Top Drawer Meds

Etomidate medication class

IV anesthetics

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Etomidate mechanism of action

Enhances activity of GABA

Etomidate half life

2 to 5 minutes

Etomidate duration of action

5 to 15 minutes

Etomidate peak

Etomidate metabolism

* Primarily through the liver by hydrolysis and ester hydrolysis
* 76% bound to albumin

Etomidate excretion

primarily through the urine with

etomidate metabolite

etomidate carboxylic acid- inactive

etomidate induction dose

0\.1-4mg/kg

Etomidate supplied dose

2mg/mL

etomidate side effects

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* temporary adrenal suppression
* cardiac stable
* Pain on injection
* Myoclonus

Ketamine class of medication

Dissociative anesthetics

ketamine mechanism of action

Modulation of various neurotransmitter systems in the brain

* Dissociative agent
* primary: antagonism of the N-methyl-D-aspartate (NMDA) receptor = inhibition of glutamate activity


* This results in a dissociative state, analgesia, and anesthesia.
* opioid receptors
* serotonin receptors
* dopamine receptors, contributing to its complex pharmacological effects. Overall, ketamine's mechanism of action involves modulation of various neurotransmitter systems in the brain.

Ketamine excretion

Urine

Ketamine half life

2 to 3 hours

Ketamine peak

5-15 min

Ketamine duration of action

30 minutes to 1 hour

ketamine onset of action

1-5 min

ketamine metabolism

Through the liver by N-demethylation

* CYP3A4, CYP2B6, and CYP2C9

Ketamine Metabolite

Norketamine > hydroxynorketamine (HNK) and other metabolites

Ketamine induction dose

0\.5-2mg/kg

Ketamine supplied dose

10mg/mL

Ketamine side effects

* N/V
* Tachycardia
* Hypertension
* Dizzy
* Hallucinations
* Confusion/disorientation
* Anxiety
* Mood changes

Propofol class of medication

IV general anesthetic

Propofol Mechanism of Action

Enhancing the inhibitory effects of gamma-aminobutyric acid (GABA). It binds to GABA-A receptors, which leads to increased chloride ion influx into neurons, hyperpolarization, and subsequent inhibition of neuronal activity. Resulting in sedation, hypnosis, and anesthesia.

Other effects on NMDA receptors

Propofol metabolism

In the liver through glucuronidation and oxidation.

* CYP 450/Glucuronidation (major): propofol is conjugated with glucuronic acid to form propofol glucuronide. Excreted in the urine
* Oxidation (minor): propofol = quinol and catechol derivatives

Propofol Metabolite

Glucuronidation: propofol glucuronide, inactive and excreted in the urine

Propofol onset

30-60 seconds

Propofol duration of action

few minutes to an hour

Propofol peak

Propofol induction dose

1\.5-2.5mg/kg

Propofol maintenance dose

25-200mcg/kg/min

* < 100mcg/kg/min for MAC sedation
* > 100mcg/kg/min for GA

Propofol supplied formula

10mg/mL

Propofol side effects

* pain at the injection site
* Hypotension
* Hypopnea
* Don’t give to patients with egg allergy

Midazolam class of medication

Benzodiazepine

Midazolam mechanism of action

Binds to GABA-A receptors, which increases the inhibitory activity of GABA. This results in the suppression of neuronal activity, leading to sedation and relaxation.

Midazolam metabolism and elimination

Hepatic metabolism through CYP450, specifically CYP3A4

Excreted in the urine/Renal

Midazolam Metabolite

Several active metabolites, including 1-hydroxymidazolam and 4-hydroxymidazolam

Midazolam onset of action

30-60 seconds

Midazolam peak

4 minutes

Midazolam duration of action

15-18 minutes

Midazolam half life

1\.5 to 2.5 hours

Midazolam Induction dose

0\.2-0.4mg/kg

Midazolam supplied dose

1mg/mL

Midazolam side effects

drowsiness, dizziness, confusion, headache, nausea, and vomiting. Other less common side effects may include respiratory depression, low blood pressure

Succinylcholine medication class

* depolarizing neuromuscular blocker
* Ultra rapid acting

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Succinylcholine mechanism of action

Mimics the action of acetylcholine and binds to the nicotinic acetylcholine receptors at the neuromuscular junction, causing sustained depolarization and subsequent muscle paralysis by preventing contraction

Succinylcholine metabolism

Hydrolysis to inactive metabolites via plasma cholinesterase produced in liver

Succinylcholine metabolite

* Succinylmonocholine and choline
* Succinylmonocholine further metabolizes to succinic acid and choline

Succinylcholine elimination

Metabolites eliminated by the kidneys

Succinylcholine half life

1-4 min

Succinylcholine onset

30-60 seconds

Succinylcholine peak

1-2 min

Succinylcholine duration of action

5-10 minutes

Succinylcholine induction dose

1-2mg/kg

Succinylcholine supplied

20mg/mL

Rocuronium medication class

* non-depolarizing neuromuscular blocking agent
* Intermediate acting
* No histamine

Rocuronium mechanism of action

Competes with ACh for alpha subunits at post-junctional nicotinic cholinergic receptors at the motor end plate resulting in absence of depolarization and skeletal muscle paralysis

Rocuroinum metabolism

metabolized by the liver through Hofmann elimination

Rocuronium metabolite

17-desacetyl-rocuronium (less active)

Rocuronium excretion

bile and renal

Rocuronium half life

1 to 1.5 hours.

Rocuronium onset

1-2 min, 30 sec for RSI

Rocuronium peak

45 min

Rocuronium duration of action

60-90 min

Rocuronium Induction Dose

0\.6mg/kg, 1.2 mg/kg for RSI

Rocuronium supplied

10mg/mL

Atracurium class of medication

* non-depolarizing neuromuscular blocking agent
* Intermediate acting
* Moderate histamine

Atracurium mechanism of action

Competitive antagonism of acetylcholine at the neuromuscular junction in the motor end plate. This leads to muscle relaxation

Atracurium metabolism

Ester hydrolysis in the plasma, primarily by Hofmann elimination. The metabolites are inactive and are excreted mainly through the kidneys.

Atracurium metabolite

Laudanosine, weak CNS stimulant and has minimal muscle relaxant properties.

Atracurium excretion

* Primarily excreted through the kidneys
* 80% of the drug is eliminated unchanged in the urine within 24 hours of administration
* Remaining 20% is metabolized in the liver and excreted in the urine as inactive metabolites.

Atracurium half life

20-30 minutes

Atracurium onset

2-3 minutes

Atracurium peak

3-5 minutes

Atracurium duration of action

20-35 minutes

Atracurium dose

0\.3-0.5mg/kg

Atracurium Supplied

10mg/mL

Cisatracurium medication class

* non-depolarizing neuromuscular blocking agent
* Intermediate acting
* No histamine

Cisatracurium mechanism of action

Competitive antagonism of acetylcholine at the neuromuscular junction in the motor end plate. This leads to muscle relaxation

Cisatracurium metabolism

Primarily by Hofmann elimination, a non-enzymatic process that occurs at physiological pH and temperature.

Cisatracurium metabolite

Laudanosine is a CNS stimulant and can accumulate in patients with renal or hepatic impairment and potentially cause seizures in high concentrations

Cisatracurium excretion

* Cisatracurium is primarily excreted unchanged in the urine
* 80% of the administered dose is eliminated within 24 hours, with about 10% excreted in the feces
* Remaining amount metabolized in the liver and plasma.

Cisatracurium half life

18-25 min

Cisatracurium onset

1\.5 min

Cisatracurium peak

1-2 min

Cisatracurium duration of action

6-16 min

Cisatracurium Dose

0\.15-0.2mg/kg

Cisatracurium supplied

2mg/mL

Vecuronium medication class

* non-depolarizing neuromuscular blocking agents
* Intermediate acting
* No histamine

Vecuronium mechanism of action

Competitively binding to the nicotinic receptors at the motor endplate, thereby preventing the binding of acetylcholine. This results in muscle relaxation and paralysis.

Vecuronium metabolism

In the liver through Hofmann elimination. This metabolic pathway involves the breakdown of vecuronium into , which is then further metabolized and excreted primarily in the urine. The exact details of vecuronium metabolism may vary depending on individual factors such as liver function and other medications being taken.

Vecuronium metabolite

3-desacetylvecuronium

Vecuronium excretion

40-70% excreted unchanged in the urine wihtin 24 hours, remaining amount through feces

Vecuronium half life

60-90 min

Vecuronium onset

2-3 min

Vecuronium Peak

3-5 min

Vecuronium duration of action

25-30 min

Pancuronium class of medication

* non-depolarizing neuromuscular blocking agent
* Long acting
* No histamine

Pancuronium mechanism of action

competitively binds to the nicotinic acetylcholine receptors at the motor endplate of the neuromuscular junction