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Module 397 lessons

Ventricular Arrhythmias

Evaluate ventricular ectopy, nonsustained and sustained VT, torsades, non-long-QT polymorphic VT, VF, electrical storm, inherited syndromes, structural substrate, ablation, and ICD-based sudden-death prevention.

01

Risk stratify PVCs and NSVT by symptoms, burden, morphology, exercise behavior, ventricular function, scar, and inherited phenotype.

02

Manage stable and unstable monomorphic VT while evaluating ischemic and scar substrate.

03

Differentiate torsades from polymorphic VT with normal QT and apply mechanism-specific recurrence prevention.

04

Execute VF and pulseless VT resuscitation and coordinate electrical-storm care beyond repeated shocks.

05

Recognize inherited, inflammatory, and cardiomyopathic ventricular-arrhythmia phenotypes and family implications.

06

Apply ICD and ablation principles to secondary and primary sudden-death prevention.

07

Select and monitor ventricular antiarrhythmics by rhythm, substrate, repolarization, conduction, organ function, interactions, and treatment goal.

39.01

Lesson

Ventricular Ectopy and Risk Assessment

PVCs, couplets, and NSVT require a substrate-first evaluation because burden, symptoms, exercise relation, ventricular function, scar, and family history change prognosis.

What to learn
  • PVC morphology and burden
  • PVC-mediated cardiomyopathy
  • NSVT
  • Structural and inherited evaluation
Ventricular rhythm spectrumVentricular ectopy ranges from isolated PVCs to sustained VT and VF, with risk defined by symptoms, substrate, burden, hemodynamics, and reversibility.
01PVCPremature ventricular activation

Assess morphology and burden

02NSVTThree or more ventricular beats

Link duration to substrate

03VTSustained organized ventricular rhythm

Stability drives acute action

04VFDisorganized ventricular activation

Immediate defibrillation

Describe the ectopy before judging it

PVC timing, morphology, coupling, multifocality, exercise response, symptoms, and ambulatory burden matter. A single morphology can suggest one focus, while multiple morphologies or exercise-triggered patterns can widen the differential.

Look for a reversible cardiomyopathy

High PVC burden can cause ventricular dysfunction, especially with broad QRS, epicardial or nonoutflow origin, long exposure, and other risk features. Exclude competing causes, suppress or ablate when appropriate, and repeat imaging to document recovery.

Place NSVT inside the substrate

NSVT is a self-terminating ventricular run, not one uniform risk state. Syncope, ischemia, reduced ejection fraction, scar, cardiomyopathy, myocarditis, inherited disease, electrolyte abnormality, and drug exposure determine urgency and prevention.

Use multimodality evaluation

Echocardiography assesses function and gross structure. Cardiac MRI can reveal scar, inflammation, or arrhythmogenic cardiomyopathy missed by echo. Coronary and exercise testing, genetic counseling, and family screening are selected by phenotype.

Quick check

0 of 1 answered
01What finding makes frequent PVCs more concerning for a reversible arrhythmia-mediated cardiomyopathy?

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39.02

Lesson

Monomorphic Ventricular Tachycardia

Sustained monomorphic VT often reflects a stable scar circuit, but immediate care follows pulse and perfusion before mechanism, drug, ablation, and device planning.

What to learn
  • Scar-mediated reentry
  • Stable wide-complex tachycardia
  • Unstable synchronized cardioversion
  • Drug and ablation strategy
Monomorphic VTStable morphology suggests one dominant circuit or focus, commonly scar-mediated reentry in structural heart disease.
01IdentifyRegular wide tachycardia

Assume VT when uncertain

02StabilizePulse and perfusion

Cardiovert instability

03DefineIschemia and scar substrate

Image and evaluate

04PreventDrug, ablation, ICD

Address recurrence and death risk

Assume VT when the cost of error is high

Wide-complex tachycardia can be VT, SVT with aberrancy or preexcitation, pacing, hyperkalemia, or sodium-channel blockade. Structural disease, AV dissociation, capture or fusion, and morphology can support VT, but uncertainty should avoid verapamil and other potentially harmful shortcuts.

Cardiovert instability

Sustained monomorphic VT with a pulse that causes hypotension, shock, ischemic discomfort, acute heart failure, or altered mental status requires prompt synchronized cardioversion. Sedate when feasible without delaying restoration of perfusion.

Treat stable VT under continuous readiness

Stable monomorphic VT permits a 12-lead and selected antiarrhythmic infusion or cardioversion. Procainamide requires avoidance in prolonged QT or heart failure and stopping for hypotension or marked QRS widening. Amiodarone and sotalol have their own substrate and interval constraints.

Address the durable circuit

In infarct or cardiomyopathy, scar channels can repeatedly support VT. Evaluate ischemia, ejection fraction, ICD need, antiarrhythmic risk, and catheter ablation. Termination alone is not sudden-death prevention.

Quick check

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01What is the immediate treatment for unstable monomorphic VT with a pulse?

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39.03

Lesson

Polymorphic Ventricular Tachycardia

The baseline QT distinguishes torsades from polymorphic VT more often driven by acute ischemia or another non-long-QT mechanism.

What to learn
  • Torsades and prolonged QT
  • Magnesium and pause control
  • Normal-QT polymorphic VT
  • Drug and congenital long QT
Polymorphic VTThe baseline QT separates torsades from polymorphic VT driven more often by acute ischemia or other non-long-QT mechanisms.
01ShockUnsynchronized defibrillation

Treat sustained episodes

02QT longTorsades mechanism

Magnesium and cause removal

03QT normalOften ischemic

Treat coronary and trigger state

04PreventCorrect pause, electrolyte, drug

Match to mechanism

Defibrillate sustained polymorphic VT

Beat-to-beat morphology prevents reliable synchronization, so sustained polymorphic VT requires unsynchronized shock. Continue resuscitation when pulseless and support perfusion when pulses return.

Treat torsades as repolarization disease

Torsades occurs with prolonged QT and often follows a pause. Give magnesium for recurrence, correct potassium and other electrolytes, stop QT-active exposures, and address bradycardia or pauses with expert rate support when necessary. Avoid further QT prolongation.

Treat normal-QT polymorphic VT as a different problem

Polymorphic VT without QT prolongation is often associated with acute ischemia. Defibrillation terminates the episode, while coronary treatment, beta blockade, and selected antiarrhythmics address recurrence. Routine magnesium is not supported when QT is normal unless another indication exists.

Assess acquired and inherited long QT

Acquired risk combines drugs, interactions, kidney or liver dysfunction, bradycardia, sex, age, structural disease, and electrolyte depletion. Congenital LQTS can be concealed on one ECG and requires trigger, family, symptom, genotype, and specialist assessment.

Quick check

0 of 1 answered
01Which finding most directly separates torsades from other polymorphic VT?

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39.04

Lesson

Ventricular Fibrillation and Electrical Storm

VF and recurrent ventricular arrhythmia demand defibrillation and CPR plus trigger correction, ischemia care, sympathetic control, device interrogation, and early expert escalation.

What to learn
  • VF resuscitation
  • Shock-refractory VF or pVT
  • Electrical storm
  • ICD shock evaluation
VF and electrical stormRepeated ventricular arrhythmia demands simultaneous resuscitation, defibrillation optimization, ischemia treatment, trigger correction, sympathetic control, and specialist escalation.
01ResuscitateCPR and defibrillation

Minimize interruption

02CorrectHs, Ts, ischemia, electrolytes

Remove recurring triggers

03SuppressAntiarrhythmic and sympathetic strategy

Reduce recurrence

04EscalateAblation and mechanical support

Use expert team

Prioritize CPR and defibrillation

VF eliminates effective output. Start high-quality CPR, defibrillate promptly, minimize interruptions, and use guideline epinephrine and amiodarone or lidocaine pathways while correcting Hs and Ts. Do not delay defibrillation for airway or IV perfection.

Optimize refractory-shock care

Verify pad contact and position, appropriate energy, rhythm recognition, compression fraction, epinephrine timing, antiarrhythmic delivery, and reversible causes. ETCO2 informs CPR and physiology but should not determine termination by itself.

Suppress electrical storm

Repeated sustained VA or appropriate ICD therapy over a short period requires monitored specialist care. Treat ischemia, heart failure, electrolytes, and drug triggers, reduce sympathetic drive, use antiarrhythmics, optimize ICD programming, provide sedation, and consider early ablation or support.

Interrogate every ICD shock

A shock may be appropriate, inappropriate, or unsuccessful. Review stored electrograms, lead and battery integrity, detection programming, AF or SVT, VT morphology, ischemia, heart failure, electrolytes, adherence, and the psychological consequences.

Quick check

0 of 1 answered
01What should happen after repeated ICD shocks over a short interval?

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39.05

Lesson

Inherited and Structural Syndromes

Brugada syndrome, CPVT, arrhythmogenic cardiomyopathy, myocarditis, cardiac sarcoidosis, and other phenotypes can present with syncope or ventricular arrhythmia before obvious structural disease.

What to learn
  • Brugada syndrome
  • CPVT
  • Arrhythmogenic cardiomyopathy
  • Inflammatory ventricular arrhythmia
Inherited and structural syndromesLong-QT, Brugada, catecholaminergic polymorphic VT, cardiomyopathy, myocarditis, and sarcoidosis require phenotype-directed family and structural evaluation.
01PhenotypeECG and trigger pattern

Do not diagnose from one clue

02StructureImaging and function

Find scar or inflammation

03FamilyHistory and genetics

Use expert counseling

04ProtectLifestyle, drugs, ablation, device

Match syndrome risk

Confirm Brugada phenotype carefully

A diagnostic type 1 pattern and clinical context guide Brugada syndrome assessment. Fever and certain drugs can unmask risk. Treat fever aggressively, avoid recognized provoking drugs, evaluate arrhythmic syncope or arrest, and use expert family and genetic counseling.

Find CPVT under adrenergic stress

CPVT often has a normal resting ECG but produces exercise- or emotion-triggered bidirectional or polymorphic VA. Exercise testing and specialist genetic evaluation support diagnosis. Nonselective beta blockade, flecainide, trigger management, and family screening are central.

Recognize arrhythmogenic cardiomyopathy

Fibrotic or fibrofatty disease can cause VT before overt failure. Multimodality imaging, rhythm morphology, exercise history, genetics, and family screening define the phenotype. Exercise can accelerate disease and arrhythmic risk in susceptible patients.

Investigate inflammation

Myocarditis and cardiac sarcoidosis can produce AV block, VT, ventricular dysfunction, and sudden death through active inflammation and scar. Cardiac MRI, PET in selected disease, biomarkers, extracardiac findings, and tissue-specific care guide treatment and device decisions.

Quick check

0 of 1 answered
01Which inherited syndrome can present with exercise-triggered polymorphic VT despite a normal resting ECG?

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39.06

Lesson

Sudden-Death Prevention

ICDs, ablation, antiarrhythmic drugs, revascularization, heart-failure therapy, and inherited-disease management address different components of ventricular-arrhythmia recurrence and mortality.

What to learn
  • Secondary-prevention ICD
  • Primary-prevention ICD
  • VT ablation
  • Longitudinal device and disease care
Sudden-death preventionICDs terminate dangerous rhythm, ablation modifies substrate, drugs reduce recurrence, and disease therapy changes the risk environment.
01SecondaryPrior arrest or sustained VA

Exclude reversible cause

02PrimaryRisk phenotype and timing

Use guideline thresholds

03AblateFocus or scar circuit

Reduce recurrent VT

04FollowProgramming, shocks, function

Treat the whole disease

Use secondary prevention after persistent risk

Survivors of cardiac arrest or sustained hemodynamically significant VT often benefit from an ICD when the event was not caused by a completely reversible factor and meaningful survival is expected. Prove whether ischemia, electrolyte disturbance, drug exposure, or acute disease was truly and durably corrected.

Respect timing in primary prevention

Primary-prevention ICD decisions use ejection fraction, cardiomyopathy, heart-failure symptoms, optimized therapy, timing after MI or revascularization, and competing mortality. Reassess ventricular function after recovery windows unless another device indication exists.

Use ablation to modify the arrhythmia substrate

Ablation can eliminate focal VA or transect scar circuits, reducing recurrent VT and ICD therapy. It does not guarantee removal of all sudden-death risk, so device follow-up and disease treatment continue.

Follow the person and the device

Programming, remote monitoring, lead and battery surveillance, shock review, heart-failure optimization, ischemia care, medication toxicity, driving and activity guidance, psychological recovery, and goals of care determine long-term value.

Quick check

0 of 1 answered
01Why can primary-prevention ICD implantation be deferred after a recent myocardial infarction?

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39.07

Lesson

Ventricular Antiarrhythmic Therapy

Procainamide, lidocaine, mexiletine, disopyramide, amiodarone, and sotalol differ in urgency, substrate fit, proarrhythmic risk, organ handling, and monitoring burden.

What to learn
  • Acute sodium channel blockade
  • Oral ventricular suppression
  • QT-active therapy
  • Whole-patient monitoring
Ventricular antiarrhythmic therapyRhythm, hemodynamics, substrate, repolarization, conduction, organ clearance, and treatment goal determine whether an antiarrhythmic helps or adds risk.
01AcuteProcainamide or lidocaine

Monitor perfusion, QRS, QT, and neurologic status

02OralMexiletine or disopyramide

Reserve for serious ventricular indications

03QT activeSotalol or amiodarone

Control repolarization, bradycardia, and interactions

04DurableAblation, ICD, disease care

Do not mistake suppression for survival

Use acute sodium channel blockers selectively

Procainamide can treat selected stable regular monomorphic wide-complex tachycardia, while lidocaine is used in selected acute ventricular arrhythmias and cardiac arrest pathways. Procainamide can widen QRS, prolong QT, lower blood pressure, and accumulate with its active metabolite. Lidocaine can produce neurologic toxicity and conduction depression, especially when clearance is reduced.

Reserve oral class I therapy for serious indications

Mexiletine is an oral class IB agent labeled for documented life-threatening ventricular arrhythmias. Disopyramide is a class IA agent with negative inotropic, anticholinergic, conduction, and QT effects. Neither belongs in routine suppression of asymptomatic ventricular ectopy, and neither substitutes for substrate treatment or mortality-reducing care.

Treat sotalol as both beta blocker and QT-active drug

Sotalol combines beta blockade with potassium channel effects. Initiation or reinitiation requires a setting with resuscitation capability and continuous ECG monitoring. Baseline QT, kidney function, potassium, magnesium, heart rate, conduction, heart failure, bronchospasm risk, and interacting drugs determine whether exposure is safe.

Separate acute amiodarone use from chronic surveillance

IV amiodarone is one option in selected ventricular arrhythmia and shock-refractory arrest pathways. Long-term oral therapy carries pulmonary, hepatic, thyroid, ocular, neurologic, bradycardic, proarrhythmic, and interaction risks. Baseline and follow-up monitoring must match the duration and route of therapy.

Quick check

0 of 1 answered
01Which finding most directly makes sotalol initiation unsafe without correction or reassessment?

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Module practice

Check the connections.

Each attempt draws 10 questions from the complete 120 question bank.

120 questions in this module bank10 questions per attempt

Each attempt draws a fresh set and rearranges the answer choices.

References

Current clinical foundation.

Core source material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.

  1. American Heart Association. 2025 Adult Advanced Life Support Guidelines
  2. American College of Cardiology. Ventricular Arrhythmias and Sudden Cardiac Death Guideline
  3. American College of Cardiology. 2022 ESC Ventricular Arrhythmia Guideline Key Points
  4. DailyMed. Procainamide Hydrochloride Injection Prescribing Information
  5. FDA. Lidocaine Hydrochloride and Dextrose Injection Prescribing Information
  6. DailyMed. Mexiletine Hydrochloride Capsules Prescribing Information
  7. DailyMed. Disopyramide Phosphate Capsules Prescribing Information
  8. DailyMed. Amiodarone Hydrochloride Tablets Prescribing Information
  9. FDA. Sotalol Hydrochloride Injection Prescribing Information
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