Y Gürkan1, H Canatay, A Toprak, E Ural, K Toker. 1. Kocaeli University School of Medicine, Department of Anesthesiology and Reanimation, Kocaeli, Turkey. yavuzg@superonline.com
Abstract
BACKGROUND: Carbon monoxide (CO) poisoning is associated with direct cardiovascular toxicity. QT dispersion (QTd) of the ECG is an indirect measure of heterogeneity of ventricular repolarization, which may contribute to ventricular arrhythmias. Our aim was to study QTd in patients with acute CO poisoning. METHODS: CO intoxication was confirmed by arterial blood gas analysis. A control group consisted of age- and sex-matched individuals admitted to the hospital for unrelated clinical conditions. 12-lead ECG's were recorded on admission and repeated 1 week after discharge from the hospital. QT dispersion was defined as the difference between the greatest and the least QT intervals in any of the 12 leads. RESULTS: Seventeen intoxicated patients, aged 5-46 years, had mean carboxyhemoglobin levels of 22.5 +/- 11.1%. On admission, corrected QT intervals of the intoxicated patients were significantly increased compared to the control group (431 +/- 18 ms vs. 404 +/- 28 ms, P = 0.008), but not the QT interval (358 +/- 25 ms vs. 345 +/- 20 ms, P = 0.17). Mean QTd and cQTd values (46 +/- 15 ms and 62 +/- 13 ms) of the intoxicated patients were significantly increased compared to the control group (17 +/- 4 ms and 33 +/- 15 ms, P < 0.0001 for both). Both QTd and cQTd decreased significantly after discharge from the hospital (P = 0.0001). CONCLUSION: Although QT dispersion increased in patients with CO poisoning, none of ECG's showed ventricular arrhythmia. Increased QTd in the absence of QT interval prolongation may have a lowered arrhythmogenic potential of CO poisoning.
BACKGROUND:Carbon monoxide (CO) poisoning is associated with direct cardiovascular toxicity. QT dispersion (QTd) of the ECG is an indirect measure of heterogeneity of ventricular repolarization, which may contribute to ventricular arrhythmias. Our aim was to study QTd in patients with acute CO poisoning. METHODS: CO intoxication was confirmed by arterial blood gas analysis. A control group consisted of age- and sex-matched individuals admitted to the hospital for unrelated clinical conditions. 12-lead ECG's were recorded on admission and repeated 1 week after discharge from the hospital. QT dispersion was defined as the difference between the greatest and the least QT intervals in any of the 12 leads. RESULTS: Seventeen intoxicated patients, aged 5-46 years, had mean carboxyhemoglobin levels of 22.5 +/- 11.1%. On admission, corrected QT intervals of the intoxicated patients were significantly increased compared to the control group (431 +/- 18 ms vs. 404 +/- 28 ms, P = 0.008), but not the QT interval (358 +/- 25 ms vs. 345 +/- 20 ms, P = 0.17). Mean QTd and cQTd values (46 +/- 15 ms and 62 +/- 13 ms) of the intoxicated patients were significantly increased compared to the control group (17 +/- 4 ms and 33 +/- 15 ms, P < 0.0001 for both). Both QTd and cQTd decreased significantly after discharge from the hospital (P = 0.0001). CONCLUSION: Although QT dispersion increased in patients with CO poisoning, none of ECG's showed ventricular arrhythmia. Increased QTd in the absence of QT interval prolongation may have a lowered arrhythmogenic potential of CO poisoning.
Authors: Ozgür Ciftçi; Murat Günday; Mustafa Calışkan; Hakan Güllü; Rafi Doğan; Aytekin Güven; Haldun Müderrisoğlu Journal: Indian J Crit Care Med Date: 2013-05