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2-2012

D. Andresen, H.-J. Trappe Applied Cardiopulmonary Pathophysiology 16: 154-161, 2012 Antiarrhythmic drug therapy in patients with
supraventricular or ventricular tachyarrhythmias in
emergencies
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 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
tricular and supraventricular tachyarrhyth-mias is essential for appropriate manage- Emergency medicine and critical care are ment. Most frequently, the diagnosis of the fields that require rapid diagnosis and inter- underlying arrhythmia is readily apparent, but vention to avoid sudden cardiac death (1).
occasionally it is necessary to use clues from These critical interventions can be life-saving the physical examination, the response to or severely debilitating depending on their maneuvers or drugs, in addition to the 12- appropriateness and timeliness. In cardiac lead surface electrocardiogram. Treatment of emergencies, accurate differentiation of ven- supraventricular or ventricular arrhythmias in Antiarrhythmic drug therapy in patients with supraventricular or ventricular tachyarrhythmias emergencies is sometimes difficult (2,3). The hypotension, severe angina, pulmonary ede- purpose of the present manuscript is to sum- ma) should be promptly cardioverted after marize new strategies for patients with administration of an anesthetic agent (Fig. 1).
supraventricular and ventricular tachyarrhyth- Cardioversion should always be performed in mias under emergency situations. a synchronized mode.
Restoration of sinus rhythm
Atrial fibrillation is the most frequent arrhyth- In patients in whom the duration of atrial fib- mia, both in surgical and cardiological inten- rillation is less than 48 hours DC-cardiover- sive care units (4). Knotzer et al. (5) found sion should be considered early. Pharmaco- that 14.8% of „ surgically ill patients" devel- logical conversion to sinus rhythm with an- oped atrial tachyarrhythmias compared to tiarrhythmic drugs is a widely used therapeu- 47.4% of patients treated in a cardiological tic alternative with different efficacy rates (6).
ICU. The goal of acute treatment of atrial fib- Amiodarone has a conversion rate in atrial rillation with rapid ventricular response is to fibrillation of up to 80% (7,8). However, the restore sinus rhythm (rhythm control). If car- time interval between amiodarone adminis- dioversion to sinus rhythm is not possible, the tration and cardioversion is long, and there- secondary goal is to slow the ventricular re- fore amiodarone is not the drug of choice for sponse, usually to a rate of less than 100 pharmacologic cardioversion in patients with beats per minute (rate control). Patients who atrial fibrillation. Iibutilide represents another are hemodynamically unstable (significant class III antiarrhythmic agent that has been history, PE, ECG
dive reflex
Figure 1: Treatment algorithm for patients with tachyarrhythmias. Abbreviations: ACS=acute corona-ry syndrome, DC=direct current, ECG=electrocardiogram, PE=physical examination D. Andresen, H.-J. Trappe reported to have high conversion rates (9).
tients, atrial flutter 2 patients, atrial tachycar- Proarrhythmic effects occur in 5-8% of pa- dia 1 patient) were randomized to diltiazem tients and careful monitoring is required. The (25 mg bolus followed by a continuous infu- conversion rates of recent-onset atrial fibrilla- sion of 20 mg/hour for 24 hours)(group I), tion to sinus rhythm with ibutilide range from amiodarone (300 mg bolus)(group II) or 50-70%. However, ibutilide is not available in amiodarone (300 mg bolus followed by 45 Germany. A new drug for atrial conversion is mg/hour for 24 hours)(group III). The primary vernakalant (10). It has been shown that the end point was a >30% heart rate reduction conversion rates are approximalety 50%; within 4 hours. The secondary end point was however, vernakalant is very expensive and a heart rate <120 beats/min. The primary end therefore of limited use in clinical practice point was achieved in 70% of group I pa- tients, 55% of patients in group II and in 75% In the setting of ineffective chemical car- of patients in group III (p=0.38). In patients dioversion, electrical cardioversion may be achieving heart rate control, diltiazem an option that will restore more patients than showed a significantly better rate reduction chemical cardioversion. In Germany electri- when compared with group II and III cal cardioversion is preferred. (p<0.01). However, premature drug discon-tinuation due to hypotension was requiredsignificantly more often in group I (30%) than Rate-control in atrial fibrillation with
in group II (0%) or group III (5%)(p<0.01). rapid ventricular response
Both a loss of atrial synchrony and the rapid ventricular response may be poorly toleratedin hemodynamically compromised patients.
Acute therapy for patients with atrial flutter in Attempts to restore sinus rhythm are fre- emergencies depends on the clinical presen- quently unsuccessful or even debatable (12).
tation. If the patient presents with acute he- Thus, heart rate control becomes the main modynamic collapse or congestive heart fail- therapeutic goal in this setting. It is well ure, emergent direct-current synchronized known for many years that treatment with in- shock is indicated (Fig. 1). Atrial flutter can travenous digoxin, verapamil, beta-blocking most often be successfully cardioverted to si- agents, or diltiazem alone or in combination nus rhythm with energies less than 50 joules.
is effective in patients with atrial fibrillation A number of drugs have been shown to be and rapid ventricular response via blocking effective in conversion of atrial flutter to sinus the AV-Node. Digoxin may be helpful for rate rhythm. Placebo controlled intravenous ibu- control with an initial dose of 0.5 mg. After tilide trials showed efficacy rates of 38-76% 30 minutes, 0.25 mg digoxin should be ad- for conversion of atrial flutter to sinus rhythm ministered again. In intensive care and emer- (14,15). For those who responded to ibu- gency medicine other therapeutic strategies tilide, the mean time interval to conversion are verapamil (5-10 mg iv), diltiazem (20 mg was 30 minutes; the efficacy of intravenous iv) or beta-blocking agents as propranolol (1- ibutilide (76%) was significantly higher than 5 mg iv,) and esmolol. However, beta-block- that of intravenous procainamide (14%)(16).
ing agents or calcium channel blockers may Several single blinded, randomized control cause additional hypotension. Delle Karth et trials comparing intravenous flecainide with al. (13) compared another pharmacological either intravenous propafenone or intra- approach for rate control: they studied the venous verapamil have shown relatively poor role of amiodarone or diltiazem in a prospec- efficacy for acute conversion (5-13%); in ad- tive, randomized trial. Sixty patients with atri- dition, the conversion rate of intravenous so- al tachyarrhythmias (atrial fibrillation 57 pa- talol varied from 20-40% depending on the Antiarrhythmic drug therapy in patients with supraventricular or ventricular tachyarrhythmias sotalol dose, but was not different from Acute management in wide
placebo. High dose (2 mg) of ibutilide was QRS complex tachycardia
more effective than sotalol (1.5 mg/kg) inconversion of patients with atrial flutter to si- The patient with wide QRS complex tachy- nus rhythm (70% versus 19%) (17).
cardia (QRS width ≥ 0,12 s) and hemody-namically unstable situation should bepromptly cardioverted with a direct current Acute management in narrow-
synchronized shock (Fig. 1). Once the hemo- QRS complex tachycardia
dynamically unstable patient has been car-dioverted and stabilized, it is important to If the patient presents with narrow QRS-com- evaluate the preconversion 12-lead ECG for plex tachycardia (QRS width < 0,12 s) with QRS configuration and signs of AV dissocia- acute hemodynamic collapse or congestive tion. For hemodynamically stable patients, a heart failure, emergent direct-current syn- 12-lead ECG should allow an accurate diag- chronized shock is indicated. However, while nosis in the majority of patients. If after preparations are made for synchronized car- analysing the ECG the diagnosis is uncertain, dioversion, it is reasonable to give adenosine.
the patient should be treated for VT. This is In hemodynamically stable situations, vagal by far the most common diagnosis in patients maneuvers should be initiated to terminate with wide complex tachycardia and VT is po- the arrhythmia or to modify AV conduction tentially life-threatening (18,19).
(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 is recommended. Valsalva manoeuvre – expira-tion against the occluded glottis – is the most In patients with sustained (duration > 30 sec) effective technique. If this fails, intravenous hemodynamically stable monomorphic ven- antiarrhythmic drugs should be administered tricular tachycardia (Fig. 2) amiodarone plays for arrhythmia termination in hemodynami- an important role to terminate ventricular cally stable patients. Adenosine, calcium tachycardia (150-300 mg in 5 min i.v., fol- channel blockers (verapamil) or beta-block- lowed by an infusion of 1000 mg/24 hrs.). Al- ing agents are the drugs of first choice. The ternatives are the administration of pro- advantage of adenosine (9-12 mg iv) relative cainamide (10 mg/kg i.v.) or ajmaline (25-50 to intravenous calcium antagonists or beta- mg i.v. over 5 min). In patients with VT and in blockers relates to its rapidity of onset and the setting of acute myocardial ischemia, li- short half-life. Longer acting agents (intra- docaine (100-150 mg i.v.) was the treatment venous calcium channel blockers or beta- of choice for long term (20). However, it is blocking agents) are of value, particularly for well known that the efficacy of ajmaline is patients with recurrences of narrow QRS higher than the effect of lidocaine, whereas li- tachycardia. It is clear to avoid concomitant docaine is associated with high risk for de- use of intravenous calcium channel blockers generation of monomorphic ventricular and beta-blocking agents because of possible tachycardia into ventricular fibrillation. There- increase of hypotensive and/or bradycardiac fore, lidocaine is no more indicated in these patients 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.

D. Andresen, H.-J. Trappe 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 V and V (triphasic appearance ofV , R to S ratio of less than 1 in V ). The AV dis- sociation and the north-west axis are also helpfulclues for the diagnosis ofventricular tachycardia. reperfusion therapy (PCI, bypass grafting) willbe helpful in terminating the arrhythmia (24). Less frequently, patients may present withpolymorphic ventricular tachycardia (Fig. 3).
Factors associated with this arrhythmia are Torsade de pointes tachycardia
electrolyte abnormalities, acute myocardialischemia, reperfusion arrhythmia, proarrhyth- Torsade de pointes is a type of polymorphic mia antiarrhythmic drugs with QT prolonga- ventricular tachycardia associated with tion. The treatment of choice of polymorphic marked QT prolongation. It may occur after ventricular tachycardia is, after coronary care administration of class Ia and class III antiar- unit monitoring, discontinuation of the of- rhythmic drugs. The tachycardia is paroxys- fending drug, and isoproterenol infusion with mal and may result in ventricular fibrillation shortening repolarization and increasing the and sudden death (25,26). Its onset is pro- heart rate (1-4 µg/min i.v.) as initial steps. Atri- moted by a slow basic rhythm and frequent- al or ventricular pacing may be an option to ly follows a pause induced by a premature suppress the polymorphic VT. In these situa- ventricular contraction. The tachycardia is tions with polymorphic ventricular tachycar- characterized by polymorphic QRS complex- dia there is also a clear indication for emer- es. Progressive lengthening of the QT interval gency treatment with amiodarone (150-300 and the development of a prominent U wave mg i.v., followed by infusion of 1000 are important warning signs. The degree of mg/day)(20,22). Despite all considerations QT prolongation that predicts torsade de about the "ideal" therapeutic strategy, in pointes tachycardia is not known. However, polymorphic VT patients evaluation of the prolonged QT syndromes may be congenital underlying disease and the mechanism of the (Romano-Ward syndrome, Jervell-Lange- arrhythmia is the most important step. In Nielsen syndrom) or acquired (class I a- and some cases, acute myocardial ischemia is class III-antiarrhythmic drugs). The treatment present ("acute coronary syndrome") and in intensive care and emergencies is stopping Antiarrhythmic drug therapy in patients with supraventricular or ventricular tachyarrhythmias Figure 3: 12-lead ECGof a patient with fastpoymorphic ventriculartachycardia after acutemyocardial infarction. the offending drug and correction of elec- tricular fibrillation. In 2010, the new resusci- trolyte abnormalities with potassium and tation guidelines reported again the chain of magnesium. Intravenous magnesium sulfate survival concept, with four links – early ac- (initial bolus of 2g i.v. over 10 min., another cess, cardiopulmonary resuscitation, defibril- bolus of 2g after 15 min if the initial bolus lation, and advanced care – as the way to ap- failed, followed by a continuous infusion of proach cardiac arrest (24). It has been point- 500 mg/h i.v.) may be effective, even if the ed out that the highest potential survival rate serum magnesium level is within the normal from cardiac arrest can be achieved only range (27,28). Although magnesium has when the following sequence of events oc- been used to treat arrhythmias for several curs as rapidly as possible: (a) recognition of decades, its mechanism of action and effica- early warning signs, (b) activation of the cy remain controversial (29,30). emergency medical services system, (c) basiccardiopulmonary resuscitation, (d) defibrilla-tion, (e) management of the airway and ven- Ventricular fibrillation and
tilation, and (f) intravenous administration of medications. Prompt cardiopulmonary resus-citation with early defibrillation either by DC- Approximately 1.000 people in the United countershock or an automated external de- States suffer from cardiac arrest each day, fibrillator (AED) significantly improves the most often as a complication of an acute my- likelihood of successful resuscitation from ocardial infarction with accompanying ven- ventricular fibrillation. According to the new D. Andresen, H.-J. Trappe guidelines, the antiarrhythmic drug of choice 2. Reinelt P, Karth GD, Geppert A, Heinz G.
Incidence and type of cardiac arrhythmias in patients with recurrent ventricular fibrilla- in critically ill patients: a single center expe- tion or fast ventricular tachycardia refractory rience in a medical-cardiological ICU. Inten- to DC defibrillation is amiodarone. It also ap- sive Care Med 2001; 27: 1466-1473 pears to improve the response to DC-coun- 3. Baine WB, Yu M, Weis KA. Trends and out- tershock. Amiodarone is a complex drug with comes in the hospitalization of older Amer- effects on sodium, potassium, and calcium icans for cardiac conduction disorders or ar- channels as well as alpha- and beta-adrener- rhythmias, 1991-1998. J Am Geratr Soc gic blocking properties. Amiodarone is a 2001; 49: 763-770 highly efficacious antiarrhythmic agent for 4. Prystowsky EN. Management of atrial fibril- many cardiac arrhythmias, ranging from atrial lation: therapeutical options and clinical de- fibrillation to malignant ventricular tachy cisions. Am J Cardiol 2000; 85: 3D-11D 5. Knotzer H, Mayr A, Ulmer H, Lederer W, arrhythmias (31). In most published studies, Schobersberger W, Mutz M, Hasibeder W.
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