Use of midazolam in seizures has been used intravenously to treat acute attack of seizure effectively. Recent studies proved its usefulness through oral and intranasal route to control acute seizure attack particularly in children. The efficacy of intranasal and oral midazolam in seizures in hospitalized patients was similar to, and even higher than, that of […]
Midazolam sedation is a useful intravenous adjunct to local or regional anesthesia for a variety of therapeutic and diagnostic procedures. Midazolam sedation in doses of 1.0 to 2.5 mg IV (onset within 30-60 sec, time to peak affect 3 to 5 minutes, duration of sedation 15 to 80 minutes) is effective for sedation. Titrated intravenous
Midazolam, 0.2 mg/kg IV, for induction of intravenous versed anesthesia produces a greater decrease in systemic blood pressure and increase in heart rate than does diazepam, 0.5 mg/kg IV. The haemodynamic effects of midazolam are significant in humans. In normal humans, midazolam, 0.15 mg/kg IV over 15 seconds, produces statistically significant reduction in systolic (5%)
Midazolam structure is characterized by pH dependent ring opening phenomenon in which the ring remains open at pH values of less than 4, thus maintaining its water solubility. The pK of midazolam is 6.15, which permits the preparations of salts to be water soluble. The parenteral solution of midazolam used clinically is buffered to an
In patients with acute renal failure, total body clearance is lower and the elimination half-life, while considering midazolam duration of action becomes longer than in patients with normal kidney function. In patients with impaired kidney function, the excretion of 1-hydroxymethyl midazolam glucuronide, the major metabolite of midazolam, is impaired. In healthy children aged 1 year
Midazolam metabolism is carried out rapidly by hepatic and small intestine cytochrome P450 (CYP3A4) enzymes to active and inactive metabolites. The principal metabolite of midazolam is 1-hydroxymidazolam, which has approximately half the activity of the parent compound. This active midazolam metabolism is rapidly conjugated to 1-hydroxymidazolam glucuronide and is subsequently cleared by the kidneys. This
The midazolam half life elimination of IM administration is comparable to that observed following the IV administration. Midazolam is approximately 97% plasma protein-bound in normal subjects. In patients with chronic renal failure, the free fraction of drug in plasma can be significantly higher than in healthy adults. In animals and humans, Midazolam has shown to
Midazolam onset of action undergoes rapid absorption from gastrointestinal tract. Only about 50% of the orally administered dose of midazolam reaches the systemic circulation, reflecting extensive first-pass metabolism. It is highly protein bound and this does not depend on the plasma concentration of the drug. The short duration of the drug is due to its
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
The molecular mechanisms underlying the diverse actions remain unclear, although some of the midazolam mechanism of action and sites of action of benzodiazepines effects are known. Benzodiazepines appear to produce all their pharmacologic effects by facilitating the actions of gamma-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the CNS. Benzodiazepines do not activate the GABAA
