general anesthetics Flashcards
definition of GA
a medically induced coma and loss of protective reflexes resulting from the administration of one or more GA agents
ideal qualities of GA
- induce smooth and rapid loss of consciousness
- allow for prompt recovery after discontinuation
- wide safety margin and no adverse effects
definition of monitored anesthesia
pt continues to maintain a patent airway and respond to commands
LA w sedation and analgesia
stages of anesthesia
analgesia, amnesia, excitement (may vomit if stimulated), surgical anesthesia, medullary depression
stages obscured by rapid onset of GA and use of other drugs
most reliable sign of surgical anesthesia
loss of motor and autonomic response to noxious stimuli
how is the effect of inhaled anesthesia produced? (A,D)
produced when we achieve the necessary BRAIN conc, depending on:
- solubility in blood (low solubility -> high arterial tension rapidly -> rapid equilibration w brain -> fast onset)
- anesthetic w moderate solubility can be given at higher conc initially to increase the rate of rise then reduced after adequate depth of anesthesia is achieved
- anesthetic conc in inspired air (higher conc -> increase rate of transfer to blood)
- rate and depth of pulm ventilation (increase absorption)
- depression of respiration by opioid analgesics will reduce onset of anesthesia
- pulm blood flow (increase blood flow -> less time for GA to diffuse into blood ->decrease rate of rise of anesthetic tension in blood)
- ateriovenous conc gradient higher -> more go to tissue instead of brain -> more time to equilibrate w brain)
determinants of rate of recovery (M,E)
excretion MAINLY through lungs (pulm blood flow, rate of ventilation impt), hepatic metab, bacteria in GI (NO)
- insoluble in blood -> excrete faster
- exposed longer -> accumulate in muscle, skin, fat -> eliminated slower
inhaled anesthetics mechanism of action
modify ion currents by direct interactions w ligand-gated ion channels
inhaled anesthetics actions on organ systems
- CVS: decreased mean arterial P
- Respi: decreased ventilation, response to hypercapnia, muco-ciliary function, bronchodilation
- brain: increased cerebral blood flow –> undesirable in pt w increased intracranial P (NO least likely to increase cerebral blood flow)
- renal: impairs renal autoregulation
- liver: reduced hepatic blood flow
- uterus: halogenated anesthetics –> potent uterine muscle relaxant
toxicity of inhaled anesthesia
repeated exposure of halothane may cause liver damage (develop hepatitis)
renal dysfunction following methoxyflurane (release of F- during metab)
malignant hyperthermia
- autosomal dominant skeletal muscle disorder (check fam history)
- increase in muscle cell Ca2+
- tx w dantrolene
- effects: hypertension, tachycardia, severe muscle rigidity, hyperthermia, acidosis
inhaled anesthetics: halothane
standard for comparison for modern inhaled anesthetic
potent
maintain anesthesia
induction of anesthesia commonly in children
relax skeletal muscles, potentiates skeletal muscle relaxants
decrease BP, may cause bradycardia, arrhythmia
may rarely cause halothane hepatitis
inhaled anesthetics: nitrous oxide
fast onset and recovery but LACKS potency
- cannot give surgical anesthesia even at max dose (80%)
used in adjunct w other inhaled anesthetics
analgesic agent for labour pain
limitation of inhaled anesthesia
require specialised vaporiser for delivery/equipment for disposal of exhaled gases
properties of IV anesthetics
onset faster – commonly used for induction
rapid recovery
lack analgesic properties – combined use w inhaled/LA for short procedures
IV anesthetics: barbiturates
increases duration of GABA Cl- channel opening
AMPA receptor to depress glutamate mediated excitation
THIOPENTAL
- commonly used for induction as it rapidly crosses BBB
- high lipid solubility
- high dose/continuous infusion: decrease arterial BP, stroke vol, C/O
- potent respi depressant
- decrease cerebral metab, O2 consumption and blood flow – desirable for pt w ^ intracranial P
benzodiazepines (pre-medication, not GA)
potentiated GABA inhibition, increases freq of GABA Cl- channel openings
diazepam, larazepam, medazolam
- pre-anesthetic medication
may cause anterograde amnesia
how to accelerate recovery from benzodiazepine
to accelerate recovery when large doses given (esp elderly), give benzodiazepine antagonist FLUMAZENIL
short duration of action (<90mins) – multiple doses
IV anesthetics: propofol
potentiate GABA receptor activity, slowing channel closing time
sodium channel blocker
most popular IV A, rapid onset as barbiturates, more rapid recovery
rapidly metab by liver, excreted by kidney
decrease BP
potent respi depressant
IV anesthetics: ketamine
dissociative anesthesia (no loss of consciousness)
only IV A w both analgesic + anesthetic properties
NMDA receptor antagonist
stimulates CVS
increase cerebral blood flow, O2 consumption, intracranial P
decrease respi rate
highly lipophilic
metab by liver, excreted by kidney + in bile
post op disorientation, illusions, dreams
neurolept analgesia
fentanyl + droperidol
detached, pain-free state
alternatives of GA
balanced anesthesia
- supervision by professional
- combination of inhaled/IV A, muscle relaxants, LA, cardiovascular drugs for control of transient autonomic responses to noxious surgical stimuli
monitored anesthesia care
- supervision by professional
- LA supplemented by IV anesthetics
- diagnostic, minor procedures
- midazolam for premedication, propofol infusion, opioid analgesics/ketamine
conscious sedation
- primarily by non-anesthesiologist
- pt maintain patent airway, responsive to commands
- benzodiazepine, propofol, opioid
reverse opioid
naloxone, opioid antagonist
