Reactions such as agitation, involuntary movements, hyperactivity and combativeness are usually reported during midazolam administration . Should such reactions occur, the response to each dose of midazolam and all other drugs, including local anesthetics, should be evaluated before proceeding with the midazolam administration of the drug. For induction of general anaesthesia in healthy patients, the […]
Midazolam produces dose-dependent decrease in ventilation with 0.15 mg/kg IV producing effect similar to diazepam 0.3 mg/kg IV. Patients with chronic obstructive pulmonary disease experience even greater midazolam respiratory depression . Transient apnoea usually follows after rapid injection of large doses of midazolam (>0.15 mg/kg IV) especially in the presence of premedication with opioids. The
For the Barbiturate therapy , High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Barbiturates decrease ICP by decreasing cerebral blood volume through drug-induced cerebral vascular vasoconstriction and an associated decrease in cerebral blood flow. This therapy in used either as a anti seizure medication
The management of methods of pain relief is and will always remain a challenging task for the clinicians. Many a times in spite of understanding the pathophysiology of pain, it becomes extremely difficult to control that pain. Most of the times the pathophysiology itself, may be shrouded in the mist of uncertain methods of pain
Beta blockade prior to instituting other vasodilator drugs in aortic dessection management is essential. The following case presentation demonstates the importance of beta blockade in Aortic dissection management. A 44-year-old man whose only past medical history consists of hypertension and unilateral cataracts presents to his local emergency department with the acute onset of severe tearing
Barbiturates mechanism of action is described here. Barbiturates most likely produce their sedative hypnotic effects through an interaction with the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the CNS. Barbiturates cause reversible depression of all excitable tissues, the CNS being exquisitely sensitive. They bind to beta subunit of the inhibitory GABA-A receptor, a site distinct from
Ketamine is associated with psychedelic effects and dependence. Well the question here arises is that Is Ketamine addictive ? These effects are dose-related and comprised of multimodal hallucinatory experiences, a sense of slowing, paranoid ideation and enhancement of sexual, musical and sensory enjoyment. The mechanisms of these phenomena are largely due to its complex multi-receptors
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
Drugs like sufentanil, alfentanil, fentanyl and other opiates although belong to phenyl piperidine group like pethidine (meperidine), their spectrum of action is more morphine-mimicking, more like mediated through β endorphin and t receptors. Actually there are some very striking differences between the two: Fentanyl and other opiates unlike, morphine, is very highly lipid soluble, so
Diazepam metabolism is carried out by hepatic microsomal enzymes using an oxidative pathway of N-demethylation with the production of desmethyldiazepam, oxazepam, and to a lesser extent temazepam as metabolites. Desmethyl diazepam is metabolized more slowly than oxazepam and is only slightly less potent than diazepam. These metabolites contribute to the sustained effect of diazepam. The
