Review Article

THE cardiac tachyarrhythmias can be divided into 2 majorgroups.

(a) Supraventricular

(b) Ventricular

The supraventricular tachyarrhythmias, commonlyseen in clinical practice are:

1. Supraventricular tachycardias.

2. Atrial flutter

3. Atrial fibrillation

Supraventricular arrythmias can be life threatening-

(a) When associated with underlying LV dys-function heart failure.

(b) In association with WPW Syndrome where rapidconduction across the accessory pathway maylead to rapid ventricular rates.

(c) In association with incessant atrial tachycardiawhichcan lead to LV Dysfunction and tachy-cardiomyopathy.

Supraventricular tachycardias

The term Supraventricular Tachycardia (SVT) refersto paroxysmal tachyarrhythmias, which require atrial oratrioventricular nodal tissue, or both, for their initiationand maintenance. Supraventricular tachycardias areoften recurrent, occasionally persistent, and a frequentcause of visits to emergency rooms and primary carephysicians. Common symptoms of supraventriculartachycardia include palpitations, anxiety, light-headed-ness, chest pain, pounding in the neck and chest, anddyspnea

Most types of tachycardia have a reentry mechanism(Fig. 1a-c) and they are classified according to thelocation of the reentry circuit. Approximately 60% of

LIFE THREATENING SUPRAVENTRICULAR ARRYTHMIAS DIAGNOSIS:PHARMACOLOGICAL AND NON-PHARMACOLOGICAL OPTIONS OF MANAGEMENT

Balbir SinghSenior Consultant, Department of Cardiology, Indraprastha Apollo Hospitals, Sarita Vihar,

New Delhi 110 076, India.

cases are due to an atrioventricular nodal reentry circuit,and about 30% are due to an atrioventricular reentrycircuit mediated by an accessory pathway–a shortmuscle bundle that directly connects the atria andventricles.Atrial tachycardia comprises about 10% ofcases and often has a focal origin.

Table 1: Supraventricular tachycardia

1. Atrioventricular nodal reentry (AVNRT)

2. Atrioventricular reentry(a) Accessory pathway mediated.(b) Permanent form of junctional reciprocating

tachycardia (PJRT)-usually seen in children

3. Atrial tachycardia

Table 2: Causes of wide QRS tachycardia

1. Ventricular tachycardia

2. Supraventricular tachycardia with aberrancy

3. Supraventricular tachycardia with underlying bundlebranch block

4. Antidromic tachycardia in patients with WPWsyndrome

AV Nodal Reentry

It is the most common mechanism of supra-ventricular tachycardias, comprising 60% of allsupraventricular tachycardias. The supraventriculartachycardia usually have narrow QRS complex unlessassociated with aberrancy. The EKG features whichhelp to distinguish various forms of supraventriculartachycardia are:

(a) Relationship of atrial and ventricular events:Presence of atrial activity and AV relationship help todistinguish reentrant tachycardia from atrial tachy-

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cardias. Reentrant tachycardias have 1:1 AVrelationship. The presence of AV block makes areentrant tachycardia unlikely.

(b) RP versus PR interval ratio: The ratio of RP to PRhelps in distinguishing various forms of supra-ventricular tachycardias. In typical AV nodal reentry,the atria and ventricles are activated simultaneously,thus the P waves are usually burried within the QRScomplexes.

In patients with orthodromic tachycardias, which aremediated through accessory pathway the P wave can beseen outside the QRS complex and the RP interval isusually shorter than the PR interval. In patients withatrial tachycardia the RP interval is generally longer thanPR interval.

Accessory pathway mediated tachycardia

The most frequently occurring arrhythmias inpatients with pre-excitation are:

(a) Circus Movement Tachycardia

A circus movement tachycardia with AV conductionover the AV node and retrograde conduction over theaccessory pathway is called an orthodromic tachycardia(Fig.1c). A tachycardia proceeding, in the reversedirection is an antidromic tachycardia.

Orthodromic tachycardia is much more frequent thanan antidromic tachycardia. Antidromic tachycardiaproduces a broad QRS complex tachycardia. The QRS iswide and starts with a clear delta wave indicating initialventricular activation outside the specific conductionsystem.

Some patients show no preexcitation during the sinusrhythm but have conduction only in the retrogradedirection (concealed accessory pathways). Thesepatients develop only orthodromic tachycardias. Theconcealed pathways may be having fast or slowretrograde conduction. The slowly conducting retro-grade pathways are uncommon and generally causeparoxysmal junctional reentrant tachycardia, which maybe incessant in children.

(b) Atrial Fibrillation

The ventricles are usually protected by the refractoryperiod of the AV node against a very rapid ventricularrate during a rapid atrial rhythm such as atrialfibrillation. In patients with accessory pathways, atrial

Fig. 1 (A-C). An impulse (Panel A, arrows), initiated normally in thesinus node, passes through two pathways–for example,the atrioventricular nodal connection and an accessorypathway. A premature atrial impulse (Panel B) occurs andreaches the accessory pathway when it is still refractorybut conduction can occur in the atrioventricular node. Theimpulse takes sufficient time to circulate through theatrioventricular node and across the ventricle to allow theaccessory pathway to recover its excitability and conductthe impulse back to the atrium (Panel C). The wave frontreenters the atrioventricular node, continually encountersexcitable tissue, and is perpetuated as a reentry circuit.

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If supraventricular tachycardia is refractory toadenosine or rapidly recurs, clinical experience indicatesthat the tachycardia can be terminated by theadministration of intravenous verapamil or a beta-blocker.

The treatment of choice for patients with atrialfibrillation and preexcitation is influenced by theventricular rate and hemodynamic consequences of thearrhythmia. Cardioversion should be done immediatelyif a rapid ventricular rhythm during AF leads tosevere circulatory impairment. If the patient ishemodynamically stable, procainamide, ajmaline, amio-darone can be given intravenously (Table 4).

Table 4: Treatment of supraventricular tachycardia

AVNRT

(a) Vagal maneuvers(b) Diltiazem 0.25 mg/kg IV)(c) Adenosine (12-20 mg IV)(d) Amiodarone (150-300 mg IV bolus)(e) Verapamil 10 mg IV over 3 minutes( f ) Ajmaline 1mg/kg IV(g) Procainamide 10 mg/kg IV

Orthodromic tachycardia (same as above)

Antidromic tachycardia (AVRT)

(a) Procainamide 10 mg/kg(b) Amiodarone (300 mg IV over 10-15 minutes)(c) Ajmaline (1 mg/kg IV)

Atrial fibrillation with WPW syndrome

Hemodynamically not well tolerated-DC shock

Hemodynamically tolerated

• Procainamide IV• Ajmaline IV

• Disopyramide IV

After the acute management, most patients can nowbe offered a cure with a radiofrequency ablationparticularly those with WPW syndrome. The successrates are high (95-98%) with low complications, makingthis a procedure of choice in these patients.

Atrial tachycardia

The atrial rate is generally 150 to 200 beats/minute

fibrillation can be an extremely dangerous arrhythmia ifthe accessory pathway has a short antegrade refractoryperiod. The ventricular rate is not only determined by theantegrade refractory period of an accessory pathway butalso by the antegrade refractory period of the AV node.Verapamil, betablockers or digoxin are contraindicatedin patients with atrial fibrillation and antegradeconduction as by blocking the AV node they increase theconduction across the accessory pathway which mayresult at times in ventricular fibrillation.

Acute Treatment of SVTs

Before discussing the choice of a drug, emphasisshould be placed upon the effectiveness of vagalmaneuvers (Table 3) that block the conduction in the AVnode in the patient with circus movement tachycardia.

Table 3: Maneuvers used to interrupt a supra-ventricular tachycardia.

• Carotid massage• Valsalva maneuver• Squatting (valsalva)• Gag reflex (finger in the throat)• Dive reflex (immersion of face in cold water)

These should be performed as quickly as possibleafter the onset of tachycardia. The longer the delay,higher the sympathetic tone and less the possibility of avagal maneuver being successful.

If vagal maneuvers are unsuccessful, the intravenousinjection of a drug that prolongs the refractory periodof the AV node (verapamil, diltiazem, adenosine, pro-pranolol or amiodarone) or produce the lengthening ofthe refractory period of the accessory pathway (ajmaline,procainamide or amiodarone) usually terminates thecircus movement tachycardia.

As with vagal maneuvers, treatment with intravenousadenosine has both diagnostic and therapeutic value.Data from randomized trials show that supraventriculartachycardia is terminated in 60 to 80% of patients treatedwith 6 mg of adenosine and in 90 to 95% of those treatedwith 12 mg. In patients with atrial tachycardias,adenosine causes a transient atrioventricular nodal blockor interrupts the tachycardia. ECG monitoring isrequired during the administration of adenosine, andresuscitation equipment should be available in the eventthat the rare complications of bronchospasm orventricular fibrillation occur.

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Drugs are less effective than these techniques. Theindications for the use of drugs in this condition are:

(a) To slow the ventricular response rate (with either abetablocker or calcium channel blocker).

(b) To enhance the efficacy of rapid atrial pacing inrestoring sinus rhythm (use of quinidine, pro-cainamide or sotalol).

(c) To enhance the likelihood that the sinus rhythm willbe sustained following effective DC cardioversion.

Selection of acute therapy for atrial flutter with eitherDC cardioversion or atrial pacing will depend on theclinical presentation of the patient and both the clinicalavailability and ease of applying either of thesetechniques. DC cardioversion has a very high likelihoodof success. It requires as low as 25 J, however, since100 J is virtually always successful and never harmful itshould be considered as the initial shock.

Atrial Fibrillation

The mechanisms involved in atrial fibrillationindicate that it results from multiple and concurrentlycirculating reentrant excitation wave fronts of theleading circile type in the atria. The electrocardiogramremains the gold standard for the diagnosis of atrialfibrillation. Classically, the EKG shows the absence ofdiscrete atrial activity, a variable RR interval and anirregular baseline between QRS complexes. Occasion-ally this rhythm may be difficult to diagnosefrom theEKG. The coarse atrial fibrillation may mimic atrialflutter.

Treatment. Once the diagnosis of atrial fibrillation isestablished, two courses of therapy are available (a)attempt to convert the rhythm to sinus rhythm using DCcardioversion or antiarrhythmic drug therapy, (b) controlthe ventricular response rate using drugs such as digoxin,betablocker or a calcium channel blocker.

The choice between these approaches depends on theclinical status of the patients. As a general rule if theclinical situation is of hypotension or pulmonary edema,where prompt restoration to sinus rhythm is essential,DC cardioversion is the treatment of choice. If electriccardioversion is to be performed then it should be doneafter the administration of a type 1A agent or amiodaroneto help maintain sinus rhythm after cardioversion. DCcardioversion establishes normal sinus rhythm in over90% of patients, but sinus rhythm remains for 12 monthsin only 30-50%. Class IA, IC and III (amiodarone,

and the P wave contour is different from that of sinus Pwave. As the atrial rate increases the degree of AV blockincreases and Wenckebach second-degree block mayensue i.e., atrial tachycardia with block.

EKG Diagnosis

Atrial tachycardia can sometimes become incessantparticularly in children and young adults when over aprolonged period of time can lead to LV Dysfunction andheart failure, this has termed as tachycardiomyopathy.This condition is reversible following the cure of thetachycardia, the LV function generally improved over aperiod of time.

DIAGNOSIS

It has been demonstrated that there are two types ofatrial flutter viz., (a) Type I or classic atrial flutter and (b)Type II or very rapid flutter.

Type I atrial flutter has an atrial rate of about 240-340bpm and can be interrupted by rapid atrial pacing.Type II atrial flutter has an atrial rate ranging from 340-440bpm and it cannot be interrupted by rapid atrialpacing. The appearance of the saw toothed flutter wavesin the EKG particularly in leads II, III and aVF remainsthe standard for the diagnosis of atrial flutter and isprobably the easiest way to establish the diagnosis. If theheart rate is fast, carotid sinus massage may be used toproduce transient AV block and allow the better analysisof the flutter waves. If the diagnosis remains unclear, thefollowing maneuvers may be used.

(a) Use of pharmacological agent-such as edrophonium,adenosine or esmolol, to increase AV conductiontransiently.

(b) Placement of an esophageal lead or an atrial lead forrecording the atrial activity. In the presence of WPWsyndrome with possibility of atrial flutter, the use ofpharmacological agents, which block the AV nodalconduction, is fraught with danger.

TREATMENT

When the diagnosis of atrial flutter is made, threetherapeutic options are available, viz.,

(a) Antiarrhythmic drug therapy.

(b) DC current cardioversion.

(c) Rapid atrial pacing to interrupt atrial flutter.

DC cardioversion or pacing is the preferred option.

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cause is severe ischemia resulting from obstructivecoronary artery disease. The management here istreating ischemia with medications or revascularisation,and there is no role anti-arrythmics drugs exceptbetablockers.

Treatment of TDP

Summary

• The major groups of cardiac tachyarrhythmiasare supraventricular and ventricular. The supra-ventricular tachyarrhythmias commonly seen areatrial tachycardia, supraventricular tachycardias,atrial flutter and atrial fibrillation.

• The common mechanisms of supraventriculartachycardias involve reentry using the AV node orreentry using a bypass tract, both producing a narrowQRS complex tachycardia. Acute management ofthese remains the same.

• For the acute management of supraventriculartachycardias, adenosine is the drug of choice,intravenous verapamil, diltiazem or beta-blockers arealso useful. Radiofrequency ablation has emerged asa modality of choice for the long term management ofthese patients.

• Ventricular tachycardia (VT) is the commonest causeof a broad QRS tachycardia. The differentialdiagnosis of a broad QRS tachycardia in theemergency room is crucial for the proper manage-ment of these patients. Sustained monomorphic andpolymorphic VT represents two distinct entities.Polymorphic VT is usually seen in patients with anunderlying heart disease, (coronary artery diseasebeing the commonest) or with QT with QTprolongation.

• The acute treatment of VT depends on thehemodynamic stability of the patient, DC cardio-version is the method of choice for those with hemo-dynamic compromise. Intravenous anti-arrhythmicdrugs (xylocaine, procainamide, amiodarone,sotalol) may be tried for those who arehemodynamically stable. Oral amiodarone is theagent most commonly used for long termmanagement.

sotalol) agents can be used to terminate acute onset atrialfibrillation and prevent recurrences of atrial fibrillation.Amiodarone appears to be superior to class IA agentsbased on the side effect profile and risk of proarrhythmia.These drugs increase the likelihood of maintaining sinusrhythm from about 30-50% to 50-70% per year aftercardioversion.

Polymorphic VT

Marked prolongation of the QT interval can beassociated with the development of a polymorphicventricular tachycardia known as torsade de pointes .This arrhythmia is caused by a specific electro-physiologic abnormality, triggered automaticity, thatarises as a result of marked prolongation of the cardiacaction potential.It is estimated that 1-8% of patientsreceiving quinidine will have torsade de pointeshypokalemia and bradyarrhythmias are risk factors, andthe arrhythmia is frequently “idiosyncratic”, occurring atlow dosages and low plasma drug concentrationsSotalol, an antiarrhythmic drug that prolongs the QTinterval, is also associated with torsade de pointes. Thisdrug is widely used in Europe and Canada and becameavailable in the United States in early 1993. Theincidence of torsade de pointes varies as a function of thedose of sotalol and may exceed 5% in patients receivingdoses of 320 mg or more twice daily. Other anti-arrhythmic agents that prolong the QT interval,including disopyramide, procainamide, and amiodarone,have also been associated with torsade de pointes. Theincidence appears quite low with amiodarone, despitethe marked prolongation of the QT interval it sometimescauses. Although, most episodes of torsade de pointesare self-limited or associated with symptoms such assyncope, they can progress to ventricular fibrillation; theincidence of such progression is not known. Mostrecognized cases of torsade de pointes occur within daysafter the offending drug is initiated and, in patients beingtreated for atrial fibrillation, after the restoration ofnormal sinus rhythm. However, some patients havetorsade de pointes during long-term therapy, raising thepossibility that fatal episodes contribute to an increase inmortality during therapy with some antiarrhythmicdrugs. Polymorphic VT can also occur without QTprolongation, under these circumstances the commonest