- Open Access
Cardiac arrest following a glucose 30% bolus: what happened?
© BioMed Central Ltd 2008
- Published: 16 January 2008
- Ventricular Fibrillation
- Central Venous Catheter
- Serum Potassium
A 74-year-old man was admitted with postoperative peritonitis. On day 45, a double-lumen central venous catheter was positioned in the patient's right subclavian vein. The distal lumen was used only for parenteral nutrition (2,000 ml/day Kabiven® 1600; Fresenius Kabi Brezin, France). Glucose 5% (250 ml) with 6 g potassium was infused, over 24 hours, via the proximal lumen. Hypokalemia was noted (K+, 3.0 mEq/l). An additional infusion of potassium was initiated (34 mEq in 10 ml, at 17 mEq/hour) via the proximal lumen.
Electrocardiographic changes are not usually seen until serum potassium exceeds 6.0–6.5 mmol/l. Disappearance of the P wave is usually seen when serum potassium exceeds 8 mmol/l . We were surprised, however, to find changes in the absence of any increase in serum potassium. There was neither hyponatremia nor hypocalcemia, both of which 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.
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