Dexmedetomidine
Dexmedetomidine (DEX) has been shown to decrease anesthetic induction doses and decreased use of intraoperative opioid and halogenated requirements for the maintenance of anesthesia. DEX decreases the preoperative concentrations of catecholamines and promotes perioperative hemodynamic stability (1 ).
Dexmedetomidine (DEX) is an alpha (2A)-adrenergic receptor with a selectivity ratio between α2: α1 receptors of 1600: 1, which is eight times more selective for the alpha (2A)-adrenergic receptor in comparison to clonidine. Dexmedetomidine is a relatively new drug approved by the end of 1999 by the Food and Drug Administration (FDA) for human use due to its sedative, analgesic and anxiolytic action, its reduction in delirium and agitation, its perioperative sympatholysis, cardiovascular stabilizing effects, and preservation of respiratory function (4 ).
Metabolism. DEX is extensively metabolized by the liver and excreted in urine. More than 90% is bound to proteins.
Pharmacokinetics . The elimination half-life (t1 / 2β) of DEX is 2 - 3 h. The context-sensitive half-life is approximately 4 min - 8 min. which allows the suspension of DEX infusion minutes before the end of the surgery.
Central Nervous System . Activation of the α2 receptor of the CNS (central nervous system) produces sedation, analgesia, and anxiolysis. Sedation is mediated by the activation of the alpha (2A)-adrenergic receptor in the locus coeruleus. Analgesic effects are mediated mainly at spinal cord level. It is known that DEX lowers the minimum alveolar concentration (CAM) of inhalation anesthetics and at higher concentrations it may affect memory and recollection.
Respiratory effects . While DEX reduces minute ventilation (VE), it maintains a ventilatory response to increased CO2 levels. DEX appears to decrease the tidal volume (VC) without affecting the respiratory rate (FR). The combination of DEX along with an opioid, improves analgesia but does not seem to enhance respiratory depression.
Cardiovascular system. Through its sympathetic effects of central action and included in cardiovascular effects, there are frequent decreases in heart rate, BP, systemic vascular resistance (SVR) and cardiac output (CO). This is believed to be the result of agonist effects on the peripheral alpha (2A)-adrenergic receptor. A bolus injection of DEX causes a biphasic response, with an initial increase in BP and a decrease in heart rate (5 )(6 ).
In cardiac surgery, DEX is a clinical alternative amidst numerous pharmacological alternatives because it does not cause depression of the respiratory centers, and furthermore reduces the use of opioids up to 66% in the postoperative period.