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Dexmedetomidine (dex) is a newly discovered drug that has gained great popularity in neuroanesthesia, intensive care unit (ICU) and cardiac anesthesia in recent years. It was approved in 1999 by the FDA as a short-acting sedative. In Europe, it was introduced to health care in 2011 [1, 2]. Dexmedetomidine is a highly selective α2-adrenergic receptors agonist with high affi nity for the α2-receptor (α2/α1 1600:1) compared with clonidine (α2/α1 200:1), which makes it a complete α2 agonist [3, 4]. Dexmedetomidine by α2-adrenergic receptor activation causes sedation similar to natural sleep, which helps in the early postoperative period [5, 6]. It also exhibits analgesic, anxiolytic and sedative effects without causing severe respiratory depression. Sedative action is responsible for the stimulation of receptors located at the sinus of the upper part of the brain stem [7]. Analgesic activity consists of a central component – stimulation of receptors in the brain stem and hind corners of the spinal cord, and peripheral – stimulation of the receptors in the nerve roots of the posterior nerve roots [8]. ABSTRACT

The pharmacodynamics of dexmedetomidine in elderly cardiac patients undergoing analgosedation in the ICU