Adequate anticoagulation is a must prior to elective electrical cardioversion in atrial arrhythmias which have lasted more than 48 hours. Some resort to cardioversion after exclusion of left atrial appendage clot by trans esophageal echocardiogram. Usual duration of anticoagulation is for about 4 weeks, which is initiated with heparin and followed up with warfarin. Anticoagulation has to be continued for 4 weeks to 6 months after the procedure as well as there is a chance for atrial stunning which may predispose to clot formation.

The procedure can be done as an outpatient procedure, but usually in the setting of an intensive care setting with standby anaesthesia cover. Person should be fasting overnight and skin should be free of any ointments or other applications. Intravenous short acting sedation is given prior to the procedure to allay the pain and anxiety of the shock. Intravenous access, continuous monitoring and emergency crash cart should be at hand. It is ideal to use adhesive pads for cardioversion rather than paddles as the latter can be used for immediate transcutaneous pacing in case of post shock bradycardia. Anteroposterior placement is also easy in case of patches rather than paddles and it improves the success rate of cardioversion.

Lower energy levels may be enough for atrial flutter which is due to a macro re-entry while higher energies are often needed for atrial fibrillation. The principle of cardioversion is to simultaneously depolarise a critical amount of myocardium so that when the spontaneous electrical activity restarts, it is the dominant pacemaker, usually the sinus node which takes over. When there is a large and scarred atrium as in uncorrected mitral valvular lesions or congenital heart disease, the chance of recurrence is high. Electrolyte imbalances and digoxin toxicity should be excluded as these may lead to more severe arrhythmias after cardioversion.

Atrial electrical stunning is the phenomenon of delayed atrial electrical activity after a cardioversion, which is rare. Atrial mechanical stunning is more commonly seen, as a delay in recovery of the contractile function of the atrium even after successful restoration of sinus rhythm. This is one of the reasons for continuing anticoagulation after a successful cardioversion. Elective cardioversion is usually done with therapeutic INR range of 2 – 3.

Even though the persons undergoing elective electrical cardioversion of atrial fibrillation can be sent home after observing for a few hours, they are asked not to drive a vehicle or make important decisions on the same day because of residual sedation.

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Atrial fibrillation with WPW syndrome (pre-excitation) is a potentially life threatening arrhythmia. Since it is a wide QRS tachycardia, it is often mistaken for ventricular tachycardia. Due to very fast rates, they often present with hemodynamic compromise requiring cardioversion. In the current strip, a small portion in aVR shows presumably sinus rhythm with pre-excitation. The QRS in general is wide and bizarre. The shortest RR interval gives an estimate of the ventricular refractory period. If it is below 250 msec, it is ominous as the ventricular rates can go very high and it can degenerate into ventricular fibrillation. The arrhythmia also responds to intravenous amiodarone, which can be considered if there is no hemodynamic compromise. Either way radiofrequency catheter ablation has to considered as an elective treatment to prevent recurrence. The ECG after cardioversion (below) shows WPW syndrome (short PR interval and delta waves) with sinus bradycardia.

WPW syndrome with sinus bradycardia

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]]> http://www.cardiophile.net/2009/10/atrial-fibrillation-with-wpw-syndrome.html/feed 0 http://www.cardiophile.net/2009/09/avnrt.html http://www.cardiophile.net/2009/09/avnrt.html#comments Sun, 20 Sep 2009 00:57:23 +0000 Johnson Francis http://www.cardiophile.net/?p=3295 Which of the following rhythms is taken as a marker of successful ablation of atrioventricular nodal re-entrant tachycardia (AVNRT)?

A. Ventricular tachycardia
B. Sinus rhythm
C. Junctional rhythm
D. Atrial fibrillation

Answer: C

Usually a short run of accelerated junctional rhythm occurs during successful radiofrequency catheter ablation of AVNRT. Non inducibility of tachycardia is an important criterion of success.

A. Takotsubo cardiomyopathy
B. Broken heart syndrome
C. Tachycardiomyopathy
D. Stress cardiomyopathy

Answer: C

All the others are eponyms for apical ballooning syndrome. Tachycardiomyopathy is secondary to long standing tachycardia as in atrial fibrillation or permanent junctional tachycardia.

Pacing through lateral cardiac vein

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ECG of pacing through lateral cardiac vein. Pacing through lateral cardiac vein was done because of prior triple valve replacement (mitral, tricuspid and aortic) which precluded trans venous right ventricular pacing. The basic rhythm is atrial fibrillation and the fifth and last beats are paced. The tall spikes before the paced QRS complexes indicates the possibility of unipolar pacing which causes tall pacing artefacts. QS complexes in lead V4-V6 indicates an activation proceeding medially form the lateral wall of the left ventricle. This is quite different from the activation seen with the basic rhythm. Another ECG showed much smaller pacing artefacts, possibly because of filter settings which could have filtered the high frequency components of the pacing artefacts, which is quite common with digital ECG machines.

MAT

Multifocal atrial tachycardia

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Multifocal atrial tachycardia is defined as three or more different types of P waves occuring at a rate more than 100 per minute. In the second rhythm strip there is a pause before the onset of sinus rhythm after the tachycardia terminates. This could be due to down regulation of the If current (funny current or pacemaker current) in the sinus node due to the tachycardia or due to a block atrial ectopic beat which is not very evident as it is superimposed on the T wave.

Multifocal atrial tachycardia and blocked atrial ectopic beat

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Sinus rhythm is seen in the middle portion of the ECG, while tachycardia is seen at both ends. Following the fourth beat in the rhythm strip, there is a pause due to a non conducted atrial ectopic beat (blocked atrial ectopic). The nearest differential diagnosis of a multifocal atrial tachycardia is atrial fibrillation (paroxysmal atrial fibrillation in this case). Multifocal atrial tachycardia (MAT) can occur in this with chronic obstructive lung disease.

Atrial fibrillation with slow ventricular rate and left ventricular hypertrophy

Atrial fibrillation with slow ventricular rate and left ventricular hypertrophy. Slow ventricular rate is due to suppresion of the atrioventricular conduction either due to drugs or due to disease of the atrioventricular node. Left ventricular hypertrophy is manifest as tall R waves with ST segment depression in lateral leads. Digoxin effect could also contribute both slow rate and ST segment changes. The coarse fibrillary waves in V1 suggest possbility of a large atrium as in mitral stenosis. Fibrillary waves of more than 1 mm amplitude indicate atrial enlargement. Left ventricular hypertrophy indicates associated lesions like mitral regurgitation or aortic valve disease as left ventricular hypertrophy does not occur in isolated mitral stenosis.

The ECG also shows the paper speed of 25 mm/s and standardisation of 10 mm / mV. The filter settings are also shown towards the right lower border. Notch filter of 50 Hz filters out alternating current (AC) interference from line voltage. 0.08 – 35 Hz gives the high pass and low pass filter settings. High pass filter passes all frequencies above it and low pass filter passes all frequencies below it. Hence the ECG amplifier with this setting picks up signals within this frequency range. Filtering lower frequencies avoids the baseline shift due to respiratory variation of thoracic impedance. Too much filtering of higher frequencies can remove important signals like pacemaker artifacts or pacing stimuli. Hence digital ECG may miss pacing stimuli if the filter settings are not optimal.

Short QT syndrome is characterized by consistently short QT intervals, usually below 300 msec, which does not lengthen with bradycardia. There is a propensity for sudden cardiac death and atrial fibrillation. Family history of sudden death may be forthcoming. Electrophysiologically short QT syndrome is characterized by short refractory periods and inducible VF (ventricular fibrillation) at EP (electrophysiological) study.

Shortening of QT interval can occur in tachycardia, hyperthermia and hypercalcemia. Digoxin can also shorten the QT interval. These should be excluded before considering a diagnosis of short QT syndrome.

Treatment options for short QT syndrome are limited. Some have reported lengthening of QT interval with quinidine. Most patients with short QT syndrome and a risk of sudden cardiac death get an ICD (implantable cardioverter defibrillator) implanted.

Myocardial factors like ischemia, infarction and myocarditis
Autonomic imbalance like sypmathetic and parasympathetic overactivity or underactivity
Electrolyte imbalance like hypokalemia and hypomagnesemia
Hypoxia
Drugs like antiarrhythmic agents and psychotropic agents
Genetic disorders – Channelopathies like Brugada syndrome, long QT syndrome and short QT syndrome

Common supraventricular tachyarrhythmias

Atrial fibrillation
Atrial flutter
AV-nodal reentrant tachycardia
Atrioventricular reentrant tachycardia
Atrial ectopic tachycardia
Preexcitation syndromes combined with atrial fibrillation
Multifocal atrial tachycardia

Common ventricular tachyarrhythmias

Ventricular tachycardia: monomorphic / polymorphic
Ventricular fibrillation

Investigations in a case of cardiac arrhythmia

ECG is ideally recorded during the arrhythmia in addition to a routine baseline recording
Holter monitoring – used for 24 to 48 hour monitoring with cassette / solid state recorder
Loop recorder is an event recorder which monitors continuously and records events
Implantable loop recorder can be used for long term recording, upto 18 months
Head up tilt test for evaluation of vasovagal syncope
Echocardiography to exclude structural heart disease
Invasive electrophysiological studies – conventional catheter mapping and programmed stimulation
Cardiac mapping using newer modalities like Carto and electroanatomical mapping

Therapy of cardiac arrhythmias

Historical aspects
1960s: Bulky pacemakers with limited battery life; Surgery for WPW, VT, SVT
1980s: Catheter ablation – direct current / radiofrequency, ICD
2000s: Refinements in radiofrequency ablatiion / ICD; newer energy sources like Cryo, Ultrasound

Management of atrial fibrillation

Options in atrial fibrillation are: Rate control with anticoagulation vs rhythm control. Termination can be achieved by synchronized DC Cardioversion. Rate control can be achieved by digoxin, beta blockers or non – dihydropyridine group of calcium channel blockers (verapamil and diltiazem). All these agents can be given orally as well as intravenously depending on the situation. Rhythm control can be achieved by amiodarone, flecainide, quinidine, sotalol or ibutilide. Anticoagulation has to initiated with heparin and maintained on warfarin with a target INR of 2 – 3.

Direct current cardioversion is indicated in atrial fibrillation if there is hemodynamic compromise with hypotension, angina or pulmonary edema. Synchronized cardioversion can be either external cardioversion or internal cardioversion. Internal cardioversion is delivered using specialised catheters has a high efficacy, but is rarely required.

Management of atrial flutter

If there is acute hemodynamic collapse or heart falure, emergent synchronized DC Version is needed.
Energies less than 50 J may be sufficient as atrial flutter is highly sensitive to cardioversion, being a macro-rentrant arrhythmia. Atrial / trans-esophageal pacing may also be able to terminate atrial flutter. Intravenous ibutilide has a 76% success rate. Rate control can be achieved by diltiazem, verapamil, beta blocker or digoxin.

Management of supraventricular tachycardia

Vagal maneuvers like caortid sinus massage or pressure over the eyeballs can be initially tried. In an infant, the dive reflex can be activated by placing ice packs over the face. Adenosine as a bolus injection of 6 -12 mg is very useful in terminating an episode of supraventricular tachycardia. If a second bolus at a higher dose is required, it should not be an add on dose, but a higher dose as the half life of adenosine is very short. Adenosine is contraindicated in asthmatics as it can induce bronchospasm, which can persist upto 30 minutes. Verapamil 5 to 10 mg IV, diltiazem: 0.25 mg/kg over 2 minutes or esmolol: 0.5 mg/kg/min for 1 minute followed by infusion at a rate of 0.05 mg/kg/min for 4 minutes are other options for termination of supraventricular tachycardia.

Management of multifocal atrial tachycardia

Three or more P waves with different morphology at a rate above 100 per minute qualify for a diagnosis of multifocal atrial tachycardia (MAT). ECG of multifocal atrial tachycardia resembles that of atrial fibrillation and flutter. Multifocal atrial tachycardia occurs in seriously ill, elderly individulas, mostly in those with chronic obstructive pulmonary disease. Treatment is that of the underlying condition.

Management of ventricular tachycardia

Lignocaine as 50 – 100 mg intravenous bolus (25 -50 mg/min)? followed by 1- 4 mg/min infusion was the sheet anchor of treatment of ventricular tachycardia earlier. Now amiodarone 150 mg bolus over 10 min followed by an infusion at a rate of 1 mg/ min 6 hrs (360 mg)? and 0.5 mg/min 18 hrs (540 mg) is more popular. A word of caution is needed regarding amiodarone infusion. Occasional serious acute pulmonary toxicity can occur and hence the duration of therapy should not exceed 24 to 48 hrs, except when absolutely necessary. Maintenance with oral dosage of amiodarone is necessary for recurrent ventricular tachycardia. Mexiletine intravenously followed by oral dosage for maintenance is another option.

Role of magnesium in the treatment of cardiac arrhythmias

Intravenous magnesium is drug which is often very useful in the management of polymorphic ventricular tachycardia. Deficiency of magnesium is associated with cardiac arrhythmias and
can precipitate refractory ventricular fibrillation. Magnesium deficiency will also hinder replenishment of intracellular potassium as magnesium is a co-factor for the enzyme involved in potassium transport.
1 – 2 g MgSO4 is helpful to suppress life-threatening ventricular tachyarrhythmias and is administered IV over 1 to 2 min. Magnesium is also reported to be useful in digitoxicity.