Midazolam sedation

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 sedation produces mild sedation and amnesia. It can be used for sedation of healthy patients receiving subarachnoid or epidural anesthesia.

Sedation occurs without loss of airway reflexes or significant cardiovascular changes. It is also useful for sedation in endoscopic procedures.

Compared to cliazepam, midazolam sedation has, a more rapid onset, more amnesia, less postoperative drowsiness, less pain on injection, less venous irritation, but time to complete recovery is similar.

The most significant side effect of midazolam sedation is depression of ventilation caused by decrease in hypoxic drive. The ventilatory depressant effect of midrolam is greater than diazepam or lorazepam.

Midazolam-induced respiratory depression is exaggerated in the presence of opioids and other CNS depressant drugs. Increasing age greatly increases the pharmacodynamic sensitivity to the hypnotic effects of midazolam.

Cardiovascular depression and clinical evidence of respiratory depression are usually absent in patients given midazolam-titrated intravenous method of administration.

Many patients in the ICU receive mechanical ventilation and require sedative medications. Anxiolysis, hypnosis, and amnesia can be considered the primary objects of sedative therapy.

Midazolam sedation is one of the most commonly used sedatives used in the intensive care setting as a continuous infusion or intermittent bolus technique. In comparison to lorazepam it leads to quicker emergence from sedation when stopped.

Midazolam sedation has the shortest t-half of the commonly used benzodiazepines, generates few active metabolites, and is water soluble at physiologic pH and thus, it is well suited for continuous infusion in the ICU. To sedate patients in the ICU, midazolam is commonly administered via titrated, continuous infusions.

Cardiorespiratory effects tend to be minimal; however, hypotension can occur in hypovolaemic patients. Prolonged sedation after cessation of the midazolam infusion may be caused by altered kinetics of the drug in critically ill patients or by accumulation of active metabolites.

Tolerance and tachyphylaxis may occur, particularly with longer-term infusions (>=3 days). Benzodiazepine withdrawal syndrome has also been associated with high dose or long-term midazolam infusions.

In addition, paradoxical and psychotic reactions have been rarely reported. In comparison to propofol, midazolam sedation results in better maintenance of sedation, yields complete amnesia, less cardiovascular depression during induction but more respiratory depression.

 

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