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Ventricular Tachycardia Last Updated: March 20, 2006 |
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| Synonyms and related keywords: 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
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AUTHOR INFORMATION
| Section 1 of 10   |
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| Author: William Ernoehazy, Jr, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Ed Fraser Memorial Hospital |
| William Ernoehazy, Jr, MD, FACEP, is a member of the following medical societies:
American College of Emergency Physicians |
| Editor(s): Steven A Conrad, MD, PhD, Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine;
Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School;
John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School;
and Charles V Pollack, Jr, MD, MA, FACEP, Chairman, Professor of Emergency Medicine, Department of Emergency Medicine, Pennsylvania Hospital, University of Pennsylvania |
Disclosure
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INTRODUCTION
| Section 2 of 10   |
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Background: Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than 120 beats per minute and wide QRS complexes. VT may be monomorphic (originating from a single focus with identical QRS complexes) or polymorphic (may appear as an irregular rhythm, with varying QRS complexes). Nonsustained VT is defined as a run of tachycardia of less than 30 seconds duration; longer runs are considered sustained VT.
No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT, including the following:
- Rate greater than 100 beats per minute (usually 150-200)
- Wide QRS complexes (>120 ms)
- Presence of atrioventricular (AV) dissociation
- Fusion beats
Ventricular tachycardia may develop without hemodynamic deterioration. Nevertheless, it often causes severe hemodynamic compromise and may deteriorate rapidly into ventricular fibrillation (VF). This tachydysrhythmia must be addressed swiftly to avoid morbidity or mortality.
Pathophysiology: VT usually is a consequence of structural heart disease, with breakdown of normal conduction patterns, increased automaticity (which tends to favor ectopic foci), and activation of re-entrant pathways in the ventricular conduction system. Electrolyte disturbances and sympathomimetics may increase the likelihood of VT in the susceptible heart. AV dissociation usually is present. Retrograde ventriculoatrial conduction may occur, which can generate an ECG complex similar to paroxysmal supraventricular tachycardia (PSVT) with aberrant conduction.
A distinctive variant of VT is torsade de pointes, with its unusual shifting-axis QRS complexes that appear (on ECG) as if the heart is rotating upon an axis. It typically occurs from drugs or conditions that prolong the QT interval (eg, type 1A antiarrhythmics, hypomagnesemia, droperidol). Arrhythmia may occur either in the presence of or in the absence of myocardial ischemia or infarction.
A second variant of VT is accelerated idioventricular rhythm. Sometimes termed slow ventricular tachycardia, this arrhythmia presents with a rate of 60-100 beats per minute. It typically occurs with underlying heart disease (ischemic or structural), is transient, and only rarely is associated with hemodynamic compromise or collapse. Treatment usually is not required unless hemodynamic impairment develops.
Recently, a catecholaminergic polymorphic VT has been described. The syndrome is characterized by exercise- or stress-induced ventricular tachyarrhythmias and is most commonly found in pediatric cases. The syndrome is apparently congenital, with both autosomal dominant and recessive patterns. Either syncope or sudden death can occur. Prophylactic beta-blocker therapy does not appear to have substantial long-term efficacy, and these patients are increasingly being managed by implantation of implantable cardioverter defibrillators (ICDs). Frequency:
- In the US: VT is one of the most frequently observed dysrhythmias.
- Internationally: VT and coronary disease are common throughout most of the developed world. In developing countries, VT and other heart diseases are relatively less common.
Mortality/Morbidity:
- Morbidity and mortality in VT arises principally from spontaneous degeneration into the more malignant VF.
- Even without such degeneration, VT can also produce congestive heart failure and hemodynamic compromise, with subsequent morbidity and mortality.
Sex:
- Currently, most patients presenting with VT are men.
- As coronary artery disease (CAD) becomes more common in women, it seems certain that the incidence of VT in women will increase.
Age:
- VT is unusual among pediatric patients. Tachydysrhythmias in this population generally are PSVT.
- VT incidence rates peak in the middle decades of life, following the incidence of structural heart disease.
History: Most patients present to the ED with symptoms of either ischemic heart disease or hemodynamic compromise. Symptoms may include the following: Physical: Findings generally reflect the degree of hemodynamic instability. - Symptoms of congestive heart failure (CHF)
- Rales from pulmonary edema
- Jugular venous distention
Causes: As noted above, VT generally is a symptom of CAD or structural heart disease. - VT can be triggered by electrolyte deficiencies (eg, hypokalemia, hypocalcemia, hypomagnesia).
- Use of sympathomimetic agents (from relatively benign caffeine to more potent agents such as methamphetamine or cocaine) may stimulate VT in vulnerable hearts.
- Drugs that prolong the QT complex (eg, type 1A antiarrhythmics, droperidol and related antiemetics) may predispose to VT, particularly torsade de pointes.
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DIFFERENTIALS
| Section 4 of 10 |
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Atrial Fibrillation
Atrial Flutter
Automatic External Defibrillation
Congestive Heart Failure and Pulmonary Edema
Hypocalcemia
Hypokalemia
Hypomagnesemia
Myocardial Infarction
Pacemaker and Automatic Internal Cardiac
Defibrillator
Premature Ventricular Contraction
Torsade de Pointes
Ventricular Fibrillation
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Lab Studies:
- When the patient presents with symptoms of frank hemodynamic compromise, defer laboratory tests until electrical cardioversion is performed and the patient stabilizes.
- Assess electrolytes of all patients with VT, including serum calcium, magnesium, and phosphate levels. Ionized calcium levels are preferred over total serum calcium. Hypokalemia, hypomagnesemia, and hypocalcemia may predispose patients to either conventional VT or torsade de pointes.
- Obtain, when appropriate, levels of therapeutic drugs (eg, digoxin).
- Evaluate for myocardial ischemia or infarction with serum cardiac troponin I, T levels, or other cardiac markers.
Imaging Studies:
- Chest radiography is indicated if symptoms suggest the possibility of congestive heart failure (CHF) or other cardiopulmonary pathology as contributing factors.
Other Tests:
- ECG is the diagnostic tool of choice for confirming the presence of VT. Simultaneous 3-channel recordings and 12-lead tracings are more helpful than rhythm strips to analyze such dysrhythmias.
- Complexes of atypical morphology often are difficult to interpret. Such tachycardias could be PSVT with aberrant conduction. If patient is unstable, or differentiation between VT and SVT is uncertain, treat rhythm as VT. Recognize that some therapies for PSVT (eg, verapamil) can be lethal when employed in VT.
- ECG criteria that support VT over SVT include AV dissociation, fusion beats at the initiation of the arrhythmia, QRS duration over 140 ms, and RS pattern in V1. Patients with underlying structural or ischemic heart disease are more likely to have VT than SVT.
- ECG criteria that support SVT over VT include a right bundle branch block (RBBB) pattern, varying bundle branch block, an R or qR pattern in V1, or an ectopic P wave preceding the dysrhythmia.
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TREATMENT
| Section 6 of 10 |
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Prehospital Care: EMTs and paramedics may be called upon to provide cardioversion 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 determine if the VT is stable or unstable, even as the ABCs are reassessed in the secondary survey. - Unstable VT is characterized by symptoms of insufficient oxygen delivery such as chest pain, dyspnea, hypotension, or altered level of consciousness, indicating that rate and stroke volume are not providing adequate cardiac output.
- Unstable VT is treated as ventricular fibrillation, with immediate synchronized cardioversion, followed by expeditious airway management (if needed), supplemental oxygenation, vascular access, and antiarrhythmic therapy. Most patients respond to low levels of energy (eg, 1-50 watt-seconds of electrical energy). Failure to synchronize the shock with the patient's QRS may precipitate ventricular fibrillation.
- Advanced cardiac life support (ACLS) drug therapy guidelines now recommend the use of amiodarone as the first line agent in the adjunctive treatment of hemodynamically unstable VT, followed by bretylium and procainamide. Replenishment of magnesium and/or other electrolytes may be a valuable adjunct to antiarrhythmic therapies.
- Stable VT patients do not experience symptoms of hemodynamic decompensation.
- Unlike other dysrhythmias, VT tends to deteriorate into unstable states and more malignant dysrhythmias; consequently, treat even stable VT with amiodarone or lidocaine, followed by procainamide in the refractory patient.
- Consider synchronized cardioversion early if medical therapy fails to stabilize the rhythm, even in stable patients.
Consultations: Following initial treatment and stabilization, VT patients generally should be referred to an internist or cardiologist for admission to a monitored bed, further studies, and definitive management.
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.
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MEDICATION
| Section 7 of 10 |
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The mainstays of treatment for clinically stable VT are the varied antiarrhythmic drugs.
Note that use of verapamil can precipitate VF in patients whose VT has been misidentified as PSVT with aberrancy. For that reason, avoid verapamil in any patient with wide-complex tachycardia of uncertain etiology.
Drug Category: Antiarrhythmics -- These agents alter the electrophysiologic mechanisms responsible for arrhythmia. Drug Name
| Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach) -- Class IB antiarrhythmics 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.
Lidocaine is still the generally accepted DOC for initial therapy of stable VT in the United States. Amiodarone appears to be replacing lidocaine as the DOC in Europe and that may occur in the United States in the future.| Adult Dose | 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 Dose | 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| Contraindications | Documented hypersensitivity; Adams-Stokes syndrome and Wolf-Parkinson-White syndrome; severe sinoatrial, AV, or intraventricular block, if artificial pacemaker is not in place |
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| Interactions | 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 |
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| Pregnancy |
B - Usually safe but benefits must outweigh the risks.
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| 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 |
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| Drug Name
| Procainamide (Procanbid, Pronestyl) -- Class IA antiarrhythmic, slows down phase 4 (diastolic) depolarization, decreases automaticity, and slows intraventricular conduction.
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 Dose | 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 Dose | 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| Contraindications | 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 |
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| Interactions | 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 |
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| Pregnancy |
C - Safety for use during pregnancy has not been established.
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| 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 |
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Drug Name
| Bretylium (Bretylol) -- Class III antiarrhythmic agent for treatment of PVCs. Has catecholamine-releasing properties and adverse effects and should not be used as initial treatment.
Limit use to PVCs refractory to class I anti-arrhythmics. Increases fibrillation threshold and causes refractory period by decreasing potassium conductance.| Adult Dose | 5 mg/kg (undiluted) IV over 1 min
10 mg/kg (undiluted) over 1 min for persistent arrhythmia
Repeat at 15-30 min intervals prn not to exceed 30-35 mg/kg/d
Maintenance dose: 1-2 mg/min| Pediatric Dose | Not established
Suggested dose:
Acute VF: 5 mg/kg (undiluted) IV over 1 min; if arrhythmia persists, administer 10 mg/kg over 1 min, repeat prn q15min to maximum of 30 mg/kg
Maintenance dose: 5-10 mg/kg q6h| Contraindications | 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 |
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| Interactions | Pressor catecholamines and digitalis may increase toxicity; coadministration with ofloxacin may increase risk of cardiotoxicity |
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| Pregnancy |
C - Safety for use during pregnancy has not been established.
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| Precautions | Hypotension has been associated with use of this drug, especially in patients with a fixed cardiac output (eg, aortic stenosis); use caution in patients with renal insufficiency, severe pulmonary hypertension, and aortic stenosis; has prolonged half-life in older persons; when renal clearance is 10-50 mL/min, administer 25-50% of dose; rapid IV injection may result in transient hypertension, nausea, and vomiting; limit injection to 5 mL (undiluted) at each injection site |
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Drug Category: Electrolytes -- These agents are considered therapeutic alternatives for refractory VT. Patients with persistent or recurrent VT following antiarrhythmic 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 antiarrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VT caused by hyperkalemia.Drug Name
| 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 Dose | 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 |
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| Pediatric Dose | 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| Contraindications | Documented hypersensitivity; heart block, Addison disease, myocardial damage, or severe hepatitis |
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| Interactions | 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 |
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| Pregnancy |
A - Safe in pregnancy
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| 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 |
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Drug Name
| Sodium bicarbonate (Neut) -- Used only when patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant or phenobarbital overdose. Routine use is not recommended. |
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| Adult Dose | Initial dose: 1 mEq/kg
Maintenance dose: 0.5 mEq/kg q10min or as indicated by ABGs| Pediatric Dose | 0.5-1 mEq/kg repeated q10min or as indicated by ABGs; rate of infusion not to exceed 10 mEq/min |
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| Contraindications | Patients with alkalosis, hypernatremia, hypocalcemia, severe pulmonary edema, and unknown abdominal pain |
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| Interactions | 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 |
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| Pregnancy |
C - Safety for use during pregnancy has not been established.
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| 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 |
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Drug Name
| Calcium chloride -- Useful to treat hyperkalemia, hypocalcemia, or calcium channel blocker toxicity, it moderates nerve and muscle performance by regulating action potential excitation threshold. |
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| Adult Dose | Known or suspected hyperkalemia (K+ >6 mEq/L): 2-4 mg/kg (10% solution) IV |
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| Pediatric Dose | 0.2 mL/kg of IV (10% solution) |
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| Contraindications | VF not associated with hyperkalemia; digitalis toxicity, hypercalcemia, renal insufficiency, cardiac disease |
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| Interactions | Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate |
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| Pregnancy |
C - Safety for use during pregnancy has not been established.
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| Precautions | Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure |
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Drug Category: Vasopressor -- Augment both coronary and cerebral blood flow present during low flow state associated with CPR.Drug Name
| Epinephrine (Adrenalin, Sus-Phrine, EpiPen) -- Considered the single most useful drug in cardiac arrest. |
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| Adult Dose | 1 mg (10 mL of 1:10,000 solution) IV push q3-5min
ET administration requires 2-2.5 times IV dose| Pediatric Dose | 0.01 mg/kg or 0.3 mg/m2 SC (repeat q4h or more frequently prn) |
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| Contraindications | 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) |
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| Interactions | Increases toxicity of beta- and alpha-blocking agents and of halogenated inhalational anesthetics |
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| Pregnancy |
C - Safety for use during pregnancy has not been established.
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| 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 |
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Drug Name
| Amiodarone (Cordarone) -- Newest of the antiarrhythmics used in treating VT, generally is considered a class III antiarrhythmic, 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. DOC 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 antiarrhythmic. This change already is well underway in Europe.| Adult Dose | 150 mg IV, infused over 10 min, then 1 mg/min constant infusion for 6 h, then maintenance infusion at 0.5 mg/min |
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| Pediatric Dose | Not established |
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| Contraindications | 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 |
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| Interactions | 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 |
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| Pregnancy |
D - Unsafe in pregnancy
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| Precautions | Hypotension (most common adverse effect), bradycardia, and AV block may occur; elevation of serum hepatic enzymes is common in VT; monitor patients carefully |
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FOLLOW-UP
| Section 8 of 10 |
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Further Inpatient Care:
- Admit patients with VT to monitored settings as a precaution against recurrent tachyarrhythmia, to facilitate workup for ischemic heart disease, and to allow timely evaluation for definitive device therapy.
- In the past, long-term antiarrhythmic medical therapy was used for suppression of VT. However, several subsets of VT patients do poorly under such an approach, with frequent recurrence of VT. As a result, cardiologists are increasingly making use of interventional therapy, with devices and procedures designed to abort VT or to remove the arrhythmogenic foci in the heart. Such interventions include the following:
- Prophylactic implantation of ICDs
- Catheter-directed radiofrequency ablation of aberrant conduction pathways
- In a recently reported case in the United Kingdom, a patient whose VT was refractory even to ICD prophylaxis underwent bilateral thoracoscopic cervical sympathectomy, which successfully stopped the recurrent VT.
Complications:
- Patients with VT may suffer CHF and its attendant morbidity as a result of hemodynamic compromise.
- VT may deteriorate to VF.
- Consider all patients with VT to have active myocardial ischemia, which should be sought and treated aggressively.
Prognosis:
- If treated rapidly, VT generally has a favorable short-term outcome.
- Long-term prognosis depends upon the underlying cardiac disease.
Patient Education:
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MISCELLANEOUS
| Section 9 of 10 |
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Medical/Legal Pitfalls:
- Failure to promptly treat hemodynamically compromised patients in a misguided effort to secure a definite diagnosis first
- Use of verapamil in a wide-complex tachycardia
- Failure to treat underlying diseases or conditions that may have precipitated the tachyarrhythmia
- Failure to aggressively assess patient for myocardial ischemia after initial stabilization
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BIBLIOGRAPHY
| Section 10 of 10 |
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American Heart Association: Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 1: Introduction to ACLS 2000: overview of recommended changes in ACLS from the guidelines 2000 conference. Circulation 2000 Aug 22; 102(8 Suppl): I86-9[Medline].
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Brennan TD, Haas GJ: The role of prophylactic implantable cardioverter defibrillators in heart failure: recent trials usher in a new era of device therapy. Curr Heart Fail Rep 2005; 2(1): 40-5[Medline].
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Francis J, Sankar V, Nair VK, et al: Catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm 2005; 2(5): 550-4[Medline].
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Hoffman JR, Votey SR: Tachyarrhythmias. In: The Clinical Practice of Emergency Medicine. 2nd ed. 1996:605.
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Hunter R: Ventricular tachycardia following naloxone administration in an illicit drug misuse. J Clin Forensic Med 2005; 12(4): 218-9[Medline].
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Kliegel A, Eisenburger P, Sterz F, et al: Survivors of ventricular tachyarrhythmias due to a transient or reversible disorder have a high recurrence rate of lethal cardiac events. Resuscitation 2002; 54(3): 237-43[Medline].
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Kudenchuk PJ, Cobb LA, Copass MK, et al: Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med 1999 Sep 16; 341(12): 871-8[Medline].
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Stevenson WG: Catheter ablation of monomorphic ventricular tachycardia. Curr Opin Cardiol 2005; 20(1): 42-7[Medline].
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Stewart RB, Bardy GH, Greene H: Wide complex tachycardia: Misdiagnosis and outcome after emergent therapy. Annals of Internal Medicine 1986; 104: 766[Medline].
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Testa A, Ojetti V, Migneco A, et al: Use of amiodarone in emergency. Eur Rev Med Pharmacol Sci 2005; 9(3): 183-90[Medline].
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Turley AJ, Thambyrajah J, Harcombe AA: Bilateral thoracoscopic cervical sympathectomy for the treatment of recurrent polymorphic ventricular tachycardia. Heart 2005; 91(1): 15-7[Medline].
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Walter PF: Cardiac arrhythmias: Their identification and management. In: Emory University Comprehensive Board Review In Internal Medicine. 1997:1.
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