His-Purkinje system

Glass lA Antiarrhythmic Agents. Class lA antiarrhythmic agents decrease automaticity, ie, depress pacemaker rates, especially ectopic foci rates produce moderate depression of phase 0 depolarization and thus slow conduction in atria, A-V node, His-Purkinje system, and ventricles prolong repolarization, ie, lengthen action potential duration increase refractoriness and depress excitabiHty. These electrophysiological effects are manifested in the ECG by increases in the PR, QRS, and QT intervals. 

First-degree AV nodal blockade occurs due to inhibition of conduction within the upper portion of the node.15 Mobitz type I second-degree AV nodal blockade occurs as a result of inhibition of conduction further down within the node.12,15 Mobitz type II second-degree AV nodal blockade is caused by inhibition of conduction within or below the level of the bundle of His.12,15 Third-degree AV nodal blockade maybe a result of inhibition of conduction either within the AV node or within the bundle of His or the His-Purkinje system.12,15 AV block may occur as a result of age-related AV node degeneration. 

Pharmacology Procainamide, a class lA antiarrhythmic, increases the effective refractory period of the atria, and to a lesser extent the bundle of His-Purkinje system and ventricles of the heart. 

Myocytes within the sinoatrial node possess the most rapid intrinsic rate of automaticity therefore, the sinoatrial node serves as the normal pacemaker of the heart. Specialized cells within the atria, atrioventricular (A-V) node, and His-Purkinje system are capable of spontaneous depolarization, albeit at a slower rate. The more rapid rate of depolarization of the sinoatrial nodal cells normally suppresses all of the other cells with the potential for automaticity. The other cells will become pacemakers when their own intrinsic rate of depolarization becomes greater than that of the sinoatrial node or when the pacemaker cells within the sinoatrial node are depressed. When impulses fail to conduct across the A-V node to excite the ventricular myocardium (heart... 

Quinidine can depress the automaticity of ventricular pacemakers by depressing the slope of phase 4 depolarization. Depression of pacemakers in the His-Purkinje system is more pronounced than depression of sinoatrial node pacemaker cells. 

Quinidine also prolongs repolarization in Purkinje fibers and ventricular muscle, increasing the duration of the action potential. As in atrial muscle, quinidine administration results in postrepolarization refractoriness, that is, an extension of refractoriness beyond the recovery of the resting membrane potential. The indirect (anticholinergic) properties of quinidine are not a factor in its actions on ventricular muscle and the His-Purkinje system. 

The electrophysiological effects of phenytoin on the His-Purkinje system resemble those of lidocaine that is. 

Flecainide (Tambocor) is a fluorinated aromatic hydrocarbon examined initially for its local anesthetic action and subsequently found to have antiarrhythmic effects. Flecainide inhibits the sodium channel, leading to conduction slowing in all parts of the heart, but most notably in the His-Purkinje system and ventricular myocardium. It has relatively minor effects on repolarization. Flecainide also inhibits abnormal auto-maticity. 

Flecainide slows conduction in the His-Purkinje system and ventricular muscle to a greater degree than in the atrium. Flecainide may also cause block in accessory A-V connections, which is the principal mechanism for its effectiveness in treating A-V reentrant tachycardia. 

Acebutolol s effects on the atria, sinoatrial and AV nodes, His-Purkinje system, and ventricular muscle are similar to those of propranolol. 

There are no changes in the PR or QRS intervals, which reflects a lack of effect on the conduction velocity. The QT interval is prolonged as a result of an increase in both the effective and functional refractory periods in the His-Purkinje system and the ventricles. The increase in the QT interval is directly related to the dofetilide dose and plasma concentration. 

Mechanism of Action An antiarrhythmic that shortens duration of action potential and decreases effective refractory period in the His-Purkinje system of the myocardium by blocking sodium transport across myocardial cell membranes. Therapeutic Effect Suppresses ventricular arrhythmias. 

Mechanism of Action An antiarrhythmic that increases the electrical stimulation threshold of the ventricles and His-Purkinje system. Decreases myocardial excitability and conduction velocity and depresses myocardial contractility Exerts direct cardiac effects. Therapeutic Effect Suppresses arrhythmias. 

Historically and romantically, the heartbeat is recognized as the quintessential hallmark of life. Normally, the heart beats at 60-100 beats per minute (bpm), with each beat yielding a ventricular contraction that ejects blood out to the body. Each heartbeat is an electrical event that originates from a collection of electrically excitable cells within the heart called the sinoatrial node (SA), anatomically located at the upper pole of the heart. The sinoatrial node is the primary pacemaker of the heart. The electrical impulse generated in the sinoatrial node spreads rapidly downward from the atria chambers of the heart and reaches the atrioventricular node (AV), a collection of electrically excitable cells that constitutes the electrical interface between the atria and ventricles of the heart. Erom the AV node, the impulse propagates throughout the ventricles via an electrical conduction system referred to as the His-Purkinje system. The electrical transmission... 

Class Ic agent that prolongs refractoriness and slows conduction in the atria, atrioventricular node (AV-node), His-Purkinje system, ventricles and accessory pathways. Predominantly blocks sodium channels in the activated state with rate-dependent block (40). 

Actions Bretylium has a number of direct and indirect electro-physiological actions, the most prominent of which are prolongation of the refractory period and raising of the intensity of the electrical current necessary to induce ventricular fibrillation in the His-Purkinje system. 

Chalvidan T, CeUarier G, Deharo JC, Cohn R, Savon N, Barra N, Peyre JP, Djiane P. His-Purkinje system reentry as a proarrhythmic effect of flecainide. Pacing Chn Electrophysiol 2000 23(4 Pt l) 530-3. 

FIGURE 17-7. Reentry mechanism of dual-AV-nodal- pathway PSVT. A. Sinus rhythm. The impulse travels from the atrium through the fast pathway (F) and then to the His-Purkinje system. The impulse also travels through the slow pathway (S) but is stopped when refractory tissue is encountered. B. Dual-AV-nodal reentry. A critically timed premature impulse ) is stopped in the fast pathway (because of prolonged refractoriness) but is able to travel antegrade down the slow pathway and retrograde through the fast pathway. 

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