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Sustained Ventricular Tachycardia (VT)
Type 1. Sustained Ventricular Tachycardia

It may arise in the conducting system below the bundle of His or in the ventricular myocardium or both (figures 104b, 104c), lasting 30s or more at rate of 100 beats/min.or more. It is generally life threatening unless there is no structural heart disease (see: fig.7, fig.8, fig.9a, fig.9b, fig.10).

With prior myocardial infarction (MI, heart attack) and ventricular aneurysm (an abnormal dilatation of a portion of the myocardium caused by a thinning of the heart muscle due to a MI, (see fig.10, fig.51a) a sustained monomorphic VT may be hemodynamically well tolerated. This type can be treated with intravenous (IV) drugs.

But with transient myocardial ischemia, the VT may be polymorphic or sinusoidal, and hemodynamically unstable with a higher risk of VF than the momomorphic type. With unstable blood pressure (BP) in acute myocardial infarction, immediate electrical cardioversion is indicated (fig. 11, fig.12).

human heart

Proarrhythmia due to prior drugs for VT should be suspected if the VT morphology is different from a prior VT form, especially if prior drugs or changes have been prescribed, with a prolonged QT (see figure 94) interval, or if the new VT has a polymorphic or torsades de pointe configuration (see fig.13).

If there are repeated recurrences after cardioversion, the possibility of proarrhythmia should be entertained and temporary pacing ( fig.84b, fig.85, fig.86, fig.87, fig.88, fig.89, fig.90, fig.91, fig.92 ) may be useful. Other causes of repeated recurrence include ischemia, heart failure, autonomic surges, or electrolyte disturbances.

Acute Management of Sustained Monomorphic VT

This form of V.T. (see figure 9b) may occur in acute or chronic ischemic heart disease, idiopathic dilated, or hypertrophic cardiomyopathy (see fig.61, fig.62) and less frequently in inflammatory or infiltration diseases, or a primary electrical disturbance .

In acute myocardial infarction, sustained VT occurs most commonly within 24 hours of the onset. It carries a risk of degenerating into ventricular fibrillation (VF ) (see figure 9b ) and must be treated aggressively. A lidocaine (heart medication) intravenous ( IV) bolus followed by a continuous infusion may be tried. If the VT does not revert immediately or if the patient is hypotensive (low blood pressure) immediate DC electrical cardioversion is required. Following the cardioversion, the IV infusion of lidocane is continued to prevent recurrences.

If the VT recurs despite lidocane, boluses of procainamide (another heart drug) are infused. If breakthroughs continue, other heart drugs like bretylium tosylate or intravenous amiodarone are indicated. The therapy may be stopped after 48-72 hours, since the risk of recurrence is small at that point.

Type2: Sustained VT in convalescent phase of acute myocardial infarction

A second category of sustained VT (see fig.9b, fig.10, fig.51a ) related to acute myocardial infarction occurs in the convalescent period, and is most common in patients with large anterior left ventricular wall infarctions. Management is similar to the above therapy. This type has a high death rate.

Long Term Management of VT in Chronic Ischemic Heart Disease

Approaches include the following:
1) Antiarrhythmic therapy guided by invasive electrophysiologic testing, exercise EKG testing, or ambulatory EKG monitoring,
2) Surgical procedures to excise or cryoablate reentrant pathways or automatic foci,
3) catheter ablation (see fig.11),
4) ICD (implantable cardioverter defibrillator) (see fig.12, fig.61, fig.62)

Type 3: Nonsustained VT

A) Repetitive Monomorphic VT

This is an uncommon form of repetitive, nonsustained VT, but it may become sustained. It is more common in women and is usually benign. The QRS in the EKG suggest a left bundle branch block (LBBB) pattern with a widened QRS (see fig.8). Treatment is indicated when there is structural disease or severe symptoms. Beta adrenoceptors and calcium (Ca 2+) entry blocking agents are effective in some patients. Catheter ablation is an option if symptomatic.

B) Nonsustained Ventricular Tachycardia (V.T.)

It represents nonsustained runs of VT (salvos of 3 to 5 consecutive impulses or nonsustained VT of 6 impulses to 30s) (see fig.7) which are considered indicators of high risk for potentially fatal arrhythmias (sustained VT or ventricular fibrillation, VF) in most clinical settings. But patients with no organic disease may not be at increased risk.

Even without increased risk, severe symptoms like transient syncope or near syncope require therapy. Some of the highest risk patients have cardiomyopathy (see fig.40b, fig.40c, fig.40d, fig.40f, fig.41, fig.43a, fig.43b) and advanced coronary heart disease (fig.51a, fig.53, fig.54, fig.55, fig.56a). Implantable cardioverder defibrillator (ICD) therapy (see fig.11, fig.12) has shown a greater decreased mortality than the best conventional therapy.


1) Brugada syndrome is an inherited genetic disorder affecting the repolarization function of the sodium channel associated with the presence of an RSR' in lead V1 with coving of the ST segment in leads VI-V3 and a normal QT interval. This syndrome is clinically characterized by ventricular tachyarrhythmias and sudden death. The symptomatic patient requires treatment with an implantable cardioverter defibrillator (ICD). A slightly different abnormality of the same gene is responsible for one of the long QTsyndromes (LQT3).

2) The "long QT syndrome" (LQTS) is associated with a prolonged QT interval during sinus rhythm signifying an inherited or acquired repolarization disorder. The inherited form of LQTS has as many as six different responsible genotypes with several phenotypes, and can predispose to a special kind of VT called "torsade de pointes". This VT has a characteristic polymorphic EKG appearance of the QRS, which appears to be" twisting about on its points" (see fig.13). A fairly specific electrophysiologic mechanism, "early afterdepolarizations", caused by a malfunctioning sodium or potassium channel, appears to be responsible for torsade de pointes, which can be treated by drugs or an ICD. Some youngsters present with seizures due to hypotension from the torsade de pointes. Some patients predisposed to drug-induced, acquired LQTS may actually have an inherited form that makes them vulnerable to the QT prolonging, proarrhythmic effects of many drugs.

3) Several types of cardiomyopathies can cause ventricular tachyarrhythmias and may show uniquely appearing EKGs during sinus rhythm. As an example, arrhymogenic right ventricular cardiomyopathy can be characterized during sinus rhythm by a epsilon wave (a notch on the terminal portion of the QRS in lead V1 due to delayed right ventricular activation) and T wave negativity in the anterior precordial leads.This disorder, due to fatty replacement of right and, less commonly, left ventricular myocardium, can result in lethal ventricular arrhythmias. Patients with hypertrophic cardiomyopahy (see fig.39a, fig.39b, fig.40a, fig.40b) can exhibit large voltages consistent with ventricular hypertrophy and deep Q waves often confused with myocardial infarction, whereas patients who have muscular dystrophy can have tall R waves in the anterior precordial leads suggestive of a true posterior myocardial infarction. Patients with dilated cardiomyopathy can have VT due to bundle branch reentry that has a LBBB contour and can be treated with radiofrequency catheter ablation.

4) Two types of VTs that occur in patients with apparently structurally normal hearts include those coming from the right ventricular outflow tract that have a LBBB-inferior axis morphology, and those coming from the left ventricular septum that have a RBBB and left axis deviation contour. Both are relatively easily eliminated with radiofrequency ablation.

Reference:Zipes.D.P.,Clinical Application of the Eleectrocardiogram,JACC Vol.36,No.6,2000:1746-8



The first use of PHT(Phenytoin) in cardiac disorders was reported by Leonard in 1958. Since it was the pioneer paper in this field, it will be summarized in some detail. It brings into focus three important points which develop throughout the literature:

1) PHT is an effective antiarrhythmic, prompt in its action;

2) PHT has a high margin of safety;

3) In the acute stage, substantial amounts of PHT may be required, adjusted to the severity of the condition.

Leonard, Archives of Internal Medicine (1958), demonstrated the beneficial effect of PHT in controlling ventricular hyperirritability complicating myocardial infarction in a patient. The patient was gravely ill with cardiographic findings of typical ventricular tachycardia. In spite of the previous history of complete heart block, it was felt that intravenous procainamide, if carefully controlled, was the treatment of choice. The patient was receiving Arterenol to maintain his blood pressure at 110/70. Procainamide was given intravenously. During a period of approximately two hours, 2300 mg of procainamide was given, in spite of several episodes of marked hypotension, but finally discontinued because of disturbing widening of the QRS complex without reversion to a normal sinus mechanism. The patient's condition remained critical, and it was considered advisable to investigate the therapeutic potential of intravenous PHT. PHT was administered slowly intravenously in a dose of 250 mg. A cardiogram recorded approximately two minutes later revealed a normal sinus mechanism coupled with premature auricular contractions. In twenty minutes ventricular tachycardia had recurred. An immediate additional dose of 250 mg of PHT was given and within moments a normal sinus mechanism appeared. Four hours later ventricular tachycardia returned and was again successfully reverted to a normal sinus rhythm with 250 mg of intravenous PHT. Because the duration of effectiveness of PHT was unknown, a constant, slow intravenous infusion of 250 mg of PHT was started. The normal sinus mechanism was maintained in this fashion for successive periods of six and four hours. At these intervals ventricular tachycardia returned, but was promptly reverted with additional intravenous doses of 250 mg of PHT. At this time it was considered advisable to supplement the intravenous therapy with 3 grains of PHT and 500 mg of procainamide every four hours orally. Eighteen hours after its initiation the intravenous PHT was discontinued. An electrocardiogram at this time showed posterior myocardial infarction with a normal sinus mechanism. On the following day procainamide was discontinued, and the patient was maintained with 3 grains of PFU orally every six hours. There was no recurrence of signs of ventricular irritability. The patient made an uneventful recovery. The author suggests that PHT may represent a drug with a wide margin of safety that is effective in controlling serious ventricular hyperirritability.

Leonard, W. A., Jr., The use of diphenylhydantoin (Dilantin) sodium in the treatment of ventricular tachycardia, A.M.A. Arch. Intern. Med., 101: 714-717,1958. Paramedic Medications, DrugCard, Revised 5/01





1. Decreases Neuron Excitability thru Increasing Sodium efflux from neurons.

2.Shortens QT interval,decreasing serum levels of quinidine, dilitiazem, disopypramide


1. Status Epilepticus

2. Digitalis induced dysrhythmias

3.Torsade de Pointes


1. Hypersensitivity
2. Bradycardia
3. High Degree HB's (2 & 3)


1. Do not administer faster that 50 mg/min.. Causes Hypotension.



1. Hypotension

2. Heart block

3. Dysrhythmias

4. Respiratory Depression

5. CNS Depression

6. Nausea, vomiting, blurry vision


Seizures: 10-20 mg/kg SLOW IVP. Do not exceed 1 gm or rate of 50 mg/min.

Dysrhythmias: 50-100 mg SLOW IV every 5-15 min as needed to max of 1 gm.


HOW SUPPLIED Ampule 250 mg/5 mi


Seizures: 10-20 mg/kg SLOW IVP. (1-3 mg/kg/min) Same Precautions as adult.

Dysrhythmias: 5 mg/kg SLOW IV. Same precautions as adult.


Last Updated: May 30. 2002

Author: Michael Bessette, MD, Associate Director, Assistant Professor, Department of Emergency Medicine. Mount Sinai School of Medicine
Coauthor(s): Sheldon Jacobson. MD, Chair, Professor, Department of Emergency Medicine, Mount Sinai Medical Center


Torsade de pointes (TDP), often referred to as torsade, is an uncommon variant of ventricular tachycardia (VT). The underlying etiology and management of torsade are, in general, quite different from those of garden-variety VT. The management of torsade with group IA antidysrhythmic drugs can have disastrous consequences. Differentiating between these entities, therefore, is critically important.


Torsade is defined as a polymorphous VT in which the morphology of the QRS complexes varies from beat to beat. The ventricular rate can range from 150 beats per minute (bpm) to 250 bpm. The original report described regular variation of the morphology of the QRS vector from positive to net negative and back again. This was symbolically termed torsade de pointes, or "twisting of the point" about the isoelectric axis, because it reminded the original authors of the torsade de pointes movement in ballet. Most cases exhibit polymorphism, but the axis changes may not have regularity.

The definition also requires that the QT interval be increased markedly (usually to 600 msec or greater).

Cases of polymorphous VT, which are not associated with a prolonged QT interval, are treated as generic VT.

Torsade usually occurs in bursts that are not sustained; thus, the rhythm strip usually shows the patient's baseline QT prolongation.

The underlying basis for rhythm disturbance is delay in phase III of the action potential. This prolonged period of repolarization and the inhomogeneity of repolarization times among myocardial fibers allow the dysrhythmia to emerge. The initiating electrophysiologic mechanism may be triggered activity or reentry.

Six genetic variants currently are recognized. Genotypes LQT1 and LQT2 have slow potassium channels, while LQT3 shows defects in the sodium channels. Treatment modalities soon may be based on the genotype of the individual.


In the US: Incidence of torsade is still unknown.


In the US, 300,000 sudden cardiac deaths occur per year. TDP probably accounts for fewer than 5%.


Women are 2-3 times more likely to develop TDP than men.
Women have more QT prolongation secondary to drug therapy.
Congenital long QT syndrome is autosomal dominant but shows greater frequency of expression and a greater lengthening of the QT interval in women than in men.


The highest frequency is in patients aged-35-50 years.


Ask patient about previous cardiac events or syncope and any medications that the patient presently is using.
History of congenital deafness or family history of sudden death may indicate a long QT syndrome.


No physical findings are typical of TDP.


Prolongation of the QT interval may be congenital, as seen in the Jervell and Lange-Nielson syndrome (ie, congenitally long QT associated with congenital deafness) and the Romano Ward syndrome (ie, isolated prolongation of QT interval). Both of these syndromes are associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation.

Prolonged QT is found in only 0.25-0.3% of deaf-mute children.

The acquired conditions that predispose one to torsade either decrease the outward potassium current or interfere with the inward sodium and calcium currents, or fluxes.

The electrolyte disturbances that have been reported to precipitate torsade include hypokalemia and hypomagnesemia.

Hypokalemia and hypomagnesemia, in turn, cause a delay in phase III (ie, reprolongation) and form the substrate for emergence of the dysrhythmia.

Antiarrhythmic drugs reported to be etiologic include class IA agents (eg, quinidine, procainamide, disopyramide), class IC agents (eg, encainide, flecainide), and class III agents (eg, sotalol, amiodarone).

Drug interactions with the antihistamines, astemizole (recalled from US market), and terfenadine (recalled from US market) can precipitate torsade; these drugs should never be used with class IA, IC, or III agents.

Astemizole and terfenadine, in high dosages or when used in combination with the azole antifungal drugs or the macrolide antibiotics, have been reported to precipitate torsade and sudden death,

Grapefruit juice has been shown to slow the hepatic metabolism of these antihistamines as well as other drugs and to prolong the QT interval in patients taking astemizole or terfenadine (recently taken off the market by the US Food and Drug Administration [FDA]).

Clinical implications of this interaction are unclear.

Other drugs that prolong the QT interval and have been implicated in cases of torsade include phenothiazines, tricyclic antidepressants, lithium carbonate, and anthracydine chemotherapeutic agents (eg, doxorubicin, daunomycin).

Risk factors:

Female gender

History of syncope or resuscitated arrest

Family history of sudden death

Lab Studies:

Potassium, magnesium, and calcium levels

Other tests:

ECG: Once in sinus rhythm, examine the QTc interval. See Picture 1 and Picture 2 below for typical examples, as well as figures fig.11, fig.12, fig.13, fig.62 and fig.94.

Picture 1 (rhythm strip including animation). A run of torsade de pointes in a 70-year-old man who developed QT prolongation (QTc = 0.61 sec) secondary to quinidine therapy. The bottom strip shows resolution with overdrive ventricular pacing (see also figures: fig.11, fig.12, fig.13, fig.62 ).

Picture 2 (rhythm strip including animation). A patient with prolonged QT and atrial ectopy. Strip shows premature beat that entrains and a run of torsade de pointes (see figures fig.11, fig.12, fig.13, fig.62 ).

Prehospital Care:

Institute immediate advanced cardiac life support (ACLS) protocol for VT,

Overdrive pacing may be necessary at a rate of up to 140 bpm to control the rhythm (see picture 1 above).

Emergency Department Care:

Torsade, an inherently unstable rhythm, is prone to revert to more stable rhythms spontaneously and prone to recurrences. Torsade also is subject to degeneration into ventricular fibrillation. Begin therapy as soon as the rhythm clearly fulfills the criteria for torsade.

Treat hypokalemia if it is the precipitating factor and administer magnesium sulfate in a dose of 2-4 g intravenously (IV) initially.

Magnesium usually is very effective even in the patient with a normal magnesium level.

If this fails, repeat the initial dose, but danger of hypermagnesemia (depression of neuromuscular function) requires close monitoring.

Other therapies include overdrive pacing and isoproterenol infusion. Most (75-82%) TDP rhythms are started by a pause. Pacing at rates up to 140 bpm may prevent the ventricular pauses that allow TDP to originate.

The patient with torsade who is in extremis should be treated with electrical cardioversion or defibrillation.

Anecdotal reports cite successful conversion with phenytoin (Dilantin) and lidocaine.

Patients with congenital long QT syndromes are thought to have an abnormality of sympathetic balance or tone and are treated with beta-blockers. If the patient breaks through this therapy and enters the ED in torsade, a short-acting beta-blocker, such as esmolol, can be tried.

A few cases of successful conversion using phenytoin and overdrive pacing have been reported.

If patient is unresponsive to conversion with phenytoin and overdrive pacing, attempt electrical cardioversion.

Cervical sympathectomy and implantable pacemaker/defibrillator have been used in some cases for long-term management.

Shortening the action potential decreases the likelihood of immediate recurrence.

Pacing or administration of isoproterenol to a rate of 90-100 bpm is effective.

Withdraw all QT-prolonging drugs.


Immediate cardiology evaluation and follow-up are required.

Magnesium and potassium are first-line therapies in the treatment of torsade de pointes. Isoproterenol and short-acting beta-blockers also have been used. For treatment of primary torsades associated with congenital prolonged QT syndromes, use a beta-blocker. In primary and secondary torsade, overdrive pacing is an appropriate secondary therapy. In treatment of recurrent torsade, implantable defibrillators are used as prophylaxis. If the patient is hemodynamically unstable, carry out electrical cardioversion or defibrillation at once.

Drug Category:

Electrolytes :

These agents are therapeutic alternatives for the treatment of torsade de pointes. Assessment of patient for underlying electrolyte abnormalities that may cause refractory dysrhythmia is important. Some of the electrolyte abnormalities associated with torsade de pointes include hypokalemia and hypomagnesemia. Electrolytes also reduce the arrhythmic effects of offending drugs.

Drug Name

Magnesium sulfate -

DOC for treatment of torsade de pointes. Acts as antiarrhythmic agent and diminishes frequency of PVCs, particularly when secondary to acute ischemia. Deficiency in this electrolyte is associated with sudden cardiac death and can precipitate refractory VF. Magnesium supplementation is used for treatment of torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF.

Adult Dose

1-2 g IV diluted in 100 mL of D5W over 1-2 min; may repeat q4h with close monitoring of deep tendon reflexes

Pediatric Dose

Torsade de pointes: Not established

Hypomagnesemia: 25-50 mg/kg/dose q4-6h for 3-4 doses; single dose not to exceed 2 g also may be administered and repeated if hypomagnesemia persists


Documented hypersensitivity; heart block; Addison disease, myocardial damage; severe hepatitis


Nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocuranne, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants and betamethasone and cardiotoxicity of ritodrine


A - Safe in pregnancy


Magnesium may alter cardiac conduction, leading to heart block in digitalized patients; respiratory rate, deep tendon reflexes, and renal function should be monitored when administered parenterally;
caution when administering since may produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia

Drug Name

Potassium chloride (Klor-Con, K-Dur, Micro-K)
-- First-line therapy in treatment of torsade de pointes. Essential for maintenance of intracellular tonicity, transmission of nerve impulses, contraction of cardiac, skeletal, and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal
excretion, through GI loss, or because of low intake. Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea (if associated with vomiting), or inadequate replacement during prolonged parenteral nutrition. Depletion sufficient to cause 1 mEq/L drop in serum potassium requires a loss of about 100-200 mEq of potassium from the total body store.

Adult Dose

Serum levels >2.5 mEq/L: 10 mEq over 1 h prn based on frequently
obtained lab values; not to exceed 200 mEq/d
Serum levels <2.5 mEq/L: 40 mEq over 1 h prn based on frequently obtained lab values; not to exceed 400 mEq/d

Pediatric Dose

1 mEq/kg IV over 1-2 h prn based on frequently obtained lab values

Medical/Legal Pitfalls:

Failure to recognize as separable from other forms of VT

If one fails to differentiate this rhythm disturbance, the therapy of the dysrhythmia is likely to include a type IA antidysrhythmic agent, such as procainamide.

Type IA agents perpetuate the rhythm disturbance in torsade.


Hyperkalemia; renal failure; conditions in which potassium is retained; oliguria; azotemia; crush syndrome; severe hemolytic reactions; anuria; adrenocortical insufficiency


ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; use caution if discontinuing a potassium preparation in patients maintained on digoxin


A - Safe in pregnancy


Do not infuse rapidly; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest;
plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when concentration >40 mEq/L infused, local pain and phlebitis may follow.

Drug Category:

Adrenergic agonist

These agents alter the electrophysiologic mechanisms responsible for arrhythmic disturbances.

Drug Name

Isoproterenol (Isuprel)

Stimulates beta l- and beta 2-adrenergic receptor activity. Binds beta-receptors of heart, smooth muscle of bronchi, skeletal muscle, skeletal vasculature, and alimentary tract. Positive inotropic and chronotropic actions.

Adult Dose

1 mL of 1:5000 solution (0.2 mg) diluted in 10 mL sodium chloride or 5% dextrose injection
0.02-0.06 mg IV (1-3 mL of diluted solution) initially
0.01-0.2 mg IV (0.5-10 mL of diluted solution) subsequent doses to
achieve heart rate of 90-100 bpm
Alternatively, 10 mL of 1:5000 solution (2 mg) diluted in 500 mL of D5W, or 5 mL of 1:5000 solution (1 mg) diluted in 250 mL of D5W 5 mcg/min (1.25 ml/min of diluted solution) subsequent doses to achieve heart rate of 90-100 bpm

Pediatric Dose

Not established
AHA recommends initial infusion rate of 0.1 mcg/kg/min; titrate to HR effect


Documented hypersensitivity; tachyarrhythmias; tachycardia or heart block caused by digitalis intoxication; ventricular arrhythmias that require inotropic therapy; angina pectoris


Bretylium increases action of vasopressors on adrenergic receptors, which may in turn result in arrhythmias; guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; tricyclic antidepressants may potentiate pressor response of direct-acting vasopressors.


C - Safety for use during pregnancy has not been established.


By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, isoproterenol may have deleterious effect on injured or failing heart; isoproterenol may worsen heart blocks or precipitate Adams-Stokes attacks in some patients, presumably with organic disease of AV node and its branches; caution with coronary artery disease, coronary insufficiency,diabetes, hyperthyroidism, patients sensitive to sympathomimetic amines; if HR exceeds 110 bpm, may be advisable to decrease infusion rate or temporarily discontinue infusion

Drug Category:

Beta-adrenergic blocker

This agent is excellent for use in patients at risk for experiencing complications from beta-blockade, particularly with reactive airway disease, mild to moderately severe left ventricular dysfunction. and peripheral vascular disease. The short half-life of 8 min allows for titration to desired effect and ability to stop quickly if needed.

Drug Name

Esmolol (Brevibloc)

Ideal for use in patients at risk for experiencing complications from beta-blockade, especially patients diagnosed with mild to moderately severe LV dysfunction and those with peripheral vascular disease. Has short half-life of 8 min; thus, easily titratable to desired effect. Therapy may be stopped quickly prn.

Adult Dose

Initially, 500 mcg/kg/min IV infusion for 1 min followed by 4-min maintenance infusion of 50 mcg/kg/min; if adequate therapeutic effect not observed within 5 min, repeat loading dose and follow with maintenance infusion of 100 mcg/kg/min; continue titration procedure, repeating loading infusion and increasing maintenance infusion by increments of 50 mcg/kg/min for 4 min

Pediatric Dose

Not established; suggested dose 100-500 mcg/kg administered over 1 min


Documented hypersensitivity: uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities


Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives may increase cardiotoxicity; digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents increase toxicity


C - Safety for use during pregnancy has not been established.


Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of
hyperthyroidism, including thyroid storm, may worsen when medication withdrawn abruptly; withdraw drug slowly and monitor patient closely

Further Inpatient Care:

Admit patient to ICU for continued monitoring and withdrawal of offending drugs.


Since ICU care is warranted, transfer patient to a facility with acute cardiac care capabilities.


Avoid QT-prolonging medications.
Patients with TDP have a 50% chance of a recurrence even with therapy.

Medical/Legal Pitfalls:

Failure to recognize as separable from other forms of VT

If one fails to differentiate this rhythm disturbance, the therapy of the dysrhythmia is likely to include a type IA antidysrhythmic agent, such as procainamide.

Type IA agents perpetuate the rhythm disturbance in torsade de pointes.