01Approach to the Critical Patient/attcp23

Immediate Stabilization

›Hemodynamic stability assessment

›SBP <80 mmHg, altered mental status, or signs of poor perfusion mandate immediate synchronized cardioversion

›Continuous cardiac monitoring and defibrillator at bedside

›IV access x2 and supplemental oxygen

›12-lead ECG during tachycardia before any pharmacologic intervention (Class I recommendation)

›Do not delay cardioversion for ECG if patient is deteriorating

Escalation Triggers

›Indications for immediate synchronized cardioversion

›Hemodynamic instability: hypotension, chest pain, pulmonary edema, altered mentation

›VT storm: three or more sustained episodes within 24 hours

›Polymorphic VT or degeneration to ventricular fibrillation

›Rate >200 bpm with impending cardiovascular collapse

›Failure of two antiarrhythmic agents

Resuscitation Targets

›Hemodynamic and metabolic targets

›SBP >90 mmHg

›SpO2 >94%

›Serum potassium >4.0 mmol/l

›Serum magnesium >0.8 mmol/l

›Corrected QT interval: monitor during antiarrhythmic therapy

Pitfalls

›Common critical pitfalls in stable VT

›Administering verapamil or diltiazem for wide-complex tachycardia of unknown origin — can cause hemodynamic collapse in VT

›Assuming wide-complex tachycardia is SVT with aberrancy without definitive criteria — VT should be the default diagnosis

›Delaying cardioversion in a deteriorating patient while awaiting pharmacologic response

›Failing to correct reversible metabolic triggers (hypokalemia, hypomagnesemia) before pharmacologic therapy

02History/hx50

Presenting Symptoms

›Symptom characterization

›Palpitations: sudden onset, rapid and regular

›Chest pain or pressure

›Dyspnea or exertional intolerance

›Lightheadedness or presyncope

›Diaphoresis and nausea

Onset and Duration

›Temporal features

›Time of symptom onset and duration of current episode

›Gradual vs. sudden onset

›Prior VT episodes and their management

›ICD shocks: number, timing, and response

Important Negatives

›Features suggesting instability

›Syncope or loss of consciousness during episode — suggests hemodynamic instability

›Seizure-like activity

›Witnessed cardiac arrest or near-arrest

›Jaw or arm pain (ischemic equivalent)

Triggers and Precipitants

›Potential precipitants

›Exertion or emotional stress

›Caffeine, energy drinks, or stimulant use

›Recent vomiting or diarrhea (electrolyte depletion)

›Recent medication changes: new antiarrhythmics, diuretic dose increase, new QT-prolonging drugs

›Cocaine or methamphetamine use

Cardiac History

›Relevant past cardiac events

03Physical Exam/exam23

Vital Signs

›Hemodynamic assessment

›Heart rate: rate, regularity, and rhythm

›Blood pressure: bilateral arm measurement to confirm stability

›SpO2 and respiratory rate

›Temperature (fever suggests myocarditis)

Cardiovascular Exam

›Cardiac examination findings

›Cannon A waves in JVP — pathognomonic for AV dissociation in VT

›Variable intensity of S1 — consistent with AV dissociation

›S3 or S4 gallop — heart failure

›Murmurs: valvular disease, HCM outflow tract obstruction

›Signs of poor perfusion: cool extremities, delayed capillary refill, mottled skin

Pulmonary Exam

›Respiratory findings

›Bibasilar crackles suggesting pulmonary edema

›Increased work of breathing or accessory muscle use

›Jugular venous distension

Neurological Exam

›Mental status and neurologic findings

›Level of consciousness and orientation

›Altered mentation indicates hemodynamic instability — triggers immediate cardioversion

›Focal neurological deficits

Skin and Extremities

›Peripheral findings

›Pitting edema suggesting heart failure

›Peripheral cyanosis or mottling

›Surgical scars: sternotomy, ICD or pacemaker pocket site

04Differential Diagnosis/ddx24

Life-Threatening Mimics

›Dangerous wide-complex tachycardia diagnoses

›Ventricular fibrillation — pulseless; immediately treated with defibrillation

›Polymorphic VT including torsades de pointes — waxing and waning QRS amplitude with QT prolongation

›VT storm — three or more sustained VT episodes in 24 hours

SVT with Aberrant Conduction

›Supraventricular tachycardia mimics

›SVT with bundle branch block (most common mimic) — look for typical BBB morphology and compare with prior ECGs

›Antidromic AVRT via accessory pathway (WPW) — delta waves on prior ECG, history of WPW

›Atrial fibrillation with pre-excitation — irregularly irregular, very rapid rates; avoid AV nodal blockers

Metabolic and Toxic Causes

›Non-primary arrhythmia etiologies

›Hyperkalemia — can produce wide-complex rhythm mimicking VT; check potassium urgently

›Sodium channel blocker toxicity: TCA overdose, flecainide — wide QRS with rightward axis

›Digoxin toxicity — bidirectional VT

›Cocaine or stimulant-induced VT

Other Diagnoses

›Additional diagnostic considerations

›Ventricular paced rhythm — check for ICD or pacemaker, compare with pacing settings

›ECG artifact — inappropriate treatments have been given; confirm with exam and rhythm strip

›Idiopathic VT: RVOT VT or fascicular (verapamil-sensitive) VT — typically in younger patients without structural heart disease

Features Favoring VT Over SVT

›ECG criteria supporting VT diagnosis (Class I: presume VT if diagnosis unclear)

›AV dissociation — cannon A waves, variable S1, P waves marching independently

›QRS duration >140 ms

›Positive or negative concordance across all precordial leads

›Monophasic R wave in aVR

›Absence of RS complex in all precordial leads, or RS interval >100 ms

05Laboratory Tests/lt21

Electrolytes

›Serum electrolytes

›Potassium: hypokalemia present in approximately 36% of VT presentations (LYTE-VT Study)

›Magnesium: hypomagnesemia potentiates ventricular arrhythmias

›Calcium: hypocalcemia prolongs QT interval

›Replete potassium to >4.0 mmol/l and magnesium to >0.8 mmol/l before or concurrent with antiarrhythmics

Cardiac Biomarkers

›Myocardial injury markers

›High-sensitivity troponin I or T: rule out acute MI as trigger

›BNP or NT-proBNP: assess for decompensated heart failure

›Serial troponins if initial negative and high suspicion for ACS

Metabolic Panel

›Organ function and metabolic assessment

›Serum creatinine and BUN: drug dosing, electrolyte context

›Lactate: hypoperfusion assessment

›ABG or VBG: acidosis worsens arrhythmia threshold

›Blood glucose

Additional Testing

›Directed additional laboratory workup

›CBC: anemia can exacerbate ischemia

›TSH: hyper- or hypothyroidism as arrhythmia trigger

›Digoxin level if patient is on digoxin

›Urine or serum toxicology screen if substance use suspected

›LFTs if amiodarone therapy anticipated (baseline)

›TFTs if amiodarone therapy anticipated (baseline)

06Diagnostic Tests/dt58

Scoring Systems

›ECG-based diagnostic algorithms

›Brugada criteria — four-step algorithm to differentiate VT from SVT with aberrancy

›Step 1: Absence of RS complex in all precordial leads — VT

›Step 2: RS interval >100 ms in any precordial lead — VT

›Step 3: AV dissociation — VT

›Step 4: Morphologic criteria in V1 and V6 — VT

›Sensitivity 98.7%, specificity 96.5% for VT

›Vereckei algorithm (aVR lead method) — four-step algorithm using aVR morphology

›Initial R wave in aVR

›Width of initial R or Q >40 ms in aVR

›Notching on descending limb of negative QRS in aVR

›Vi/Vt ratio less than or equal to 1

›RBBB morphology favoring VT: monophasic R or qR in V1, QS in V6

›LBBB morphology favoring VT: R >30 ms in V1, R-to-nadir of S >70 ms, Q wave in V6

MRI

›Cardiac MRI

›Gold standard for structural substrate characterization

›ARVC: fatty infiltration, RV dilatation, fibrosis on late gadolinium enhancement (LGE)

›Myocarditis: subepicardial or midmyocardial LGE pattern

›Cardiac sarcoidosis: patchy LGE particularly of the basal septum

›Ischemic scar: subendocardial or transmural LGE in coronary territory

›Typically performed after acute stabilization, not during acute VT episode

›Useful for risk stratification and ablation planning in recurrent VT

CT

›CT-based cardiac imaging

›CT coronary angiography: alternative to invasive angiography in select stable patients to rule out obstructive CAD

›Sensitivity for obstructive CAD approximately 95-99%

07Disposition/dispo20

ICU or CCU Admission

›High-acuity admission criteria

›New-onset sustained VT regardless of structural heart disease status

›Known structural heart disease with VT episode

›Reduced LVEF or decompensated heart failure

›Required cardioversion for termination

›Hemodynamic instability at any point during the episode

›VT storm: three or more episodes in 24 hours

›Ongoing ischemia or elevated troponins

›Complex antiarrhythmic initiation requiring monitoring

Telemetry Admission

›Lower-acuity monitored admission

›Young patient with idiopathic VT and structurally normal heart after successful pharmacologic termination

›Pending electrophysiology consultation and further outpatient workup planning

›Stable, first-episode VT without identifiable acute trigger

Consultation Requirements

›Mandatory consultations

›Cardiology or electrophysiology consultation for all patients with sustained VT

›EP consultation for VT storm, recurrent VT, ICD evaluation, or ablation candidacy

›Cardiac surgery consultation if structural disease requires surgical intervention

Discharge

›Disposition to home

›Essentially no scenario exists in which documented sustained VT is discharged from the ED without inpatient evaluation

›Exception: incidentally found non-sustained VT (less than 30 seconds) in a young, structurally normal heart may be referred urgently to outpatient cardiology within 24-48 hours

08Treatment/t69

Immediate Interventions

›Stabilization and monitoring

›Continuous cardiac monitoring with defibrillator at bedside

›IV access and supplemental oxygen

›12-lead ECG during tachycardia — obtain before pharmacologic therapy

›Correct reversible causes concurrently

›IV potassium chloride: replete to >4.0 mmol/l

›IV magnesium sulfate 2 g over 5-10 minutes if hypomagnesemia

Synchronized Cardioversion

›DC cardioversion

›Synchronized DC cardioversion: most efficacious treatment at any point

›Monomorphic VT: initial energy 100-200 J biphasic

›Escalate to 200-360 J biphasic if initial attempt fails

›Procedural sedation required

›Propofol 0.5-1.5 mg/kg IV

›Etomidate 0.1-0.3 mg/kg IV (preferred if hemodynamically borderline)

›Midazolam 0.02-0.05 mg/kg IV with fentanyl

›If patient deteriorates at any point during pharmacologic therapy, proceed directly to cardioversion

Procainamide

›Procainamide IV (preferred first-line pharmacologic agent, Class IIa)

›Dosing protocol

›10 mg/kg IV at 50-100 mg/min infusion rate

›Monitor BP and QRS duration every 5 minutes during loading

›Hold if SBP falls below 90 mmHg

›Hold if QRS widens more than 50% from baseline

›Hold if QT prolongation occurs

›Maintenance infusion after termination: 1-4 mg/min

›One RCT (PROCAMIO trial) found procainamide superior to amiodarone for termination of stable VT

›Contraindications

›Pre-existing QT prolongation or torsades de pointes

›Complete heart block

›Severe renal impairment — dose reduction required

Amiodarone

›Amiodarone IV (Class IIb for acute stable VT)

›Loading dose: 150 mg IV over 10 minutes

›Slow onset compared to procainamide

›Risk of hypotension during loading — monitor BP closely

›Maintenance infusion

›1 mg/min IV for 6 hours

›Then 0.5 mg/min IV for 18 hours

›Total first 24-hour dose typically not to exceed 2.2 g

›Cautions

›Avoid use of multiple antiarrhythmics concurrently (arrhythmogenic risk)

›Thyroid, hepatic, and pulmonary toxicity with chronic use — baseline labs before initiation

›QT prolongation monitoring required

Sotalol

›Sotalol IV (Class IIb)

›IV formulation provides acute pharmacologic option

›Generally without significant hypotension compared to amiodarone

›Contraindications

›Pre-existing QT prolongation

›Decompensated heart failure

›Bradycardia or AV block

›Severe renal impairment

Idiopathic VT Management

›Pharmacologic options for VT without structural heart disease

›RVOT VT (outflow tract VT)

›Adenosine 6 mg IV rapid push, may repeat 12 mg x2 — terminates some RVOT VT

›IV beta-blocker: metoprolol 5 mg IV q5 min x3

›Fascicular VT (verapamil-sensitive, left fascicular VT)

›Verapamil 5-10 mg IV over 2 minutes ONLY if this specific diagnosis is confirmed by arrhythmia expert

›Contraindicated if diagnosis of VT type is uncertain — can cause cardiovascular collapse

Long-Term Management

›Secondary prevention and ongoing therapy

›ICD implantation for secondary prevention in structural heart disease with sustained VT (Class I)

›Antiarrhythmic therapy for recurrence prevention

›Amiodarone: most effective for recurrence prevention in structural heart disease

›Sotalol: alternative in patients with preserved LVEF

›Mexiletine: adjunct therapy, particularly with amiodarone

›Catheter ablation for recurrent VT or VT storm (Class IIa in structural heart disease)

›Optimize heart failure therapy: beta-blockers, ACEi or ARB, SGLT2 inhibitors

›Treat underlying cause: revascularization if ischemia-mediated VT

Contraindicated Treatments

›Medications to avoid

›Verapamil and diltiazem — potentially fatal in wide-complex tachycardia of uncertain origin; can cause cardiovascular collapse in VT

›Lidocaine — less effective than procainamide, amiodarone, or sotalol; may be considered only in acute MI-related VT

›Class IC agents (flecainide, propafenone) — contraindicated in structural heart disease

09Special Populations/sp31

Pregnancy

›VT in pregnancy

›Physiologic changes increasing arrhythmia risk

›Increased plasma volume, heart rate, and cardiac output

›Hormonal changes and autonomic shifts alter electrophysiology

›Pharmacologic considerations

›Procainamide: limited data but generally considered acceptable in acute setting

›Amiodarone: avoid if possible — associated with fetal thyroid suppression, growth restriction, and neonatal bradycardia; use only if life-threatening arrhythmia with no alternative

›Sotalol: generally considered acceptable; used for fetal arrhythmia treatment

›Adenosine: safe in pregnancy for termination of SVT and diagnostic use

›Synchronized cardioversion: safe at all gestational ages; fetal monitoring required before and after

›Idiopathic VT (RVOT VT): most common VT type in pregnancy; often manageable with IV beta-blocker

Geriatric

›VT in older adults

›Higher prevalence of structural heart disease, prior MI, and cardiomyopathy

›Ischemic cardiomyopathy predominates as substrate for sustained monomorphic VT

›Pharmacokinetic considerations

›Reduced renal clearance: procainamide and sotalol dose reduction required

›Increased sensitivity to hypotension from amiodarone loading

›Polypharmacy and drug interactions: review for QT-prolonging drugs

›ICD decisions require discussion of goals of care, functional status, and life expectancy

›Higher risk of procedure-related complications from ablation

Pediatrics

›VT in children and adolescents

›Idiopathic VT is more common than in adults — structural heart disease less prevalent

›RVOT VT: most common form of idiopathic VT in children

›Fascicular VT: second most common idiopathic VT in children

›Inherited channelopathies: long QT syndrome, CPVT, Brugada syndrome more likely substrate than in adults

10Background/b35

Epidemiology

›Epidemiology of ventricular tachycardia

›VT defined as three or more consecutive ventricular complexes at rate greater than or equal to 100 bpm with QRS greater than or equal to 120 ms

›Sustained VT: duration greater than 30 seconds or requiring termination due to hemodynamic compromise

›Structural heart disease present in approximately 70-75% of patients presenting with sustained VT

›Prior MI with scar is the most common substrate for sustained monomorphic VT

›Recurrence rate up to 40% within 2 years in patients with structural heart disease without definitive therapy

›Idiopathic VT accounts for approximately 10% of all VT presentations

›Hypokalemia present in approximately 36% of patients presenting with ventricular arrhythmia (LYTE-VT Study)

Pathophysiology

›Mechanisms of ventricular tachycardia

›Reentry (most common mechanism in structural heart disease)

›Scar from prior MI creates zones of slow conduction allowing reentrant circuits

›Monomorphic VT typically reflects a stable reentrant circuit around a fixed anatomic substrate

›Triggered activity

›Early afterdepolarizations (EADs): long QT states, hypokalemia, bradycardia

›Delayed afterdepolarizations (DADs): digoxin toxicity, catecholaminergic states, heart failure

›Abnormal automaticity

›Enhanced automaticity in partially depolarized myocardium: ischemia, metabolic disturbance

›Idiopathic VT from RVOT: cyclic AMP-mediated triggered activity

›Structural substrates

›Ischemic cardiomyopathy: transmural scar after MI

›ARVC: fibro-fatty replacement of RV myocardium, most common cause of sudden death in young athletes

›HCM: asymmetric hypertrophy with myocyte disarray and fibrosis

›Cardiac sarcoidosis: patchy granulomatous inflammation

Therapeutic Considerations

›Evidence base for acute and long-term management

›PROCAMIO trial: randomized controlled trial demonstrating procainamide superior to amiodarone for termination of stable monomorphic VT in the ED

11Patient Discharge Instructions/pdi27

copy discharge instructions

›Discharge instructions for ventricular tachycardia

›Your diagnosis is ventricular tachycardia — an abnormal fast heart rhythm starting in the lower chambers of your heart

›You were treated in hospital and your heart rhythm returned to normal

›You must follow up with a heart specialist (cardiologist or electrophysiologist) as arranged before discharge

Medications

›Medication instructions at discharge

›Take all new and existing heart medications exactly as prescribed

›Do not stop any heart rhythm medication without first speaking with your doctor

›If you are prescribed a new antiarrhythmic (e.g., amiodarone, sotalol), report any new symptoms of dizziness, slow heart rate, or breathing problems

›Avoid medications known to prolong the QT interval unless approved by your cardiologist

Activity Restrictions

›Activity and lifestyle instructions

›Avoid driving until cleared by your cardiologist — sudden recurrence can be dangerous

›No strenuous exercise or heavy lifting until follow-up appointment

›Avoid alcohol and excessive caffeine intake

›Avoid cocaine, methamphetamine, and stimulant substances

Return to Emergency Department

›Red flag symptoms requiring immediate return to the ED

›Recurrence of rapid heartbeat, palpitations, or fluttering in the chest

›Dizziness, lightheadedness, or fainting (syncope)

›Chest pain or pressure

›Significant shortness of breath or difficulty breathing at rest

›ICD shock: one shock — call your cardiologist immediately; multiple shocks — return to ED by ambulance

›Confusion or altered mental status

Follow-Up

›Outpatient follow-up instructions

›Cardiology or electrophysiology appointment within 1-2 weeks of discharge

12References/r16

Guidelines and Key Sources

›Primary guidelines

›Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Journal of the American College of Cardiology. 2018. https://doi.org/10.1016/j.jacc.2017.10.054

›Wigginton JG, Agarwal S, Bartos JA, et al. Part 9: Adult Advanced Life Support: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001376

›European Heart Rhythm Association, Heart Rhythm Society, Zipes DP, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Journal of the American College of Cardiology. 2006. https://pubmed.ncbi.nlm.nih.gov/16949478

›Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS Expert Consensus Statement on Catheter Ablation of Ventricular Arrhythmias. Heart Rhythm. 2020. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8453449/

Key Clinical Studies

›Landmark trials and clinical evidence

›Laslett DB, Cooper JM, Greenberg RM, et al. Electrolyte Abnormalities in Patients Presenting With Ventricular Arrhythmia (From the LYTE-VT Study). The American Journal of Cardiology. 2020. https://pubmed.ncbi.nlm.nih.gov/32565090

›Long B, Koyfman A. Best Clinical Practice: Emergency Medicine Management of Stable Monomorphic Ventricular Tachycardia. The Journal of Emergency Medicine. 2017. https://pubmed.ncbi.nlm.nih.gov/27751700

›Shivkumar K. Catheter Ablation of Ventricular Arrhythmias. The New England Journal of Medicine. 2019. https://www.nejm.org/doi/full/10.1056/NEJMra1615244

›John RM, Tedrow UB, Koplan BA, et al. Ventricular Arrhythmias and Sudden Cardiac Death. Lancet. 2012. https://pubmed.ncbi.nlm.nih.gov/23101719

›Tisdale JE, Chung MK, Campbell KB, et al. Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association. Circulation. 2020. https://www.ahajournals.org/doi/abs/10.1161/CIR.0000000000000905

›Koplan BA, Stevenson WG. Ventricular Tachycardia and Sudden Cardiac Death. Mayo Clinic Proceedings. 2009. https://pubmed.ncbi.nlm.nih.gov/19252119

›William J, Xiao X, Shirwaiker A, et al. Diagnostic Evaluation of Unexplained Ventricular Tachyarrhythmias in Younger Adults. Journal of Cardiovascular Electrophysiology. 2023. https://onlinelibrary.wiley.com/doi/10.1111/jce.15868

›Lampert R, Chung EH, Ackerman MJ, et al. 2024 HRS Expert Consensus Statement on Arrhythmias in the Athlete. Heart Rhythm. 2024. https://doi.org/10.1016/j.hrthm.2024.05.018

›Elias Hanna. Approach to Narrow and Wide QRS Complex Tachyarrhythmias. Practical Cardiovascular Medicine 2e. 2022. https://onlinelibrary.wiley.com/doi/10.1002/9781119832737.ch8

›Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI. Ventricular Arrhythmias in the Absence of Structural Heart Disease. Journal of the American College of Cardiology. 2012. https://pubmed.ncbi.nlm.nih.gov/22575310

Evidence & Review

Evidence & Review