Propofol Class
Hypnotic
Propofol Clinical Use
- Induction, maintenance of general anesthesia, and monitored anesthesia care
- Anticonvulsant and antiemetic
Propofol MOA
Mimics GABA at the receptor, directly activating chloride channels, which hyperpolarizes the postsynaptic membrane.
Propofol Doses
- Induction of GA: 1-2.5 mg/kg
- Maintenance of GA: 25-300 mcg/kg/min IV
- Sedation: 25-100 mcg/kg/min
- Antiemetic 10-20 mg can repeat every 5-10 minutes, or start infusion of 10 mcg/kg/min
Propofol Pharmacokinetics
- Onset after induction dose: 30 seconds
- DOA induction dose: 5 – 15 minutes
- Metabolized via hepatic and extra hepatic metabolism (mostly lungs), no active metabolite
- Excreted by the kidney
Propofol Contraindications
- Allergy to propofol or its contents
- Caution with cardiac dysfunction and hypovolemia.
- Can cause severe hypotension
Propofol Considerations
- There is no evidence that propofol should be avoided in egg or soy allergic patients
- Contains sulfites
- Painful on injection
- Thrombophlebitis and extravasation risk
- Bacterial infection risk
- Can trigger propofol infusion syndrome
If given >48 hours, especially with pedi - Raises seizure threshold
Etomidate Class
Hypnotic
Etomidate Clinical Use
Induction of anesthesia
Considered for CV stability and trauma
Etomidate MOA
Binds to the GABA-a receptor, increasing chloride conduction
Lower doses: potentiates GABA at its receptors
Higher doses: directly stimulates the GABA receptor
Etomidate Dose
Induction Dose: 0.3 mg/kg
Etomidate Pharmacokinetics
Onset: 1 minute
Duration: 5 -15 minutes
Metabolism: Hepatic P450 enzymes and plasma esterases
No active metabolite
Excretion: kidneys and in bile
Etomidate Contratindications
Seizures – can induce further seizures
Avoid if adrenally suppressed
Porphyria
Etomidate Considerations
Reduces ICP/CBR, CMO2
Minimal cardiac effects
Does not blunt SNS response to laryngoscope
Hyperventilation –> apnea and mild resp depression
INHIBITS CORTISOL; ADRENAL SUPPRESSION VIA 11 BETA-HYDROXYLASE
N/V in 30-40% of patients
Ketamine Class
phencyclidine derivative
Ketamine Clinical Use
May be used for GA induction and maintenance, and monitored anesthesia care.
Used as an anesthetic, analgesic and antidepressant.
Ketamine MOA
non competative NMDA receptor antagonist.
Blocks postsynaptic reflexes in the spinal cord and inhibits excitatory neurotransmitters in selected areas of the brain. Dissociates thalamus from the limbic system involved in awareness.
It also binds with opioid, MAO, serotonin, NE, muscarinic and sodium channels.
Ketamine Dose
IV Induction 1-2 mg/kg
IM Induction 4-6 mg/kg
Onset: 20 minutes
Sedation 1-3 mcg/kg/min or 0.5-1 mg/kg boluses as needed
Multimodal infusion – 3-5 mcg/kg/minute
Ketamine Pharmacokinetics
IV Onset: 2-5 minute
IV DOA: 10-20 minutes (may require an hour for full orientation)
Metabolism = P450 enzymes in the liver
Chronic ketamine use induces enzymes that metabolize it
Active metabolite: norketamine is 1/3 as potent as ketamine and is renally excreted
- Excretion = kidneys
Ketamine Contraindications
- Hypertension
- Angina
- CHF
- Increased intracranial pressure
- Increased ocular pressure
- Auditory/Visual hallucinations
- Airway problems d/t increase secretions
- Emergence reactions
vivid dreams, hallucinations (lasts 1-3 hours) and can be reduced with propofol and/or benzodiazepines
Ketamine Considerations
Increases CMRO2, CBF, ICP
Dissociative, analgesic, depression, emergence delirium, nightmares and hallucinations
SNS stimulant. Increased SVR, HR, myocardial O2 consumption, PVR, mild cardiac depression
Bronchodilator, maintains RR, preserves reflexes low dose, increases secretions (pair with antisialagogue)
Causes nystagmus
Dexmedetomidine Class
Selective alpha 2 adrenergic agonist
Dexmedetomidine Use
May be used for induction, monitored anesthesia care, analgesia and prevention of emergence delirium
Dexmedetomidine MOA
Centrally and peripherally alpha 2 adrenergic receptor agonist thereby producing sedation by decreasing sympathetic nervous system activity and the level of arousal.
Regulates the cardiovascular system by inhibiting norepinephrine release
Reduces blood pressure and heart rate by decreasing the tonic levels of sympathetic outflow from the CNS and augmenting cardiac vagal activity.
