Week 3 General Anesthetics Flashcards
Stage I-Analgesia
subsequent amnesia and inability to feel pain
Stage II- Excitement
delirium, combative behavior, elevated BP and resp rate; not common now b/c short-acting anesthetic given before
Stage III- surgical anesthesia
reg respiration, skeletal muscle relaxation, decrease in eye reflexes and movements, fixed pupils; loss of motor and autonomic response to pain
Stage IV- Medullary paralysis
NOT GOOD; depression of respiratory and vasomotor centers; leads to DEATH
Low blood solubility
Leads to faster induction time b/c the drug isnt staying in the blood- also leads to faster elimination
Tissue uptake
highly vascularized tissues rapidly reach steady state
Adipose tissue
accumulates anesthetics more slowly b/c lower perfusion rate- most anesthetics have high lipid solubility
Meyer & Overton Rule
higher lipid solubility the more potent the volatile anesthetic
Potency
amt of drug required to produce its effect
Efficacy
max strength of the effect of the drug @ saturating concentrations (like Vmax?)
Minimum Alveolar Concentrations (MAC)
potency of anesthetics; alveolar concentrations that renders 50% of subjects to strong noxious stimulation’ 1 MAC: Nitrous oxide=100%(not possible), Isoflurane=1.4%(much more potent than NO)
Drug elimination
lower blood/gas partitioning coefficient & tissue solubility- faster the elimination; clearance by lungs major route of elimination
Analgesia
dorsal horn
Sedation
frontal cortex
Hypnosis
Thalamus
Immobility
Ventral horn neurons (motor neurons)
MOA- Inhaled anesthetics-volatiles
ion channels are important targets; potentiate GABAa, glycine receptors, K+ channels; inhibit glutamatergic ionotropic receptors and neuronal nAChRs- stop movement
MOA- Nitrous Oxide
blocks NMDA-R like ketamine; powerful analgesic
Organ system effects- volatiles
CV- decrease BP; Resp- mucous accumulates, decreased response to hypoxia- must be on ventilator; GI-nausea vomitting; CNS- dec metabolic rate, inc. cerebral blood flow & intracranial pressure; Liver/kidneys- dec blood flow; Uterus- dec contractions
Organ system effects- N20
CV- no change; Resp- diffusional hypoxia, can diffuse into pneumothorax; GI- nausea/vomiting; CNS- inc cerebral blood flow & intracranial pressure; Liver/kidneys- dec blood flow
Volatile anesthetics- malignant hyperthermia
mutation in Ryanodine receptor- activated by inhaled anesthetic; leads to uncontrolled release of Ca2+ from sarc retic; succinylcholine can also cause it; Tx- dantrolene (blocks Ca2+ release @ ryanodine receptor), cooling, oxygen, correction of acid-base disturbances
Premedication (balanced anesthesia)
Midazolam (I.V. benzodiazepine)
Induction (balanced anesthesia)
Fentanyl (IV opioid), Propofol (IV anesthetic), Curare-like neuromuscular blocker (Pancuronium or Succinyl CoA); tracheal intubation
Maintenance (balanced anesthesia)
Inhalational Anesthetics (combo)- Sevoflurane (not strong analgesic) + Nitrous Oxide (very good analgesic w/ less side effects)
Premedication (Total intravenous anesthesia-TIVA)
MIdazolam (I.V. benzodiazepine); Give TIVA if malignant hyperthermia has occured before
Induction (Total intravenous anesthesia-TIVA)
Remifentanil (instead of fentanyl; shorter acting), Propofol
NMJ blockade (Total intravenous anesthesia-TIVA)
Rocuronium; tracheal intubation after this
Maintenance (Total intravenous anesthesia-TIVA)
Remifentanil, Propofol (more to keep asleep?)
Benzodiazepines (Midazolam)
use prior to induction of anesthesia- reduce anxiety, induce amnesia & sedation; used for sedation for non general anesthesia; used in perioperative period; 15-60 min before anesthesia to produce amnesia; given IV; rapid onset & shorter duration of action
Opioids (Fentanyl)
induction & maintenance in TIVA; epidural anesthesia together w/ local anesthetics; ICU-conscious and deep sedation; potent respiratory depression; chest wall & laryngeal rigidity-impaired ventilation; dec HR & BP
Barbiturate anesthetics (Thiopental)
lipophilic rapidly entres & depresses CNS (<1min); short acting b/c it diffuses out of brain rapidly; used during induction of anesthesia & deep sedation; NOT good analgesic; dec cerebral metabolism & blood flow; dec cardiac output & BP; potent respiratory depression
Propofol
most common for induction & maintenance or day surgery; potentiates GABAa receptors; onset rapid as other barbiturates-recovery more rapid; rare postop vomiting; potent resp depression; dec periperheral resistance; dec intracranial pressure; not a good analgesic
Good analgesics
Nitrous oxide, Ketamine, Fentanyl
Ketamine
PCP analog; blocks NMDA receptors; GOOD analgesic; catatonia, amnesia, analgesia w/out loss of consciousness; short procedures; ONLY IV anesthetic that increases HR & cardiac output; minimal effect on respiration; inc intracranial pressure; postop hallucinations
Etomidate
potentiates GABAa receptors; minimal CV depression; used for someone experiencing shock; causes: vomitting, pain on injection, myoclonus; use as anesthetic induction for pts @ risk of hypotension (elderly)
Dexmetodine
short term sedation of intubated & ventilated ICU pt or during regional anesthesia; alpha adrenergic receptor agonist (tizanidine); analgesia b/c activation of receptors in spinal cord; hypnosis produced’
Increase cranial pressure
Volatiles (sevoflurane, desflurane, isoflurane), Nitrous oxide, Fentanyl (in head trauma pts), Ketamine
Decrease cranial pressure
Thiopental, Propofol, Etomidate,
