlying structural heart disease or a risk of SCA, echocardiography is recommended for evaluation of cardiac structure and function. (Level of Evidence: B-NR)
Class IIa

1. In patients presenting with VA who are suspected of having structural heart disease, cardiac magnetic resonance imaging (MRI) or computed tomography (CT) can be useful to detect and characterize underlying structural heart disease. (Level of Evidence: C-EO)

Cardiac magnetic resonance imaging allows for evaluation of structural heart disease and assessment of LV and RV function including quantification of LVEF, LV mass and volume, valvular structure and coronary anatomy. Cardiac MRI can be useful in the evaluation for myocardial scar and infiltrative processes evident as late gadolinium enhancement and is particularly useful in arrhythmogenic right ventricular cardiomyopathy and hypertrophic cardiomyopathy.

The 2022 ESC guideline places greater emphasis on CMR as part of the diagnostic evaluation, including in hypertrophic cardiomyopathy, in inconclusive cases, and in patients with suspected PVC-induced cardiomyopathy to rule out underlying structural heart disease.[12]

#### Electrophysiological Study (2017 AHA/ACC/HRS)

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Class IIa

1. In patients with ischemic cardiomyopathy, NICM, or adult congenital heart disease who have syncope or other VA symptoms and who do not meet indications for a primary prevention ICD, an electrophysiological study can be useful for assessing the risk of sustained VT. (Level of Evidence: B-R)
Class III: No Benefit

1. In patients who meet criteria for ICD implantation, an electrophysiological study for the sole reason of inducing VA is not indicated for risk stratification. (Level of Evidence: B-R)
2. An electrophysiological study is not recommended for risk stratification for VA in the setting of long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome, or early repolarization syndromes. (Level of Evidence: B-NR)

With the advent of the ICD and its proven benefit in the primary and secondary prevention of SCD, there are fewer indications for programmed stimulation to provoke VA. Patients with heart failure and LVEF ≤35% generally will have an indication for an ICD and specific induction of VT/VF before implantation is not necessary. Patients with LVEF 35% and unexplained syncope or near-syncope may benefit from an electrophysiological study to determine if VT/VF is the cause of symptoms and to guide further therapy.

### Management of Special Patient Populations:

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#### 2017 AHA/ACC/HRS and 2023 HRS Guidelines for Ventricular Arrhythmias in Pregnancy[13]

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Class I

1. In mothers with long QT syndrome, a beta blocker should be continued during pregnancy and throughout the postpartum period including in women who are breastfeeding. (Level of Evidence: B-NR)
2. In the pregnant patient with sustained VA, electrical cardioversion is safe and effective and should be used with standard electrode configuration. (Level of Evidence: C-EO)
Class IIa

1. In pregnant patients needing an ICD or VT ablation, it is reasonable to undergo these procedures during pregnancy, preferably after the first trimester. (Level of Evidence: B-NR)

The risk of SCA or SCD is significantly higher during the 9 months after delivery, most notably among women with LQT2. A large retrospective analysis from the long QT syndrome registry demonstrated an odds ratio of 40.8 for syncope, SCA, or SCD among women with long QT syndrome in the 9 months postpartum; treatment with beta blockers during pregnancy was independently associated with decreased risk.

The 2023 HRS Expert Consensus Statement on the Management of Arrhythmias During Pregnancy provides more detailed and expanded recommendations for ventricular arrhythmias in pregnancy:[14]

Class I

1. In pregnant patients with sustained VT and hemodynamic compromise, direct current cardioversion is recommended, with energy dosing as in the nonpregnant patient. (Level of Evidence: C-LD)
2. In pregnant patients with idiopathic VT and hemodynamic stability, intravenous beta blocker or adenosine for outflow tract VT and intravenous verapamil for fascicular VT are recommended as first-line options. (Level of Evidence: C-LD)
3. In pregnant patients with hemodynamically stable VT, when pharmacological therapy is deemed necessary, intravenous procainamide is recommended for acute therapy. (Level of Evidence: C-LD)
4. In pregnant patients with sustained VT refractory or with contraindications to beta blockers and/or other antiarrhythmic drugs, synchronized cardioversion is recommended, with energy dosing as in the nonpregnant patient. (Level of Evidence: C-LD)
5. In pregnant patients who meet indications for ICD placement due to sustained ventricular arrhythmias or due to high risk for sudden cardiac death, device implantation is recommended with attention to and techniques for eliminating or minimizing radiation exposure to as low as reasonably achievable. (Level of Evidence: C-LD)
6. In pregnant patients with ICDs prior to pregnancy, it is recommended to continue routine ICD care according to the underlying cardiac substrate. (Level of Evidence: C-LD)
7. In women who are considering pregnancy and would otherwise meet indications for ICD, pacemaker, or cardiac resynchronization therapy device placement, these procedures should be performed prior to pregnancy and according to the underlying cardiac substrate. (Level of Evidence: C-LD)
8. In pregnant patients with chronic or recurrent VT, beta blockers, alone or in combination with other antiarrhythmic drugs, are recommended for arrhythmia suppression due to their overall safety profile in pregnancy. (Level of Evidence: C-LD)
9. In pregnant patients with recurrent VT refractory or with contraindications to beta blockers who require additional antiarrhythmic drug therapy, treatment with flecainide, sotalol, or mexiletine is recommended with the choice of drug based on the underlying cardiac substrate. (Level of Evidence: C-LD)
Class IIa

1. In pregnant patients with recurrent symptomatic or hemodynamically unstable VT in whom pharmacological therapy is either ineffective or contraindicated, catheter ablation is reasonable with an experienced operator and with attention to and techniques for eliminating or minimizing radiation exposure to as low as reasonably achievable. (Level of Evidence: C-LD)
2. In pregnant patients with recurrent VT associated with hemodynamic impairment or ICD shocks, amiodarone is reasonable for arrhythmia suppression if alternative therapies, including ablation, are contraindicated or ineffective. (Level of Evidence: C-LD)
Class IIb

1. In pregnant patients who meet indications for sudden death prevention due to high-risk features or VT that may be of a reversible etiology, such as peripartum cardiomyopathy, a wearable cardioverter defibrillator may be reasonable. (Level of Evidence: C-LD)

#### 2017 AHA/ACC/HRS Guideline for Older Patients With Comorbidities

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The 2017 AHA/ACC/HRS guideline provides the following recommendation for older patients (defined as ≥75 years) with comorbidities:

Class IIa

1. For older patients and those with significant comorbidities, who meet indications for a primary prevention ICD, an ICD is reasonable if meaningful survival of greater than 1 year is expected. (Level of Evidence: B-NR) (Systematic Review)

The guideline notes that neither age nor comorbidities alone should be exclusions for an ICD. However, older adults are prone to higher complication rates, shorter life expectancies (and thus, fewer years during which they could derive benefit from an ICD), and varying preferences. For these reasons, a particularly nuanced and patient-centered approach is important in treating these patients.

##### Shared Decision-Making (2017 AHA/ACC/HRS)

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Class I

1. In patients with VA or at increased risk for SCD, clinicians should adopt a shared decision-making approach in which treatment decisions are based not only on the best available evidence but also on the patients' health goals, preferences, and values. (Level of Evidence: B-NR)
2. Patients considering implantation of a new ICD or replacement of an existing ICD for a low battery should be informed of their individual risk of SCD and nonsudden death from heart failure or noncardiac conditions and the effectiveness, safety, and potential complications of the ICD in light of their health goals, preferences, and values. (Level of Evidence: B-NR)

The guideline emphasizes that ICD replacement is an important point in time where patients and clinicians should discuss whether replacing an ICD is still consistent with the patients' goals. What made sense at 70 years of age may not make sense at 80 years of age. The possibility of deactivation of an existing ICD should be discussed with patients who have terminal illnesses.

#### Updated Recommendations: 2021 PACES Expert Consensus Statement for Pediatric Patients

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The 2021 PACES Expert Consensus Statement on the Indications and Management of Cardiovascular Implantable Electronic Devices in Pediatric Patients (developed in collaboration with HRS, ACC, AHA, and AEPC) provides updated recommendations for ICD therapy in pediatric patients (defined as ≤21 years of age):Shah MJ, Silka MJ, Avari Silva JN, Balaji S, Beach CM, Benjamin MN, Berul CI, Cannon B, Cecchin F, Cohen MI, Dalal AS, Dechert BE, Foster A, Gebauer R, Gonzalez Corcia MC, Kannankeril PJ, Karpawich PP, Kim JJ, Krishna MR, Kubuš P, LaPage MJ, Mah DY, Malloy-Walton L, Miyazaki A, Motonaga KS, Niu MC, Olen M, Paul T, Rosenthal E, Saarel EV, Silvetti MS, Stephenson EA, Tan RB, Triedman J, Von Bergen NH, Wackel PL (2021). "2021 PACES Expert Consensus Statement on the Indications and Management of Cardiovascular Implantable Electronic Devices in Pediatric Patients". Heart Rhythm. 18 (11): 1888–1924. doi:10.1016/j.hrthm.2021.07.038. PMID 34794667 Check `|pmid=` value (help).

##### General Recommendations for ICD Therapy in Pediatric Patients (2021 PACES)

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Class I

1. ICD implantation is indicated for survivors of SCA due to VT/VF if completely reversible causes have been excluded and an ICD is considered to be more beneficial than alternative treatments that may significantly reduce the risk of SCA. (Level of Evidence: B-NR)
Class IIb

1. ICD implantation may be considered for patients with sustained VT that cannot be adequately controlled with medication and/or catheter ablation. (Level of Evidence: C-EO)
2. ICD therapy may be considered for primary prevention of SCD in patients with genetic cardiovascular diseases and risk factors for SCA or pathogenic mutations and family history of recurrent SCA. (Level of Evidence: C-EO)
Class III: Harm

1. ICD therapy is not indicated for patients with incessant ventricular tachyarrhythmias due to risk of ICD storm. (Level of Evidence: C-EO)
2. ICD therapy is not indicated for patients with ventricular arrhythmias that are adequately treated with medication and/or catheter ablation. (Level of Evidence: C-LD)
3. ICD therapy is not indicated for patients who have an expected survival <1 year, even if they meet ICD implantation criteria specified in the above recommendations. (Level of Evidence: C-EO)
4. Endocardial leads should be avoided in patients with intracardiac shunts except in select cases, when there should be an individualized consideration of the risk/benefit ratio. In these exceptional cases anticoagulation is mandatory, but thromboembolism remains a risk. (Level of Evidence: B-NR)

The 2021 PACES statement emphasizes that ICD implantation should be a shared decision between the patient, family, and physician considering specific pediatric characteristics including age, size of the patient, need for an epicardial device, religious/cultural beliefs, and patient quality of life. This includes the physical as well as the psychological impact of an ICD on the patient's well-being. A pediatric cardiologist should be involved in the decision to implant an ICD in pediatric patients, and the procedure should be performed by a cardiologist or cardiothoracic surgeon with special training and/or experience in CIED implantation in the pediatric age group.

##### ICD Indications for Nonischemic Dilated Cardiomyopathy in Pediatric Patients (2021 PACES)

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Class I

1. ICD implantation is indicated in patients with NIDCM who either survive SCA or experience sustained VT not due to completely reversible causes. (Level of Evidence: B-NR)
Class IIb

1. ICD implantation may be considered in patients with NIDCM and syncope or an LVEF ≤35%, despite optimal medical therapy. (Level of Evidence: C-LD)
Class III: Harm

1. ICD implantation is NOT recommended in patients with medication-refractory advanced heart failure who are not cardiac transplantation or left ventricular assist device candidates. (Level of Evidence: C-EO)

The 2021 PACES statement notes that the annual incidence of SCD in pediatric patients with NIDCM is only 1%–5%, which is significantly less than in adult patients. In contrast to some studies of adult patients with NIDCM and LVEF ≤35%, there is no clear evidence that ICDs implanted for primary prevention improve survival for pediatric patients with NIDCM. The Sudden Death in Childhood Cardiomyopathy study showed that the cumulative incidence of SCD at 15 years was 5% for idiopathic dilated cardiomyopathy compared to 23% for left ventricular noncompaction.

##### ICD Indications for Arrhythmogenic Cardiomyopathies in Pediatric Patients (2021 PACES)

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Class I

1. ICD implantation is indicated in patients with arrhythmogenic cardiomyopathy (ACM) who have been resuscitated from SCA or sustained VT that is not hemodynamically tolerated. (Level of Evidence: B-NR)
Class IIa

1. ICD implantation is reasonable in patients with ACM with hemodynamically tolerated sustained VT, syncope presumed due to ventricular arrhythmia, or an LVEF ≤35%. (Level of Evidence: B-NR)
Class IIb

1. ICD implantation may be considered in patients with inherited ACM associated with increased risk of SCD based on an assessment of additional risk factors. (Level of Evidence: C-LD)

SCD occurs in 2%–15% of young patients with ACM. The 2021 PACES statement notes that arrhythmogenic cardiomyopathy encompasses a spectrum of primary myocardial disorders including genetic disorders such as arrhythmogenic right/left ventricular cardiomyopathy, lamin A/C mutations, filamin-C, phospholamban, and cardiac amyloidosis. These entities are infrequent before puberty and often overlap with other cardiomyopathies.

2006 ACC/AHA/ESC Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) [15]

### Diagnostic Evaluation

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#### Electrocardiographic Techniques and Measurements (DO NOT EDIT)[15]

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| Class IIa

"1. It is reasonable to use TWA to improve the diagnosis and risk stratification of patients with ventricular arrhythmias or who are at risk for developing lifethreatening ventricular arrhythmias. (Level of Evidence: A) "
Class IIb

"1. ECG techniques such as signal-averaged ECG (SAECG), heart rate variability (HRV), baroflex sensitivity, and heart rate turbulence may be useful to improve the diagnosis and risk stratification of patients with ventricular arrhythmias or who are at risk of developing life-threatening ventricular arrhythmias. (Level of Evidence: B) "

#### Resting Electrocardiogram (DO NOT EDIT)[15]

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Class I

"1. Resting 12-lead ECG is indicated in all patients who are evaluated for ventricular arrhythmias. (Level of Evidence: A). "

#### Ambulatory Electrocardiography Recommendations (DO NOT EDIT)[15]

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Class I

"1. Ambulatory ECG is indicated when there is a need to clarify the diagnosis by detecting arrhythmias, QT interval changes, T-wave alternans (TWA), or ST changes, to evaluate risk, or to judge therapy. (Level of Evidence: A) "
"2. Event monitors are indicated when symptoms are sporadic to establish whether or not they are caused by transient arrhythmias. (Level of Evidence: B) "
"3. Implantable recorders are useful in patients with sporadic symptoms suspected to be related to arrhythmias such as syncope when a symptom-rhythm correlation cannot be established by conventional diagnostic techniques. (Level of Evidence: B) "

#### Exercise Testing Recommendations (DO NOT EDIT)[15]

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Class I

"1. Exercise testing is recommended in adult patients with ventricular arrhythmias who have an intermediate or greater probability of having CHD by age, gender, and symptoms* to provoke ischemic changes or ventricular arrhythmias. (Level of Evidence: B) *See Table 4 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for further explanation of CHD probability."
"2. Exercise testing, regardless of age, is useful in patients with known or suspected exercise-induced ventricular arrhythmias, including catecholaminergic VT, to provoke the arrhythmia, achieve a diagnosis, and determine the patient’s response to tachycardia. (Level of Evidence: B)"
Class III

"1. See Table 1 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for contraindications. (Level of Evidence: C)"
Class IIa

"1. Exercise testing can be useful in evaluating response to medical or ablation therapy in patients with known exercise-induced ventricular arrhythmias. (Level of Evidence: B)"
Class IIb

"1. Exercise testing may be useful in patients with ventricular arrhythmias and a low probability of CHD by age, gender, and symptoms.* (Level of Evidence: C) *See Table 4 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for further explanation of CHD probability."
"2. Exercise testing may be useful in the investigation of isolated premature ventricular complexes (PVCs) in middle-aged or older patients without other evidence of CHD. (Level of Evidence: C)"

#### Left Ventricular Function and Imaging (DO NOT EDIT)[15]

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Class I

"1. Echocardiography is recommended in patients with ventricular arrhythmias who are suspected of having structural heart disease. (Level of Evidence: B)"
"2. Echocardiography is recommended for the subset of patients at high risk for the development of serious ventricular arrhythmias or SCD, such as those with dilated, hypertrophic, or RV cardiomyopathies, AMI survivors, or relatives of patients with inherited disorders associated with SCD. (Level of Evidence: B)"
"3. Exercise testing with an imaging modality (echocardiography or nuclear perfusion [single-photon emission computed tomography (SPECT)]) is recommended to detect silent ischemia in patients with ventricular arrhythmias who have an intermediate probability of having CHD by age, symptoms, and gender and in whom ECG assessment is less reliable because of digoxin use, LVH, greater than 1-mm ST-segment depression at rest, WPW syndrome, or LBBB. (Level of Evidence: B)"
"4. Pharmacological stress testing with an imaging modality (echocardiography or myocardial perfusion SPECT) is recommended to detect silent ischemia in patients with ventricular arrhythmias who have an intermediate probability of having CHD by age, symptoms, and gender and are physically unable to perform a symptom-limited exercise test. (Level of Evidence: B)"
Class IIa

"1. MRI, cardiac computed tomography (CT), or radionuclide angiography can be useful in patients with ventricular arrhythmias when echocardiography does not provide accurate assessment of LV and RV function and/or evaluation of structural changes. (Level of Evidence: B)"
"2. Coronary angiography can be useful in establishing or excluding the presence of significant obstructive CHD in patients with life-threatening ventricular arrhythmias or in survivors of SCD, who have an intermediate or greater probability of having CHD by age, symptoms, and gender. (Level of Evidence: C)"
"3. LF imaging can be useful in patients undergoing biventricular pacing. (Level of Evidence: C)"

#### Electrophysiological Testing (DO NOT EDIT)[15]

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Class I

"1. EP testing is recommended for diagnostic evaluation of patients with remote MI with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. (Level of Evidence: B)"
"2. EP testing is recommended in patients with CHD to guide and assess the efficacy of VT ablation. (Level of Evidence: B)"
"3. EP testing is useful in patients with CHD for the diagnostic evaluation of wide QRS complex tachycardias of unclear mechanism. (Level of Evidence: B)"
Class IIa

"1. EP testing is reasonable for risk stratification in patients with remote MI, NSVT, and LVEF equal to or less than 40%. (Level of Evidence: B)"

### Management of Special Patient Populations

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#### Management of Ventricular Arrhythmias in Pregnancy (DO NOT EDIT)[15]

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Class I

"1. Pregnant women developing hemodynamically unstable VT or VF should be electrically cardioverted or defibrillated. (Level of Evidence: B) (See Section 7.)"
"2. In pregnant women with the LQTS who have had symptoms, it is beneficial to continue beta-blocker medications throughout pregnancy and afterward, unless there are definite contraindications. (Level of Evidence: C)"

#### Management of Ventricular Arrhythmias in Elderly Patients (DO NOT EDIT)[15]

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Class I

"1. Elderly patients with ventricular arrhythmias should generally be treated in the same manner as younger individuals. (Level of Evidence: A)"
"2. The dosing and titration schedule of antiarrhythmic drugs prescribed to elderly patients should be adjusted to the altered pharmacokinetics of such patients. (Level of Evidence: C)"
Class III

"1. Elderly patients with projected life expectancy less than 1 y due to major comorbidities should not receive ICD therapy. (Level of Evidence: C)"

#### Management of Ventricular Arrhythmias in Pediatric Patients (DO NOT EDIT)[15]

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Class I

"1. An ICD should be implanted in pediatric survivors of a cardiac arrest when a thorough search for a correctable cause is negative and the patients are receiving optimal medical therapy and have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)"
"2. Hemodynamic and EP evaluation should be performed in the young patient with symptomatic, sustained VT. (Level of Evidence: C)"
"3. ICD therapy in conjunction with pharmacological therapy is indicated for high-risk pediatric patients with a genetic basis (ion channel defects or cardiomyopathy) for either SCD or sustained ventricular arrhythmias. The decision to implant an ICD in a child must consider the risk of SCD associated with the disease, the potential equivalent benefit of medical therapy, as well as risk of device malfunction, infection, or lead failure and that there is reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)"
Class III

"1. Pharmacological treatment of isolated PVCs in pediatric patients is not recommended. (Level of Evidence: C)"
"2. Digoxin or verapamil should not be used for treatment of sustained tachycardia in infants when VT has not been excluded as a potential diagnosis. (Level of Evidence: C)"
"3. Ablation is not indicated in young patients with asymptomatic NSVT and normal ventricular function.(Level of Evidence: C)"
Class IIa

"1. ICD therapy is reasonable for pediatric patients with spontaneous sustained ventricular arrhythmias associated with impaired (LVEF of 35% or less) ventricular function who are receiving chronic optimal medical therapy and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: B)"
"2. Ablation can be useful in pediatric patients with symptomatic outflow tract or septal VT that is drug resistant, when the patient is drug intolerant or wishes not to take drugs. (Level of Evidence: C)"

## Resources

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1\. Zipes DP, Camm AJ, Borggrefe M, et al., ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)Circulation 2006;114;e385-e484

2\. Kesh Hebbar A, Hueston WJ, Management of Common Arrhythmias: Part II.Ventricular Arrhythmias and Arrhythmias in Special Populations Am Fam Physician 2002;65:2491-6.

## References

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1. ↑ Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". J Am Coll Cardiol. 72 (14): e91–e220. doi:10.1016/j.jacc.2017.10.054. PMID 29097320.
2. ↑ Könemann H, Ellermann C, Zeppenfeld K, Eckardt L (2023). "Management of Ventricular Arrhythmias Worldwide: Comparison of the Latest ESC, AHA/ACC/HRS, and CCS/CHRS Guidelines". JACC Clin Electrophysiol. 9 (5): 715–728. doi:10.1016/j.jacep.2022.12.008. PMID 37225314 Check `|pmid=` value (help).
3. ↑ Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, Priori SG, Quinones MA, Roden DM, Silka MJ, Tracy C (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". J Am Coll Cardiol. 48 (5): e247–346. doi:10.1016/j.jacc.2006.07.010. PMID 16949478.
4. ↑ Natale A, Raviele A, Al-Ahmad A, Alfieri O, Aliot E, Almendral J, Breithardt G, Brugada J, Calkins H, Callans D, Cappato R, Chiang CE, Coumel P, Della Bella P, Delacretaz E, Di Biase L, Haissaguerre M, Hindricks G, Ho SY, Jackman W, Jalife J, Jais P, Kalman J, Keane D, Kim YH, Kirchhof P, Klein G, Kottkamp H, Kumagai K, Lindsay BD, Mansour M, Marchlinski FE, McCarthy PM, Mont JL, Morady F, Nademanee K, Nam GB, Packer DL, Pappone C, Prystowsky E, Reddy V, Ruskin JN, Scanavacca M, Shivkumar K, Soejima K, Stevenson W, Swarup V, Tanner H, Thibault B, Tung R, Verma A, Wilber DJ, Yamane T (2010). "Venice Chart International Consensus Document on Ventricular Tachycardia/Ventricular Fibrillation Ablation". J Cardiovasc Electrophysiol. 21 (3): 339–79. doi:10.1111/j.1540-8167.2009.01686.x. PMID 20487903.
5. ↑ Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI (2012). "Ventricular Arrhythmias in the Absence of Structural Heart Disease". J Am Coll Cardiol. 59 (20): 1733–44. doi:10.1016/j.jacc.2012.01.036. PMID 22575310.
6. ↑ Katritsis DG, Zareba W, Camm AJ (2012). "Nonsustained Ventricular Tachycardia". J Am Coll Cardiol. 60 (20): 1993–2004. doi:10.1016/j.jacc.2011.12.063. PMID 23083773.
7. ↑ Kennedy HL, Whitlock JA, Sprague MK, Kennedy LJ, Buckingham TA, Goldberg RJ. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med 1985;312:193-7.
8. ↑ Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med 1991;324:781-8
9. ↑ Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. The Cardiac Arrhythmia Suppression Trial II Investigators. N Engl J Med 1992;327:227-33.
10. ↑ Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". J Am Coll Cardiol. 72 (14): e91–e220. doi:10.1016/j.jacc.2017.10.054. PMID 29097320.
11. ↑ Könemann H, Ellermann C, Zeppenfeld K, Eckardt L (2023). "Management of Ventricular Arrhythmias Worldwide: Comparison of the Latest ESC, AHA/ACC/HRS, and CCS/CHRS Guidelines". JACC Clin Electrophysiol. 9 (5): 715–728. doi:10.1016/j.jacep.2022.12.008. PMID 37225314 Check `|pmid=` value (help).
12. ↑ Könemann H, Dagres N, Merino JL, Sticherling C, Zeppenfeld K, Tfelt-Hansen J, Eckardt L (2023). "Spotlight on the 2022 ESC Guideline Management of Ventricular Arrhythmias and Prevention of Sudden Cardiac Death: 10 Novel Key Aspects". Europace. 25 (5): euad091. doi:10.1093/europace/euad091. PMID 37102266 Check `|pmid=` value (help).
13. ↑ Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". J Am Coll Cardiol. 72 (14): e91–e220. doi:10.1016/j.jacc.2017.10.054. PMID 29097320.
14. ↑ Joglar JA, Kapa S, Saarel EV, Dubin AM, Gorenek B, Hameed AB, Halperin HR, Levine GN, Levy WC, Natale A, Page RL, Passman RS, Russo AM, Saul JP, Shen WK, Siu SC, Stevenson WG, Vetter VL (2023). "2023 HRS Expert Consensus Statement on the Management of Arrhythmias During Pregnancy". Heart Rhythm. 20 (10): e175–e264. doi:10.1016/j.hrthm.2023.05.017. PMID 37182560 Check `|pmid=` value (help).
15. ↑ 15.00 15.01 15.02 15.03 15.04 15.05 15.06 15.07 15.08 15.09 Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M; et al. (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (10): e385–484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)

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Electrocardiography

Overview|

History of the EKG • EKG interpretation basics • Normal sinus rhythm

EKG Complexes|

P wave • QRS complex • ST Segment • T wave • T wave alternans • Tombstone T wave • U wave

Osborn wave • H wave • K wave • Delta wave

NSSTW changes

EKG Intervals|

PR Interval • QRS Interval • ST Interval • QT Interval

Conduction System & Bradycardia|

Cardiac pacemaker • SA node • AV node• Bundle of His • Purkinje fibers • Sinus bradycardia • First Degree AV Block • Second Degree AV Block • Complete or Third-Degree AV Block • Concealed conduction • AV Junctional Rhythms • LBBB • LAHB • LPHB • RBBB • Trifascicular block

Atrial Arrhythmias|

Sinus tachycardia • Premature Atrial Contractions (PACs) • Ectopic Atrial Rhythm • Paroxysmal Atrial Tachycardia (PAT) • Paroxysmal Atrial Tachycardia (PAT) with Block • Multifocal Atrial Tachycardia (MAT) • Atrial Flutter • Atrial Fibrillation • Wandering atrial pacemaker

Ventricular Arrhythmias|

Differential Diagnosis of Tachycardia with a Wide QRS Complex • Accelerated Idioventricular Rhythm • Ventricular Parasystole • Premature Ventricular Contractions (PVCs) • Ventricular tachycardia • Ventricular Fibrillation • Sudden cardiac death

EKG Abnormalities in Disease States|

Hypertrophy & Dilatation • Right atrial enlargement • Left atrial enlargement • Biatrial enlargement • Left Ventricular Hypertrophy • Right Ventricular Hypertrophy • Biventricular Hypertrophy •

Acute myocardial infarction • NSTEMI • STEMI • Tombstone ST elevation • Right ventricular myocardial infarction • Atrial infarction

Pre-excitation Syndromes • Wolff-Parkinson-White Syndrome • Lown Ganong Levine Syndrome • Mahaim Type Preexcitation

Cardiomyopathies • Arrhythmogenic Right Ventricular Dysplasia • Dilated Cardiomyopathy • Hypertrophic Cardiomyopathy

Drug Effects on the EKG • Adenosine • β-blockers • Digitalis • Quinidine • Procainamide • Disopyramide • Lidocaine • Tocainide and Mexiletine • Phenytoin • Encainide, Flecainide and Propafenone • Amiodarone • Bretylium • Ca Channel Blockers • Phenothiazines • Tricyclic Antidepressants • Lithium

Congenital Heart Disease • Dextrocardia • Atrial Septal Defect • Ventricular Septal Defect • Tetralogy of Fallot • Conjoined Twins or Siamese Twins • Congenital heart block

Electrolyte Disturbances • Hyperkalemia • Hypokalemia • Hypercalcemia • Hypocalcemia • Nonspecific Changes

Other Heart Diseases • Pericarditis • Myocarditis • Tamponade • Heart Transplantation • Sick Sinus Syndrome • Long QT Syndrome

Inherited Disease • Brugada Syndrome

Systemic Diseases • CNS Disease • Cardiac Tumors

Heart Transplantation • EKG Changes in patient with Heart Transplantation

Exogenous Effects • Hypothermia • Chest Trauma • Insect Bites • Electric Injuries

Technical Issues and Potential Errors in Interpretation|

Artifacts • Lead Placement Errors • The EKG in a Patient with a Pacemaker • EKG in athletes

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