Anesthesia Flashcards
(34 cards)
Barbiturates, MOA, Uses, SE, OD treatment, CI
Pheno-, pento-, secobarbital; thiopental
Increase DURATION of Cl- channel opening -> Increased GABA action
Sedatives for anxiety, seizures, insomnia, anesthesia induction (thiopental)
SE: Resp + CV depression, CNS depression exacerbated by EtOH, Dependence, P450 inducer
Supportive treatment for OD
CI: Porphyria
Benzodiazepines, MOA, Uses, SE, OD treatment, CI
Diazepam (Valium), midazolam (Versed), -zepams, -zolams
Increase FREQUENCY of Cl- channel opening -> Increased GABA action
Anxiety, spasticity, status epilepticus (lorazepam, diazepam), DT detox, night terrors, sleepwalking, general anesthesia (amnesia, muscle relaxation), insomnia
SE: Dependence (short-actings: midazolam, oxazepam, triazolam), CNS depression exacerbated by EtOH. Less risk of OD than barbiturates.
Treat OD w/ flumazenil (competitive GABA antagonist at BZD receptor)
Non-BZD hypnotics, MOA, use, SE
Zolpidem, Zaleplon, Eszopiclone (ZZZs)
Same mechanism as BZDs, effects reversed by flumazenil
Insomnia
SE: Ataxia, headaches, confusion
Short duration from rapid liver metabolism. Lower dependence risk than BZDs
To act in the CNS, drugs must be…
Lipophilic or transported across BBB
Low drug solubility in blood causes?
Rapid induction and recovery
High drug solubility in lipid causes?
Increased potency (1/MAC)
MAC
Minimal Alveolar Concentration of inhaled anesthetic to prevent half of subjects from moving in response to noxious stimuli.
Inhaled anesthetics, MOA, effects, severe SE
Halothane, -fluranes (Desflurane, Sevoflurane), NO2
Unknown mechanism
Cause CV + Resp depression, nausea/emesis, increased cerebral blood flow/decreased cerebral metabolic demand
SE: Halothane = hepatotoxicity, Methoxyflurane = nephrotoxicity, Enflurane = convulsions, NO2 = gas expansion in body cavity. All + SCh except NO2 = Malignant hyperthermia (high fever, MSK contractions, treat w/ dantrolene)
IV anesthesics
Barbiturate (thiopental), BZDs (midazolam), Ketamine, Opioids, Propofol
What induces anesthesia?
Sedative (Propofol) + Narcotic
Thiopental for anesthesia, use, distribution, effects
High lipid solubility = high potency
For induction, short surgical procedures
Rapidly redistributes into muscle & fat to terminate effects (not metabolized to stop effects)
Decreases cerebral blood flow
BZDs (midazolam) for anesthesia, use, SE
Used adjunctively w/ gaseous anesthetics and narcotics
SE: Severe post-op CV/Resp depression (treat OD w/ flumenazil), anterograde amnesia
Ketamine for anesthesia, mechanism, SE
PCP analog = dissociative anesthetic
Blocks NMDARs
CV stimulant, Increase cerebral blood flow
SE: Disorientation, hallucination, bad dreams
Opioids for anesthesia
Morphine, fentanyl used w/ other CNS depressants during general anesthesia
Propofol use, mechanism, SE
For sedation, rapid anesthesia induction, short procedures
Potentiates GABAa
Less post-op nausea than thiopental
Local anesthetics, MOA, admin, considerations, uses, SE
Procaine, cocaine, tetracaine (esters); Lidocaine, mepivacaine, bupicvacaine (amides, 2 I’s in names)
Block Na+ channels from cytoplasmic side (penetrate membrane uncharged, form ion in cytosol to stay in neuron and bind channel)
Preferentially bind activated Na+ channels = best in rapidly firing neurons
Give w/ vasoconstrictors (epi) to enhance local action - less bleeding, systemic escape, and SE + more anesthesia. Don’t give epi for ears, fingers, nose, penis, toes
In infected tissue (more H+), alkaline anesthetics are charged before penetrating membrane = need more
For minor procedures, spinal anesthesia
Give amides if allergic to esters
SE: CNS excitation, CV toxicity (bupivacaine), hypertension, hypotension, arrhythmias (cocaine)
Order of nerve blockade
Small diameter -> Large; Myelinated -> Unmyelinated
Overall size predominates over myelination:
Small myelinated -> Small unmyelinated -> Large myelinated -> Large unmyelinated
Order of loss: Pain -> Temp -> Touch -> Pressure
Depolarizing neuromuscular blockers, target, MOA, phases, antidotes, SE
Both non-/depolarizers are for paralysis in surgery/mechanical ventilation, selective for motor nicotinic receptor (not autonomic)
Succinylcholine: Strong AChR agonist -> Sustained depolarization -> Prevent muscle contraction
Phase I (prolonged depolarization) - no antidote, potentiated by AChE inhibitors
Phase II (repolarized but blocked) - AChRs available, but desensitized; Antidote is AChE inhibitors
SE: High Ca++, K+, Malignant hyperthermia
CI: Peds due to risk of undiagnosed DMD
Nondepolarizing neuromuscular blockers, mechanism, antidotes
Curare derivatives (e.g. -curium, -curonium [steroids])
Competitive AChR antagonists
Reversal of blockade w/ AChE inhibitors (Neostigmine - Must give w/ atropine to prevent muscarinic effects such as bradycardia; edrophonium; etc.)
Dantrolene use, MOA
Prevents Ca++ release from SR of skeletal muscle
For malignant hyperthermia and neuroleptic malignant syndrome (tox of antipsychotics)
Components of anesthesia
Analgesia (pain relief), amnesia (memory loss), immobilization
Accomplished by narcotic + propofol + muscle relaxant
Induction agents + CV effects, CIs
Propofol - decrease SVR, BP, HR. CI in hypotension (sepsis, shock, bleeding, severe CHF)
Etomidate - slight BP decrease, no HR change. Good in adrenal suppression, hypotension, severe CHF. CI in CAD
Ketamine - increases BP, HR; sympathomimetic. Good in hypotension.
Indications for a-line
Continuous direct beat-to-beat BP measurement
Severe CV disease
Potential need for vasoactive infusions
Frequent blood sampling
Potential hemodynamic instability
Inability to use noninvasive BP (obese, burns)
Indications for central line
Surgeon request for post-op Potential need for vasoactive infusions Need for multiple ports Secure IV access unavailable elsewhere Measure pulmonary artery pressures
