Pacemaker failure procainamide

Procainamide INa (primary) and IKr (secondary) blockade Slows conduction velocity and pacemaker rate prolongs action potential duration and dissociates from INa channel with intermediate kinetics direct depressant effects on sinoatrial (SA) and atrioventricular (AV) nodes Most atrial and ventricular arrhythmias drug of second choice for most sustained ventricular arrhythmias associated with acute myocardial infarction Oral, IV, IM eliminated by hepatic metabolism to /V-acetylprocainamide (NAPA see text) and renal elimination NAPA implicated in torsade de pointes in patients with renal failure Toxicity Hypotension long-term therapy produces reversible lupus-related symptoms... 

Interference with ventricular pacing occurred in a patient with a pacemaker who developed severe procainamide toxicity with a serum concentration of 36 ptglml the QRS widened from 0.20 to 0.26 sec and a delay of 0.18 sec appeared between the pacing stimulus and the QRS. Subsequently, periodic variation of the Wenkenbach type developed in the stimulus-QRS interval with intermittent failure to pace. Failure of pacemaker inhibition also occurred. Administration of 160 mM sodium bicarbonate intravenously led to immediate improvement in the abnormalities (37 ). 

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