Cardiac Arrhythmias

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5.9 Cardiac Arrhythmias

Normal conduction system

The normal heartbeat is initiated by an impulse which originates from the sinoatrial (SA) node located in the wall of the right atrium near the superior vena cava junction. The impulse is then propagated via conducting cells that form a specialised system throughout the heart. Initially the impulse travels across the atria and via transatrial internodal pathways that converge on the atrioventricular (AV) node. The impulse proceeds down the bundle of His to the right and left bundle branches; the impulse then finally spreads throughout the Purkinje fibres to depolarise the ventricular muscle. The conducting cells of this specialised system have a rapid conduction velocity to rapidly propagate the electrical impulse throughout the heart. The various parts of this conduction system are also capable of spontaneous depolarisation and impulse generation under abnormal conditions.

The SA node is normally the dominant (fastest) cardiac pacemaker but this can change if sinus node dysfunction occurs or if other parts of the conduction system develop increased automaticity. As stated above, the SA node is located near the junction of the superior vena cava (SVC) and the right atrium. The SA node is innervated by both sympathetic and parasympathetic nerve endings. Parasympathetic tone predominates during rest. Children are known to have relatively greater parasympathetic tone than adults and are also known to have developmental and age-dependent differences in action potential amplitude and conduction speed. Accordingly, there are age-dependent normal values for resting heart rate as well as PR interval and QRS duration, in addition to many other electrophysiology parameters (see Table 5.9.1).

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Depolarisation initiated in the SA node spreads rapidly through the internodal pathways to converge on the AV node. Usually, the atria and ventricles are electrically separated from one another by a ring of fibrous tissue at the atrioventricular junction (the annulus fibrosis). Accordingly, in usual circumstances, the impulse must pass to the His bundle via the AV node. The AV node is located in the inferomedial wall of the right atrium near the insertion of the septal leaflet of the tricuspid valve. Conduction through the AV node is slow to allow completion of atrial systole (and ventricular diastole). This delay (and therefore potentially the completeness of ventricular filling) can be reduced during sympathetic stimulation.

After leaving the AV node the impulse travels along the bundle of His for 1–2 cm along the posteroinferior margin of the membranous portion of the interventricular septum, before dividing into the right and left bundle branches. These extensions of the conducting system spread subendocardially across the ventricular chambers to the base of the papillary muscles. The left bundle separates into two distinct fascicles (anterior and posterior). From these specialised fibres the impulse spreads from endocardium to epicardium throughout the right and left ventricles.

Abnormally situated embryonic remnants of conducting tissue can persist as accessory tracts. These are most commonly found around the AV node and are capable of conducting electrical activity between the atria and ventricles thus bypassing the AV node. These remnants are the anatomical substrate for re-entrant tachyarrhythmias.

The cardiac action potential

The cardiac action potential is divided into five phases: 0, 1, 2, 3, 4.

Vaughan Williams antiarrhythmia drug classification

Antiarrhythmic drugs are classified into five classes in the Vaughan Williams classification by the mechanism or channel that they most reliably affect during in vitro studies. There is, however, considerable overlap.

Class 1 drugs block the fast inward sodium channels and thereby increase the refractory period. This class is further subdivided into:

It is fair to say that these are infrequently used in paediatrics, though lignocaine is still an option in the ventricular fibrillation protocol and flecainide may sometimes be used in supraventricular tachyarrhythmias.

Class 2 agents are β-blockers, which act by a combination of β-antagonism and a quinidine-like membrane stabilising effect. There is a slowing of conduction velocity, prolonging of action potential duration and a reduction of automaticity Their main clinical use is in treating supraventricular tachyarrhythmias (SVT, atrial fibrillation, atrial flutter) by increasing the refractory period of the AV node. Propranolol or atenolol may be used but in acute situations many clinicians favour esmolol, a very short-acting parenteral β-1-antagonist (half life 9 minutes), which can be useful in supraventricular tachycardia (SVT) and possibly ventricular tachycardia (VT).

Class 3 drugs act primarily as potassium channel blockers and basically prolong the phase 3 repolarisation phase, thereby causing a prolongation of the action potential and increase in the effective refractory period. This class of drug is particularly useful in ventricular tachyarrhythmias and includes amiodarone and sotalol.

Amiodarone is one of these antiarrhythmics with a plethora of effects, in that it is primarily class 3 (i.e. potassium channel blocker) but also has sodium channel blocking, β-antagonism and calcium channel blocking effects. Oral amiodarone has unusual pharmacokinetics, with clinical effect only apparent after several days of treatment and a half life of 3–15 weeks. Side effects are frequent and serious (corneal photosensitivity, hyper- or hypothyroidism, pulmonary fibrosis and pro-arrhythmia). Intravenous amiodarone is used in the acute management of post-operative tachyarrhythmias (usually junctional ectopic tachycardia, JET). In the adult ventricular fibrillation protocol, a randomised comparison between amiodarone and lignocaine found a greater chance of successful resuscitation (but not survival) with amiodarone. Therefore some authorities have recommended amiodarone as the agent of choice to help effect defibrillation after adrenaline (epinephrine). In haemodynamically stable VT the agent of choice is probably sotalol unless there is impaired ventricular function (EF <40%, signs of congestive heart failure) when amiodarone is recommended. In unstable or polymorphic VT the recommended agent depends a little on the initial trace. If it looks like torsade de pointes with the trace oscillating around the baseline (or in polymorphic VT with a normal QT interval), the clear recommendation is intravenous (IV) magnesium. If it is not torsade-like and the QT interval can be determined and is not prolonged, amiodarone is a second-line agent to β-blockers. If the QT interval is prolonged, then IV magnesium, followed if necessary by lignocaine, would be the recommended approach.

Sotalol is classified as a class 3 drug, although it is a non-selective β-blocker with additional class 3 properties. It therefore combines the β-blocking effect on the SA and AV nodes with prolongation of AP duration and lengthening of refractory period elsewhere in the heart. It is valuable acutely and long term in preventing SVT of all sorts and is the agent of choice in monomorphic stable VT with apparent normal ventricular function. Like amiodarone, it does increase the QT interval and is therefore pro-arrhythmic as well as having the other risks of hypotension and bradycardia, presumably resulting from its β-blocking effects.

Class 4 agents are calcium channel blockers and the prototype remains verapamil, which has wide-ranging effects on shortening the plateau phase and reducing contractility. Verapamil is primarily used in the adult setting because of its reduction of conduction velocity in the AV node, thereby controlling the ventricular response rate to SVT, atrial flutter or atrial fibrillation. Even in that situation it is still a second-line agent to adenosine for SVT termination in adults, provided there is good left ventricular (LV) function. However, because of serious bradycardia, hypotension and cardiac arrest in infants, it is not used in children. Instead, β-blockers are used in Wolff–Parkinson–White (WPW) syndrome and digoxin in non-WPW patients.

Finally, Class 5 agents are a miscellaneous group and include adenosine and digoxin. Adenosine is an endogenous purine nucleoside with a very rapid half life (less than 5 seconds). It acts by depressing slow calcium channels and enhancing potassium conduction. Its main effects are to depress sinus node and AV node activity with a shortening of atrial refractoriness. Because of its effect in blocking AV nodal activity, adenosine is superbly suited to block re-entry phenomena, the most frequent cause of SVT in children. Series show that adenosine terminates 90–100% of SVTs but the arrhythmia re-initiates in approximately 25%. Other atrial tachycardias like multifocal atrial tachycardia, atrial flutter or atrial fibrillation are almost always resistant to adenosine. Adenosine is given in increasing doses from 50–200 mcg kg–1 every 2 minutes, using a two-syringe technique so that it can be flushed rapidly into the circulation. Side effects can be facial flushing, bronchospasm or sinus arrest. Adenosine is essentially very safe, although there is a single case report of VF occurring after a dose of adenosine in a neonate with a concealed WPW syndrome previously treated with digoxin.

Although adenosine is unlikely to be controlling in supraventricular tachycardias other than re-entrant SVT, the acute injection of adenosine may transiently slow AV nodal activity and allow the flutter wave or P wave morphology to be assessed. This may be very valuable in diagnosing the specific rhythm. In a haemodynamically stable wide complex tachycardia of uncertain origin, the differential diagnosis is primarily between VT and SVT with aberrant conduction. Adenosine administration might be discussed as a way of making this distinction (i.e. effective in the latter but not in the former). In the adult literature, unless SVT origin is strongly suspected, this practice is discouraged because of the potential for brief hypotension, and accelerated accessory pathway conduction following adenosine injection.

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