antiarrhythmic drug therapy in patients with ...€¦ · key words:tachyarrhythmias, intensive...

154 D. Andresen, H.-J. Trappe

Introduction

Emergency medicine and critical care arefields that require rapid diagnosis and inter-vention to avoid sudden cardiac death (1).These critical interventions can be life-savingor severely debilitating depending on theirappropriateness and timeliness. In cardiacemergencies, accurate differentiation of ven-

tricular and supraventricular tachyarrhyth-mias is essential for appropriate manage-ment. Most frequently, the diagnosis of theunderlying arrhythmia is readily apparent, butoccasionally it is necessary to use clues fromthe physical examination, the response tomaneuvers or drugs, in addition to the 12-lead surface electrocardiogram. Treatment ofsupraventricular or ventricular arrhythmias in

Applied Cardiopulmonary Pathophysiology 16: 154-161, 2012

Antiarrhythmic drug therapy in patients with supraventricular or ventricular tachyarrhythmias inemergencies

Dietrich Andresen, Hans-Joachim Trappe*

Klinik für Kardiologie, Allgemeine Innere Medizin und konservative Intensivmedizin, Vivan-tes Klinikum am Urban und im Friedrichshain, Berlin, Germany; *Medizinische Klinik II(Kardiologie und Angiologie), Ruhr-Universität Bochum, Herne, Germany

Abstract

Atrial fibrillation (AF), atrial flutter, AV-nodal reentry tachycardia (AVNRT) with rapid ventricu-lar response, atrial ectopic tachycardia and preexcitation syndromes (AVRT) sometimes com-bined with AF or ventricular tachyarrhythmias (VTA) are typical arrhythmias in emergency pa-tients. Most frequently, the diagnosis of the underlying arrhythmia is possible from the 12-leadsurface electrocardiogram, the physical examination and the response to manoeuvres or drugs.In unstable hemodynamics, immediate DC-cardioversion is indicated. Conversion of AF to si-nus rhythm (SR) is possible using antiarrhythmic drugs. Amiodarone has a conversion rate inAF of up to 80%. A new drug for AF conversion is vernakalant. Acute therapy of atrial flutter(Aflut) in intensive care pts depends on the clinical presentation. It can most often be success-fully cardioverted to SR with DC-energies less than 50 joules. In narrow complex tachycardia,if the patient is hemodynamically stable, treatment should start with vagal manoeuvre. If tachy-cardia persists and atrial flutter is excluded, use of adenosine (6 mg as rapid i.v. bolus) is sug-gested. Successful termination by vagal manoeuvre or adenosine indicates that it was AVNRTor AVRT. If there is no response to adenosine (even after a second bolus) a longer-acting drug(e.g. verapamil, diltiazem) is recommended. Drugs like procainamide, sotalol, amiodarone ormagnesium are recommended for treatment of VTA pts. However, today only amiodarone isthe drug of choice in VTA pts and also effective even in pts with defibrillation-resistant out-of-hospital cardiac arrest.

Key words: tachyarrhythmias, intensive care, emergency medicine

155Antiarrhythmic drug therapy in patients with supraventricular or ventricular tachyarrhythmias

emergencies is sometimes difficult (2,3). Thepurpose of the present manuscript is to sum-marize new strategies for patients withsupraventricular and ventricular tachyarrhyth-mias under emergency situations.

Atrial fibrillation

Atrial fibrillation is the most frequent arrhyth-mia, both in surgical and cardiological inten-sive care units (4). Knotzer et al. (5) foundthat 14.8% of „ surgically ill patients“ devel-oped atrial tachyarrhythmias compared to47.4% of patients treated in a cardiologicalICU. The goal of acute treatment of atrial fib-rillation with rapid ventricular response is torestore sinus rhythm (rhythm control). If car-dioversion to sinus rhythm is not possible, thesecondary goal is to slow the ventricular re-sponse, usually to a rate of less than 100beats per minute (rate control). Patients whoare hemodynamically unstable (significant

hypotension, severe angina, pulmonary ede-ma) should be promptly cardioverted afteradministration of an anesthetic agent (Fig. 1).Cardioversion should always be performed ina synchronized mode.

Restoration of sinus rhythm

In patients in whom the duration of atrial fib-rillation is less than 48 hours DC-cardiover-sion should be considered early. Pharmaco-logical conversion to sinus rhythm with an-tiarrhythmic drugs is a widely used therapeu-tic alternative with different efficacy rates (6).Amiodarone has a conversion rate in atrialfibrillation of up to 80% (7,8). However, thetime interval between amiodarone adminis-tration and cardioversion is long, and there-fore amiodarone is not the drug of choice forpharmacologic cardioversion in patients withatrial fibrillation. Iibutilide represents anotherclass III antiarrhythmic agent that has been

tachyarrhythmias

history, PE, ECG

supraventricular ventricular

stable unstable unstable stable

vagal maneuvers drugs DC cardioversion

drugs

amiodarone

ajmaline

procainamide

isoprenaline

magnesium

sulfate

carotid sinus

massage

gagging

valsalva

trendelenburg

dive reflex

adenosine

ajmaline

procainamide

verapamil

digitalis

DC cardioversion

DC cardioversion

Figure 1: Treatment algorithm for patients with tachyarrhythmias. Abbreviations: ACS=acute corona-ry syndrome, DC=direct current, ECG=electrocardiogram, PE=physical examination


reported to have high conversion rates (9).Proarrhythmic effects occur in 5-8% of pa-tients and careful monitoring is required. Theconversion rates of recent-onset atrial fibrilla-tion to sinus rhythm with ibutilide range from50-70%. However, ibutilide is not available inGermany. A new drug for atrial conversion isvernakalant (10). It has been shown that theconversion rates are approximalety 50%;however, vernakalant is very expensive andtherefore of limited use in clinical practice(11).

In the setting of ineffective chemical car-dioversion, electrical cardioversion may bean option that will restore more patients thanchemical cardioversion. In Germany electri-cal cardioversion is preferred.

Rate-control in atrial fibrillation withrapid ventricular response

Both a loss of atrial synchrony and the rapidventricular response may be poorly toleratedin hemodynamically compromised patients.Attempts to restore sinus rhythm are fre-quently unsuccessful or even debatable (12).Thus, heart rate control becomes the maintherapeutic goal in this setting. It is wellknown for many years that treatment with in-travenous digoxin, verapamil, beta-blockingagents, or diltiazem alone or in combinationis effective in patients with atrial fibrillationand rapid ventricular response via blockingthe AV-Node. Digoxin may be helpful for ratecontrol with an initial dose of 0.5 mg. After30 minutes, 0.25 mg digoxin should be ad-ministered again. In intensive care and emer-gency medicine other therapeutic strategiesare verapamil (5-10 mg iv), diltiazem (20 mgiv) or beta-blocking agents as propranolol (1-5 mg iv,) and esmolol. However, beta-block-ing agents or calcium channel blockers maycause additional hypotension. Delle Karth etal. (13) compared another pharmacologicalapproach for rate control: they studied therole of amiodarone or diltiazem in a prospec-tive, randomized trial. Sixty patients with atri-al tachyarrhythmias (atrial fibrillation 57 pa-

tients, atrial flutter 2 patients, atrial tachycar-dia 1 patient) were randomized to diltiazem(25 mg bolus followed by a continuous infu-sion of 20 mg/hour for 24 hours)(group I),amiodarone (300 mg bolus)(group II) oramiodarone (300 mg bolus followed by 45mg/hour for 24 hours)(group III). The primaryend point was a >30% heart rate reductionwithin 4 hours. The secondary end point wasa heart rate <120 beats/min. The primary endpoint was achieved in 70% of group I pa-tients, 55% of patients in group II and in 75%of patients in group III (p=0.38). In patientsachieving heart rate control, diltiazemshowed a significantly better rate reductionwhen compared with group II and III(p<0.01). However, premature drug discon-tinuation due to hypotension was requiredsignificantly more often in group I (30%) thanin group II (0%) or group III (5%)(p<0.01).

Atrial flutter

Acute therapy for patients with atrial flutter inemergencies depends on the clinical presen-tation. If the patient presents with acute he-modynamic collapse or congestive heart fail-ure, emergent direct-current synchronizedshock is indicated (Fig. 1). Atrial flutter canmost often be successfully cardioverted to si-nus rhythm with energies less than 50 joules.A number of drugs have been shown to beeffective in conversion of atrial flutter to sinusrhythm. Placebo controlled intravenous ibu-tilide trials showed efficacy rates of 38-76%for conversion of atrial flutter to sinus rhythm(14,15). For those who responded to ibu-tilide, the mean time interval to conversionwas 30 minutes; the efficacy of intravenousibutilide (76%) was significantly higher thanthat of intravenous procainamide (14%)(16).Several single blinded, randomized controltrials comparing intravenous flecainide witheither intravenous propafenone or intra-venous verapamil have shown relatively poorefficacy for acute conversion (5-13%); in ad-dition, the conversion rate of intravenous so-talol varied from 20-40% depending on the


sotalol dose, but was not different fromplacebo. High dose (2 mg) of ibutilide wasmore effective than sotalol (1.5 mg/kg) inconversion of patients with atrial flutter to si-nus rhythm (70% versus 19%) (17).

Acute management in narrow-QRS complex tachycardia

If the patient presents with narrow QRS-com-plex tachycardia (QRS width < 0,12 s) withacute hemodynamic collapse or congestiveheart failure, emergent direct-current syn-chronized shock is indicated. However, whilepreparations are made for synchronized car-dioversion, it is reasonable to give adenosine.In hemodynamically stable situations, vagalmaneuvers should be initiated to terminatethe arrhythmia or to modify AV conduction(Fig. 1). Carotid sinus massage is by applyingpressure over the carotid artery on one side.If it is not working, use of the opposite side isrecommended. Valsalva manoeuvre – expira-tion against the occluded glottis – is the mosteffective technique. If this fails, intravenousantiarrhythmic drugs should be administeredfor arrhythmia termination in hemodynami-cally stable patients. Adenosine, calciumchannel blockers (verapamil) or beta-block-ing agents are the drugs of first choice. Theadvantage of adenosine (9-12 mg iv) relativeto intravenous calcium antagonists or beta-blockers relates to its rapidity of onset andshort half-life. Longer acting agents (intra-venous calcium channel blockers or beta-blocking agents) are of value, particularly forpatients with recurrences of narrow QRStachycardia. It is clear to avoid concomitantuse of intravenous calcium channel blockersand beta-blocking agents because of possibleincrease of hypotensive and/or bradycardiaceffects.

Acute management in wideQRS complex tachycardia

The patient with wide QRS complex tachy-cardia (QRS width ≥ 0,12 s) and hemody-namically unstable situation should bepromptly cardioverted with a direct currentsynchronized shock (Fig. 1). Once the hemo-dynamically unstable patient has been car-dioverted and stabilized, it is important toevaluate the preconversion 12-lead ECG forQRS configuration and signs of AV dissocia-tion. For hemodynamically stable patients, a12-lead ECG should allow an accurate diag-nosis in the majority of patients. If afteranalysing the ECG the diagnosis is uncertain,the patient should be treated for VT. This isby far the most common diagnosis in patientswith wide complex tachycardia and VT is po-tentially life-threatening (18,19).

Monomorphic ventricular tachycardia

In patients with sustained (duration > 30 sec)hemodynamically stable monomorphic ven-tricular tachycardia (Fig. 2) amiodarone playsan important role to terminate ventriculartachycardia (150-300 mg in 5 min i.v., fol-lowed by an infusion of 1000 mg/24 hrs.). Al-ternatives are the administration of pro-cainamide (10 mg/kg i.v.) or ajmaline (25-50mg i.v. over 5 min). In patients with VT and inthe setting of acute myocardial ischemia, li-docaine (100-150 mg i.v.) was the treatmentof choice for long term (20). However, it iswell known that the efficacy of ajmaline ishigher than the effect of lidocaine, whereas li-docaine is associated with high risk for de-generation of monomorphic ventriculartachycardia into ventricular fibrillation. There-fore, lidocaine is no more indicated in thesepatients and should be avoided. Other antiar-rhythmic drugs like sotalol (20 mg in 5 mini.v.), propafenone (1-2 mg/kg i.v.) or fle-cainide (1-2 mg/kg i.v.) do not play a role as“first line” drugs in stable monomorphic VT(21-23). In 2012, these drugs are rarely usedin monomorphic VT.


Polymorphic ventricular tachycardia

Less frequently, patients may present withpolymorphic ventricular tachycardia (Fig. 3).Factors associated with this arrhythmia areelectrolyte abnormalities, acute myocardialischemia, reperfusion arrhythmia, proarrhyth-mia antiarrhythmic drugs with QT prolonga-tion. The treatment of choice of polymorphicventricular tachycardia is, after coronary careunit monitoring, discontinuation of the of-fending drug, and isoproterenol infusion withshortening repolarization and increasing theheart rate (1-4 µg/min i.v.) as initial steps. Atri-al or ventricular pacing may be an option tosuppress the polymorphic VT. In these situa-tions with polymorphic ventricular tachycar-dia there is also a clear indication for emer-gency treatment with amiodarone (150-300mg i.v., followed by infusion of 1000mg/day)(20,22). Despite all considerationsabout the “ideal” therapeutic strategy, inpolymorphic VT patients evaluation of theunderlying disease and the mechanism of thearrhythmia is the most important step. Insome cases, acute myocardial ischemia ispresent (“acute coronary syndrome”) and

reperfusion therapy (PCI, bypass grafting) willbe helpful in terminating the arrhythmia (24).

Torsade de pointes tachycardia

Torsade de pointes is a type of polymorphicventricular tachycardia associated withmarked QT prolongation. It may occur afteradministration of class Ia and class III antiar-rhythmic drugs. The tachycardia is paroxys-mal and may result in ventricular fibrillationand sudden death (25,26). Its onset is pro-moted by a slow basic rhythm and frequent-ly follows a pause induced by a prematureventricular contraction. The tachycardia ischaracterized by polymorphic QRS complex-es. Progressive lengthening of the QT intervaland the development of a prominent U waveare important warning signs. The degree ofQT prolongation that predicts torsade depointes tachycardia is not known. However,prolonged QT syndromes may be congenital(Romano-Ward syndrome, Jervell-Lange-Nielsen syndrom) or acquired (class I a- andclass III-antiarrhythmic drugs). The treatmentin intensive care and emergencies is stopping

Figure 2: 12-lead-ECG ofa patient with wide QRScomplex tachycardia. Thetracing shows right bund-le branch block morpholo-gy. Note the typical QRSfeatures in leads V1 and V6(triphasic appearance ofV1, R to S ratio of lessthan 1 in V6). The AV dis-sociation and the north-west axis are also helpfulclues for the diagnosis ofventricular tachycardia.


the offending drug and correction of elec-trolyte abnormalities with potassium andmagnesium. Intravenous magnesium sulfate(initial bolus of 2g i.v. over 10 min., anotherbolus of 2g after 15 min if the initial bolusfailed, followed by a continuous infusion of500 mg/h i.v.) may be effective, even if theserum magnesium level is within the normalrange (27,28). Although magnesium hasbeen used to treat arrhythmias for severaldecades, its mechanism of action and effica-cy remain controversial (29,30).

Ventricular fibrillation and cardiac arrest

Approximately 1.000 people in the UnitedStates suffer from cardiac arrest each day,most often as a complication of an acute my-ocardial infarction with accompanying ven-

tricular fibrillation. In 2010, the new resusci-tation guidelines reported again the chain ofsurvival concept, with four links – early ac-cess, cardiopulmonary resuscitation, defibril-lation, and advanced care – as the way to ap-proach cardiac arrest (24). It has been point-ed out that the highest potential survival ratefrom cardiac arrest can be achieved onlywhen the following sequence of events oc-curs as rapidly as possible: (a) recognition ofearly warning signs, (b) activation of theemergency medical services system, (c) basiccardiopulmonary resuscitation, (d) defibrilla-tion, (e) management of the airway and ven-tilation, and (f) intravenous administration ofmedications. Prompt cardiopulmonary resus-citation with early defibrillation either by DC-countershock or an automated external de-fibrillator (AED) significantly improves thelikelihood of successful resuscitation fromventricular fibrillation. According to the new

Figure 3: 12-lead ECGof a patient with fastpoymorphic ventriculartachycardia after acutemyocardial infarction.


guidelines, the antiarrhythmic drug of choicein patients with recurrent ventricular fibrilla-tion or fast ventricular tachycardia refractoryto DC defibrillation is amiodarone. It also ap-pears to improve the response to DC-coun-tershock. Amiodarone is a complex drug witheffects on sodium, potassium, and calciumchannels as well as alpha- and beta-adrener-gic blocking properties. Amiodarone is ahighly efficacious antiarrhythmic agent formany cardiac arrhythmias, ranging from atrialfibrillation to malignant ventricular tachy -arrhythmias (31). In most published studies,intravenous amiodarone has been adminis-tered in patients with ventricular tachy -arrhythmias only after failure of other antiar-rhythmic drugs. In 1999, Kudenchuk de-scribed in 504 randomized patients with out-of-hospital cardiac arrest due to refractoryventricular arrhythmias (ARREST study) thattreatment with amiodarone (single 300 mgdose of intravenous amiodarone) resulted ina higher rate of survival to hospital admission(44%) compared to placebo (34%) (p=0.03)(32).

Conclusions

In all patients with tachyarrhythmias, evalua-tion of the underlying etiology and the de-gree of left ventricular function (dysfunction)is essential. Correct treatment is based on anunderstanding of the mechanism that causedthe situation. In hemodynamic unstable situ-ation DC cardioversion/defibrillation is indi-cated. In hemodynamic stable patients thereis still a place for antiarrhythmic drug treat-ment. However, in 2012 only few specific an-tiarrhythmic drugs are recommended. Amio-darone is the drug of choice in life-threaten-ing ventricular tachyarrhythmias.

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Correspondence address:Prof. Dietrich Andresen, M.D.Klinik für Kardiologie, Allgemeine Innere Medizin und konservative IntensivmedizinVivantes Klinikum am UrbanDieffenbachstr. 1, 10967 [email protected]

antiarrhythmic drug therapy in patients with ...€¦ · key words:tachyarrhythmias, intensive...

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