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.