recurrent well tolerated atrial flutter if combined with an AV node blocking

recurrent, well-tolerated atrial flutter if combined with an AV node- blocking agent and if no significant structural cardiac disease is present. Generic procainamide requires dosing every 6 to 8 hours; its cost is increased when switched to the sustained-release form, but adherence is improved. For disopyramide, mexiletine, procainamide sustained-release, propafenone, and tocainide, a dose that is missed should be taken as soon as it is remembered, unless the next dose is due in 4 hours or less. For flecainide, the missed dose should be taken unless the next dose is due in 6 hours, and for sotalol, 8 hours. For quinidine and standard formulations of procainamide, the separation is 2 hours. Procainamide occasionally is associated with a lupus-like syndrome. Joint swelling and rashes should be reported. There are many drug interactions with metformin ( Table 21-12 ). Carbonic anhydrase inhibitors may increase the risk for lactic acidosis and should be used cautiously. Cationic drugs that are eliminated by renal secretion (e.g., amiloride, digoxin, morphine, procainamide, quinidine, ranitidine, triamterene, trimethoprim, and vancomycin) may compete with metformin for its elimination pathway.

58 Uses This medication is used to treat a certain serious, life-threatening irregular heartbeat (ventricular tachycardia ). It is used to restore normal heart rhythm and to keep a regular, steady heartbeat. Procainamide is known as an anti-arrhythmic drug. It works by blocking certain electrical signals in the heart that can cause an irregular heartbeat. POWERPOINT : Antiarrhythmic Agents: Membranes stabilizing agents (sodium channel blockers): procainimide 40.Primary and Secondary HTN The level of BP is strongly familial, and studies of rare genetic disorders affecting BP have led to the identification of genetic abnormalities associated with several rare forms of HTN. Genetic polymorphisms have also been discovered that may harbor genes contributing to primary HTN. To date, none of these genetic abnormalities has been shown, either alone or in combination, to be responsible for a clinically significant portion of HTN in the general population. Although 90% to 95% of all cases of HTN are primary in nature with no identifiable cause, there are identifiable causes of HTN in which a cure may be effected by appropriate diagnosis and treatment. POWERPOINT: ▪ Prima ry or “essential” (95%) HTN ▪ Ather osclerosis

59 ▪ Secon dary (5%) HTN ▪ Adren al, renal ▪ BP relies on balance between CO and PVR 41.CCBs CALCIUM CHANNEL BLOCKERS Calcium is a vital component in the excitation-contraction process in muscles, in electrical excitation, and in facilitating myocardial relaxation. Calcium enters cells via three types of voltage-dependent calcium channels (L-type, N-type, and T-type). The L-type, or long- lasting, channels are predominant in cardiac and smooth muscle and are the ones blocked by most calcium channel blockers (CCBs). CCBs have