IV sedatives-hypnotics Flashcards
Advantage of propofol
More rapid return of consciousness with minimal residual effects compared to other induction agents
Propofol MOA
Increases GABA affinity for GABAa receptor - prolonged channel opening, increased Cl- influx
Effect of increased Cl- influx
Neuronal cell hyperpolarization - inhibition of the cell
Propofol metabolism
P450 - water soluble metabolites excreted via kidneys. <0.3% excreted unchanged in urine
Propofol induction dose:
MAC dose:
TIVA dose:
I: 1.5-2.5 mg/kg
MAC: 25-100 mcg/kg/min
TIVA: 100-300 mcg/kg/min
Propofol PONV dose:
Subhypnotic: 10-15 mg IV
Propofol CNS effects:
Decreased - CMRO2, CBF, ICP
DOES NOT EFFECT - cerebral autoregulation
Propofol cardiovascular effects:
Decreased - SVR, inotropy
DOES NOT EFFECT - HR
Decreased SVR may be augmented in hypovolemic, elderly, compromised LV function
Propofol SNS effect:
Suppression of sympathetic nervous system activity
Propofol effects respiratory:
Dose-dependent decrease ventilation
Propofol effects intraocular pressure:
Decreased immediately after induction of anesthesia
Etomidate MOA:
Increases GABA affinity for GABAa receptor - prolonged channel opening, increased Cl- influx
Etomidate metabolism:
Hepatic microsomal enzymes and plasma esterases
Etomidate induction dose:
0.2-0.4 mg/kg IV
Etomidate cardiovascular effects:
Minimal changes in - HR, SV, CO
Decreases - up to 15% decrease in MAP d/t decrease in SVR
5 Benzodiazepine effects:
Anxiolysis, sedation/hypnosis, anticonvulsant, anterograde amnesia, SK muscle relaxation
Benzodiazepine MOA:
Increased GABA affinity for GABAa receptor - increased frequency of channel opening, increased Cl- influx
Benzodiazepine amnesic effect?
Amnestic effect is greater than sedative effect - patients may be awake, but remain amnestic for events and conversations
Midazolam Vd elderly and obese:
Increased Vd resulting from enhanced distribution into peripheral adipose tissue
Midazolam metabolism:
Rapidly metabolized by hepatic and small intestine P450 (CYP3A4) - hydroxymidazolam (1/2 potency) is rapidly conjugated and renally excreted
Drugs that decrease midazolam metabolism?
cimetidine, erythromycin, calcium channel blockers, antifungal drugs - inhibit P450
Midazolam CNS effects:
Decreases CMRO2, CBF. Autoregulation is preserved.
Solo midazolam induction:
Increased ICP associated with laryngoscopy is not blunted
Midazolam respiratory effects:
Dose-dependent decrease in ventilation by decreasing hypoxic drive
Midazolam cardiovascular effects:
Decrease in BP, SVR. Increase in HR.
Midazolam doses:
Induction: 0.1-0.2 mg/kg
IV sedation: 1-2.5 mg
Onset 30-60 sec, Peak 5.5 minutes, Duration 15-80 min
Flumazenil MOA:
Benzodiazepine antagonist at GABA receptor sites, however lacks agonist activity
Flumazenil dose:
0.2 mg, subsequent doses of 0.1 mg q1min
Ketamine MOA:
Produces dissociative anesthesia by interrupting signals between the thalamus and cerebral cortex. Patient is amnesic and analgesic
Limit as sole anesthetic:
High frequency of emergence delirium
Ketamine specific targets:
NMDA: inhibits activation by glutamate and prevents presynaptic release of glutamate
GABAa: only weak actions compared to propofol
Ketamine dose:
Intubating: 1-2 mg/kg IV
Analgesia: 0.2-0.5 mg/kg IV
Ketamine CNS effects:
Mildly increased ICP, can be maintained with normal ventilation
Ketamine cardiovascular effects:
SNS stimulation - increases systemic and arterial blood pressure, HR, CO, myocardial O2 demand
Ketamine respiratory effects:
DOES NOT decrease ventilation. Bronchodilates. Increased salivary and pulmonary secretions - glyco
Ketamine cardioprotective effects:
R(-) isomer blocks cardiac preconditioning
Dexmedetomidine MOA:
Alpha-2 agonist - sedation produced by a reduction in SNS tone
Dexmedetomidine ventilation effects:
Dose not reduce ventilation
