Carbon monoxide poisoning increases Tpeak-Tend dispersion and QTc dispersion : cardiovascular topic

Abstract

SummaryObjectiveCarbon monoxide (CO) poisoning leads to cardiac dysrhythmia. Increased heterogeneity in ventricular repolarisation on electrocardiogram (ECG) shows an increased risk of arrhythmia. A number of parameters are used to evaluate ventricular repolarisation heterogeneity on ECG. The aim of our study is to investigate the effect of acute CO poisoning on indirect parameters of ventricular repolarisation on ECG.MethodsSixty-seven patients were included in this case–control study. Thirty patients with acute CO poisoning were assigned to group 1 (19 females, mean age: 30.8 ± 11.3 years). A control group was formed with patients without known cardiac disease (group 2, n = 37; 25 females, mean age: 26.0 ± 5.2 years). Twelve-lead ECG and serum electrolyte levels were recorded in all patients. Also, carboxyhaemoglobin (COHb) levels were recorded in group 1. Tpeak–Tend (TpTe) interval, TpTe dispersion, TpTe/QT ratio, QT interval and QTd durations were measured as parameters of ventricular repolarisation. Corrected QT (QTc) and QTc dispersion (QTcd) intervals were determined with the Bazett’s formula.ResultsThe mean COHb level in group 1 was 27.6 ± 7.4% and mean duration of CO exposure was 163.5 ± 110.9 min. No statistically significant difference was found in age, gender, serum electrolytes or blood pressure levels between the groups. QRS, QT, QTc, TpTe interval and TpTe/QT ratio were similar between the groups (p > 0.05). QTcd (65.7 ± 64.4 vs 42.1 ± 14.2 ms, p = 0.003) and TpTe dispersion (40.5 ± 14.8 vs 33.2 ± 4.9 ms, p = 0.006) were significantly longer in group 1 than group 2. COHb level was moderately correlated with TpTe dispersion (r = 0.29; p = 0.01).ConclusionTo our knowledge, this is the first study to investigate TpTe interval and dispersion in CO poisoning. Our results showed that TpTe dispersion and QTc dispersion increased after CO poisoning.

Predictive Role of QTc Prolongation in Carbon Monoxide Poisoning-Related Delayed Neuropsychiatric Sequelae

“…Acute CO poisoning frequently affects the repolarisation of myocardium electrophysiology, resulting in abnormal ECG findings such as QTc prolongation and QTc dispersion [ 16 , 18 , 19 , 24 ]. These changes may lead to life-threatening cardiac arrhythmia or proarrhythmia effects [ 19 ].…”

“…This subsequently resulted in prolongation of the action potential and the associated intracellular Ca2 + transients, leading to disruption of ventricular myocyte repolarisation and QT prolongation [ 2 , 15 ]. Studies have also suggested that prolonged QTc and QTc dispersion increased the risk of atrial and ventricular arrhythmia in patients with CO poisoning [ 2 , 16 ]. However, no study has linked QTc interval or QTc dispersion with the prediction of DNS in patients with CO poisoning.…”

Carbon monoxide poisoning and its effect on QTc prolongation

“…CO has been reported to have arrhythmogenic potential likely due to its action on the cardiac membranes [4]. A few studies have highlighted the association between QT prolongation and CO poisoning but none of them has reported prolongation to the degree highlighted in the case we present with complete resolution 24 h later [5,6].…”

Can indices of myocardial damage predict carbon monoxide poisoning outcomes?

“…Carbon monoxide reduces the oxygen-carrying capacity of blood and binds with cardiac myoglobin, causing a rapid decrease in myocardial oxygen reserves 6 . Several studies have shown that carbon monoxide intoxication causes increased QT intervals and QT dispersion [6][7][8] . This study showed that QTc dispersion and carboxyhemoglobin are signi cantly related.…”