Ketamine respiratory effects

In 1962, chemists at Parke-Davis labs who were searching for a replacement for phencyclidine synthesized ketamine hydrochloride. In 1965, scientists learned that ketamine was a useful anesthetic. Marketed under the brand name Ketalar , it was a promising anesthetic because it suppressed breathing much less than most other available anesthetics did. Ketamine, like PCP, produces minimal cardiac and respiratory effects, and it wears off soon after administration.50... 

The respiratory effects of ketamine are perhaps the best indication for its use. Induction doses of ketamine produce small and transient decreases in minute ventilation, but respiratory depression is less severe than with other general anesthetics. Ketamine is a potent bronchodilator due to its indirect sympathomimetic activity and perhaps some direct bronchodilating activity. Thus, ketamine is particularly well suited for anesthetizing patients at high risk for bronchospasm. 

At low doses, ketamine may result in impairment of attention, learning ability, and memory, and at high doses it has been associated with delirium, amnesia, impaired motor function, hypertension, depression, and respiratory depression (Krystal et al. 1994). Another mechanism of action appears to be a blocking of the reuptake of catecholamines. This effect leads to an increase in heart rate and blood pressure (Reich and Silvay 1989). 

Figure 1 illustrates the dose-dependent effects of ketamine on these three endpoints. A dose of 20 mg/kg significantly delayed tonic limb extension but did not protect against the lethality associated with this severe convulsive response. Higher doses significantly delayed the initial clonic convulsive response and prevented tonic limb extension. At these doses, the tonic extension response was replaced-with the abrupt onset of continuous clonic limb convulsions, which persisted until death from apparent respiratory depression. The onset of the continuous clonic convulsions and lethality was also delayed in a dose-dependent manner, at the higher doses of ketamine. 

Physical effects of high doses of ketamine include decreased respiration and heart rate, increased blood pressure, and the possibility of vomiting and convulsions. These can lead to cardiac and respiratory arrest, coma, and death. The risk of ketamine overdose is much greater when it is mixed with other drugs such as alcohol, Ecstasy, caffeine, or cocaine. Overdoses of ketamine have been reported when people boost the drug (take another dose before the first dose wears off) to prolong its psychedelic effects. 

In very large quantities, DXM can cause effects similar to those of ketamine and PCP because these drugs affect similar sites in the brain. These effects can include impaired motor function, numbness, nausea/vomiting, and increased heart rate and blood pressure. On rare occasions, hypoxic brain damage—caused by severe respiratory depression and a lack of oxygen to the brain—has occurred due to the combination of DXM with decongestants often found in the medication. 

Adverse effects noted with the anesthetic use of ketamine include the sudden loss of respiratory function, spasms of the trachea or larynx, and vomiting. Literature on the emergency treatment of ketamine overdose is rare. Clinical recommendations advise making sure the airway is clear, that breathing is continually monitored, and that the heart rate remains steady. 

Ketamine is not a significant respiratory depressant and the ventilatory response to hypoxia is maintained. Ketamine has a bronchodilatory effect subsequent to sympathetic stimulation. Airway reflexes are well maintained after ketamine administration. However, since ketamine is not used as... 

The pharmacological effects of tiletamine plus zolazepam are very similar to the effects produced by ketamine. When used as the sole anesthetic in the horse, tiletamine plus zolazepam can cause excitation and hyperresponsiveness. This combination is only used in the horse after adequate sedation. In general, it produces a dose-related loss of consciousness, characterized as a cataleptic state, and analgesia. Ocular and airway reflexes are well maintained. The combination induces mild cardiovascular stimulation secondary to centrally mediated sympathetic nervous system stimulation. There is minimal respiratory depression. 

In the horse, induction with thiopental usually results in a brief increase in heart rate and a decrease in cardiac output but no significant change in arterial blood pressure. Arterial blood pressure is typically lower after thiopental induction than in ketamine-based anesthetic techniques (Bennett et al 1998, Muir et al 2000). However, when horses are placed on inhalation anesthetics for maintenance of anesthesia, the hemodynamic effects of the induction agents is short lived and the hypotension and reduced cardiac output typical of inhalation anesthesia predominates (Bennett et al 1998, Wagner et al 1996). Respiratory depression is significant with an accompanying increase in Paco2 and decrease in pH. 

Known as special K, jet, green, and other names on the street, ketamine is sometimes injected, but can be evaporated to solid crystals, powdered, and smoked, snorted, or swallowed. Marijuana cigarettes are sometimes soaked in the ketamine solution, allowed to dry, and then smoked. Ketamine has become popular as a rave club drug. Side effects include signiflcant transient increases in blood pressure and heart rate, respiratory depression, airway obstruction, apnea, muscular hypertonia, psychomotor and psychotomimetic effects, and acute dystonic reactions. Following overdose, seizures, polyneuropathy, increased intracranial pressure, respiratory arrest, and cardiac arrest may occur. 

Ketamine produces a different effect to other intravenous anaesthetics analgesia, sensory loss, amnesia and muscle paralysis are produced without loss of consciousness, so-called dissociative anaesthesia, and with minimal respiratory depression. 

Ketamine is a respiratory depressant like morphine, but less potent, and its effects can be additive with morphine. The manufacturer notes that prolonged recovery time may occur if opioids are used with ketamine. ... 

Another study in healthy subjects using various experimental pain models found that ketamine antagonised the respiratory depressant effect of remifentanil. Remifentanil alone produced analgesic effects with all pain tests, but ketamine only enhanced the effect of remifentanil on intramuscular electrical stimulation. Acute remifentanil-induced hyperalgesia and tolerance were detected only by the pressure pain test and were not suppressed by ketamine. The combined effects of remifentanil and ketamine probably depend on the type of pain. ... 

Ketamine may be ideal to treat post-operative pain after adenotonsillectomy. It avoids the feared risks of bleeding with NSAIDs and respiratory depression with opioids. Ketamine at a dose of 0.5 mg/kg IV reduces post-operative pain and need for other analgesics. Peritonsillar infiltration at the same dose has a similar effect to the intravenous dose. The time of administration either before the start or the conclusion of surgery has no bearing on the analgesic effect. If prolonged pain is anticipated a ketamine infusion of 0.3 6 mg/kg per h can be started after the administration of a loading dose of 0.5 mg/kg. 

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