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Báo cáo y học: "Cardiac arrest following a glucose 30% bolus: what happened"

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Available online http://ccforum.com/content/12/1/401 Letter Cardiac arrest following a glucose 30% bolus: what happened? Philippe Goutorbe1, Nadia Kenane1, Julien Bordes1, Christophe Jego2, Ambroise Montcriol1 and Eric Meaudre1 1HIA Ste Anne Daru, Bd Ste Anne, 83000 Toulon, France 2HIA Ste Anne Cardiology, Bd Ste Anne, 83000 Toulon, France Corresponding author: Philippe Goutorbe, philippe.goutorbe@neuf.fr Published: 16 January 2008 Critical Care 2008, 12:401 (doi:10.1186/cc6216) This article is online at http://ccforum.com/content/12/1/401 © 2008 BioMed Central Ltd A 74-year-old man was admitted with postoperative peritonitis. beginning cardiac resuscitation showed serum potassium of On day 45, a double-lumen central venous catheter was 5.1 mmol/l, ionised calcium of 1.1 mmol/l, and serum sodium positioned in the patient’s right subclavian vein. The distal of 140 mmol/l. The empty ampoule was checked, and had lumen was used only for parenteral nutrition (2,000 ml/day contained the correct solution. The cardiac rhythm had been Kabiven® 1600; Fresenius Kabi Brezin, France). Glucose 5% normal before the glucose bolus was given, but sinus arrest (250 ml) with 6 g potassium was infused, over 24 hours, via with junctional or idioventricular escape rhythm developed at the proximal lumen. Hypokalemia was noted (K+, 3.0 mEq/l). the end of bolus administration, immediately followed by An additional infusion of potassium was initiated (34 mEq in ventricular fibrillation (Figure 1). The patient was discharged 10 ml, at 17 mEq/hour) via the proximal lumen. 2 weeks later without any sequelae. One hour later hypoglycemia was detected, and 20 ml of Electrocardiographic changes are not usually seen until 30% glucose was given intravenously. At the end of the serum potassium exceeds 6.0–6.5 mmol/l. Disappearance of injection, ventricular fibrillation developed. Cardiopulmonary the P wave is usually seen when serum potassium exceeds resuscitation successfully restored adequate circulation 8 mmol/l [1]. We were surprised, however, to find changes in within 12 minutes. Blood analysis performed using an ABL the absence of any increase in serum potassium. There was 700 (Radiometer, Copenhagen, Denmark) 1 minute after neither hyponatremia nor hypocalcemia, both of which Figure 1 Traces of the monitoring storage during glucose injection. The upper trace is an electrocardiogram showing sinus arrest, idioventricular or junctional escape rhythm immediately followed by ventricular fibrillation. The lower trace is the blood pressure. Page 1 of 2 (page number not for citation purposes)
Critical Care Vol 12 No 1 Goutorbe et al. increase sensitivity to hyperkalemia [2,3]. Even if serum potassium was normal, we think it possible there could have been local hyperkalemia, which led to sinus arrest and then to ventricular fibrillation. The mechanism of this hyperkalemia, we postulate, is that the high potassium concentration (1,074 mmol/l) in the deadspace of the tubing was flushed by the glucose, corresponding to a 11 mEq intravenous bolus of K+ . The present case highlights a dangerous aspect of using concentrated solutions for K+ therapy. Although an infusion rate of 17 mEq/hour is usually considered safe, in the particular situation here, with a central venous catheter in an intrathoracic position, flushing the catheter created a bolus injection. Theoretically, such a poorly mixed bolus can cause dangerous concentrations in the coronary arteries. When using potassium supplements, catheters with minimum dead- space are preferable, and bolus injections should be avoided. Competing interests The authors declare that they have no competing interests. References 1. Bonvini RF, Hendiri T, Anwar A: Sinus arrest and moderate hyperkalemia. Ann Cardiol Angeiol (Paris) 2006, 55:161-163. 2. Mehta NJ, Chhabra VK, Khan IA: Sinus arrest or sinoventricular conduction in mild hyperkalemia. J Emerg Med 2001, 20:163- 164. 3. Johnston HL, Murphy R: Agreement between an arterial blood gas analyser and a venous blood analyser in the measure- ment of potassium in patients in cardiac arrest. Emerg Med J 2005, 22:269-271. Page 2 of 2 (page number not for citation purposes)

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