Heart ventricular action potential

Figure 4.2 Cartoon representation of an ECC trace and ventricular cardiac action potential, (a) A representation of an ECC trace with its five typical deflections (PQRST) arising from the spread of electrical activitythrough the heart. The QRS wave denotes the ventricular depolarization, while the T wave represents ventricular repolarization. The QT interval therefore estimates the duration of a ventricular action potential, (b) Schematic of the five phases of a ventricular action potential. Phase 0 is the rapid depolarization phase due to a large influx of Na+ ions (Ina). Phase 1 occurs with the inactivation of Na+ channels and the onset of transient outward (repolarizing) currents (/to)...

Schematic representation of the heart and normal cardiac electrical activity (intracellular recordings from areas indicated and ECG). Sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells display pacemaker activity (phase 4 depolarization). The ECG is the body surface manifestation of the depolarization and repolarization waves of the heart. The P wave is generated by atrial depolarization, the QRS by ventricular muscle depolarization, and the T wave by ventricular repolarization. Thus, the PR interval is a measure of conduction time from atrium to ventricle, and the QRS duration indicates the time required for all of the ventricular cells to be activated (ie, the intraventricular conduction time). The QT interval reflects the duration of the ventricular action potential.

Fig. 22. Reduction in dispersion of the ventricular action potential duration by the synthetic antiarrhythmic peptide AAP10. The distribution of the action potential duration (assessed as the epicardial activation-recovery interval, ARI) on the surf ace of an isolated rabbit heart before and after treatment with AAP10. Note the greater variability of the epicardial action potential duration (ARI) before administration of AAP10 [Dhein et al., 1997c]. 

Class 1C drugs (flecainide, moricizine, propafenone) block sodium channels but do not affect potassium current. Therefore, they do not prolong the ventricular action potential or increase the QT interval. However, this class of drugs is quite proarrhythmic, and its use should be reserved for patients who have arrhythmias refractory to other treatments. Additionally, these drugs should not be used in patients with underlying heart disease. 

The ECG can be used as a rough guide to some cellular properties of cardiac tissue (1) Heart rate reflects sinus node automaticity, (2) PR-interval duration reflects AV nodal conduction time, (3) QRS duration reflects conduction time in the ventricle, and (4) the QTinterval is a measure of ventricular action potential duration. 

Fleca.inide, Elecainide acetate, a fluorobenzamide, is a derivative of procainamide, and has been reported to be efficacious in suppressing both supraventricular and ventricular arrhythmias (26—29). The dmg is generally reserved for patients with serious and life-threatening ventricular arrhythmias. Elecainide depresses phase 0 depolarization of the action potential, slows conduction throughout the heart, and significantly prolongs repolarization (30). The latter effect indicates flecainide may possess some Class III antiarrhythmic-type properties (31). 

Second, as in the ventricular muscle fibres of the heart, opening of L-type channels can generate sustained plateau potentials following the initial Na +-mediated action potential — for example, in the rhythmically firing neurons of the inferior olive (Fig. 2.7). 

Procainamide (Class IA antiarrhythmic drug) is an effective agent for ventricular tachycardia. Its mechanism of action involves blockade of the fast Na+ channels responsible for phase 0 in the fast response tissue of the ventricles. Therefore, its effect is most pronounced in the Purkinje fibers. The effects of this drug s activity include a decrease in excitability of myocardial cells and in conduction velocity. Therefore, a decrease in the rate of the phase 0 upstroke and a prolonged repolarization are observed. As a result, duration of the action potential and the associated refractory period is prolonged and the heart rate is reduced. These effects are illustrated by an increase in the duration of the QRS complex. 

Lidocaine Sodium channel (INa) blockade Blocks activated and inactivated channels with fast kinetics does not prolong and may shorten action potential Terminate ventricular tachycardias and prevent ventricular fibrillation after cardioversion IV first-pass hepatic metabolism reduce dose in patients with heart failure or liver disease Toxicity Neurologic symptoms... 

Amiodarone Blocks IKr, JNa/ Ica-L channels, adrenoceptors Prolongs action potential duration and QT interval slows heart rate and AV node conduction low incidence of torsade de pointes Serious ventricular arrhythmias and supraventricular arrhythmias Oral, IV variable absorption and tissue accumulation hepatic metabolism, elimination complex and slow Toxicity Bradycardia and heart block in diseased heart, peripheral vasodilation, pulmonary and hepatic toxicity hyper- or hypothyroidism. Interactions Many, based on CYP metabolism... 

Cardiovascular System. Atropine is sometimes used to block the effects of the vagus nerve (cranial nerve X) on the myocardium. Release of acetylcholine from vagal efferent fibers slows heart rate and the conduction of the cardiac action potential throughout the myocardium. Atropine reverses the effects of excessive vagal discharge and is used to treat the symptomatic bradycardia that may accompany myocardial infarction.4 Atropine may also be useful in treating other cardiac arrhythmias such as atrioventricular nodal block and ventricular asystole. 

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