01Approach to the Critical Patient/attcp25

Immediate Stabilization

›Immediate threat recognition

›Pulseless VT treated as cardiac arrest: CPR + defibrillation per ACLS protocol

›Hemodynamic instability defined as SBP <80 mmHg, altered mentation, syncope, chest pain, or signs of acute heart failure

›Polymorphic VT always treated as unstable regardless of blood pressure

Electrical Therapy Priorities

›Cardioversion strategy by VT type

›Monomorphic VT with pulse: synchronized cardioversion, 100 J biphasic initial energy

›Polymorphic VT (irregular, no discernible QRS): unsynchronized defibrillation at maximum energy (200 J biphasic)

›Torsades de Pointes: magnesium sulfate 2 g IV over 15 minutes prior to cardioversion if time permits

›Pulseless VT: unsynchronized defibrillation 200 J biphasic, follow ACLS protocol

Monitoring and Access

›Resuscitation setup

›Cardiac monitor with defibrillator pads applied immediately

›Two large-bore IV lines or central venous access

›Continuous pulse oximetry, end-tidal CO2 if intubated

›12-lead ECG prior to cardioversion if patient allows; do not delay cardioversion

›Arterial line for hemodynamic monitoring post-stabilization

Team Activation

›Consult triggers

›Cardiology for all sustained VT

›Electrophysiology for VT storm, recurrent VT, ICD evaluation, or ablation candidacy

›Interventional cardiology if ST elevation or acute coronary syndrome suspected

›Cardiac surgery if mechanical circulatory support or CABG indicated

Key Decision Points

›Post-cardioversion management

›If VT recurs after cardioversion: amiodarone 150 mg IV over 10 minutes then infusion

›If STEMI present after conversion: activate cardiac catheterization lab

02History/hx35

Symptom Characterization

›Presenting complaint features

›Sudden-onset palpitations, racing heart, pounding in chest

›Chest pain, pressure, or tightness

›Syncope or near-syncope

›Presyncope, lightheadedness, dizziness

›Dyspnea, orthopnea

›Sense of impending doom

Onset and Temporal Features

›Episode characteristics

›Onset: sudden vs. gradual

›Duration: sustained (>30 seconds) vs. nonsustained

›Prior episodes and frequency

›Prior ICD shocks (single or multiple)

›Triggers: exertion, emotional stress, caffeine, illicit drug use

Associated Symptoms

›Systemic features

›Diaphoresis and pallor

›Nausea, abdominal pain

›Altered consciousness or seizure-like activity from hypoperfusion

›Lower extremity edema

›Worsening dyspnea or orthopnea preceding episode

Cardiac History

›Prior cardiac diagnoses and procedures

›Prior myocardial infarction, coronary artery disease, PCI or CABG

›Known cardiomyopathy: ischemic, nonischemic, ARVC, HCM

›Prior VT or VF episodes, cardiac arrest

›ICD or pacemaker in place: device type, last interrogation date

03Physical Exam/exam28

Vital Signs

›Hemodynamic assessment

›Blood pressure: hypotension defined as SBP <80 mmHg in unstable VT

›Heart rate: typically 150-250 bpm in VT

›Respiratory rate: tachypnea suggesting pulmonary edema or hypoperfusion

›Oxygen saturation: hypoxia with pulmonary edema or cardiogenic shock

General Appearance

›Perfusion status

›Altered mental status, agitation, or unresponsiveness

›Diaphoresis, pallor, cyanosis

›Respiratory distress

Neck Examination

›Venous and AV dissociation findings

›Cannon A waves: intermittent prominent jugular venous pulsations indicating AV dissociation, pathognomonic for VT

›Elevated jugular venous pressure suggesting heart failure or right heart strain

Cardiac Examination

›Auscultation and palpation

›Rapid regular rhythm at 150-250 bpm

›Variable S1 intensity: hallmark of AV dissociation in VT

›S3 gallop: heart failure or cardiomyopathy

›Murmurs: structural heart disease, papillary muscle dysfunction

Pulmonary Examination

›Respiratory findings

›Crackles or rales: pulmonary edema from cardiogenic shock

›Decreased breath sounds: pleural effusion

Peripheral Examination

›Perfusion and vascular findings

›Cool, mottled extremities

04Differential Diagnosis/ddx16

Wide Complex Tachycardia Mimics

›Most important differential diagnoses

›SVT with aberrant conduction due to bundle branch block: most common mimic of VT

›Antidromic AVRT via accessory pathway (pre-excited tachycardia)

›Atrial flutter with 1:1 conduction and aberrancy

Polymorphic VT Variants

›Distinct subtypes requiring specific management

›Torsades de Pointes: polymorphic VT with QT prolongation; requires magnesium and overdrive pacing

›Polymorphic VT without QT prolongation: often ischemia-related; requires defibrillation

›Ventricular fibrillation: disorganized, no discernible QRS; requires immediate defibrillation

Device and Artifact-Related

›Non-arrhythmia causes of wide complex tracing

›Pacemaker-mediated tachycardia

›ECG artifact mimicking VT: confirm with pulse check and rhythm strip

Differentiating ECG Criteria

›Brugada algorithm for VT vs SVT

›Absence of RS complex in all precordial leads: diagnose VT

›RS interval >100 ms in any precordial lead: diagnose VT

›AV dissociation on ECG or clinically (cannon A waves): diagnose VT

›Morphologic criteria in V1-V2 and V6: positive concordance favors VT

05Laboratory Tests/lt20

Electrolytes

›Electrolyte panels for arrhythmia substrate

›Serum potassium: hypokalemia (<3.5 mmol/l) lowers threshold for VT

›Target potassium >4.0 mmol/l in sustained VT

›Serum magnesium: hypomagnesemia (<0.7 mmol/l) exacerbates VT

›Target magnesium >0.8 mmol/l

›Serum calcium: hypocalcemia prolongs QT interval

Cardiac Biomarkers

›Ischemia and myocardial injury markers

›Troponin I or T: elevated in acute MI-related VT or demand ischemia from prolonged VT

›Serial troponins at 0 and 3 hours to detect evolving ACS

›BNP or NT-proBNP: elevated in decompensated heart failure causing VT

Metabolic and Hematologic Studies

›Systemic metabolic assessment

›Arterial blood gas or venous blood gas: lactic acidosis in hypoperfusion

›Lactate: elevated >2.0 mmol/l suggests inadequate cardiac output

›Serum creatinine: baseline renal function, electrolyte context

›Complete blood count: anemia contributing to demand ischemia

Toxicology and Drug Levels

›Proarrhythmic substance screening

›Digoxin level if on therapy or toxicity suspected

›Urine drug screen: cocaine and amphetamine detection

›TSH: thyroid dysfunction as VT trigger

›Coagulation studies if cardiac catheterization anticipated

06Diagnostic Tests/dt40

Scoring Systems

›Clinical decision tools for VT identification

›Brugada criteria (1991): four-step algorithm differentiating VT from SVT with aberrancy

›Step 1: absence of RS in any precordial lead confirms VT

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

›Step 3: AV dissociation confirms VT

›Step 4: morphologic criteria in V1-V2 and V6 confirm VT

›Vereckei algorithm: four-step alternative to Brugada criteria for wide complex tachycardia

›AV dissociation in step 1 confirms VT

›Initial R wave in aVR confirms VT

›Left or right bundle branch block morphology inconsistency confirms VT

›Vi/Vt ratio less than 1 confirms VT

MRI

›Cardiac MRI indications in VT evaluation

›Late gadolinium enhancement imaging: scar characterization for VT substrate mapping

›Identifies ischemic and nonischemic fibrosis as reentry circuit substrate

›Guides catheter ablation planning

›ARVC diagnosis: fatty infiltration, RV dilation, wall motion abnormalities on cMRI

›Task Force Criteria include major criterion: RV ejection fraction <40% on cMRI

›Cardiac sarcoidosis: patchy LGE in non-coronary distribution

›Not indicated in acute unstable VT; reserved for post-stabilization evaluation

CT

›CT imaging in VT evaluation

›CT coronary angiography: non-invasive assessment of coronary anatomy if catheterization not immediately performed

›Sensitivity 95-99% for obstructive CAD (>50% stenosis) in stable post-VT evaluation

›CT pulmonary angiography: exclude pulmonary embolism as VT trigger in select cases

›Cardiac CT for structural evaluation: pericardial disease, congenital anomalies

›Not used in the acute unstable phase; reserved for outpatient or post-stabilization workup

07Disposition/dispo24

ICU Admission

›Intensive care unit criteria

›All hemodynamically unstable VT requiring immediate cardioversion

›VT storm: three or more VT episodes in 24 hours

›Post-cardiac arrest requiring post-resuscitation care

›Ongoing antiarrhythmic infusions (amiodarone, lidocaine)

›Cardiogenic shock or mechanical circulatory support

Step-Down or Telemetry

›Monitored bed criteria post-stabilization

›Converted VT with identified and corrected reversible cause

›Stable hemodynamics with no ongoing antiarrhythmic infusion required

›Continuous telemetry monitoring for minimum 48 hours post-conversion

Inpatient Monitoring Requirements

›Minimum inpatient workup

›Serial troponins and electrolyte monitoring

›Echocardiography for LVEF assessment if not obtained in ED

›Cardiac MRI for scar characterization when appropriate

›EP consultation for ICD implantation and ablation planning

›Device interrogation if ICD or pacemaker in situ

Discharge Criteria

›Contraindications to ED discharge

›Unstable VT patients are never discharged directly from the ED

›All patients with sustained VT require inpatient admission

Specialist Consultation Triggers

›Consultation requirements by severity

›Cardiology: all patients with sustained VT

›Electrophysiology: VT storm, recurrent VT, ICD evaluation, catheter ablation candidacy

›Interventional cardiology: suspected acute coronary syndrome as trigger

08Treatment/t61

Immediate Electrical Therapy

›Cardioversion and defibrillation protocol

›Monomorphic VT with pulse: synchronized cardioversion

›Initial energy 100 J biphasic

›Escalate to 150-200 J if no conversion

›Procedural sedation with etomidate 0.3 mg/kg IV or ketamine 1-2 mg/kg IV prior to cardioversion in conscious patients

›Polymorphic VT or VF: unsynchronized defibrillation

›Energy 200 J biphasic (maximum energy)

›Follow ACLS sequence with CPR between shocks

›Pulseless VT: unsynchronized defibrillation 200 J biphasic, then CPR

Amiodarone

›First-line antiarrhythmic post-cardioversion for refractory or recurrent VT

›Loading dose: 150 mg IV over 10 minutes

›Class I recommendation for hemodynamically unstable VT refractory to cardioversion

›May repeat 150 mg IV bolus once for breakthrough VT

›Maintenance infusion: 1 mg/min for 6 hours

›Then 0.5 mg/min for 18 hours

›Maximum 2.2 g IV over 24 hours

›Monitor for hypotension during bolus administration

›Monitor for QT prolongation: risk of Torsades de Pointes with excessive dosing

Lidocaine

›Alternative antiarrhythmic, preferred in acute MI setting

›Loading dose: 1-1.5 mg/kg IV bolus

›May repeat 0.5-0.75 mg/kg IV every 5-10 minutes

›Maximum cumulative loading dose 3 mg/kg

›Maintenance infusion: 1-4 mg/min

›Reduce to 1-2 mg/min in hepatic impairment or low cardiac output

›Monitor for CNS toxicity: perioral numbness, tremor, seizure

›Lower toxicity threshold in elderly or low cardiac output states

Procainamide

›Alternative for stable VT, use with caution in unstable patients

›Loading dose: 20-50 mg/min IV

›Maximum total dose 17 mg/kg

›Stop if hypotension, QRS widens >50%, or VT terminates

›Maintenance infusion: 1-4 mg/min

›Risk of hypotension limits use in hemodynamically unstable VT

›Preferred over amiodarone for monomorphic VT in stable patients per ACC/AHA guidelines

Magnesium Sulfate

›Torsades de Pointes and hypomagnesemia

›Loading dose: 2 g IV over 15 minutes for Torsades de Pointes

›May repeat once at 2 g IV if no response

›Effective for terminating Torsades de Pointes even with normal serum magnesium

›Follow with electrolyte repletion to maintain magnesium >0.8 mmol/l

Beta-Blockers

›Particularly useful for polymorphic VT storm and ischemia-related VT

›Esmolol: 500 mcg/kg IV bolus over 1 minute

›Maintenance infusion 50 mcg/kg/min

›Titrate 25-50 mcg/kg/min every 5 minutes

›Maximum 300 mcg/kg/min

›Metoprolol: 5 mg IV every 5 minutes, up to three doses

›Contraindicated in cardiogenic shock, severe decompensated heart failure, reactive airway disease

VT Storm Management

›Three or more VT episodes in 24 hours

›IV amiodarone plus IV beta-blocker combination

›Deep sedation with propofol or benzodiazepine to reduce sympathetic drive

›Consider stellate ganglion block for refractory VT storm

›Urgent EP consultation for catheter ablation

›Mechanical circulatory support (IABP, Impella) if cardiogenic shock

Electrolyte Therapy

›Substrate modification

›Potassium repletion: target >4.0 mmol/l

›KCl 10-20 mmol/h IV via central line for severe hypokalemia

›Magnesium repletion: target >0.8 mmol/l

›Calcium gluconate 1 g IV for hypocalcemia-associated QT prolongation

Contraindicated Medications

›Drugs to avoid in wide complex tachycardia

›Verapamil and diltiazem: absolutely contraindicated in wide complex tachycardia of unknown origin

›Risk of profound hypotension, cardiogenic shock, and cardiac arrest

›Additional QT-prolonging agents in Torsades de Pointes

›Concurrent use of multiple antiarrhythmics: increased proarrhythmic risk

09Special Populations/sp36

Pregnancy

›VT in pregnancy

›Physiologic changes increasing arrhythmia risk

›Increased blood volume, heart rate, and cardiac output in pregnancy

›Hormonal changes may trigger or exacerbate cardiomyopathy

›Peripartum cardiomyopathy: VT may be presenting arrhythmia

›Cardioversion safety in pregnancy

›Synchronized cardioversion is safe in all trimesters for unstable VT

›Fetal monitoring before and after cardioversion if fetus viable

›Medication considerations

›Amiodarone: crosses placenta; associated with neonatal hypothyroidism and bradycardia; use only if no alternative in life-threatening VT

›Lidocaine: preferred antiarrhythmic alternative in pregnancy

›Beta-blockers: generally safe; metoprolol or esmolol preferred

›Procainamide: limited data; avoid if alternatives available

Geriatric

›VT in elderly patients

›Increased prevalence of structural heart disease and medication-related proarrhythmia

›Higher burden of ischemic cardiomyopathy and prior MI

›Polypharmacy increases QT prolongation risk

›Reduced drug clearance and distribution volume

›Lidocaine toxicity threshold lower: reduce infusion to 1-2 mg/min

›Amiodarone accumulation risk with prolonged use

›ICD considerations

›Age alone is not a contraindication to ICD implantation

›Goals of care discussion essential in frail elderly patients

Pediatrics

›VT in pediatric patients

›Etiology differs from adults

10Background/b28

Epidemiology

›Incidence and prevalence data

›Sustained VT occurs in 1-3% of post-MI patients per year

›Prior MI or ischemic cardiomyopathy is the most common cause of sustained monomorphic VT accounting for approximately 70% of cases

›Reduced LVEF (<35%) is the strongest predictor of VT and sudden cardiac death

›Sudden cardiac death accounts for approximately 300,000 deaths annually in the United States, with VT/VF as the underlying arrhythmia in the majority

›In-hospital mortality for VT storm exceeds 30% without aggressive management

›Patients with structural heart disease and recurrent VT have >40% recurrence within 2 years

Pathophysiology

›Mechanisms of VT generation

›Reentry: most common mechanism in scar-related VT post-MI

›Scar tissue creates unidirectional conduction block and slow conduction zone

›Reentry circuit requires zone of slow conduction surrounded by viable myocardium

›Triggered activity: early and delayed afterdepolarizations

›Early afterdepolarizations: responsible for Torsades de Pointes with QT prolongation

›Delayed afterdepolarizations: digoxin toxicity, catecholaminergic VT (CPVT)

›Enhanced automaticity: abnormal pacemaker activity in diseased myocardium

›Occurs in ischemia, hypoxia, and electrolyte abnormalities

›Polymorphic VT: most commonly ischemia-related; multiple changing reentry circuits

›VT storm: sympathetic hyperactivation perpetuating arrhythmia cascade

Therapeutic Considerations

›Evidence base for VT management

›2017 AHA/ACC/HRS Guideline for Management of Ventricular Arrhythmias and SCD: primary reference for VT management

›Class I recommendation: immediate synchronized cardioversion for hemodynamically unstable VT

›Class I recommendation: amiodarone IV for recurrent VT refractory to cardioversion

›2025 AHA ACLS Guidelines: updated defibrillation and antiarrhythmic protocols

›Amiodarone 300 mg IV for shock-refractory VF/pulseless VT during cardiac arrest

›ICD therapy: Class I indication for secondary prevention of sudden cardiac death in survivors of VT/VF

11Patient Discharge Instructions/pdi25

copy discharge instructions

›Discharge instructions for Ventricular Tachycardia (Unstable)

›This was a serious and potentially life-threatening heart rhythm problem called ventricular tachycardia

›You required emergency treatment to restore your heart to a normal rhythm

›It is critical that you keep all follow-up appointments with your cardiologist or heart specialist

Medications

›Medication instructions after discharge

›Take all heart rhythm medications exactly as prescribed

›Do not stop any medication without speaking to your cardiologist

›Avoid all medications that can prolong the QT interval unless specifically approved by your heart doctor

›Provide a complete list of all medications to every healthcare provider

Activity Restrictions

›Activity and driving guidance

›Do not drive until cleared by your cardiologist, typically restricted for at least 6 months following a VT event

›Avoid strenuous exercise until cleared by your heart doctor

›Avoid stimulants including cocaine, methamphetamine, and high-dose caffeine

ICD Instructions

›Implantable cardioverter-defibrillator guidance if applicable

›If you have an ICD: a single shock that you felt requires urgent medical evaluation

›Multiple ICD shocks in a short period require immediate 911 activation

›Keep all ICD follow-up appointments for device checks

Return to Emergency Department

›Red flags requiring immediate 911 activation or return to emergency department

›Loss of consciousness or fainting

›Rapid or racing heartbeat lasting more than a few seconds

›Chest pain, pressure, or tightness

›Severe shortness of breath or difficulty breathing

›ICD shock, especially multiple shocks

12References/r12

Guidelines and Key Sources

›Primary clinical guidelines for unstable VT management

›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. J Am Coll Cardiol. 2018. https://pubmed.ncbi.nlm.nih.gov/29097294

›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

›Panchal AR, Bartos JA, Cabanas JG, et al. Part 3: Adult Basic and Advanced Life Support: 2020 AHA Guidelines for CPR and Emergency Cardiovascular Care. Circulation. 2020. https://www.ahajournals.org/doi/abs/10.1161/CIR.0000000000000916

›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/

Supporting Literature

›Key supporting studies and reviews

›Shivkumar K. Catheter Ablation of Ventricular Arrhythmias. N Engl J Med. 2019. https://www.nejm.org/doi/full/10.1056/NEJMra1615244

›Jentzer JC, Noseworthy PA, Kashou AH, et al. Multidisciplinary Critical Care Management of Electrical Storm: JACC State-of-the-Art Review. J Am Coll Cardiol. 2023. https://pubmed.ncbi.nlm.nih.gov/37257955

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

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

›Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for Management of Adult Patients With Supraventricular Tachycardia. J Am Coll Cardiol. 2016. https://linkinghub.elsevier.com/retrieve/pii/S0735-1097(15)05840-4

›Riley MP, Marchlinski FE. ECG Clues for Diagnosing Ventricular Tachycardia Mechanism. J Cardiovasc Electrophysiol. 2008. https://onlinelibrary.wiley.com/doi/10.1111/j.1540-8167.2007.01007.x

Evidence & Review

Evidence & Review