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<< Tachyarrhythmias In The ED: Best Evidence

Management Of Specific Tachyarrhythmias

Supraventricular Tachycardia

Vagal Maneuvers

A number of tools in the therapeutic arsenal are effective against SVT. Vagal maneuvers such as the Valsalva maneuver and carotid sinus massage achieve conversion in approximately 28% of SVT cases, with no clear advantage of one maneuver over the other.32 Carotid sinus massage is performed beneath the angle of the mandible with the patient supine and the head tilted slightly to the opposite side. Gently massage the carotid body for 1 seconds. If the maneuver is unsuccessful, it can be repeated on the other side. Because of rare case reports of ventricular fibrillation and stroke, carotid sinus massage is contraindicated in patients with a history of transient ischemic attack, stroke, or carotid bruit.33, 34, 78 Unreferenced admonitions in various textbooks advise against carotid sinus massage in patients with digoxin toxicity, suggesting it may result in bradyasystole and cardiac arrest.

To perform the Valsalva maneuver, ask the patient toinhale maximally and then “strain” against a closed glottis. The increase in intrathoracic pressure reduces venous return. When airway pressure is released, there is an overshoot phenomenon resulting in supranormal systolic and pulse pressures. It is this post-Valsalva increase in blood pressure that stimulates the carotid bodies causing increased vagal tone. One electrophysiologic study found greater efficacy in the supine (54% conversion) than the standing (20% conversion) patient.35 One disadvantage of the Valsalva maneuver is that it is effort-dependent. You might objectify the effort by having the patient blow into a sphygmomanometer tubing to verify that airway pressure reaches 40 mmHg for a period of at least 30 seconds.32 If vagal maneuvers are unsuccessful, proceed to pharmacologic conversion. Other vagal maneuvers, such as applicationof the pneumatic anti shock garment and digital rectal examination, are mentioned in the literature but are not well-studied (or appreciated by patients).


The ACLS guidelines recommend adenosine (Adenocard) as the first-line pharmacologic agent in stable patients with narrow regular SVT. (See “Clinical Pathway:Narrow Complex Tachycardia”.) Adenosine is a naturally occurring and rapidly metabolized compound that blocks conduction at the AV node. Multiple studies show that adenosine in doses of 6-12 mg will terminate SVT in 85%-93% of patients within 30 seconds.36-39 (See Table 6.)

Adenosine can serve a diagnostic as well as therapeutic role. Patients with SVT involving AV nodal reentry or AV reciprocating tachycardia will likely convert. Those with atrial flutter and 2:1 conduction without visible flutter waves will have a transient increase in the degree of AV nodal block, causing flutter waves to become more visible. Individuals with sinus tachycardia or SVT not involving AV nodal reentry (ectopic atrial tachycardia or junctional tachycardia) will not convert but will have transient slowing of the ventricular rate. When using adenosine, always run a paper rhythm strip documenting the response to therapy.

Because it has a half-life of only seconds, adverse effects (dyspnea, chest pain, or ventricular pauses) are brief. Syncope due to prolonged ventricular pauses is rare.40 During a prolonged ventricular pause, urge the patient to cough, as this may maintain cerebral perfusion until the adenosine wears off.41 Bronchospasm is a theoretical concern, but clinically significant exacerbation is unusual.42 Rarely, ventricular fibrillation can occur following adenosine administration. Most reported cases were associated with the concomitant use of digoxin and,less frequently, with digoxin and verapamil.43 For this reason, resuscitation equipment should be available immediately whenever adenosine is given.

Administer adenosine via the largest and most proximal intravenous line possible and via rapid IV push followed by a rapid saline flush. Although it is not well-studied by this route, if given through a central line, the initial dosage should be 3 mg.44 If, after administering adenosine to a patient with narrow complex tachycardia,you do not see conversion or a transient slowing of the ventricular rhythm, suspect inadequate delivery of medication to the cardiac tissues due to inadequate IV size, peripheral location of the IV, failure to administerthe drug via rapid IV push, or inadequate dose. Remember that theophylline is an antagonist of adenosine;patients taking theophylline may require higher doses—up to 20 mg of adenosine. (Be sure that the narrow tachycardia isn’t due to theophylline toxicity!)

Besides the previously mentioned problem with digoxin and verapamil, there are several possible drug interactions with adenosine. Because disopyramide potentiates the effects of adenosine, use a small initial dose, 3-6 mg, in patients taking disopyramide (Norpace, Rythmodan).38 Several letters to the editor in a variety of journals warn about profound symptomatic bradycardiain patients who are taking dipyridamole (found in Aggrenox and Persantine) who receive adenosine.45,46,79 While most reports involve patients receiving adenosine for cardiac stress testing, the possibility of an adverse drug interaction may exist in the ED.

Adenosine should not be used in patients with preexcited atrial fibrillation or flutter since it may precipitate hemodynamically unstable ventricular fibrillation or flutter.14

Calcium-Channel Blockers

Multiple studies also support the use of calcium-channel blockers for the acute termination of hemodynamically stable paroxysmal SVT. Calcium-channel blockers slow conduction at the AV node, interrupting any reentry circuit that involves the AV node, including AV nodal reentry and AV reciprocating tachycardia. These agents will not convert atrial and junctional tachycardias, but they are effective in controlling rate. Calcium-channel blockers have no direct effect on accessory bypass tract conduction.47 Verapamil, the first-line drug in the days before adenosine, terminates paroxysmal SVT in 66%-91% of cases when given via peripheral IV in doses of5.0-7.5 mg.36,37,48 When compared head-to-head with adenosine in patients with SVT, verapamil has shown similar efficacy but more clinically significant adverse side effects.36,37

Multiple placebo-controlled or comparative trials show that intravenous diltiazem in doses of 0.25-0.45mg/kg successfully terminates 90%-100% cases of SVT. Although verapamil and diltiazem are the calcium-channel blockers most studied in the management of acute SVT, no calcium-channel blocker has demonstrated superiority over the others.47,49-51 Symptomatic hypoten-sion is seen in approximately 6% of patients and responds to intravenous cry stalloid. Pretreatment with intravenous calcium (1-3 cc of calcium chloride or 5-10 cc of calcium gluconate) before giving the calcium-channel blocker may prevent hypotension in those with a marginal blood pressure.80,81 Because of their negative inotropic effects, the 2000 ACLS guidelines state that calcium-channel blockers should not be used in patients with SVT who have clinical findings of congestive heart failure or a known ejection fraction less than 40%. Verapamil is contraindicated in patients younger than 1year of age due to case reports of hemodynamic collapse after IV administration.


Beta-blockers suppress automaticity and slow conduction through the AV node. The 2000 ACLS guidelines state that beta-blockers can be used as an alternative to calcium-channel blockers in patients with narrow complex tachycardia and intact left ventricular function(when vagal maneuvers and adenosine are not effective).Very few studies, however, have assessed their efficacy in the acute treatment of SVT.

Esmolol is an intravenous, cardioselective, ultra-short-acting, beta-adrenergic blocking agent. It has a nine-minute half-life, rapid clinical onset and offset of action, and can easily be titrated to the desired effect. Despite these theoretical benefits, one study of 50 hemodynamically stable patients with paroxysmal SVT treated with esmolol or diltiazem was terminated prematurely due to the marked superiority of diltiazem.51 While there is little evidence to support the use of beta-blockers for SVT, they are reasonable rate-control agents in patients with intact left ventricular function.


Amiodarone is a potent class III antiarrhythmic that is FDA-approved for the management of ventricular tachycardia and fibrillation. It is recommended in the new ACLS guidelines for stable patients with SVT who fail vagal maneuvers and adenosine and who have clinical signs of congestive heart failure or a known ejection fraction less than 40%. Studies have also sug-gested its effectiveness against atrial fibrillation. Amiodarone has little negative inotropic effect and is theoretically a good choice in patients with SVT and poor left ventricular function who fail vagal maneuvers and adenosine. However, controlled randomized studies have not demonstrated efficacy in patients with SVT.


Digoxin is not useful to convert SVT and is not recommended in patients with atrial or junctional ectopic tachycardia (since these rhythms may themselves be a manifestation of digoxin toxicity). Digoxin is best reserved for chronic rate control of atrial fibrillation,primarily in elderly patients who have poor left ventricular function.

Multifocal Atrial Tachycardia

The first step in treating multifocal atrial tachycardia is to treat the underlying disorder. Hypoxia due to chronic obstructive pulmonary disease, pulmonary embolus, or congestive heart failure is the usual precipitant, and correction of hypoxemia is the first priority. Correction of underlying metabolic abnormalities, specifically hypokalemia and hypomagnesemia, is generally recom-mended. Judicious use of beta-agonist nebulizers or inhalers is recommended, as overuse of these agents has been thought to cause multifocal atrial tachycardia in some patients. Remember that multifocal atrial tachycardia does not typically cause hemodynamic instability, and cardioversion is not recommended in the treatment of this condition. Symptoms such as ischemic chest pain,syncope, hypotension, or uncompensated pulmonary edema should not be attributed solely to the multifocal atrial tachycardia. Because of the uncommon nature of the rhythm, there are no controlled studies demonstrating the clinical significance of multifocal atrial tachycardia and no data to support the assumption that acute orchronic pharmacologic treatment of multifocal atrial tachycardia provides a beneficial effect.

Wide Complex Tachycardia

The phrase “first do no harm” was tailor-made for the scenario of regular wide complex tachycardia. Such patients may have either SVT with aberrancy or ventricular tachycardia—conditions with very different prognoses and therapies. If the physician misidentifies ventricular tachycardia as SVT with aberrancy and treats it with adenosine, the ventricular tachycardia will likely persist (or worsen).52 More importantly, if the physician misidentifies ventricular tachycardia as SVT with aberrancy and treats it with verapamil, the patient will very likely suffer hemodynamic collapse (or worse) and require cardioversion.

When the patient’s condition permits, urgent consultation with a cardiologist may be useful when the etiology of a wide complex tachycardia remains in doubt. Some of these rhythms are complex, and the potent therapies may have life-threatening complications. Fax machines in the ED enhance communication.

If the patient truly, unquestionably, indisputably, has SVT with aberrancy (proven by an electrophysiologic study or by an old ECG showing the same bundle branch block), verapamil is probably safe. However, if you are wrong, and the patient has either ventricular tachycardia or SVT with aberrancy due to an accessory pathway,administration of verapamil can be catastrophic. In the case of ventricular tachycardia, the verapamil may precipitate hemodynamic collapse. In the case of an accessory pathway, verapamil will slow conduction through the AV node but not the accessory pathway,actually speeding the ventricular response, or inducea malignant ventricular arrhythmia. Because thepotential for error is so great, many authorities feel that it is best to avoid verapamil in any patient with a wide complex tachycardia.8,20,53,54

The approach to wide complex tachycardia is determined by the underlying diagnosis. Unstable wide complex tachycardia requires cardioversion (or defibrillation if the patient has no pulse) regardless of its presumed etiology. Stable wide complex tachycardia that is most likely SVT can be treated with adenosine in the same way as narrow complex SVT. Before giving adenosine, be sure that the wide complex tachycardia is regular,as adenosine is contraindicated in atrial fibrillation when an accessory pathway exists (a double-speed ECG may help clarify the issue of regularity). Stable wide complex tachycardia that is most likely ventricular tachycardia(which is most cases of wide complex tachycardia) is discussed in a subsequent section. In those cases where the cause for the wide complex tachycardia remains uncertain, the best approach is to presume ventricular tachycardia and treat with procainamide or amiodarone. Both agents are effective against both supraven tricularand ventricular dysrhythmias.

Procainamide is a class Ia agent that must be infused slowly in order to avoid adverse effects of hypotension and QT prolongation. The ACLS recommendation is20 mg/min IV until either the wide complex tachycardia resolves, the patient becomes hypotensive, the QRS complex is widened by 50% of its original width,or a total dose of 17 mg/kg is infused. Procainamide should be avoided in patients with clinical evidence of congestive heart failure or a known ejection fraction less than 40%.

The class III agent amiodarone is the drug of choice in patients with compromised function of the ventricles. Give 150 mg over the first 10 minutes. Then begin a slow IV infusion of 1 mg/min for the next six hours (total dose infused = 360 mg).

After conversion to sinus rhythm, examine the ECG for signs of ischemia or a prolonged corrected QT (QTc) interval. Also examine the sinus rhythm ECG for down sloping elevation of the ST segment inleads V1 -V3 with or without right bundle branch block. These findings suggest a diagnosis of the “Brugada syndrome,” a recently recognized inherited syndrome characterized by typical ECG appearance and a history of syncope or sudden cardiac death due to polymorphic ventricular tachycardia or ventricular fibrillation.55

Atrial Fibrillation

A complete discussion of atrial fibrillation appears in the August 2002 issue of Emergency Medicine Practice, “Atrial Fibrillation In The ED: Cardioversion, Rate Control,Anticoagulation, And More .”

Monomorphic Ventricular Tachycardia

Certain patients with monomorphic ventricular tachycardia can be pharmacologically converted. Such “stable”patients are without ischemic-sounding pain or dyspnea,evidence of heart failure, hypotension, or relative hypotension as evidenced by altered mental status. The2000 ACLS guidelines recommend procainamide or sotalol for patients with preserved heart function and amiodarone or lidocaine for patients with impaired cardiac function. (See “Clinical Pathway: Stable Ventricular Tachycardia: Monomorphic And Polymorphic”.) Both are FDA-approved for the treatment of sustained ventricular tachycardia. Sotalol is currently available only in oral form in the United States, though an intravenous formulation is pending FDA approval.

Only a handful of trials have studied sustained ventricular tachycardia in a randomized, controlled fashion. One study compared lidocaine (a Vaughn-Williams class Ib agent; see Table 7) and intravenous sotalol (a non selective beta-blocker with class II and III properties) in 33 patients with sustained ventricular tachycardia. The study was terminated due to a marked superiority of sotalol, with a conversion rate of 20% in the lidocaine group and 69% in the sotalol group.56Anotherstudy compared lidocaine 1.5 mg/kg IV to procainamide10 mg/kg at 100 mg/min in 29 cardiac care patients with sustained ventricular tachycardia and found procainamide superior, with efficacy rates of 21.5% for lidocaine vs. 80% for procainamide.57 Amiodarone has not been studied specifically for termination of hemodynamically stable monomorphic ventricular tachycardia. It is recommended based on a placebo-controlled prehospital study administering amiodarone to patients with pulse less ventricular tachycardia and ventricular fibrillation.58 Based on the evidence currently available,patients with stable sustained ventricular tachycardia should be treated with IV procainamide (or IV sotalol where available). For those with known or suspected ejection fraction under 40%, treat with amiodarone 150mg IV over 10 minutes followed by a drip of 1 mg/min for six hours, then 0.5 mg/min.


Polymorphic Ventricular Tachycardia

Polymorphic ventricular tachycardia associated with a prolonged QT interval, either congenital or acquired, is known as torsades de pointes. Other cases of polymorphic ventricular tachycardia are associated with a normal QT interval and result from ischemia, reperfusion, myocarditis,or idiopathic causes. The distinction between torsades de pointes and normal QTc polymorphic ventricular tachycar-dia may not be possible in the ED.

Asymptomatic, self-terminating polymorphic ventricular tachycardia should be treated by correcting any underlying electrolyte abnormalities and discontinuing pharmacologic agents known to cause the rhythm.(See Table 2.) Symptomatic but hemodynamically stable polymorphic ventricular tachycardia can be treated medically. For patients with polymorphic ventricular tachycardia and a prolonged baseline QT interval, the 2000 ACLS guidelines recommend correction of relevant electrolyte abnormalities followed by intravenous magnesium, overdrive pacing, or intravenous isoproterenol, phenytoin, or lidocaine. (See “Clinical Pathway: Stable Ventricular Tachycardia: Monomorphic And Polymorphic”.) There are no prospective controlled trials documenting the absolute or relative efficacy of any of these modalities in the treatment of torsades de pointes. Several retrospective uncontrolled case series totaling 31 patients report the effectiveness of magnesium 2g IV, repeated if needed in 5-15 minutes.59 Scattered case reports have documented the resolution of torsades de pointes after transthoracic or transvenou spacing and after the use of intravenous isoproterenol, phenytoin, or lidocaine. Because magnesium is safe,rapidly available, and less noxious than electrical pacing,it should be considered the treatment of choice for stable long-QT polymorphic ventricular tachycardia. Magnesium is cleared via the kidneys and should be used with caution in patients with renal insufficiency. It is not thought to be effective against polymorphic ventricular tachycardia in the setting of a normal Qtc interval.

Patients with polymorphic ventricular tachycardia and a normal baseline QTc interval may have an ischemic basis for their dysrhythmia. After correction of underlying electrolyte abnormalities and treatment of any evident ischemia, the 2000 ACLS guidelines recommend beta-blockers, lidocaine, amiodarone, procainamide, orsotalol. There is no evidence that supports the superiority of any individual agent. Note that amiodarone, procainamide, and sotalol also cause long-QT polymorphic ventricular tachycardia. If a patient presents with polymorphic ventricular tachycardia and is currently on chronic therapy with one of these agents, giving additional drugs is contraindicated.

Pulseless Ventricular Tachycardia /Ventricular Fibrillation

As soon as a defibrillator is available, defibrillate with 200J, 300J, and 360J (or equivalent biphasic) in rapid succession as needed. If pulseless ventricular tachycardia or ventricular fibrillation persists after three precordial shocks, the 2000 ACLS guidelines recommend securing the airway, establishing IV access, and administering either 1 mg of epinephrine (1:10,000 every 3-5 minutes) or40 U of vasopressin once intravenously. The vasopressin recommendation is based on a single randomized study of 40 patients with out-of-hospital ventricular fibrillation that showed greater 24-hour (but not long-term) survival among patients receiving vasopress in compared to those receiving epinephrine.60 Another precordial shock at 360Jis then delivered.

If pulseless ventricular tachycardia or ventricular fibrillation persists, the 2000 ACLS guidelines recommend amiodarone. A 1999 study by Kudenchuk et al in 504 patients with prehospital ventricular fibrillation or pulseless ventricular tachycardia despite three precordial shocks found significant improvement in survival to hospital admission (but not discharge) in patients receiving amiodarone 300 mg IV push vs. placebo.58 A subsequent trial (ALIVE) compared amiodarone to lidocaine for shock-resistant out-of-hospital cardiac arrest and found that despite higher rates of survival to hospital admis-sion, the survival to discharge and neurological outcome were the same in both groups.61 Lidocaine and procainamide may be considered, but there is no literature to document their efficacy in this setting.

For patients who have return of spontaneous circulation, the question of whether to initiate intravenous prophylactic anti arrhythmic therapy has not been clarified in the literature. (But it certainly seems reason-able when you’re treating a patient who’s already been dead once today.) For recurrent ventricular fibrillation or pulseless ventricular tachycardia, the 2000 ACLS guide-lines list amiodarone as a class II b recommendation(defined in their classification as fair-to-good evidence of effectiveness and safety and no evidence of harm).

Several studies tend to support this recommendation.62 Lidocaine and procainamide are listed as class indeterminate (defined as insufficient evidence to support are commendation for clinical use).For a more complete discussion of how to manage pulseless ventricular tachycardia and ventricular fibrillation, see the November 2002 issue of Emergency Medicine Practice, Cardiac Arrest: Current Concepts, Controversies, And Evidence .”



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