INTRADIALMIC CARDlAC ARRHYTHMIAS: II

M.F., a 62-year-old black female, began hemodialysis on August 4, 1990. End-stage renal disease (ESRD) was caused by diabetic glomerulosclerosis proved by renal biopsy. Past history was remarkable for insulin-requiring Type II diabetes mellitus for more than 20 years and hypertension of approximately the same duration. The patient had documented coronary artery disease for at least five years, having culminated in two non-Q wave myocardial infarcts, one year and three years prior to initiating dialysis. Cardiac systolic function was decreased with lefi ventricular ejection fraction being 45% when determined in fate 1989. Functional capacity gradually deteriorated to Class III on the New York Heart Association (NYHA) scale just prior to the initiation of dialysis. For the first two months after hemodialysis was begun, the patient gradually improved. Ultrafiltration decreased the patient's blood pressure and use of antihypertensive medication. On September 24, 1990, towards the end of a routine dialysis, the patient became hypotensive and had a cardiac arrest. The first rhythm strip showed ventricular tachycardia that quickly degenerated into fibrillation. She responded to defibrillation by electrical counter shock and was admitted to the coronary core unit (CCU). The subsequent hospital course ruled out a new ischemic event. Subsequent dialysis in the CCU with the patient being monitored showed the development of multifocal premature ventricular contractions (PVC) in the second hour of dialysis. These were subsequently quantitated at >300/hr. Medications at the time of arrest included Isordil 20 mg thrice daily, digoxin.125 mg thrice weekly, nifedipine XL 60 mg a day, multivitamins, ferrous sufate, and calcium citrate. At the conclusion of the aforementioned dialysis a renal profile and a set of blood gases were obtained. Serum K+ was 2.8 mEq/l, blood pH 7.48 with unremarkable paO2 and paCO2 values. A serum digoxin level at admission was 1.8 mg/ml. Serum calcium was normal. Digoxin was discontinued and the dialysate potassium level increased to 3.0 mEq/l. The patient was continuously monitored during the next several dialyses. The number of PVCs decreased but were still greater than 150/hr. They were most frequent immediately after dialysis and gradually decreased in number to 30/hr prior to the next dialysis. At this point, a serum magnesium was checked before and after dialyses and found to be 2.5 and 1.0 mg/dl respectively. Dialysate magnesium was increased from 0.75 to 1.25 mg/dl with almost complete resolution of the PVCs postdialysis. Since discharge from the hospital, the patient has done well and no further hemodynamic problems have been documented on dialysis.