Arrhythmias reentrant

Verapamil. Verapamil hydrochloride (see Table 1) is a synthetic papaverine [58-74-2] C2qH2 N04, derivative that was originally studied as a smooth muscle relaxant. It was later found to have properties of a new class of dmgs that inhibited transmembrane calcium movements. It is a (+),(—) racemic mixture. The (+)-isomer has local anesthetic properties and may exert effects on the fast sodium channel and slow phase 0 depolarization of the action potential. The (—)-isomer affects the slow calcium channel. Verapamil is an effective antiarrhythmic agent for supraventricular AV nodal reentrant arrhythmias (V1-2) and for controlling the ventricular response to atrial fibrillation (1,2,71—73). 

Furthermore, under certain conditions (e.g. local unidirectional block) it is possible that the activation wavefront is delayed and encounters areas already repolarized. This may result in a circulating wave-front (= reentrant circuit reentrant arrhythmia), from which centrifugal activation waves originate and elicit life-threatening ventricular fibrillation. 

Supraventricular bradycardia is treated by implantation of a pacemaker device or has been treated pharmacologically with atropine. Supraventricular paroxysmal tachycardia is treated with aj marine or praj marine. Supraventricular tachyarrhythmias or AV reentrant arrhythmia typically can be terminated using adenosine. 

Reentrant arrhythmia occurs when due to inhomogeneous repolarization or unidirectional block, heart tissue which is no longer refractory is close beside tissue which is still activated. This may result in a circuit propagation of activation serving as a reverberator. 

Potassium Increases K+ permeability, K+ currents Slows ectopic pacemakers slows conduction velocity in heart Digitalis-induced arrhythmias arrhythmias associated with hypokalemia Oral, IV Toxicity Reentrant arrhythmias, fibrillation or arrest in overdose... 

In summary, longitudinal propagation seems to be more sensitive to reduced sodium channel availability especially in nonuniform anisotropic tissue, and under these conditions reentrant arrhythmia can be initiated due to discontinuous propagation, whereas transverse propagation is more sensitive to un-... 

What is the role of the gap junctions By coupling the myocardial cells in both directions (longitudinal and transverse) they are responsible for the biophysical properties of the tissue. A reduction in gap junction distribution or a closure of the gap junction channels causes nonuniformities and discontinuities which alter the biophysical properties of the tissue and make it more prone to nonuniform anisotropic reentry. According to the model proposed by Krinsky [1966], a reduction in gap junctions or a closure of gap junction channels will lead to local slowing of conduction, thereby allowing smaller perimeters of reentrant arrhythmia. In addition, slowing of conduction is generally believed to be a risk factor for initiation of reentry. Since in many... 

Furthermore, synchronization of contraction is facilitated by gap junctional communication as well as synchronization of electrical activation. The electrical coupling between cardiomyocytes mitigates differences in the membrane potential between these cells, for example in the course of an action potential if both cells repolarize at different timepoints. This results in smaller differences in the repolarization times thereby causing a reduction in the dispersion of the action potential duration. Since increased dispersion is known to make the heart more prone to reentrant arrhythmia, sufficient gap junctional communication can be considered as an endogenous arrhythmia-preventing mechanism. For a detailed discussion of the role of gap junctional communication in the biophysics of cardiac activation as related to anisotropy, nonuniformity and stochastic phenomena, see chapter 1 for a discussion of their role in arrhythmia, see chapter 6, and for a possible pharmacological intervention at the gap junctions for suppression of arrhythmia, refer to chapter 7. 

On the other hand arrhythmia due to uncoupling may be prevented. If coupling is enhanced selectively in the previously uncoupled area only within that area cellular uncoupling would be antagonized, which means that the surrounding tissue would not be affected in the way described above. There might be a similar effect in the close border zone between diseased and normal tissue, but the effect would be confined to that zone. Inhomogeneities within the diseased zone would be smoothened whereas the normal tissue behavior would probably be less affected. This could especially smooth differences in action potential duration and thereby prevent, in some situations, from reentrant arrhythmia, since this is often related to differences in action potential duration, to dispersion. Another important factor in the initiation of reentry... 

Freysz M., Timour Q., Mazze R. I., et al. (1989) Potentiation by mild hypothermia of ventricular conduction disturbances and reentrant arrhythmias induced by bupivacaine in dogs. Anesthesiology 70, 799-804. 

Ca + CHANNEL BLOCK The major electrophysiological effects resulting from block of cardiac Ca + channels are in slow-response tissues, the sinus and AV nodes. Dihydropyridines such as nifedipine, which are used commonly in angina and hypertension, preferentially block Ca + channels in vascular smooth muscle their cardiac effects, such as heart rate acceleration, result principally from reflex sympathetic activation secondary to peripheral vasodilation. Only verapamil, diltiazem, and bepridil block Ca + channels in cardiac cells at clinically used doses. These drugs generally slow heart rate, although hypotension can cause reflex sympathetic activation and tachycardia. The velocity of AV nodal conduction decreases, so the PR interval increases. AV nodal block occurs as a result of decremental conduction and increased AV nodal refractoriness, which form the basis for the use of channel blockers in reentrant arrhythmias whose circuit involves the AV node, such as AV reentrant tachycardia. 

Nodal tachycardia A common reentrant arrhythmia that travels through the AV node it may also be conducted through atrial and ventricular tissue as part of the reentry circuit... 

Reentrant arrhythmia Arrhythmia of abnormal conduction involves the repetitive passage of an impulse through tissue previously excited by the same impulse... 

I. Pharmacology. Bretylium is a quaternary ammonium compound that is an effective type III antifibrillatory dmg and also suppresses ventricular ectopic activity. It increases the threshold for ventricular fibrillation and reduces the disparity in action potential duration between nonnal and ischemic tissue, which is believed to abolish boundary currents responsible for reentrant arrhythmias. Its pharmacologic actions are complex. Initially, norepinephrine is released from sympathetic neurons this is followed by a block of further norepinephrine release. In addition, norepinephrine uptake is inhibited at adrenergic neurons. The result is a transient increase in heart rate, blood pressure, and cardiac output that may last from a few minutes to 1 hour. Subsequent adrenergic blockade produces vasodilation, which may result in hypotension. 

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