CRNA Drugs

to study for CRNA interview/school, and advance knowledge of meds commonly used in ICU settings

Propofol MOA

Class: Anesthetic

Positive modulation of the inhibitory function of the neurotransmitter gama-aminobutyric acid (GABA) through GABA-A receptors (ligand-gated ion channels) leading to hyperpolarization of neurons, caused by an influx of chloride ions, resulting in decreased excitability and fewer action potentials, which contributes to its sedative and anesthetic effects. Propofol does not bind to GABA-A receptors directly, instead it enhances the affinity of GABA receptors to GABA, increasing the duration of GABA-activated chloride channel opening.

Propofol Pharmacokinetics and Special Considerations

Only available IV.

Dose (ICU): 5-50 mcg/kg/min

Rapid onset (15-30 seconds), short duration (3-10 minutes), half-life of approximately 2 hours

May cause hypotension and respiratory depression. Lipid emulsion susceptible to bacterial growth-tubing must be changed every 12 hours. Also, taken into consideration when preparing enteral and parenteral nutrition-contributes to calories and triglycerides.

Midazolam (Versed) MOA

Class: Benzodiazepine

A benzodiazepine that enhances the effects of GABA at the GABA-A receptor, leading to sedative, anxiolytic, muscle relaxant, and amnesic properties, commonly used for procedural sedation. It is a positive allosteric modulator, meaning it binds to a different site than GABA, and increases the frequency of chloride channel opening triggered by GABA, causing an influx of chloride ions, resulting in decreased excitability and fewer action potentials.

Midazolam Pharmacokinetics and Special Considerations

Available IV, IM, IN, oral, buccal, rectal

Dose (ICU): 1-2.5 mg IV

Onset 3-5 minutes, duration 1-6 hours, half-life of 1.5-2.5 hours.

May cause hypotension and respiratory depression.

Reversal agent: Flumazenil

Norepinephrine MOA

Sympathomimetic

Noradrenaline acts on both alpha-1 and alpha-2 adrenergic receptors to cause vasoconstriction. Its effect in-vitro is often limited to the increasing of blood pressure through antagonising alpha-1 and alpha-2 receptors and causing a resultant increase in systemic vascular resistance.