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Ventricular Tachyarrhythmias And Nonpharmacological Treatment Of Arrhythmias


Ventricular Tachyarrhythmias And Nonpharmacological Treatment Of Arrhythmias
Tachyarrhythmias originating  in  the ventricles  are  most often associated with ischaemic heart disease and primary or secondary heart failure (i.e. dilated cardiomyopathies). They are common during and up to 24 h after acute myocardial infarction (MI), when increases in sympathetic activity and extracellular [K+] as well as slowed conduction favour their initiation. Such peri-infarction arrhythmias may be immediately life-threatening, and indeed the vast majority of deaths associated with MI are caused by ventricu- lar fibrillation occurring before the individual reaches the hospital. If survived, these arrhythmias generally do not recur and are not associated with a subsequent increased risk over and above that conferred by the MI itself. Subsequently, however, the border zone of the healed infarct scar may serve as a substrate for the development of dangerous re-entrant ventricular tachyarrhythmias which can recur or become incessant weeks to years after the MI. Their seriousness and prognostic significance are related to the extent of cardiac damage and impairment of ventricular function that has been sustained. These late arrhythmias themselves confer an additional risk of death, and must be treated either with drugs or with an implantable defibrillator (see below). Ventricular tachyarrhythmias can also be associated with cardiomyopathy, and valvular and congenital heart disease, although idiopathic varieties may occur in structurally normal hearts.

Ventricular Tachyarrhythmias And Nonpharmacological Treatment Of Arrhythmias, Ventricular tachycardia, Torsade de pointes, Ventricular fibrillation, Radiofrequency catheter ablation, Implantable defibrillators, Electronic pacemakers,

Specific ventricular tachyarrhythmias Premature ventricular contractions (PVCs) are caused by a ventricular ectopic focus and can occur randomly or following every (bigeminy; Figure 50a) or every second (trigeminy) normal beat. Because depolarization is initiated at a site within ventricular muscle, it spreadsthroughouttheventriclesmoreslowly thannormalimpulses which are distributed rapidly by the specialized His–Purkinje conduction system. Thus, the QRS complex is broad and abnormally shaped. PVCs may be of no prognostic consequence, but can predispose to more serious arrhythmias if they develop during or after MI, and/or occur during the T wave of the preceding beat.

Ventricular tachycardia (VT) originates in the ventricles, and is defined as a run of successive ventricular ectopic beats occurring at a rate of >100 beats/min (usually 120–200 beats/min). VT is classified as non-sustained or sustained based on whether it lasts for >30 s. Depending on the heart rate, VT can cause symptoms such as syncope, angina and shortness of breath, and if sustained can compromise cardiac pumping, leading to heart failure and death. VT can also deteriorate into ventricular fibrillation (see below), particularly with a heart rate of >200 beats/min.
The ECG in VT demonstrates high frequency, bizarrely shaped QRS complexes which are abnormally broadened (>120 ms in duration). Normal atrial activation may continue to be driven by the SAN (Figure 50b), or the abnormal ventricular pacemaker may cause atrial tachycardia via retrograde impulses traversing the AVN. The configuration of the QRS complex can be used to classify VT into two broad categories. In monomorphic VT (Figure 50b), the QRS complexes all have a similar configuration and the heart rate is generally constant, whereas in polymorphic VT both the QRS configuration and the heart rate vary continually. Mono-morphic VT generally indicates the presence of a stable re-entrant pathway, the substrate for which is typically an MI-related scar (see Chapter 48). Polymorphic VT is thought to be caused by multiple ectopic foci or re-entry in which the circuit pathway is continually varying, and most often occurs during or soon after an MI.

Torsade de pointes (‘twisting of the points’) is a type of polymorphic VT in which episodes of tachycardia, which may give rise to fibrillation and sudden death, are superimposed upon intervals of bradycardia, during which the QT interval (indicative of the ventricular action potential duration) is prolonged (Figure 50c). During the tachycardia, the ECG has a distinctive appearance in which the amplitude of the QRS complexes alternately waxes and wanes. Torsade de pointes may be caused by drugs or conditions that delay ventricular repolarization (e.g. class IA and III antiarrhythmics, hypokalaemia, hypomagnesaemia). It is also associated with congenital long QT (LQT) syndrome, which can be caused by mutations in KvLQT1 or HERG, genes coding for cardiac K+ channels mediating repolarization, or SCN5A, the gene coding for the cardiac Na+ channel. In congenital LQT syndrome, torsades de pointes is often triggered by sympathetic activity (e.g. caused by stress), which may give rise to early or delayed afterde-polarizations, and may also involve functional re-entry mediated by spiral waves of depolarization (see Chapter 48).

Ventricular fibrillation (VF) is achaotic ventricularrhythm(Figure 50d) incompatible with a cardiac output which will rapidly cause death unless the patient is resuscitated. VF may follow episodes of VT or acute ischaemia, and frequently occurs during MI. It is the main cause of sudden death, which is responsible for 10% of all mortality. VF is generally associated with severe underlying heart disease, including ischaemic heart disease and cardiomyopathy.

Focal VT and fascicular tachycardia are forms of VT that are idiopathic (i.e. can occur in structurally normal hearts). Focal VT most commonly originates in the right ventricular outflow tract (RVOT tachycardia; Figure 50e, left) and is associated with increases in sympathetic activity. This is thought to raise intracellular [cyclic AMP] and therefore [Ca2+]i, initiating delayed afterdepolarizations. Fascicular tachycardia may in some cases be caused by a re-entrant circuit involving the Purkinje system. Idiopathic VTs generally have a good prognosis, and can usually be successfully eliminated with radiofrequency catheter ablation (see below). VF occasionally occurs idiopathically, for example in people with LQT syndrome or Brugada syndrome (Figure 50e, right). This latter condition is associated with ion channel mutations (e.g. in SCN5A) which shorten the action potential in epicardial but not endocardial cells of the right ventricle, a situation favouring the development of re-entry.

Non-pharmacological treatment for arrhythmias
Direct current (DC) synchronized cardioversion allows rapid cardioversion (reversion to sinus rhythm) of haemodynamically unstable VT and SVT. Shocks of 50–200 J are delivered in synchrony with the R wave of the QRS complex to the anaesthetized patient via adhesive defibrillator pads placed below the right clavicle and over the apex of the heart.

Radiofrequency catheter ablation (RCA) has assumed a central role in treating many types of arrhythmias. In RCA, the pathways or focally automatic sites causing certain tachyarrhythmias are ablated (destroyed) by focal heating delivered via a catheter. The catheter is inserted through a vein and the tip is located at the surface of the endocardium at the site of the abnormality. Radi- ofrequency energy is delivered to the tip and dissipated to a large indifferent plate, usually over the back. The tip temperature is set to 60–65°C, resulting in a lesion 8–10 mm in diameter and of a similar depth. This technique is curative in >90% of certain supraventricular arrhythmias. RCA is also increasingly being used to treat VT when an appropriate target site (e.g. a slowly-conducting ‘isthmus’ in a myocardial scar) can be identified.
Although seldom causing complications, RCA of sites very close to the AV node can potentially cause inadvertent AV nodal damage and therefore permanent block, requiring pacemaker implantation. This can be avoided using cryoablation, in which the catheter tip is cooled rather than heated. Cooling the tip briefly to −30°C causes a focal block of electrical activity that is reversible and so cannot cause permanent damage. If this stops the arrhythmia without causing undesirable effects the tip is then further cooled to −60°C, which causes a permanent lesion and ablation of the abnormal rhythm.

Implantable defibrillators consist of a generator connected to electrodes placed transvenously in the heart and superior vena cava. A sensing circuit detects arrhythmias, which are classified as tachycardia or fibrillation on the basis of rate. The treatment algorithm is either as burst pacing, which can terminate VT with a high degree of success, or by the delivery of a shock at up to 40 J, which can cardiovert VT and VF. Shock delivery is between an electrode in the right ventricle and another in the superior vena cava or to the body of the generator (active can). Refinements in detection allow the distinction of supraventricular and ventricular arrhythmias, so that several tiers of progressively more aggressive therapy can be set up. The AVID study reported in 1997 that in patients with malignant ventricular arrhythmia, this approach improved survival by 31% over 3 years compared with anti-arrhythmic drug therapy (mainly amiodarone).

Electronic pacemakers can be used either temporarily or permanently to initiate the heart beat by imposing repeated cardiac depolarizations. Temporary pacing is generally accomplished using a catheter-tipped electrode introduced transvenously and provides for the rapid treatment of bradycardias. A temporary pacemaker can also be used to terminate a persistent arrhythmia by pacing the heart at a rate somewhat faster than that of the arrhythmia; sinus rhythm is often restored when this overdrive pacing is stopped. Permanent pacemakers are usually implanted to treatbradycardias, forexample due to AV block or sick sinus syndrome (see Chapter 13). The pacemaker is implanted under the skin on the chest, and stimulates the heart through leads introduced into the heart transvenously, usually through the subclavian vein. Contemporary pacemakers are able to pace both the atria and ventricles to maintain AV synchronization, and to adjust the pacemaking frequency to respond to changes in physical activity by sensing parameters such as respiration and the interval between the stimulated depolarization and the T wave, a measure of sympathetic nervous system activity.

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