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Electrophysiology and pacing

Irina SumanHorduna and Sabine Ernst

National Heart and Lung Institute, Imperial College; Royal Brompton and Harefield Hospital, London, UK
Arrhythmias Sinus rhythm
Under normal circumstances, the sinus node drives Buy fluconazole 150 mg no prescription the normal rhythm with electrical activation spreading through atrial conduction fibers towards the atrioventricular node (AVN). The electrical impulse leaving the AVN reaches the ventricular myocardium through the His bundle, right and left bundle branches, and Purkinje network. The Purkinje system fans out throughout the ventricular endocardium, allowing the impulse to proceed from the specialized conduction system to the myocardial muscle.
The polarity of the sinus P wave is consistent with the sinus node location, thus positive in leads I, II, III, and aVF, and isoelectrical in lead V1.

Mechanisms Focal tachycardias

Automaticity is the property of a cell cheap diflucan online to undergo spontaneous depolarization. Enhanced normal automaticity refers to the acceleration of the discharge rate of normal pacemaker tissue, either the primary pacemaker of the heart, the sinus node, or the other latent pacemakers identified in the atrial myocardium, AVN or HisPurkinje system.
Reentrant tachycardias
Reentry is the most common mechanism of arrhythmias; it requires two anatomically and functionally separated pathways, a unidirectional block in one pathway, and an excitable gap (the time interval between the tail of the circuit and the leading edge of the next impulse). In the electrophysiology laboratory, reentrant arrhythmias can be reproduced by introducing a premature stimulus that penetrates the excitable gap, blocks one pathway, and
Cardiovascular Clinical Trials: Putting the Evidence into Practice, First Edition. Edited by Marcus D. Flather, Deepak 
Electrophysiology and pacing

Figure 7.1 Concept of reentrant tachycardia induction: example of orthodromic atrioventricular reentrant tachycardia (AVRT). (A) During sinus rhythm the activation travels from the sinus node (SN) antegradely across the atrioventricular node (AVN). The accessory pathway (AP) is concealed and therefore there is no evidence of ventricular preexcitation.
(B) The electric impulse enters the AP retrogradely and thereby returns the activation back to the atria. (C) The impulse returns to the AVN antegradely and the loop is closed and an orthodromic AV reentrant tachycardia is established.

Slowly conducts antegradely over the other pathway. If the wave travels slowly enough to allow the blocked pathway to recover, the electrical activation can be retrogradely conducted to close the loop, resulting in a single beat of reentry called an echo beat. If these echo beats are perpetuated, tachycardia results.

Supraventricular tachycardia (SVT) refers to regular, narrow QRS complex tachycardias, usually faster than 100 beats/min. These tachycardias are divided into three main categories: atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT) due to an accessory pathway, and atrial tachycardia (AT).
AVNRT is a re entrant tachycardia involving two functionally different pathways within the AVN with different conduction properties. The most commonly encountered form of AVNRT (typical slow/fast AVNRT) requires a "dual nodal pathway physiology": one slow pathway (SP) with lowvelocity conduction and a shorter refractory period, and one fast pathway (FP) that conducts faster and with a longer refractory period. The atrial activation (up the FP) occurs almost simultaneously with the ventricular activation (down the SP); therefore, on the surface electrocardiogram (EKG), the retrograde negative P wave is buried in the QRS complex and is thus invisible, or recorded as a small indentation at the end of the QRS complex (pseudo r in the V1 and pseudo s wave in the inferior leads).
AVRT is a reentrant tachycardia that utilizes at least one accessory pathway as one limb. The association between manifest preexcitation in sinus rhythm and episodes of paroxysmal tachycardia defines the WolffParkinsonWhite (WPW) syndrome. If the accessory pathway is only capable of conducting retrogradely, the terminology used is "concealed accessory pathway."
176 Cardiovascular Clinical Trials
The vast majority of accessory pathways are rapidly conducting with no decremental properties. Sixty percent of these pathways are located at the level of the left free wall, 27% are posteroseptal, 5% are anteroseptal, and 8% are at the level of the right free wall [1]. In the common form of AVRT (orthodromic AVRT), the antegrade conduction is assured by the AVN, thus leading to a QRS complex similar to that recorded in sinus rhythm, whereas the retrograde limb is represented by the accessory pathway. AVRT, which uses the accessory pathway as the antegrade limb and the AVN or a second accessory as the retrograde limb, is a rare form of tachycardia designated antidromic AVRT.
Atrial t achycardia
The mechanism of this tachycardia, which is confined to the atrial myocardium, may be focal or reentrant (often related to atrial scaring). Focal ATs have preferential anatomical locations, like the crista terminalis, coronary sinus ostium, AV annulus, atrial appendages, and pulmonary veins.
Atrial flutter
Atrial flutter is a macroreentrant arrhythmia with either an isthmusdependent (typical or common) or a noni sthmus dependent (uncommon) re entrant circuit. The typical atrial flutter circuit has an obligatory critical component in the cavotricuspid isthmus (between the tricuspid annulus and inferior vena cava) and can turn in the clockwise (positive P waves in the inferior leads) or counterclockwise (negative P waves in the inferior leads) direction.
Atrial fibrillation
AF is the most common sustained arrhythmia encountered in clinical practice. Its prevalence increases with age, affecting less than 1% of those aged 5059 years in the Framingham study but 9% of those aged 8089 years [2].
On the EKG, P waves are replaced by rapid oscillations or fibrillatory waves that vary in amplitude, shape, and timing, and are associated with an irregular, frequently rapid ventricular response when atrioventricular (AV) conduction is intact. The ventricular response to AF depends on the electrophysiological properties of the AV node and other conducting tissues, the level of vagal and sympathetic tone, the presence or absence of accessory conduction pathways, and the action of drugs.
Table 7.1 Definitions of atrial fibrillation (AF).
Type    Duration    Termination
Paroxysmal AF    <7 days    Spontaneously
Persistent AF    >7 days    Requires medication or electrical cardioversion
Permanent AF    >1 year    No more attempts at cardioversion made
Longstanding persistent AF    >1 year    Only by catheter ablation
Electrophysiology and pacing 177
The current understanding of the pathogenesis of AF involves an arrhythmia trigger and substrate that allows for tachycardia perpetuation. The trigger for AF is usually located in the left atrium at the junction with one or more pulmonary veins 3]. The atrial tissue represents the substrate and this is prone to mechanical and electrical remodeling when additional factors like hypertension, aging, congestive heart failure or AF recurrence itself concur.

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