Junctional ectopic tachycardia (JET) is a unique postoperative arrhythmia, especially in children after cardiac surgery. JET is often difficult to treat. It is likely to recur after cardioversion. Sedation and cooling (hypothermia) are helpful.

It is always better to take a 12 lead ECG for evaluation of postoperative cardiac arrhythmia rather than taking a decision from the monitor tracing, except in a dire emergency. If P waves are not seen well on surface ECG, an electrogram from the atrial pacing wire is useful.

Synchronized cardioversion is to be used for any tachycardia with a well formed QRS. Overdrive pacing is useful in re-entrant tachycardia. DC shock is also useful in re-entry. There is no point in giving a DC shock for tachycardia due to enhanced automaticity like JET – it will recur soon.

Postoperative complete heart block (CHB)

Edema in the region of the conduction system may contribute to CHB. May wait 10-15 days prior to permanent pacemaker implantation. Steroids have been tried to treat CHB due to inflammatory edema.

Prophylactic treatment for prevention of postoperative atrial fibrillation

While drugs like sotalol and amiodarone have been used, evidence is more in favour of beta blockers in preventing postoperative atrial fibrillation.

Traditionally it is thought that sympathoadrenergic system activation is compensatory in heart failure. This is true in acute heart failure. But in chronic heart failure, sympathoadrenergic system becomes counter productive and maladaptive. It increases the afterload and myocardial cell necrosis as well down regulation of beta receptors. This is why betablockers have been considered in the treatment of chronic heart failure. Studies have shown that if you treat 100 patients with heart failure, it will prevent 4 deaths and 4 hospitalisations. Carvedilol, bisoprolol and metoprolol succinate have been shown to improve the survival in heart failure in various studies, but bucindolol failed to do so in the BEST trial. Even though COMET trial showed superiority of carvedilol over metoprolol tartarate, there were several criticisms about the methodology of the trial questioning whether it was a fair comparison. Metoporolol tartarate was a short acting preparation compared to the metoprolol succinate extended release preparation which was shown to be useful in heart failure earlier. Hence the superiority of carvedilolol over metoporlol in heart failure is not yet fully accepted. Betablockers are indicated in all patients with symptomatic heart failure. But they have to be started only only when they are stable and not on inotropic support or intravenous diuretics.

What is the role for devices in heart failure management?

All patients need optimal pharmacological therapy and life style modifications. But in a small subset, there is a definite role for devices. Ventricular tachycardia in a scar of old myocardial infarction may necessitate the implantation of an implantable cardioverter defibrillator (ICD). Hypotensive ventricular tachycardia in heart failure is an important cause for sudden cardiac death (SCD) as it can degenerate into ventricular fibrillation in a short time. Those who have survived a SCD are those at a higher risk of recurrence and benefit maximum with an ICD implantation. ICD improves the life expectancy by 6 years in these high risk individuals.

Intraventricular dyssynchrony in the presence of severe left ventricular dysfunction is an important indication for cardiac resynchronization therapy (CRT). Delay between the contractions of the septum and the lateral left ventricular wall causes reduced left ventricular stroke volume. The important surrogate of ventricular dyssynchrony is an increased QRS duration. In CRT, septum and lateral left ventricular wall contracts simultaneously producing improvement in the left ventricular stroke volume. This is achieved by pacing the lateral wall of the left ventricle through a coronary vein along with right ventricular endocardial pacing. CRT improves the symptomatic status and survival of heart failure patients with left ventricular dyssynchrony. But still there is a 30% non-responder rate of patients who do not respond to CRT.

What is the implication of Starlings law of the heart?

It is the volume of the heart which determines the force of contraction. Increase in muscle fibre length increases the force of contraction upto a certain level. Beyond this level, further increase in the volume of the heart produces deterioration of cardiac output. 2.2 microns is the critical sarcomere length at which there is optimal force of contraction, due to good overlap of actin and myosin filaments.