Introduction: Ketamine is commonly used in emergency department procedural sedation. Mild to moderate transient increases in blood pressure, heart rate, and cardiac output are common due to ketamine causing an increase in sympathetic activity. There is a concern that these physiological changes could result in an increased myocardial oxygen demand that may exacerbate underlying cardiac disease.
Methods: Convenience sample of patients older than 50 years receiving ketamine for procedural sedation in the emergency department was used (n = 31). Patients were selected to receive ketamine based on provider discretion. Primary outcome was incidence of new myocardial ischemia apparent on an electrocardiogram (ECG). ECGs were obtained prior to sedation and during the sedation approximately one minute after administration of ketamine. ECGs were reviewed by a board-certified emergency medicine physician and a board-certified cardiologist.
Results: New onset ischemia was found in 9.7% (3/31) of ECGs. Of these, one was in a patient who had previously received ketamine without evidence of ischemia on the repeat ECG. There were no statistically significant differences between the groups. Evidence of ischemia on ECG did not impact patient disposition.
Conclusions: Ketamine is a useful medication in procedural sedation; however, careful attention should be made in patient selection when ketamine is the desired agent. Consideration might be made in using the lowest possible dose of ketamine to obtain adequate sedation in order to hopefully lessen the occurrence of ECG changes suggestive of myocardial ischemia. Based on this small sample, single-site study, no evidence of statistically or clinically significant ischemia was seen with the use of ketamine for procedural sedation. Ketamine remains a safe medication option in adults undergoing procedural sedation.
Chronic kidney disease (CKD) occurs in approximately one-third of patients with non-valvular atrial fibrillation (AF). The presence of CKD, particularly advanced CKD, confers increased risk of both thromboembolism and major bleeding in this group of patients who are already at risk for ischemic stroke and systemic embolism and at risk of bleeding due to anticoagulation. Studies assessing the effect of warfarin on risk of ischemic stroke, systemic embolism, and major bleeding have produced disparate results, particularly in patients with advanced CKD including those treated with hemodialysis. The direct oral anticoagulants (DOAC's) have been studied in patients with stage III (moderate) CKD and appear to be as effective or more effective (dabigatran 150 mg twice daily) than warfarin in preventing ischemic stroke or embolism in this group. Two of the DOAC's, apixaban and edoxaban, confer lower risk of major bleeding than warfarin with appropriate dose adjustments. Substantial gaps exist in our knowledge of anti-thrombotic therapy in patients with AF and CKD, primarily due to exclusion of patients with advanced CKD from randomized controlled trials comparing DOAC's with warfarin.
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