Serotonin selective reuptake inhibitors (SSRIs) have widely replaced older tricyclic antidepressants (TCAs) in the treatment of depression and anxiety over the years, given their safer cardiac profile [Glassman, 1998]. Even at therapeutic doses, TCAs commonly cause a slowing of intraventricular conduction through their sodium-channel blocking properties, leading to prolonged PR, QRS and QT intervals [Pacher and Kecskemeti, 2004]. Similarly, in vitro and animal studies have shown that citalopram and escitalopram, through their cardiotoxic metabolite, didesmethylcitalopram, can delay ventricular repolarization, prolong QT, and increase the risk of torsade de pointes by directly blocking potassium-hERG channels in cardiomyocytes [Overa, 1989; Witchel et al. 2002]. In 2011–2012, the US Food and Drug Administration (FDA) released a safety communication regarding citalopram and escitalopram and their increased risk for QTc prolongation and cardiac outcomes, especially in elderly and patients with comorbid medical illnesses [FDA, 2012]. The new FDA recommendations state that citalopram should not be used at doses greater than 40 mg per day in healthy adults, and not exceed 20 mg per day in the elderly, patients with hepatic impairment, or patients taking a CYP2C19 inhibitor. Health Canada released a similar warning for escitalopram in 2012, stating that doses greater than 10 mg should be avoided in these latter high-risk populations [Health Canada, 2012]. A retrospective cross-sectional study in elderly surgical patients published in 2014 showed no association between citalopram and escitalopram and cardiac outcomes in this vulnerable population [van Haelst et al. 2014]. However, this association has never been assessed in a sample of acutely medically ill inpatients, another highly vulnerable population.