The mechanisms for ketamine induced cardiovascular effects are complex and also Ketamine effect on blood pressure characteristics. Direct stimulation of the CNS leading to increased sympathetic nervous system outflow seems to be the most important mechanism for cardiovascular stimulation. One of the characteristic of Ketamine is related to blood pressure and is therefore termed as […]
Ketamine cardiovascular effects resemble sympathetic nervous system stimulation. Indeed, a direct negative cardiac inotropic effect is usually overshadowed by central sympathetic stimulation. HR and BP rise were similar between S(+)ketamine and racemic mixture. Systemic blood pressure, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements all are increased after IV administration of ketamine cardiovascular
Emergence from ketamine anesthesia in the postoperative period may be associated with audiovisual ketamine hallucinations , confusional state, which may progress to delirium, proprioceptive disturbances (feelings of detachment from the body) and slightly reduced ability to recall objects seen after administration of the drugs. The ability to recall objects seen immediately before drug exposure remains
Ketamine produces effective sedation, hence also known as Ketamine sedation . In pediatric patients for short surgical procedures or for putting intravenous catheters before IV induction ketamine has shown effective for producing sedation. It is highly effective with a wide margin of safety, and uniquely preserves protective airway reflexes and also does not require intravenous
Ketamine Preemptive Analgesia is an antinociceptive treatment targeted to block CNS hyperexcitability, and thereby leads to a reduced postoperative pain state. Excitatory amino acids aspartate, released by the C fibers, interacts with the NMDA receptors of the dorsal horn neurons, and thus, leads to increase in intracellular calcium ions, which is thought to be the
When administered intrathecal ketamine shows local anesthetic effects in both animals and humans. Intrathecal ketamine when used as a sole agent (0.7-0.95 mg/kg) with or without epinephrine for intrathecal use, although produces motor and sensory block but the analgesia is inadequate and of short duration along with varied psychomimetic disturbances. When added to the intrathecal
Epidural ketamine and its active enantiomer S(+)ketamine have been used intrathecally and epidurally (caudally) for the management of perioperative pain and in a variety of chronic pain syndromes. Although ketamine has been reported to interact with opioid receptors, binding to local opiate receptors seems to play only a minor role, whereas significant analgesia after even
Ketamine is metabolized extensively by hepatic microsornal enzymes. Ketamine metabolism is demethylated to the corresponding N-desmethyl compound to form norketamine (about 60%) the main metabolite. Norketamine rapidly appears (approximately within 5 minutes) in plasma following ketamine administration and had a terminal half-life of 63.6 +1- 23.9 minutes. In animals, norketamine is one-fifth to one-third as
Ketamine analgesia produces intense analgesia at sub anesthetic doses and prompt induction of anesthesia when administered IV at higher doses. Ketamine analgesia has an analgesic action at many sites both centrally and peripherally. These actions are mediated via multiple receptor subtypes, including opioid, NMDA, kainate, and GABAA receptors. Ketamine also inhibits serotonin and dopamine reuptake.
The pharmacokinetics of ketamine is characterized by rapid onset of action, relatively short duration of action, and high lipid solubility. Ketamine half life has a pK of 7.5 at physiologic pH. Ketamine half life can be given by multiple routes: IV, TM, SC, oral, sublingual, rectal, nasal, transdermal, epidural, or intrathecal. Peak plasma concentrations of
