Intravenous anesthetics 3 Flashcards
Choose the statements that demonstrate an accurate understanding of thiopental. Select 2
a. it causes a reflex tachycardia
b. prompt awakening is the result of hepatic metabolism
c. it provides neuroprotection against global ischemia
d. there is a sulfur molecule in the second position
a. it causes a reflex tachycardia
d. there is a sulfur molecule in the second position
Barbiturates should be avoided in patients with
acute intermittent prophyria
The mechanism of action of sodium thiopental is
GABA-A agonist
The onset of action of sodium thiopental is
30-60 seconds
The duration of action of sodium thiopental is
5-10 minutes
The clearance of sodium thiopental is
liver
The active metabolite of sodium thiopental is
none
The induction dose of sodium thiopental is
2.5-5 mg/kg IV
The respiratory effects of sodium thiopental include
decreased respiratory drive
histamine release can cause bronchoconstriction
The CV effects of sodium thiopental include
hypotension
myocardial depression
preserves the baroreceptor reflex so can lead to reflex tachycardia
The CNS effects of sodium thiopental include
decreased ICP
can cause hyperalgesia
decreased CMRO2
decreased cerebral blood flow
decreased EEG activity
Intra-arterial injection of sodium thiopental can cause
intense vasoconstriction and crystal formation leading to tissue necrosis
Treatment of intra-arterial injection of sodium thiopental includes
treatment with a vasodilator (phentolamine or phenoxybenazamine) or stellate ganglion nerve block (sympathectomy of upper extremity)
_______ is the gold-standard for ECT. It decreases the seizure threshold and produces a better-quality seizure.
Methohexital
Repeated doses of sodium thiopental can lead to
tissue accumulation–> prolonged wake up time + hangover effect
Compared to propofol, what effect does thiopental have on hypotension?
it produces less hypotension than propfol
Describe the neuroprotective effects of sodium thiopental?
focal ischemia: yes (examples include carotid endarterectomy, temporary occlusion of cerebral arteries)
global ischemia: no (example: cardiac arrest)
Acute intermittent porphyria is made worse by stimulation of
ALA synthase
emotional stress
prolonged NPO status
CYP450 induction
Signs and symptoms of acute intermittent prophyria include
GI: severe abdominal pain (most common & typically first), N/V
CNS: anxiety, confusion, seizures, psychosis, coma
PNS: skeletal muscle weakness (risk of respiratory muscle failure), bulbar weakness (risk of aspiration)
What drugs should be avoided with acute intermittent porphyria?
barbiturates, etomidate, ketamine, ketorolac, amiodarone, calcium channel blockers, birth control pills
Anesthetic management of acute intermittent porphyria includes
liberal hydration
glucose supplementation
heme arginate
prevention of hypothermia
With acute intermittent porphyrias, regional anesthesia is not
contraindicated, but many clinicians avoid it since it might be difficult to distinguish block-related complications from an acute porphyria attack
The methohexital induction dose is
1-1.5 mg/kg
Phenobarbital is excreted
unchanged in the urine (the hepatic P450 enzymes metabolize all of the other barbiturates)
