Electrocardiographic changes in carbon monoxide poisoning

Prediction of Extravascular Burden of Carbon Monoxide (CO) in the Human Heart

“…15,85 Also, in recent years, myocardial injury, myocardial infarction, myocardial dysfunction and cardiac arrest have been reported in patients with mild to severe CO poisoning. 2,17,26,36,47,62,74,78,87 Myocardial injury in CO-poisoned victims, 26,47,74,87 was indicated by the presence of elevated cardiac injury biomarkers, e.g., troponin I, b-natriuretic peptide, creatinine kinase, and creatinine kinase-MB (myocardial band) and by ECG abnormalities, e.g., ST segment and T wave changes, sinus tachycardia, and premature atrial and ventricular contractions. 17,26,50,62 Observations of decreased left ventricular ejection fraction and right ventricular dysfunction after CO exposure imply myocardial dysfunction in these CO-poisoned patients.…”

A Case of Carbon Monoxide Poisoning Presenting with Supraventricular Tachycardia

“…Decreased left ventricular ejection fraction and right ventricular dysfunction also can be observed in CO-poisoned patients (2, 7-9). Ar-rhythmias, e.g., sinus tachycardia, atrial fibrillation, premature atrial complexes, conduction abnormalities, premature ventricular complexes and, ventricular fibrillation have been reported in patients with mild to severe CO poisoning (10,11).…”

Carbon monoxide exposure in the urban environment: An insidious foe for the heart?

“…The risk of the worsening of symptoms after CO exposure increases in patients with cardiovascular syndromes such as coronary artery disease, injury after I/R, heart failure (Varon et al, 1999;Wellenius et al, 2004) and metabolic disease (Bell et al, 2009). General cardiac effects include modifications of the electrocardiogram (ECG) pattern and arrhythmias (Cosby and Bergeron, 1963;Henry et al, 2006). Although CO favours cardiac fibrosis (Henry et al, 2008;Peers and Steele, 2012), ECG alterations can result from changes in ion currents at the cellular level or from the altered regulation of heart function by the autonomic nervous system (ANS) (Dales, 2004;Goulopoulou et al, 2006;Tarkiainen et al, 2003).…”

“…In fact, ECG recordings reveal that acute or chronic CO exposure alters cardiac electrical conduction and rhythm. Acute poisoning has been associated with several instances of sinus tachycardia (Carnevali et al, 1987;Cosby and Bergeron, 1963), supra-ventricular tachycardia, and conduction defects with bundle branch block (Parenti , 2006). Following chronic exposure, P-wave dispersion, which reflects non-homogeneous conduction in sinoatrial tissue, has been shown to increase in healthy male indoor-barbecue workers employed in different restaurants for at least 3 years (Hb CO levels ≈6.5% vs. 2% in the control population) (Sari et al, 2008) increasing the risk of developing atrial fibrillation (AF) (Dilaveris et al, 1998).…”

“…In addition, the QT interval is also increased after acute (Onvlee-Dekker et al, 2007) and chronic CO poisoning (QT max ) (Sari et al, 2008). These perturbations of atrial and ventricular electrocardiographic parameters are directly linked to the increased susceptibility to AF (Anderson et al, 1967), the high incidence of premature ventricular contraction (Gandini et al, 2001;Sheps et al, 1990) and the lower threshold for the development of ventricular fibrillation (VF) (Carnevali et al, 1987;Cosby and Bergeron, 1963;DeBias et al, 1976) observed after CO poisoning. Several clinical observations have excluded ischaemia or hypoxia as the cause of these arrhythmias because ECG modifications do not correlate with Hb CO levels in these patients (Carnevali et al, 1987;Gandini et al, 2001).…”