Cardiovascular 8: Tachycardia Treatment Portal*
The approach to the patient with tachycardia must include a careful analysis of many critical questions. (See Vol I—Tachycardia Algorithm.)
- Is this a sinus tachycardia? Typical upper limits of sinus tachycardia can be calculated by subtracting the patient’s age in years from 220 (eg, 220-50 = 170 for a 50-year-old).2 If the rhythm is likely to be sinus tachycardia, attempt to identify and correct the underlying cause (fever, hypoxia, hypovolemia, etc). Rarely does a sinus tachycardia need to be treated as an arrhythmia.
- Is the tachycardia causing such serious signs or symptoms that the patient must be immediately cardioverted, or can the patient's tachycardia be evaluated and considered for treatment with medications? Heart rates of < 150 bpm usually do not cause serious signs and symptoms unless the tachycardia continues for a prolonged period of time or the patient has other underlying heart disease.
- What is the safest way to treat the patient’s tachycardia? All antiarrhythmic medications may cause a proarrhythmic effect, regardless of their Vaughn-Williams classification. The use of more than one antiarrhythmic in the same patient exponentially increases the risk of side effects.
- What is the patient’s specific rhythm that is causing the
tachycardia?
- Is the tachycardia of supraventricular or ventricular origin?
- Is the basic rhythm atrial flutter or atrial fibrillation?
- Is the narrow complex supraventricular tachycardia due to abnormal automaticity as in ectopic atrial tachycardia or multifocal atrial tachycardia (MAT) or due to re-entrant circuits as in AV nodal re-entrant tachycardia (AVNRT)?
- Does the patient have an accessory AV pathway as seen in Wolff-Parkinson-White Syndrome?
- Does the patient have torsades de pointes?
- Is the patient’s left ventricular function significantly impaired (ejection fraction of < 40% or signs of CHF)? Antiarrhythmic medications must be used with caution in patients with depressed left ventricular function or overt CHF. Many of the antiarrhythmic medications further depress the left ventricular function and thus will worsen or precipitate CHF. Amiodarone and sotalol are the least likely, of the antiarrhythmic medications, to worsen or precipitate CHF. Amiodarone is now often the first agent to be used to treat tachycardias due to its lesser negative inotropic effect and its broad antiarrhythmic activity. In many situations, if one antiarrhythmic fails to convert the rhythm, early electrical cardioversion should be the next intervention.
- Does the patient have an identifiable cause for the arrhythmia such as hypokalemia, hypoxia, acute MI, or CHF?
I. Atrial Fibrillation-Atrial Flutter
For
patients with atrial fibrillation/atrial flutter, the clinician must
first assess whether the patient is hemodynamically unstable and
experiencing serious signs and symptoms (ie, hypotension, angina) from
a very rapid ventricular rate. If serious signs and symptoms are
present, immediate electrical cardioversion is necessary, regardless of
the duration of the atrial fibrillation/flutter (Class I).
(
See Vol I—Atrial Fibrillation-Atrial Flutter Algorithms.)
For hemodynamically stable patients, the initial evaluation must focus on four primary features. These features include:
-
Is there an underlying reversible cause for the AF?
Acute medical conditions that might cause atrial fibrillation/atrial flutter include hypoxia, CHF, hypokalemia, hypertension, anemia, hypomagnesemia, mitral regurgitation, acute MI, digoxin toxicity, or thyrotoxicosis. If one or more of these conditions are present, they must be treated as part of the management of the AF. -
Is the cardiac function impaired?
Patients with symptomatic CHF or an ejection fraction of < 40% need special cautions when medications are used to treat the AF. Many of the antiarrhythmic medications have negative inotropic and proarrhythmic properties that manifest particularly in patients with an ejection fraction of < 40%. -
Does the patient have Wolff-Parkinson-White (WPW) syndrome?
Patients with WPW have an accessory conduction pathway between the atria and the ventricle, capable of conducting at extremely rapid rates when the AV node is blocked. Many antiarrhythmic medications have the potential of increasing AV block and causing a paradoxical increase in the ventricular rate in patients with WPW. This risk occurs primarily in the setting of wide-complex atrial fibrillation with very rapid ventricular response. -
Has the patient been in AF for less than or greater than 48 hours?
If the patient has been in AF for greater than 48 hours, there is an increased risk of systemic embolization with conversion to sinus rhythm if the patient has not been anticoagulated for at least three weeks. The management of a patient with hemodynamically stable AF has three main focuses. These include control of the ventricular rate, assessment of the need for anticoagulation, and conversion of the AF to sinus rhythm.
- Ventricular rate control
- In patients with normal left ventricular function, either IV calcium channel blockers (CCB) (Class I) or IV beta blockers (Class I) are recommended for ventricular rate control if the heart rate is > 120 bpm. Diltiazem IV is often used first. Digitalis has some effect on slowing the ventricular rate in AF but is much less potent and has a slow onset of action.
- In patients with a decreased LV function, beta blockers and CCB need to be used with caution, if at all, because of their negative inotropic effect. In these patients, digoxin (Class IIb) may be the preferred AV nodal blocking agent due to its positive inotropic effects, but its usefulness is limited due to its relative lack of potency, especially in a high adrenergic state found in CHF. The negative inotropic effects of diltiazem appears to be less than with verapamil or beta blockers and therefore may be considered for use in patients with rapid AF in the setting of reduced LV function (Class IIb).
- Amiodarone IV is also effective in controlling the ventricular rate in AF (Class IIb)2 and may convert the patient to sinus rhythm.
- If the duration of AF has been longer than 48 hours, medications that may convert the rhythm to sinus rhythm (including amiodarone) must be used with great caution in patients who have not been adequately anticoagulated for at least three weeks because of the risk of systemic emboli. In this setting, amiodarone should be used only if other measures of rate control are ineffective or contraindicated and the risks of its use thought to be justified.
- In patients with WPW (wide-complex atrial fibrillation with very rapid response), the following drugs may cause a paradoxical increase in the ventricular rate and therefore should not be used (Class III): digitalis, verapamil, diltiazem, adenosine, and possibly beta blockers. If the patient has a normal left ventricle, either DC cardioversion or an antiarrhythmic medication that has direct effects on the conduction of the accessory pathway like procainamide, propafenone, flecainide, sotalol, or amiodarone may be used (Class IIb). If the patient with WPW and in AF has a decreased LV function, either DC cardioversion or amiodarone (Class IIb) may be used. The other agents have too great a risk of being proarrhythmic to be recommended.
Caution: Do not give beta blockers IV and calcium channel blockers IV within 30 minutes of each other due to the risk that the combination may induce severe bradycardia or asystole.
- Determination of the need for anticoagulation
- If the patient is in AF for more than 48 hours, there is a significant risk that thrombi may form in the atria. Especially at the time of conversion of the AF to sinus rhythm, a piece of these thrombi may break off and embolize systemically. Therefore, if the AF has been present for longer than 48 hours, the patient should be adequately anticoagulated for at least three weeks before performing DC cardioversion or attempting chemical cardioversion.
- If the patient is hemodynamically unstable, DC cardioversion will need to be performed even if the patient is not anticoagulated and the AF has lasted more than 48 hours.
- In special situations with patients in AF longer than 48 hours who are moderately symptomatic, transesophageal echocardiography may be used to exclude the presence of atrial thrombi. This reduces the risk of emboli from DC cardioversion in a non-anticoagulated patient who must be converted to sinus rhythm on a semi-emergency basis.
- After successful cardioversion of an anticoagulated patient who had been in AF for more than 48 hours, anticoagulations should be continued for an additional four weeks.
- Conversion of AF to Sinus Rhythm
- If a patient has been in AF for more than 48 hours, maintain anticoagulation at proper levels for 3 weeks before attempting cardioversion either electrically or with antiarrhythmic agents.
- Electrical cardioversion is the method of choice for cardioversion of patients with atrial fibrillation/atrial flutter.
- In patients with a normally functioning left ventricle, consider chemical cardioversion using one of the following agents: IV ibutilide (Class IIa), IV flecainamide (Class IIa), IV propafenone (Class IIa) IV procainamide (Class IIa), IV amiodarone (Class IIa), and IV sotalol (Class IIa).
- In patients with an impaired left ventricle (ejection fraction < 40% or CHF is present) DC cardioversion is the preferred method of cardioversion. If DC cardioversion cannot be accomplished, IV amiodarone may be tried.
- For patients in AF with WPW, cardioversion is best accomplished with DC cardioversion. Acceptable chemical agents to use include: IV amiodarone (Class IIb), IV procainamide (Class IIb), IV flecainamide (Class IIb), IV propafenone (Class IIb), and IV sotalol (Class IIb). If the patient has decreased left ventricular function, IV amiodarone is the chemical agent of choice.1
Overdrive pacing may also be considered as a means of converting atrial fibrillation to sinus rhythm in some patients.
Pharmacological Agents-Atrial Fibrillation-Atrial Flutter
Rate Control
Vagal Maneuversa (ice water or Valsalva maneuver) or Adenosine (6 to 12 mg IV) temporarily slows the ventricular rate to confirm presence of atrial flutter. In this setting, vagal maneuvers and adenosine are used for diagnostic purposes only.
Calcium Channel Blockersa
Diltiazem:
0.25 mg/kg IV over 2 minutes. If ventricular rate does not slow in 15
minutes, give 2nd dose of 0.33 mg/kg IV over 2
minutes. If
hypotension occurs with these agents, place patient in Trendelenburg
position or slowly infuse calcium chloride 0.5 to 1.0 g IV.
Beta Blockersa
Propanolol
(Inderal): 0.5 to 1.0 mg/min IV to maximum total dose of 0.1
mg/kg.
Esmolol
(Brevibloc): Load with 0.5 mg/kg IV over 1 minute, then infuse 0.05 to
0.2 mg/kg/min IV as needed to slow the ventricular rate.
Metroprolol
(Lopressor): 5 mg IV over 2 to 5 minutes. Repeat at
5-minute intervals to a total dose of 15 mg.
Atenolol
(Tenormin): 5 mg IV over 5 min. May repeat in 10 min to total
dose of 10 mg.
(Use extreme caution with use of beta blockers after use of calcium
channel blockers.)
Digoxina (Lanoxin): Give 0.25 to 0.5 mg IV followed by 0.125 to 0.25 mg every 2 hours as needed to a maximum total dose of 0.75 to 1.5 mg (10 to 15 μg/kg) in the first 24 hours.
Chemical Cardioversion
Ibutilide
(Corvert): (Class III antiarrhythmic agent) Infuse 1 mg IV over 10
minutes. (For patients < 60 kg, use 0.01 mg/kg.) May repeat the
1 mg
infusion 10 minutes after completing the first infusion.
Propafenone
(Rythmol): (Class Ic antiarrhythmic agent) Initial dose of 150 mg PO
every 8 hours; may increase every 3 to 4 days up to 300 mg every 8
hours.
Amiodarone
(Cordarone): (Class III antiarrhythmic agent) Load
with 800 to 1000 mg per day PO for 1 to 3 weeks, then 400 to 800 mg per
day for 2 to 4 weeks, then 100 to 400 mg per day as maintenance.
Sotalol
(Betapace): (Class II and III antiarrhythmic agent) Initial dose of 80
mg bid PO; increase to a maximum total daily dose of 320 mg/day.
Flecainide
(Class Ic antiarrhythmic agent) Load with 2 mg/kg IV slow infusion at
rate up to 10 mg/min. Must
be infused slowly. (The IV form not approved
in the United States.)
Procainamide (Class Ia antiarrhythmic agent) Loading dose
of 20 to 30
mg/min IV to max of 17 mg/kg.
Anticoagulants
Heparin, Enoxaparin (Lovenox), Warfarin (Coumadin),
and Dabigatran
(Pradexa)
Caution
If
any of these agents are used for treatment of patients with atrial
fibrillation or atrial flutter, monitor the patient observing for
prolongation of the QT interval. This may indicate that the patient is
at risk for developing a serious arrhythmia. If this happens, consider
discontinuing the offending drug.
II. Narrow Complex Supraventricular Tachycardia
Narrow complex supraventricular tachycardias include paroxysmal supraventricular tachycardia (PSVT) caused by a re-entrant circuit, as in AV nodal reentrant tachycardia (AVNRT) or AV reentrant tachycardia (AVRT), automatic atrial tachycardia caused by abnormal automaticity in the atria, and (rarely) junctional tachycardia. While the mechanism causing the tachycardia helps to dictate the most appropriate treatment, frequently the mechanism of the arrhythmia may be difficult to determine. (See Vol I—Acute Care Portals, Paroxysmal Supraventricular Tachycardia Algorithm.)
PSVT is a regular tachycardia, with or without P waves with a rate greater than 120 bpm. It usually has an abrupt onset and an abrupt termination. PSVT may include AVNRT and AVRT mediated by a concealed or manifest accessory pathway.
Distinguishing the type of the narrow complex supraventricular tachycardia can be difficult. In frequency of presentation, PSVT is much more common than the automatic atrial tachycardia, especially the junctional tachycardia (that is very rare). The automatic atrial tachycardia has a more gradual onset (warm up) and termination while PSVT tends to have abrupt onsets and terminations.
In approaching patients with narrow complex supraventricular tachycardia, the first concern is to assess the stability of the patient to determine if immediate electrical cardioversion is necessary or if other slower but less aggressive means may be used.
In hemodynamically stable patients, the next concern is to establish a specific diagnosis of either PSVT, ectopic atrial tachycardia, multifocal atrial tachycardia (MAT), or junctional tachycardia with the use of one or more of the following diagnostic tools. This is important since the therapeutic approach is different for the different types of tachycardia.
-
Evaluation of the 12-lead ECG with special attention to the P-waves. Ectopic atrial tachycardia has abnormal P-wave configuration and P-wave axis. MAT is irregular like atrial fibrillation but has three or more different P-wave morphologies identifiable preceding the QRS complexes.
-
Clinical information may also help in the differentiation. PSVT tends to have an abrupt onset and termination while the automatic atrial tachycardias tend to start and stop more gradually. Many patients with PSVT have previously been diagnosed as having PSVT or an accessory pathway.
-
The initial use of vagal maneuvers can also help to differentiate the type of the tachycardia and will convert a PSVT to NSR in about 25% of cases. Vagal maneuvers cause slowing of conduction through the AV node by an increase in parasympathetic tone. The simplest and safest vagal maneuver is the Valsalva maneuver (bearing down). The patient may be instructed to blow into a soda straw with the end occluded by a fingertip (“blow my finger away”). Other vagal maneuvers that may be tried include coughing, induction of the gag reflex, or facial immersion in ice water. 4. Adenosine IV may also be helpful (providing that there are no contraindications) both in differentiating the type of tachycardia (ie, making the P-waves evident) and possibly in terminating the tachycardia. Remember that adenosine must be used with great caution, if at all, in patients with reactive airway disease because it may precipitate bronchospasm.
Success in the use of adenosine to terminate PSVT is dependent on proper administration. Rapidly give 6 mg of adenosine IV push in a proximal arm vein followed by a 20 mL fluid flush to deliver the drug to the AV node. If the first dose is not successful, give a second dose of 12 mg IV push 1 to 2 minutes later. The patient may demonstrate a few seconds of asystole during the conversion process. Many patients complain of a few seconds of chest pain when the adenosine is given.
If the adenosine is injected into a central venous catheter, the effect on the AV node is more pronounced than if it is injected in a peripheral vein. In this case, the initial dose of adenosine should be 3 mg and the second dose 6 mg. It is important to remember that other drugs that the patient is receiving may influence the effects of the adenosine and thus alter the appropriate doses of adenosine. For example, dipyridamole (persantine) potentiates the action of adenosine by blocking its uptake so the initial dose should be 2 to 3 mg rather than 6 mg, and the second dose should be 6 mg rather than 12 mg. Theophylline causes a decrease in the AV node blocking action of adenosine; therefore, increase the initial dose to 9 mg and the second dose to 18 mg.
If the patient remains in a supraventricular tachycardia (SVT) at this point, the provider team now needs to decide which form of SVT the patient has and proceed with appropriate treatments. In addition, the functional state of the patient’s left ventricle is also important to consider when making a decision of next most appropriate approach to the patient with an ejection fraction of < 40% being a concern that will alter the therapeutic approach.
Treatment
Approaches to PSVT Refractory to Adenosine
-
In patients with normal LV function AV nodal blocking agents including calcium channel blockers (diltiazem, verapamil) and beta blockers (metoprolol, esmolol, atenolol) are usually used first. Digoxin has also been used but is less potent and slower to act than other drugs. If the AV nodal blockers are not successful in converting the PSVT, DC cardioversion should be considered. Alternative IV medications include procainamide (Class IIa), amiodarone (Class IIa), propafenone (Class IIa), flecainide (Class IIa), and sotalol (Class IIa), but all of these medications may cause hypotension and have a proarrhythmic potential. Therefore, the use of AV blockers and DC cardioversion are preferred initial treatments. There is some evidence that IV propofenone may be more effective than IV amiodarone for AVNRT or AVRT.3
-
In patients with decreased LV function (ejection fraction of < 40%), the preferred conversion treatment is DC cardioversion. Medications with a significant negative inotropic effect (verapamil, beta blockers, procainamide, propafenone, flecainide, and sotalol) should be used only with great caution. Safer medications include digitalis, amiodarone, and probably diltiazem. Flecainide and propafenone should be avoided in patients with documented coronary artery disease.
Treatment Approaches to Automatic Atrial Tachycardia (Ectopic Atrial Tachycardia and Multifocal Atrial Tachycardia)
-
Automatic atrial tachycardias are due to an increase in automaticity. They require a different treatment approach than reentry supraventricular arrhythmias (PSVT, atrial fibrillation, and atrial flutter).
-
Multifocal atrial tachycardia (MAT) may be seen in patients with hypokalemia, COPD, theophylline toxicity, digitalis toxicity, or myocardial ischemia/infarction. Initial treatment of MAT includes treating the underlying disease process.
-
Synchronized electrical cardioversion is not effective for the treatment of automatic atrial arrhythmias (Class III).
-
In patients with a normal left ventricular function, beta blockers, and calcium channel blockers (diltiazem and verapamil), slow the heart rate by increasing the AV block and help conversion to normal sinus rhythm. Digitalis may slow the heart rate but will not help terminate the automatic atrial tachycardia.
-
In patients with a normal left ventricular function, acceptable medications to use include beta blockers (Class IIb), calcium channel blockers (Class IIb), digitalis (Class indeterminate), amiodarone (Class IIb), IV propafenone (Class IIb), and IV flecainide (Class IIb).
-
In patients with a left ejection fraction of < 40%, medications with a significant negative inotropic effect (beta blockers, verapamil, propafenone, and flecainide) need to be avoided. In these patients, safer drugs to use include amiodarone (Class IIb), diltiazem (Class IIb), and digitalis (Class indeterminate).
Treatment of Junctional Tachycardia
-
True junctional tachycardia is usually due to digitalis toxicity, theophylline toxicity, or exogenous catecholamines. Treatment in these cases consists of removal of the offending agent.
-
If no cause can be identified for the junctional tachycardia, IV amiodarone, beta blockers, and calcium channel blockers may be used for treatment.
III. Wide Complex Tachycardia of Unknown Etiology
The treatment of patients with wide complex tachycardia may be controversial. The accuracy of determining if the tachycardia is ventricular versus supraventricular with aberrant conduction based on ECG criteria is often unreliable. Giving verapamil or diltiazem to a patient with VT may cause hemodynamic collapse. Therefore treat wide complex tachycardia as if it is VT unless the team is absolutely certain that the rhythm is PSVT. Most cases of wide-complex tachycardia are of ventricular origin.
The initial approach to wide-complex tachycardia is to determine if the patient is hemodynamically stable. The criteria for hemodynamically stable wide-complex tachycardia include1:
- Regular tachycardia at a rate greater than the upper limit of sinus tachycardia (>120 bpm)
- Uniform (monomorphic) QRS configuration of > 120 milliseconds in duration
- No signs or symptoms of impaired consciousness or tissue hypoperfusion
If the patient is hemodynamically unstable, perform immediate electrical cardioversion. (See Vol I—Electrical Cardioversion Algorithm.)
In hemodynamically stable patients, the first order of treatment is to attempt to distinguish if the patient has hemodynamically stable VT or supraventricular tachycardia with aberrancy. Useful clues to help in this decision include:
-
If the patient has a history of coronary artery disease or other structural heart disease, the rhythm is more likely to be ventricular in origin.
-
A history of aberrant rhythms, preexisting bundle branch blocks (BBB) or rate dependent BBB, or accessory pathways suggests SVT with aberrancy if the QRS matches that observed with the tachycardia.
-
Carefully evaluate a 12-lead ECG for AV dissociation. The loss of the normal 1 to 1 association between P-waves and QRS complexes is a reliable criterion of ventricular tachycardia.
-
The classification of the most common forms of wide-complex tachycardia include1:
Ventricular tachycardia
SVT with aberrancy due to intraventricular conduction delay. These
include:
1. Sinus tachycardia
2. Atrial tachycardia (ectopic or reentry)
3. Atrial flutter with a fixed AV block
4. AV nodal reentry tachycardia
5. Junctional tachycardia
Preexcitation tachycardias (associated with or mediated by an accessory pathway) including:
1. Atrial tachycardia
2. Atrial flutter
3. AV reentry tachycardia
-
If a specific diagnosis of the wide complex tachycardia can be made, follow the algorithm that matches the diagnosis.
In hemodynamically stable patients, if supraventricular tachycardia with aberrancy is suspected, adenosine can be tried as a diagnostic and/or therapeutic agent.
Treatment of Regular Wide Complex Tachycardia of Unknown Etiology
If adenosine does not terminate the arrhythmia or reveal a supraventricular tachycardia, the most likely diagnosis is ventricular tachycardia. Amiodarone, procainamide, or sotalol are the recommended drug choices. Both procainamide and amiodarone have negative inotropic and vasodilatory effects so may destabilize a hemodynamically stable patient. In patients with a left ventricular ejection fraction of < 40% or signs of CHF, amiodarone is a better choice than procainamide. In patients not responding to medications, electrical cardioversion is always an option.
IV. Ventricular Tachycardia (Stable)
Although it is often difficult to be sure if a wide complex tachycardia is VT or not, there are some clues that will help in making this decision. Clues that suggest ventricular tachycardia include:
- Presence of AV dissociation
- Fusion/capture beats
- Left axis deviation in the frontal plane on the 12-lead ECG
- QRS width ≥ 140 ms
- Clinical history of coronary artery disease
Treatment
-
The approach to patients assumed to be in VT is largely determined by the hemodynamic stability of the patient. VT in patients in full cardiac arrest is treated like VF. (Vol III—CV5 Ventricular Fibrillation/Pulseless Ventricular Tachycardia) Patients with VT who have a pulse but are hemodynamically unstable must be immediately cardioverted. (Vol III CV9 Electrical Cardioversion)
-
In hemodynamically stable ventricular tachycardia, the form of the VT needs to be differentiated between monomorphic VT and polymorphic VT. In polymorphic VT, the QRS morphology varies, is irregular in rate, and is likely to degenerate into VF.
-
In the treatment of monomorphic ventricular tachycardia with a normal left ventricular ejection fraction (>40%), use just one agent to avoid adverse side effects like proarrhythmic effects of combination therapy. Agents to consider for use in the treatment of monomorphic ventricular tachycardia with preserved left ventricular ejection fraction include:
Preferred medications
- Procainamide IV(Class IIa intervention)
- Sotalol IV(Class IIa intervention)
- Amiodarone IV (Class IIb intervention)
Other acceptable medications
-
Lidocaine IV (Class IIb intervention) While commonly used in the past, it appears to be much less effective than the newer antiarrhythmics.
-
In monomorphic ventricular tachycardia with reduced left ventricular function (ejection fraction < 40% or CHF) the drug of choice is amiodarone IV. (See dosage below.) If drug treatment is ineffective, use DC cardioversion.
- Treatment of polymorphic
VT with normal
baseline QT interval. (No evidence for torsades de pointes.) This
rhythm is frequently precipitated by acute coronary syndromes (ACS),
which need to be treated with anti-ischemic medications. Correct
electrolyte abnormalities. Other potentially effective medications
include: ( Use only one of
these.)
- beta blockers (if ACS) (Class indeterminate)
- amiodarone (Class IIb)
- procainamide (Class IIb)
- sotalol (Class IIb)
If the polymorphic VT is associated with reduced left ventricular function (ejection fraction < 40% or CHF), the drug of choice is IV amiodarone. (See dosage below.) If drug therapy is not successful or the patient becomes unstable, unsynchronized countershock (defibrillation) at the usual defibrillation energy level is recommended.
- Treatment of polymorphic VT with a prolonged baseline
QT interval or torsades de pointes. Torsades de pointes is a special
form of polymorphic VT with a characteristic ECG appearance described
as twisting of the
points. This form of VT is seen especially in
patients with a prolonged QT interval. Torsades de pointes is often
associated with hypokalemia, use of many antiarrhythmic drugs, and
tricyclic agents. The recognition of torsades de pointes is important
because the treatment approach is different from the usual
uniform morphology VT. If the patient is unstable hemodynamically,
immediate defibrillation will need to be used to attempt conversion.
Defibrillation is frequently not successful in converting the torsades
de pointes to a normal rhythm, thus medications and/or overdrive pacing
will need to be used to attempt to convert this difficult
rhythm.
- Correct any electrolyte abnormalities.
- Stop or avoid any medications that may prolong the QT interval. The preferred drug choice for torsades de pointes is magnesium given at a dose of 1 to 2 g IV over 1 to 2 minutes. Doses of up to 4 to 6 g may be necessary to terminate torsades de pointes. Following successful termination of torsades de pointes with magnesium sulfate, start an infusion of 1 to 2 g IV/h.
- If magnesium sulfate is not effective in terminating the patient’s VT, then attempt overdrive pacing (Class indeterminate) of the atrium or ventricle to suppress the episodes of torsades de pointes. Transcutaneous pacing may be tried until a transvenous pacemaker can be inserted.
- In patients free of coronary artery disease, isoproternol (Class indeterminate) may be administered as interim measure to accelerate the heart until temporary pacing can be started.
- Beta blockers may be used with the pacing. Lidocaine (Class undetermined) is of uncertain value.
- In all cases of VT, look for a cause such as hypokalemia, hyperkalemia, myocardial ischemia, acidosis, or hypoxia. Correct if possible.
Use of Amiodarone
Detailed Dosing Schedule
of Amiodarone (Class IIb intervention) in Patients with Reduced Left
Ventricular Function (EF < 40% or CHF) with Stable VT
- 150 mg IV slow bolus over 10 minutes
- Repeat 150 mg IV (over 10 minutes) every 10 to 15 minutes as needed.
- Alternative infusion: 360 mg over 6 hours (1 mg/min over 6 hours), then 540 mg over the remaining 18 hours (0.5 mg/min).
- Maximum total dose: 2.2 grams in 24 hours. This means that all doses (including those used in resuscitation) should be added together, so the total cumulative dose per 24 hours is limited to 2.2 grams.
References
- Hazinski MF, Samson R, Schexnayder S, eds. 2010 Handbook of Emergency Cardiovascular Care. Dallas, Tx: American Heart Association, 2010.
- ECC Subcommittee, Subcommittees and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S750-S756.
- ACLS: Principles and Practice. ACLS - The Reference Textbook. Dallas, TX: American Heart Association, 2003.
- Bertini G, Conti A, Fradella G, et al. Propafenone versus amiodarone in field treatment of primary atrial tachydysrhythmias. J Emerg Med. 1990;8:15-20.