Incidence and factors associated with dexmedetomidineinduced hypotension and bradycardia at Moi Teaching and Referral Hospital intensive care unit Eldoret, Kenya

Abstract

Dexmedetomidine is the preferred drug for light sedation in intensive care units (ICU) where sedation plays an important role in patient comfort. Its advantages include shorter weaning time and earlier extubating from mechanical ventilation without respiratory depression. However, dexmedetomidine has been associated with over 50% incidence of hemodynamic adverse effects (hypotension and bradycardia) that has led to poor clinical outcomes. This limits its widespread use. Factors such as age, comorbidities, concomitant medications, dosage, baseline mean arterial pressure (MAP) and heart rate (HR) have been associated with adverse effects. Despite the high number of reported adverse effects, there is limited data on incidence and associated factors in resource limited settings. Therefore, its burden at Moi Teaching and Referral Hospital (MTRH) remains unknown. Knowledge on incidence and associated factors may inform future practice on safe use of dexmedetomidine at MTRH. Objective: To determine incidence and clinical factors associated with dexmedetomidine induced adverse effects among patients sedated with dexmedetomidine at MTRH ICU. Methods: This was a prospective observational study done at MTRH ICU. Hemodynamically stable eligible participants on dexmedetomidine were enrolled through census method between mid-April and mid-October 2022.The dependent variable was incidence of dexmedetomidine induced hemodynamic adverse effects. Data on MAP, HR were collected at selected time points within 24 hours. Independent variables which included factors such as age, gender, comorbidities, concomitant medication, renal, liver functions and drug dosages were obtained from patient records. Cutoff for hypotension was a MAP less than 60mmHg or a drop in MAP of 30% within the first hour, while bradycardia was a HR less than 60bpm or a drop in HR of 30% within first hour of drug administration. Continuous, data was summarized using means, medians and categorical data as frequencies and proportions. Fisher’s exact test and Kruskal Wallis test was used to assess for associations between categorical variables and continuous independent variables. The association between the clinical factors and development of dexmedetomidine induced hemodynamic adverse effects was analyzed using logistic regression model. Results: A total of 61 participants were recruited and 41% had traumatic brain injury. The mean age was 37 years and males were 63.9%. All participants had baseline HR>60bpm and MAP>60mmHg during drug initiation. Five patients (8.2%) developed hypotension and one (1.6%) developed bradycardia at the first hour. Mean baseline MAP was 90.49mmHg and mean decline was 5.16mmHg at 1hour. Mean baseline HR was 98.75bpm and mean decline was 0.91bpm within the first hour. Majority of patients received drug doses ranging from 0.2 to 0.7mcg/kg/hr for less than 24 hours. Lower baseline MAP <70mmHg was significantly associated with dexmedetomidine hemodynamic adverse effects (OR 2.17[95%CI 1.08-2.97, p<0.01]). However, there was no significant association between gender (0.21), baseline HR (0.88), comorbidities (0.19), concomitant medications (0.15), dose and duration (1), renal (0.28), liver functions (0.17) and occurrence of hemodynamic adverse effects. Conclusion: This study reported a low incidence of dexmedetomidine induced adverse effects compared to previous studies. Lower baseline MAP<70mmHg was an independent predictor of dexmedetomidine induced hypotension and bradycardia.