Author:
Emily M.Mills
Rama A.Salhi
Description
- A wide complex tachydysrhythmia (WCT):
- ≥3 consecutive QRS complexes with ventricular rate >100 bpm and QRS duration >120 ms
- Rapid, regular depolarization of the ventricles independent of atria and normal conduction system
- Considered sustained if lasts >30 s, produces syncope or arrest, or requires cardioversion/pacing
- Monomorphic VT - single, stable QRS morphology
- Polymorphic VT - changing QRS morphology:
- Torsades de pointes:
- Polymorphic form of VT
- Alternating electrical polarity and amplitude
- Long QT present on baseline ECG
- Acquired or congenital
- Bidirectional VT - beat-to-beat alternation in QRS frontal plane axis:
- Digitalis toxicity
- Catecholaminergic polymorphic VT (inherited, rare, highly lethal)
Etiology
- Wide complex tachycardia:
- 80% likelihood of being VT
- 20% supraventricular tachycardia (SVT) with a baseline left bundle branch block (LBBB) or aberrancy
- Wide complex tachycardia and a history of MI:
- >98% likelihood of being VT
- Age >35: 80% risk of VT
- Age <35: 75% risk of SVT
- Incidence of nonsustained VT:
- Associated with increased risk for sudden cardiac death (SCD)
- Mechanisms for VT:
- Reentrant:
- Occurs commonly in structural heart disease (dilated cardiomyopathy, ischemia, infiltrative heart disease, previous MI, scarring, prior surgery)
- Unidirectional conduction
- Fixed or functional conduction block
- Region of “slow conduction”
- Abnormal automaticity:
- Abnormal impulse generated by region of ventricular cells at accelerated rate
- Triggered activity:
- Due to early or late after-depolarizations
- Polymorphic VT causes:
- Acquired (drug-induced or electrolyte abnormalities)
- Congenital (long QT syndrome)
- Ischemia
- Organic heart disease
- Regardless of the mechanism, all VT may degenerate to ventricular fibrillation (VF)
Signs and Symptoms
History
- Asymptomatic
- Syncope/near syncope
- Lightheadedness/dizziness
- Shortness of breath
- Palpitations
- Chest discomfort/pain
- CHF
Physical Exam
- Establish presence of pulses, mental status, and vital sign abnormalities
- Auscultation of heart will reveal tachycardia
- Diaphoresis
- Cannon A-waves
- Hypotension
- Beat-to-beat variability of systolic BP
- Variability in heart tones, especially S1
Essential Workup
- ECG is the most important initial test
- ECG criteria favoring monomorphic VT:
- QRS complexes >140 ms for RBBB
- QRS complexes >160 ms for LBBB
- A-V dissociation (fusion complexes, capture beats)
- Extreme axis deviation (-90°-+180°)
- Concordant precordial R-wave progression pattern
- RBBB pattern with R > R' in V1
- LBBB pattern with Q or QS in V6
- Brugada Criteria for VT (stepwise algorithm, only need one to diagnose VT)
- Absence of RS complex in precordial leads
- R-S interval >100 ms in one precordial lead
- A-V dissociation
- Morphology criteria for VT present in both V1-V2 and V6 (see Additional Reading)
- ECG indicators of SVT with abnormal conduction:
- Normal-axis QRS <140 ms
- Absence of Q-waves
- RBBB in V1 with rsR′ triphasic pattern
- AV nodal blockade: Slowing of impulse conduction velocity seen with antiarrhythmic drugs is more pronounced at faster rates, so may result in wide complex SVT (SVT with aberrancy)
- Torsades de pointes:
- Polymorphic VT that rotates its axis every 10-20 beats
Diagnostic Tests & Interpretation
Lab
- Cardiac enzymes
- Electrolytes, BUN, creatinine, glucose
- Magnesium level
- Calcium level
- Digoxin level if toxicity suspected
Imaging
CXR:
- Cardiomegaly or other cardiac anomalies may be apparent
ECHO:
- Assess LV function
- Structural disease may be identified
Diagnostic Procedures/Surgery
Esophageal pacing catheters:
- Might detect atrial activity to establish AV dissociation and therefore diagnose VT
- Catheters can then be used to overdrive pace if refractory to cardioversion/antiarrhythmics
Differential Diagnosis
- SVT with aberrancy or baseline LBBB
- Proarrhythmia secondary to antidysrhythmia medications; suspect if:
- Morphology different from previous VT episodes
- Recent medications changes
- QT interval is >440 ms
- Torsades de pointes
- If VT continues to recur after cardioversion
Prehospital
- Cautions:
- Transport stable patients suspected of being in VT without attempting cardioversion
- Synchronized cardioversion for unstable patients with a pulse
- Defibrillation for pulseless VT
- Prophylactic lidocaine administration is not recommended (class III: Harm)
Initial Stabilization/Therapy
ABCs, IV, O2, monitor, ECG
ED Treatment/Procedures
- Pulseless VT:
- Defibrillate immediately and follow ACLS pVT treatment plan
- Amiodarone may be considered for pVT unresponsive to CPR, defibrillation, and vasopressor therapy (class IIb)
- Lidocaine may be considered as alternative (class IIb)
- Routine use of Magnesium is not recommended (class III: No benefit)
- No antiarrhythmic drug has yet been shown to increase survival/neurologic outcomes after cardiac arrest due to pVT/VF
- Unstable VT with pulse:
- Definition:
- Initiate immediate synchronized cardioversion with 100 J, quickly progressing to 200 J, 300 J, and 360 J if no response:
- If the VT is polymorphic, begin cardioversion at 200 J
- Sedate before cardioversion if possible
- If unable to terminate VT, administer amiodarone (class IIb) and repeat cardioversion:
- Lidocaine may be considered as alternative (class IIb)
- After successful return of sinus rhythm, begin infusion
- Overdrive pacing if Torsades not responsive to IV magnesium
- If defibrillator not immediately available, consider precordial thump for witnessed, monitored, unstable VT (class IIb)
- Calcium channel blockers are potentially harmful when given for WCT of unknown origin (class III: Harm)
- Adenosine should not be given for unstable, irregular, or WCT, as it may cause degeneration to VF (class III)
ALERT |
| Procainamide received a stronger recommendation for use by both 2017 AHA/ACC/HRS and 2015 ESC guidelines and recent research has shown its efficacy, however amiodarone is the only medication listed in most recent ACLS guidelines for pVT treatment and is more frequent first-line choice in the US for VT with pulse. Further research is needed |
- Stable monomorphic VT:
- Normal cardiac function at baseline:
- Amiodarone (class IIb) if suspected new HF or acute MI, then infusion
- Procainamide (class IIa) - avoid if HF, acute MI, or prolonged QT (class III)
- Consider sotalol (class IIb) - avoid if evidence of HF or prolonged QT (class III)
- Lidocaine is less effective, but consider if nonresponsive to other measures
- Impaired cardiac function at baseline:
- Amiodarone bolus, then infusion
- If antiarrhythmic therapy unsuccessful, consider synchronized cardioversion or expert consultation
- Stable polymorphic VT/Torsades:
- Normal QT interval at baseline:
- Correct electrolyte abnormalities, especially K and Mg
- Treat ischemia if present (most likely cause)
- Amiodarone may be effective (class IIb)
- Magnesium less effective in patients with normal QT (class IIb)
- IV β-blockers may be useful in ischemia (class IIa)
- Prolonged QT:
- Correct electrolytes
- IV magnesium (class I)
- Overdrive pacing if not responsive to magnesium
- If history of congenital long QT syndrome, β-blockers may be appropriate, seek expert consultation
- Recurrent Torsades due to acquired QT prolongation and bradycardia not suppressed with IV magnesium can be treated with pacing or isoproterenol if the patient has no history of coronary artery disease or congenital long QT syndrome (class I)
- Catecholaminergic polymorphic VT:
- Seek expert consultation
- If adequately tolerated β-blockers previously, may require combination medical therapy, cardiac sympathetic denervation, or ICD (class I)
- Impaired cardiac function at baseline:
- Amiodarone (or lidocaine) bolus, then synchronized cardioversion
Pregnancy Prophylaxis |
- Increased risk of VT in patients with underlying structural heart disease
- If history of long QT syndrome, β-blockers should be continued during pregnancy (class I)
- Treat with cardioversion if unstable (class I)
- Consider sotalol or procainamide in stable monomorphic VT (class IIa)
- Can use amiodarone if refractory to electrical cardioversion, unstable, or not responding to other drugs (class IIa)
- Note: Amiodarone is category D in pregnancy
- Catheter ablation may be considered
|
Pediatric Considerations |
- Primary cardiac arrest and VT are rare in children
- Usually secondary to hypoxia and acidosis
- VT is tolerated for longer periods in children than adults and is less likely to degenerate to VF
- Infants in VT most commonly present with CHF
- VT in children results from:
- Cardiomyopathy
- Congenital structural heart disease
- Congenital prolonged QT syndromes
- Coronary artery disease secondary to vasculitis
- Toxins, poisons, drugs
- Severe electrolyte imbalances, especially of potassium
- Either amiodaroneorlidocaine is acceptable for treatment of shock-refractory pVT (class IIb)
- Cardioversion starting energy dose 0.5-1.0 J/kg, if fails increase to 2 J/kg
- Pulseless VT starting energy dose 2-4 J/kg, if fails may increase, but do not exceed 10 J/kg or adult maximum dose
|
Medication
First Line
- Amiodarone: 300 mg IV bolus for pulseless VT, second dose 150 mg IV. 150 mg IV bolus for stable VT, followed by infusion 1 mg/min × 6 hr, then 0.5 mg/min × 18 hr. Max cumulative dose of 2.2 g in 24 hr. (Peds: 5 mg/kg IV/IO over 20-60 min. Max dose 15 mg/kg/d)
- Procainamide: 20-50 mg/min IV (up to max dose 17 mg/kg) or 100 mg over 2 min (every 5 min) until arrhythmia suppressed, followed by maintenance infusion 1-4 mg/min. (Peds: 15 mg/kg IV/IO over 30-60 min). Avoid if prolonged QT, HF, or acute MI. Requires ECG and BP monitoring, stop if hypotension or QRS duration increased by >50%
- Magnesium: 2 g in D5W over 5-10 min followed by infusion of 0.5-1 g/hr IV, titrate to control Torsades (Peds: 25-50 mg/kg IV/IO over 10 min, max dose 2 g)
Second Line
- Lidocaine: 1-1.5 mg/kg bolus IV push first dose, 0.5-0.75 mg/kg second dose, and q5-10min for a max of 3 mg/kg; tracheal administration 2-4 mg/kg; maintenance infusion 1-4 mg/min if converted. Not recommended for ACS induced VT (Peds: 1 mg/kg bolus with infusion 20-50 mcg/kg/min)
- Isoproterenol: 2-10 mcg/min, titrate to heart rate (peds: 0.1 mcg/kg/min). Note: Do not give with epinephrine, may precipitate VT/VF (no longer part of ACLS protocol), do not give if prolonged QT
- Sotalol: 100 mg IV (1.5 mg/kg) over 5 min. (Peds: Use not recommended for initial management). Note: Do not give if prolonged QT. Not always readily available
Disposition
Admission Criteria
- Admit sustained VT to a critical care setting
- Admit nonsustained VT and a history of MI or dilated cardiomyopathy for electrophysiologic studies
Discharge Criteria
- Rare patients with nonsustained VT and a previous evaluation that revealed no structural heart disease can be discharged:
- Patients with automatic internal cardiac defibrillators that are well functioning can also be discharged
Issues for Referral
All patients discharged with VT should be followed by a cardiologist within 48 hr
Follow-up Recommendations
Patients should follow-up with a cardiologist
- Al-KhatibSM, StevensonWG, AckermanMJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society . Circulation. 2018;138(13):e415-e418.
- NeumarRW, ShusterM, CallawayCW, et al. Part 1: Executive summary: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care . Circulation. 2015;132:S315-S367.
- OrtizM, MartinA, ArribasF, et al. Rand omized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide WRS tachycardia: The PROCAMIO study . Eur Heart J. 2017;38:1329-1335.
- PellegriniCN, ScheinmanMM. Clinical management of ventricular tachycardia . Curr Probl Cardiol. 2010;35:453-504.
- PrioriSG, Blomstrom-LundqvistC, MazzantiA, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death . Eur Heart J. 2015;36:2793-2867.
The authors gratefully acknowledge Jennifer Audi, Shannon Straszewski, and Daniel C. McGillicuddy for their contribution to the previous edition of this chapter.
ICD9
427.1 Paroxysmal ventricular tachycardia
ICD10
I47.2 Ventricular tachycardia
SNOMED