The importance of identifying patients at risk of dexmedetomidine-associated hypotension.

The use of dexmedetomidine in the intensive care setting has risen dramatically in recent years, which can be attributed to the benefits of decreased ventilator dependence,[1] shortened Intensive Care Unit (ICU) stays, and decreased costs of hospitalization associated with these improvements.[2] However, the hypotension and bradycardia associated with dexmedetomidine administration is well documented and can limit its use in critically ill patients. To date, scant evidence is available to predict which patients will suffer these potentially life–threatening effects. With increasing emphasis on cost–effective healthcare delivery, determining the patient populations and characteristics that would most benefit from dexmedetomidine use is critical both for patient safety and optimal resource utilization.

The authors have made a valiant endeavor to address this deficit in literature while raising other important clinical questions.[3] When reviewing the association between dexmedetomidine and hypotension, many researchers use different definitions of hypotension, either based on systolic blood pressure or mean arterial pressure, with different numeric cutoffs for these values. By limiting their review to a single institution, the authors avoid this discrepancy. In addition, the study includes both cardiac surgical and medical ICU patients, which acknowledges that these are two distinct patient populations with potentially different vulnerabilities and underlying comorbidities. This study also serves to illustrate that more acute patients are more prone to dexmedetomidine-associated hypotension, which reinforces an already accepted tenant that sick patients are prone to getting sicker and that utilization of more recent therapies in the ICU setting should probably be limited to less acute patients.

This study also raises several interesting questions. While the authors determine existing hypotension to be a risk factor for persistent hypotension after dexmedetomidine use, they are unable to differentiate the etiology of the initial hypotension as they lack data regarding volume status or cardiac function before ICU admission. Several studies have exhibited the susceptibility to hypotension and bradycardia in both medical and surgical patients with cardiac dysfunction,[4] but data also show that routine surgical patients not undergoing cardiac procedures do not suffer any adverse effect from transient dexmedetomidine-induced hypotension,[5] which may suggest that hypotension secondary to hypovolemia is less of a risk factor for dexmedetomidine-associated hypotension than coronary artery disease or cardiac dysfunction. The assertion that dexmedetomidine use should be limited in volume–depleted patients, while potentially prudent, has no basis on the data presented in this study. In addition, this study and many prior studies do not address pulmonary comorbidities in critically ill patients even though respiratory failure brings a significant number of patients to the ICU and one of the chief benefits of dexmedetomidine use is shortened ventilator dependence. Are coronary artery disease and hypotension independent from pulmonary comorbidities as risk factors for dexmedetomidine-associated hypotension? The authors also fail to mention the clinical significance of the hypotension in the 40% of their patients who had this complication. Did these patients require initiation of pressor support, or was pressor support only necessary for patients who were on pressors before dexmedetomidine use?

Determining the risk factors that predispose patients to dexmedetomidine-associated hypotension is an important clinical question, and this study achieves great strides in providing a foundation for that dialog. Further study into both predisposing factors and the effects of patient factors and comorbidities to this complication are necessary to optimize the use of dexmedetomidine in the critical care setting.