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Class I agents interfere with the sodium (Na +) channel. Class II agents are anti-sympathetic nervous system agents. Most agents in this class are beta blockers. Class III agents affect potassium (K +) efflux. Class IV agents affect calcium channels and the AV node. Class V agents work by other or unknown mechanisms.
While procainamide and quinidine may be used in the conversion of atrial fibrillation to normal sinus rhythm, they should only be used in conjunction with an AV node blocking agent such as digoxin or verapamil, or a beta blocker, because procainamide and quinidine can increase the conduction through the AV node and may cause 1:1 conduction of ...
Drugs that slow the conduction of the electrical signal through AV node, such as beta-blockers, digoxin, calcium channel blockers, and amiodarone, can cause heart block if they are taken in excessive amounts, or the levels in the blood get too high.
The underlying anatomical causes of PSVT, specifically atrioventricular nodal reentry, involve the presence of two functionally distinct conduction pathways within the AV node and the formation of a reentrant circuit that sustains the tachycardia. [8] These pathways within the AV node are known as the fast pathway and the slow pathway. [9]
The most common causes of first-degree heart block are AV nodal disease, enhanced vagal tone (for example in athletes), myocarditis, acute myocardial infarction (especially acute inferior MI), electrolyte disturbances and medication. The medications that most commonly cause first-degree heart block are those that increase the refractory time of ...
If there is a blockage between the AV node and the SA node, the atria may not contract at all. [6] [7] Junctional rhythm can be diagnosed by looking at an ECG: it usually presents without a P wave or with an inverted P wave. Retrograde, or inverted, P waves refers to the depolarization from the AV node back towards the SA node. [8]
Third-degree atrioventricular block (AV block) is a medical condition in which the electrical impulse generated in the sinoatrial node (SA node) in the atrium of the heart can not propagate to the ventricles. [1] Because the impulse is blocked, an accessory pacemaker in the lower chambers will typically activate the ventricles.
The AV node's normal intrinsic firing rate without stimulation (such as that from the SA node) is 40–60 times/minute. [13] This property is important because loss of the conduction system before the AV node should still result in pacing of the ventricles by the slower pacemaking ability of the AV node.