Successful Transitory External Cardiac Electrostimulation in a Patient with Excessive Hyperkalemia and Bradycardia

This article is also accessible online at: http://BioMedNet.com/karger Dear Sir, We present the case of a young hypertensive patient (35 years old, body weight 73.5 kg) with insulin-dependent diabetes mellitus diagnosed 18 years ago and multiorgan complications related to diabetes such as retinopathy with advanced chronic renal failure, metabolic ‘renal’ acidosis, blindness, and excessive hyperkalemia (9.0 mmol/l). The blood glucose concentration and arterial pressure were not satisfactorily controlled, 1 year ago (HbA1c 17.5%, mean arterial pressure varies between 118 and 144 mm Hg). At the same time, chronic azotemia was detected (creatinine blood concentration 150 Ìmol/l). During the last few months, the chronic azotemia progressed to advanced uremia. Because of repeated bilateral intravitreal hemorrhages, the patient was treated four times in Moscow, Russia (Fjodorov Institute). In August 1996, advanced nephrotic syndrome was detected with simultaneous aggravation of the renal function (blood urea nitrogen 12–21 mmol/l, serum creatinine 250–540 Ìmol/l, total urinary proteins 6.4– 2.9 g/l). The patient’s general health status worsened abruptly in October 17, 1996 (unconsciousness, hypotonia to 80/50 mm Hg, depressed heart beats, excessive bradycardia to 25 beats/min, bradypnea to 10 breaths/min). Routine laboratory analyses demonstrated acute hyperglycemia to 35 mmol/l, hyperkalemia to 9.0 mmol/l, blood urea nitrogen to 28 mmol/l, advanced anaemia to 64 g/l for hemoglobin, 2.0 ! 1012/l for RBC, and 0.17 for hematocrit. The decompensated renal and ketometabolic acidosis (urine-positive glucose and acetone) was characterized by pH 6.8, BE –30.1 mmol/l, and total HCO3 6.3 mmol/l. After that, the patient was admitted to the Department of Nephrology (Medical Faculty, Skopje). Before acute dialytic therapy, the patient was initially treated (Medical Center Gostivar) with subcutaneous application of 4 mg atropine, 16 U crystal insulin and intravenous perfusion with orciprenaline (1 mg in total) because of excessive bradycardia (24–32 beats/min) [1] hyperglycemia to 29 mmol/l, and advanced arterial hypotension (0/0, 80/40, 95/40 mm Hg) [2] (fig. 1, 2). Because of acute transverse cardiac failure dyspnea, painful hepatomegaly, anasarca, and ascites related to diabetic myocardiopathy, hyperkalemia, and acidosis, a transitory extracorporeal cardiac electrostimulation was performed through the right subclavian vein with regular ventricular response and sufficient circulatory stability (mean arterial tension 85 mm Hg, heart rate 74/min). In the meantime, a femoral venous catheter was placed and 3-hour hemodialysis instituted with good results (K+ 9.0–4.5 mmol/l, blood urea nitrogen 28–18, PO4 2.2–1.6, blood sugar, 35–20.4 mmol/l, pH 6.8–7.4, BE –30.1 to –5.6 mmol/l, total HCO3 6.3–17.0 mmol/l) and normalization of cardiac performance (clinical, ECG, and echographic monitoring). The calculated creatinine clearance [3] was 15.6 ml/min and the measured clearance from the 24-hour urine and blood creatinine (5.2 Ìmol/l) was three times lower (only 6.1 ml/min). During the next 3 weeks, the patient was regularly treated with hemodialysis and insulin. After 3 U RBC, hemoglobin was 98 g/l, RBC 3.4 ! 1012 and hematocrit 0.29. Besides frequent nonmalignant ventricular extrasystolies during the first 7 days after the patient was admitted to the hospital, cardiac function was normal and stable with

[1]  R. Tannen The influence of potassium on blood pressure. , 1987, Kidney international. Supplement.

[2]  S. Linas,et al.  Hemodynamic effects of potassium. , 1987, Seminars in Nephrology.

[3]  T. Bjornsson Use of Serum Creatinine Concentrations to Determine Renal Function1 , 1979, Clinical pharmacokinetics.