eMedicine Specialties > Emergency Medicine > Cardiovascular
Ventricular Tachycardia: Treatment & Medication
Updated: Sep 17, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
EMTs and paramedics may be called upon to provide cardioversion/defibrillation in the field if they have sufficient training and if appropriate protocols exist.
- Rapid transport to an ED is essential.
- EMS personnel must pay adequate attention to the primary survey and address the ABCs as necessary. Beyond those steps, vascular access, supplemental oxygen, and ECG rhythm strip monitoring are all-important but should not delay rapid transport to the ED for definitive care.
Emergency Department Care
During the initial assessment, once real-time cardiac monitoring or 12-lead ECG has established VT as the diagnosis, one should determine if the VT is stable or unstable as the ABCs are reassessed in the primary survey.
- Pulseless VT
- Pulseless VT, in contrast to other unstable VT rhythms, is treated with immediate defibrillation. High-energy, unsynchronized energy should be used. The initial shock dose on a biphasic defibrillator is 150-200 J followed by an equal or higher shock dosage for subsequent shocks. If a monophasic defibrillator is used, the initial and subsequent shock dosage should be 360 J. Shock administration should be followed by immediate chest compressions, airway management with supplemental oxygen, and vascular access with administration of vasopressor agents. In cases of shock-resistant pulseless VT, one can consider use of antidysrhythmic medications.
- Vasopressors can include epinephrine at 1 mg IV given every 3-5 minutes, or in lieu of epinephrine, vasopressin 40 U IV as a one-time dose.
- Advanced cardiac life support (ACLS) drug therapy guidelines recommend the use of intravenous amiodarone or lidocaine as the first-line adjunctive antidysrhythmic treatment of shock-resistant pulseless VT.
- Unstable VT
- Unstable VT is characterized by signs/symptoms of insufficient oxygen delivery to vital organs such as chest pain, dyspnea, hypotension, or altered level of consciousness, which indicate that rate and stroke volume are not providing adequate cardiac output.
- In this situation, the dysrhythmia should be immediately treated with synchronized cardioversion, usually at a starting energy dose of 100 J.
- In contrast, unstable polymorphic VT is treated with immediate defibrillation. The defibrillator may have difficulty recognizing the varying QRS complexes and therefore synchronizing the delivery of energy may not occur.
- Antidysrhythmic therapy as outlined above for shock-resistant pulseless VT may be administered to those with shock-resistant unstable VT.
- Stable VT
- Stable VT usually denotes monomorphic VT with adequate vital end-organ perfusion. These patients do not experience signs/symptoms of hemodynamic compromise.
- Although DC cardioversion is probably the most effective treatment of stable VT, it causes obvious discomfort and requires systemic analgesia/anxiolysis. Alternatively, stable VT can be treated with intravenous amiodarone, procainamide, or sotalol. Some evidence indicates that procainamide may be more effective than amiodarone in the treatment of stable VT.4,5 In situations involving torsade de pointes, magnesium sulfate may be effective if there exists a long QT interval at baseline.
- Consider synchronized cardioversion early if medical therapy fails to stabilize the rhythm. Initial monophasic shock energy should be 100 J, followed by higher shock energies if the response is inadequate.
Consultations
Following initial treatment and stabilization, patients with ventricular tachycardia (VT) generally should be referred to a cardiologist for admission to a monitored bed, further studies such as electrophysiologic study (EPS), and definitive management such as automatic internal cardioverter/defibrillator (AICD) placement.
Only rarely will a patient with stable, recurrent episodes of VT have his or her dysrhythmia treated in the ED and be discharged with appropriate follow-up care. This decision must be made in consultation with a cardiologist.
Medication
The mainstays of treatment for clinically stable VT are the various antidysrhythmic drugs.
Note that use of verapamil can precipitate ventricular fibrillation (VF) in patients whose VT has been misidentified as PSVT with aberrancy. For that reason, avoid verapamil (and all calcium channel blockers) in any patient with wide-complex tachycardia of uncertain etiology.6
Antidysrhythmics
These agents alter the electrophysiologic mechanisms responsible for arrhythmia.
Amiodarone (Cordarone)
Newest of the antidysrhythmics used in treating VT, generally is considered a class III antidysrhythmic, yet it has pharmacologic characteristics of all 4 classes.
Now is considered a class I intervention by the American College of Cardiology's practice guidelines for managing acute MI. Drug of choice in treatment of refractory, hemodynamically unstable VT. Prehospital studies suggest amiodarone is safe for use in prehospital setting, and its adoption in the new ACLS guidelines will increasingly lead EMS authorities to adopt it as their first-line antidysrhythmic. This change already is well underway in Europe.
Adult
150 mg IV, infused over 10 min, then 1 mg/min constant infusion for 6 h, then maintenance infusion at 0.5 mg/min
Pediatric
Not established
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; ritonavir, sparfloxacin, and disopyramide increase cardiotoxicity; coadministration with calcium channel blockers may cause additive effects, further decreasing myocardial contractility; cimetidine may increase amiodarone levels
Documented hypersensitivity; systemic lupus erythematosus, digitalis-induced arrhythmias, complete heart block, or second- or third-degree heart block if a pacemaker is not in place; torsade de pointes
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Hypotension (most common adverse effect), bradycardia, and AV block may occur; elevation of serum hepatic enzyme levels is common in VT; monitor patients carefully
Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach)
Class IB antidysrhythmics stabilize cell membranes, blunts phase 0 of the action potential, and shortens repolarization. Their net effect is to decrease firing of ectopic foci to allow a normal rhythm to reassert itself.
However, amiodarone appears to be replacing lidocaine as the drug of choice.
Adult
1-1.5 mg/kg IV push, followed by 0.5-0.75 mg/kg IV push, not to exceed 3 mg/kg
Start continuous 1-4 mg/min infusion after arrhythmia is suppressed
Pediatric
1 mg/kg IV/ET/IO loading dose; may repeat twice at 10- 15-min intervals prn
Following loading dose, start continuous IV infusion 20-50 mcg/kg/min
Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Documented hypersensitivity; Adams-Stokes syndrome and Wolff-Parkinson-White syndrome; severe sinoatrial, AV, or intraventricular block, if artificial pacemaker is not in place
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly patients; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities
Procainamide (Procanbid, Pronestyl)
Class IA antidysrhythmic, slows down phase 4 (diastolic) depolarization, decreases automaticity, and slows intraventricular conduction. May be considered first-line medical therapy for treatment of stable VT.
Second-line therapy used for VT refractory to defibrillation, epinephrine, and lidocaine, it increases refractory period of atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Adult
20-30 mg/min IV at continued infusion rates until either arrhythmia is suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or a maximum dose of 17 mg/kg is administered
Once arrhythmia is suppressed, may infuse at a continuous rate of 1-4 mg/min
Pediatric
Not established; the following doses have been suggested:
15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
3-6 mg/kg/dose IV infused over 5 min
Maintenance: 20-80 mcg/kg/min administered as continuous infusion; not to exceed 100 mg/dose or 2 g/d
Can expect increased levels of procainamide metabolite, NAPA, in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; may increase effect of skeletal muscle relaxants, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may significantly increase its blood levels; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity
Documented hypersensitivity; complete heart block or second- or third-degree heart block, if pacemaker is not in place; torsade de pointes; documented hypersensitivity; systemic lupus erythematosus
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor patients for hypotension; plasma concentration of procainamide and its active metabolite, NAPA, may be increased in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; use caution in patients with complete AV block, digitalis intoxication, organic heart disease, renal disease, or hepatic insufficiency
Sotalol (Betapace)
Class III antidysrhythmic agent, which blocks potassium channels, prolongs action potential duration (APD) and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.
Adult
0.2 mg/kg to 1.5 mg/kg IV over 5 min
80 mg PO bid and increase dose gradually q2-3d to 240-320 mg/d
Pediatric
200 mg/m2/24 h up to 80 mg/dose divided bid maximum
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity of sotalol may increase when administered concurrently with sparfloxacin, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of sotalol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Documented hypersensitivity; sinus bradycardia, second- and third-degree AV block
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor patient closely; caution in hypokalemia, peripheral vascular disease, hypomagnesemia, congestive heart failure, and congestive heart failure
Electrolytes
These agents are considered therapeutic alternatives for refractory VT. Patients with persistent or recurrent VT following antidysrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmia. Some electrolyte abnormalities associated with VF include hyperkalemia, hypokalemia, and hypomagnesemia. Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VT secondary to other medications. Magnesium sulfate acts as an antidysrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VT caused by hyperkalemia.
Magnesium sulfate (Magnesium)
DOC for torsade de pointes, it also may be useful to treat conventional VT, especially where hypomagnesemia is confirmed.
When treating with magnesium sulfate, monitor for hypermagnesemia since an overdose can cause cardiorespiratory collapse and paralysis.
Adult
1-2 g diluted in 100 mL of D5W over 1-2 min for refractory VT and known or suspected hypomagnesemia (Mg+2 <1.4 mEq/L); not to exceed 30-40 g/d; maximum rate of infusion for maintenance not to exceed 1-2 g/h
Pediatric
Not established:
Suggested dose: 25-50 mg/kg q4-6h for 3-4 doses; maximum single dose of 2 g also may be administered and repeated if hypomagnesemia persists
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and other agents causing neuromuscular antagonism; may increase CNS depressant effects
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Monitor for hypotension and follow DTRs; if depressed DTRs observed, modify or halt dosage; may lead to heart block in digitalized patients; renal impairment may lead to accumulation and toxicity
Sodium bicarbonate (Neut)
Used only when patient is diagnosed with bicarbonate-responsive acidosis with pH ≤7.0, hyperkalemia, tricyclic antidepressant or phenobarbital overdose. Routine use is not recommended.
Adult
Initial dose: 1 mEq/kg
Maintenance dose: 0.5 mEq/kg q10min or as indicated by ABGs
Pediatric
0.5-1 mEq/kg repeated q10min or as indicated by ABGs; rate of infusion not to exceed 10 mEq/min
Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; conversely, use increases levels of amphetamines, anorexiants, mecamylamine, ephedrine, pseudoephedrine, flecainide, quinidine, and quinine
Patients with alkalosis, hypernatremia, hypocalcemia, severe pulmonary edema, and unknown abdominal pain
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Only to be used to treat documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances such as patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, should avoid extravasation since can cause tissue necrosis
Calcium chloride
Useful to treat hyperkalemia, hypocalcemia, or calcium channel blocker toxicity, it moderates nerve and muscle performance by regulating action potential excitation threshold.
Adult
Known or suspected hyperkalemia (K+ >6 mEq/L): 2-4 mg/kg (10% solution) IV
Pediatric
0.2 mL/kg of IV (10% solution)
Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate
VF not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure
Vasopressor
These agents augment both coronary and cerebral blood flow present during low flow state associated with CPR.
Epinephrine (Adrenalin, Sus-Phrine, EpiPen)
Considered the single most useful drug in cardiac arrest, although it has never been shown to affect mortality.
Adult
1 mg (10 mL of 1:10,000 solution) IV push q3-5min
ET administration requires 2-2.5 times IV dose
Pediatric
0.01 mg/kg or 0.3 mg/m2 SC (repeat q4h or more frequently prn)
Increases toxicity of beta- and alpha-blocking agents and of halogenated inhalational anesthetics
Documented hypersensitivity; cardiac arrhythmias or angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; do not use during labor (may delay second stage of labor)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in elderly patients, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
Vasopressin
May improve vital organ blood flow, cerebral oxygen delivery, ability to be resuscitated, and neurologic recovery.
Adult
40 U IV single dose
Pediatric
Not established
Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, and carbamazepine may potentiate effects
Documented hypersensitivity; coronary artery disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia
More on Ventricular Tachycardia |
| Overview: Ventricular Tachycardia |
| Differential Diagnoses & Workup: Ventricular Tachycardia |
 Treatment & Medication: Ventricular Tachycardia |
| Follow-up: Ventricular Tachycardia |
| Multimedia: Ventricular Tachycardia |
| References |
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References
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[Guideline] Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. Sep 5 2006;114(10):e385-484. [Medline].
Further Reading
Keywords
ventricular tachycardia, VT, tachydysrhythmia, ventricular ectopic focus, fusion beats, atrioventricular dissociation, AV dissociation, wide QRS complexes, ventricular fibrillation, VF, paroxysmal supraventricular tachycardia, PSVT, torsade de pointes, accelerated idioventricular rhythm, congestive heart failure, pulmonary edema, jugular venous distention,hypotension, CAD, structural heart disease, hypokalemia, hypocalcemia, hypomagnesia, methamphetamine, cocaine, genetic arrhythmia syndrome, cardiac channelopathy
