Hypnotics Flashcards
(29 cards)
Propofol Class
Hypnotic
Propofol Indications
induction, maintenance of anesthesia, MAC, anticonvulsant, antiemetic
Propofol Mechanism of Action
mimics GABA @receptor, directly activates cl- channels –> hyper-polarizes the postsynaptic membrane
Propofol Dosing
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 onset/duration/metabolism/elimination
Onset w/ induction dose: 30 seconds
DOA w/ induction dose:5-15 minutes
Metabolized: hepatic and extra-hepatic (lungs), no active metabolite
Excreted: Kidney
Propofol Considerations
no evidence that it should be avoided with egg or soy allergy contains sulfites painful w/ injection thrombophlebitis bacterial infection risk
Propofol Systemic Effects
CNS: Rapid onset and emergence Raises seizure threshold Reduces cerebral blood flow, CMRO2, ICP and IOP No analgesia Myoclonus may occur
Pulmonary: Dose dependent respiratory depression Infusion will decrease TV and increase RR Decrease reflexes Shifts CO2 response curve to the right Bronchodilation
Cardiovascular:
Decreases BP r/t decrease SNS and vasodilation
Decrease myocardial contractility and SVR
Decrease venous tone - > lower preload
Metabolism and Elimination:
Hepatic and extra hepatic metabolism
Renally excreted
Propofol has the potential to change urine color (green or cloudy)
Muscles:
Does not prolong neuromuscular blockade but can offer adequate intubation conditions
Ketamine Class
phencyclidine derivative
Ketamine Uses:
GA induction, GA maintenance, MAC, analgesia , antidepressant
Ketamine MOA:
Non-competitive antagonist at NMDA receptor ion channels.
Ketamine blocks the open channel, inhibiting the excitatory response to glutamate.
Provides amnesic and potent analgesia.
Produces a “dissociative state” by depressing the cerebral cortex and thalamus and stimulating the hippocampus.
Bind w/ opioid, MAO, serotonin, NE, muscarinic and sodium channels
Ketamine inhibits neuronal sodium channels (producing a modest local anesthetic action) and calcium channels (causing cerebral vasodilatation)
Ketamine pre-medication
benzo and antisaligogue
Ketamine Dose/Onset/DOA for IV induction
1-2mg/kg
onset: 2-5minutes
DOA: 10-20 minutes (may require 1 hour for full orientation)
Ketamine IM induction dose/onset
4-6mg/kg
onset:20 minutes
Ketamine Sedation/multimodal dose
Sedation: 1-3mcg/kg/min or 0.5-1mg/kg boluses as needed
Multimodal infusion: 3-5 mcg/kg/min
Ketamine metabolism
P450 enzyme in liver, chronic ketamine use induces enzymes that metabolize it
Active metabolite: norketamine 1/3 as potent and renally excreted
Excretion: kidneys
least protein bound of all induction agents
Ketamine effects on organs
CNS:
Increased CMRO2, CBF, ICP
Dissociative
Analgesic
Depression
Associated with emergence delirium, nightmares and hallucinations
Benzodiazepines are an effective means of prevention
Risk factors: age > 15, female gender, personality disorder, dose > 2mg/kg
Cardiovascular:
SNS stimulant
Increased SVR, HR, myocardial O2 consumption, PVR
Mild myocardial depression
Respiratory:
Bronchodilator
Maintains respiratory rate
Preserves reflexes at low dose
Increased secretions, often paired with an antisialogue like glycopyrrolate
Ocular
Nystagmus
Caution use of Ketamine in patients with:
HTN, angina, CHF, increased ICP, increased IOP, auditory/visual hallucinations, airway problems r/t increased secretions, emergence reactions
Etomidate Class
Carboxylated imidazole derivative
Hypnotic
Etomidate uses:
induction of anesthesia, considered CV stable and good for traumas
Etomidate MOA
Binds to GABA-a receptor
Lower doses: potentiates GABA at receptors
Higher doses: directly stimulates the GABA receptor
Etomidate dose/onset/duration
- 3mg/kg
onset: 1 minutes
doa: 5-15 minutes
Etomidate metabolism
hepatic p450 enzymes and plasma esterases
extreted by kidneys and in bile
Etomidate Organ Effects
CNS
Reduces intracranial pressure, cerebral blood flow, CMO2
Myoclonia likely related to an imbalance of excitatory and inhibitory pathways in the thalamacortical tract and can induce EEG seizure foci
No analgesia
Cardiovascular:
Hemodynamically stable
Minimal/no cardiac depression
Does not blunt sympathetic response to laryngoscopy
Pulmonary:
Brief hyperventilation followed by apnea
Mild respiratory depression (less than propofol)
No histamine release
Endocrine:
inhibits cortisol; adrenal suppression via suppression of 11-beta hydroxylase
GI – N/V in 30-40% of patients
Hematologic:
May induce acute intermittent porphyria
Dexmedetomidine Class
selective alpha 2 adrenergic agonist
