Submodule
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.
- PVC morphology and burden
- PVC-mediated cardiomyopathy
- NSVT
- Structural and inherited evaluation
Assess morphology and burden
Link duration to substrate
Stability drives acute action
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
Submodule
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.
- Scar-mediated reentry
- Stable wide-complex tachycardia
- Unstable synchronized cardioversion
- Drug and ablation strategy
Assume VT when uncertain
Cardiovert instability
Image and evaluate
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
Submodule
Polymorphic Ventricular Tachycardia
The baseline QT distinguishes torsades from polymorphic VT more often driven by acute ischemia or another non-long-QT mechanism.
- Torsades and prolonged QT
- Magnesium and pause control
- Normal-QT polymorphic VT
- Drug and congenital long QT
Treat sustained episodes
Magnesium and cause removal
Treat coronary and trigger state
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
Submodule
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.
- VF resuscitation
- Shock-refractory VF or pVT
- Electrical storm
- ICD shock evaluation
Minimize interruption
Remove recurring triggers
Reduce recurrence
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
Submodule
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.
- Brugada syndrome
- CPVT
- Arrhythmogenic cardiomyopathy
- Inflammatory ventricular arrhythmia
Do not diagnose from one clue
Find scar or inflammation
Use expert counseling
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
Submodule
Sudden-Death Prevention
ICDs, ablation, antiarrhythmic drugs, revascularization, heart-failure therapy, and inherited-disease management address different components of ventricular-arrhythmia recurrence and mortality.
- Secondary-prevention ICD
- Primary-prevention ICD
- VT ablation
- Longitudinal device and disease care
Exclude reversible cause
Use guideline thresholds
Reduce recurrent VT
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
Module test
Check the connections.
Each attempt draws 10 questions from the complete 100 question bank.
Each attempt draws a fresh set and rearranges the answer choices.
References
Current clinical foundation.
Lecture material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.