Abstract P183: Predictors of Myocardial Injury in Patients with Carbon Monoxide Poisoning
Introduction: Carbon monoxide (CO) is the most common cause of death from poisoning in the United States. Cardiovascular complications and their contribution to acute outcomes are yet to be defined.
Methods: We retrospectively reviewed all the cardiovascular manifestations of CO poisoning in patients presented to St Vincent Charity Medical Center, the regional center for CO poisoning treatment between the periods of January 2009 to September 2012. Patients demographics, comorbidities, electrocardiograms (EKG), laboratory results and echocardiograms were identified from chart review and retrieved for analysis.
Results: We identified 55 patients, mean age 49.3 years and majority were male (72%)(40 of 55). The mean hospital stay was 2.6 days. The average carboxyhemoglobin (COHb) level was 24.9% (4-63). Intentional poisoning was in 21% of patients (12 of 55), while 24%(14 of 55) were unconscious on presentation (UOP) and 19% (10 of 55) were intubated. Cardiovascular risk factors in these patients were DM 9% (5 OF 55), HTN in 36% (20 of 55), dyslipidemia 6% (3 of 55), smoking 32% (18 OF 55) and family history of premature CAD 4% (2 OF 55). Obesity was present in 19% (10 OF 55) while 5% (3 of 55) had documented history of CAD and 14% (8 of 55) with cocaine abuse prior to admission. Troponin I was found to be greater than 0.2 ng/mL in 35 % (19 of 55) of patients and more than 1 ng/mL in 20% (11 of 55). Ischemic EKG changes were found in 6 % (3 of 55) of patients. Corrected QT interval (QTc) was prolonged (>460 msec) in 40% (22 of 55) of patients. Echocardiogram was done in 9% (5 of 55) of patients and 4% (2 of 55) had depressed left ventricular ejection fraction which recovered after hyperbaric oxygen treatment (HBO) that 93% (51 of 55) of patients received.
Two patients died by anoxic brain injury that was unrelated to their cardiac status. There was no correlation between COHb level and troponin or QTc (r = -0.2 and 0.02 respectively). Patients who had significant myocardial injury (Troponin I >1 ng/mL were older (61.7 Vs. 46.6 years; P=0.02,RR=2.1,CI=1.27[[Unable to Display Character: –]]3.94) and had more history of CAD (33.3% (4 OF 11) Vs.0% (0 of 44); P=0.001;RR=3 CI=1.67[[Unable to Display Character: –]]5.94). They were more to be UOP (66.7%(7 of 11) Vs.17.5%(8 of 44) ; P=0.003;RR=3.6 CI= 1.96 [[Unable to Display Character: –]] 3.66) and necessitated more intubation (66.7%(7of11) Vs.7.7%(3 of 44); P<0.001; RR=20;CI=2.27 [[Unable to Display Character: –]] 82.45). CAD was the only predictor of significant QTc prolongation with 70% (6 of 8) of CAD group having a QTc >460 msec (P=0.016).
Conclusion: Myocardial damage in patients presenting with CO poisoning is common and manifested by increased troponin and prolonged QTc. There is no correlation between COHb level and myocardial injury. In these patients, Age, CAD, UOP and intubation are the significant predictors of troponin elevation while CAD is associated with more QTc prolongation. This damage is usually transient and is reversed with urgent HBO therapy.
- © 2013 by American Heart Association, Inc.