VT with Hemodynamic Instability (Crashing BP)

Step 1: Immediate - Electrical Cardioversion (Do NOT wait for drugs)

• If the patient is conscious, sedate first (e.g., midazolam + ketamine) before synchronized cardioversion, if time allows.
• Do NOT delay the shock waiting for sedation if the patient is losing consciousness.

"QRS synchronous electrical cardioversion should be performed in case of impaired consciousness, hypotension, or pulmonary edema, after sedation if possible if the patient is conscious." - Braunwald's Heart Disease

Step 2: Simultaneous Resuscitation

• IV access x 2, continuous ECG monitoring
• High-flow oxygen, secure airway if obtunded
• Call for crash cart/defibrillator immediately
• Start CPR if pulseless at any point

Step 3: Post-Cardioversion / If Temporarily Stable - Antiarrhythmic Drugs

Drug Options (in order of evidence):

1. Amiodarone - 150 mg IV over 10 minutes (loading), then 1 mg/min x 6 hours, then 0.5 mg/min
   • Better at preventing recurrence (more effective at slower rates)
   • Can cause hypotension - watch BP
2. Procainamide - 10 mg/kg IV (up to 1000 mg) over 20 minutes
   • Superior to amiodarone for acutely terminating wide-complex tachycardia in randomized trials
   • Avoid in renal failure (metabolite causes QT prolongation and Torsades)
   • Also a vasodilator - can worsen hypotension in up to 30% of patients
3. Lidocaine - 50 mg IV bolus (1-1.5 mg/kg)
   • More effective at faster heart rates
   • Good in acute ischemia/MI-related VT
   • Less effective for preventing recurrence

Step 4: Find and Fix the Cause

"The most important factors in preventing early recurrence are the prompt identification and reversal of any precipitating causes." - Goldman-Cecil Medicine

Step 5: If VT Keeps Coming Back (Electrical Storm)

• Esmolol 500 mcg/kg IV bolus, then 50-200 mcg/kg/min infusion (preferred - short half-life beta-blocker)
• Continue amiodarone infusion
• Consider intra-aortic balloon pump for hemodynamic support
• Treat ischemia - reperfusion if coronary occlusion
• Catheter ablation if refractory to all the above

Critical Warnings

• Do NOT give IV verapamil or diltiazem for VT (unless you are 100% certain it is idiopathic fascicular VT in a structurally normal heart) - can cause irreversible hemodynamic collapse
• Adenosine can be used diagnostically for stable wide-complex tachycardia of uncertain origin, but only in a hemodynamically stable patient
• Magnesium is specifically for Torsades de Pointes (polymorphic VT with long QT) - give 2g IV over 1-2 minutes

• Braunwald's Heart Disease, p. 556
• Goldman-Cecil Medicine, p. 590
• Tintinalli's Emergency Medicine, p. 145

ECG Diagnosis of Polymorphic VT (PMVT)

Core ECG Features

"Polymorphic VT has a continually changing QRS morphology indicating a changing ventricular activation sequence." - Harrison's Principles of Internal Medicine 22E

Real ECG Examples

Three examples of monomorphic VT - note consistent beat-to-beat QRS morphology (Tintinalli's Emergency Medicine)

A = Polymorphic VT (chaotic, randomly changing QRS). B = Torsades de Pointes (QRS amplitude waxes and wanes, appearing to "twist" around the baseline) (Tintinalli's Emergency Medicine)

The Two Subtypes of Polymorphic VT

1. Polymorphic VT WITHOUT QT Prolongation

• QRS changes randomly and chaotically in shape, amplitude, and axis
• Baseline (sinus rhythm) ECG shows normal QT interval
• Occurs in: acute MI/ischemia, structural heart disease, catecholaminergic PMVT
• Key trigger: Ischemia, adrenergic surge

2. Torsades de Pointes (TdP) - PMVT WITH QT Prolongation

1. Ventricular rate >200 beats/min
2. Undulating QRS axis - the polarity of the complexes appears to shift around the baseline (the "twisting of the points")
3. Paroxysms typically <90 seconds in duration (often self-terminating)
4. On the preceding sinus beats: prolonged QT interval (>450 ms in males, >470 ms in females)

• QRS complexes appear to rotate around the isoelectric baseline
• Amplitude gradually increases then decreases in a cyclical, sinusoidal fashion
• Best seen in a single continuous rhythm strip

How to Identify TdP on ECG - Step by Step

1. Look at the rhythm strip - see wide, fast, chaotic complexes
2. Is the QRS morphology changing beat to beat? → Yes = PMVT
3. Is there a spindle/waxing-waning pattern? - complexes appear to "twist" around the baseline → suggests TdP
4. Go back to the sinus beats BEFORE the episode - is the QT prolonged?
5. Look for the "short-long-short" initiating sequence - TdP is often triggered by a PVC following a long R-R pause (pause-dependent mechanism)

Causes to Look for After Diagnosis

Key Clinical Point: TdP vs VF

• TdP - recognizable organized "twisting" pattern, usually self-terminates, then recurs
• VF - completely chaotic, no discernible QRS, no organized pattern at all
• TdP can degenerate into VF if sustained

Treatment Reminder (Based on Diagnosis)

• PMVT with normal QT (ischemic) - cardioversion + treat ischemia; beta-blockers
• TdP - IV MgSO₄ 2g immediately (even if Mg is normal); correct K+; stop QT-prolonging drugs; overdrive pacing if bradycardia-dependent; avoid Class IA/IC antiarrhythmics (they worsen QT prolongation)
• Tintinalli's Emergency Medicine, p. 156-157
• Harrison's Principles of Internal Medicine 22E, p. ~1248
• Rosen's Emergency Medicine, p. 1063

Torsades de Pointes (TdP)

What It Is

Classic ECG Appearance

Torsades de Pointes: classic spiraling of QRS complexes around the baseline (Rosen's Emergency Medicine)

Mechanism

1. Prolonged QT = prolonged action potential phase 2/3
2. During this prolonged repolarization window, abnormal Ca²⁺ and late Na⁺ influx generate EADs
3. EADs reach threshold and trigger an ectopic beat (usually the initiating PVC)
4. This sets up a reentrant circuit with constantly shifting activation wavefronts → the "twisting" appearance

Two Types: Acquired vs Congenital

Type 1: Acquired (Pause-Dependent) - MOST COMMON

Type 2: Congenital (Adrenergic-Dependent) - triggered by exercise/emotion

• Women are at greater risk than men for TdP due to naturally longer QTc

Clinical Features

• Episodes of palpitations, dizziness, presyncope, syncope
• Often self-terminates (<90 seconds) then recurs repeatedly
• Can degenerate into VF and sudden cardiac death
• Patients may present with recurrent "blackouts" that are misdiagnosed as seizures

Treatment

Acute Management

Drugs to AVOID in TdP

• Class IA antiarrhythmics (quinidine, procainamide, disopyramide) - prolong QT further
• Class IC (flecainide, propafenone)
• Amiodarone (lengthens QT, use with caution)

Long-Term Management

"An ICD is recommended for patients who present with aborted cardiac arrest. About 25% of patients continue to experience ventricular arrhythmias on full doses of beta-blocker therapy and require an ICD." - Goldman-Cecil Medicine

Key Points to Remember

1. QT prolongation is the substrate - always check QTc on the prior ECG
2. Mg first, always - even if serum Mg is normal
3. Isoproterenol for acquired/pause-dependent TdP; beta-blockers for congenital LQTS (opposite treatments!)
4. Never give Class IA/IC drugs - they make it worse
5. Short-long-short initiating pattern is pathognomonic
6. Women > men for risk; concurrent QT-prolonging drugs multiply risk dramatically

• Rosen's Emergency Medicine, p. 1063
• Goldman-Cecil Medicine, p. 590-591
• Lippincott Pharmacology
• Washington Manual of Medical Therapeutics