BMS 450 Lecture Notes - Atrioventricular Block, Beta Blocker, Amiodarone
Document Summary
Predominately block k+ channels, thereby prolonging the action potential. Do not affect na+ channels, therefore conduction velocity is not decreased. Break the reentrant circuit and allow the sa node to take over. Arrhythmia: ap prolongation is generally associated with inducing. Primary effect is to slow av nodal conduction. Some decrease in cardiac contractility, especially with verapamil. Use: decrease ventricular response to atrial fibrillation (does not stop atrial fibrillation, only the ventricular response) Cardiac contractility can be a problem in heart failure, especially with verapamil. Av nodal block with high doses or susceptible individuals. Use will be similar to calcium channel blockers. Can terminate supraventricular tachycardias involving the av node (e. g. atrial fibrillation) Half-life of about 5 seconds (give iv only) Leads to poor oxygenation of the myocardium (ischemic heart disease) Decrease heart rate, contractility, afterload (tpr), preload (blood volume), venous return. Happens automatically when cardiac output (and bp) drops during heart failure through the baroreceptor reflex.
