general anesthetics Flashcards by H B

are pts less responsive during anesthesia or sleep?

pts are less responsive during anesthesia

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Halogens like HCCl3 (Chloroform)
di-ethyl ether
CH3CH2OH (ethanol)

how do these structures act ?

depress nervous system and prevent action potential (achieved via state of unconsciousness)

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What type of experiences are different for anesthesia vs sleep

no dreams
perception of the time
“emerging from anesthesia “ aka waking up
PONV: post op n/v caused from anesthesia

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How many stages of anesthesia

stage 1-4

CNS depression increases as dose and level of sedation increases

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stage 1

starts as analgesia w/o amnesia
late stage 1 has BOTH

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stage 2

excitement stage
amnesia occurs, enhanced reflexes, irregular respiration, vomiting, the duration of this stage in limited by increasing anesthetic concentration

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stage 3 (something changes here is red flag during surgery)

surgical anesthesia
achieved via induction
GOAL stage
regular respiration; patient is unconscious; no pain reflexes, BP is maintained

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stage 4

medulla depression
COMA
respiratory and cardiac depression requiring respirator and pharm support (not a stage we want)

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loss of consciousness

thalamic and cortical involved in CNS depression
thalamic injury cause vegetative state
thalamic stimulation improves response
removal or cortex abolishes effect on thalamus

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amnesia

pt does not remember
common during anesthesia
part of hippocampus response via GABAa receptor

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immobility and diminished muscle tone

do not want the patient to move
direct effect on spine
activates descending pathways which inhibit spinal reflexes
reticulospinal pathways
descending pathways from rostral ventromedial medulla

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inhaled anesthetics

aerosolized
start in lungs and target CNS

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solubility in blood

important; quicker the drug equalibertaes w/ blood the quicker it passes into brain producing anesthetic affect
blood gas partition coefficient (larger=more time spent in blood= longer time to get to the cns=longer onset)

picture: halo thane and n2o respiratory and brain/CNS compartment same size
BLOOD compartment changes size

when drug likes to be in drug compartment like halo thane; it is slower to enter brain meaning onset
of anesthesia would be slower

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induction of anesthesia effect

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elimination of anesthesia

anesthesia is terminated of the drug from the BRAIN to the BLOOD and elimination of drug through the LUNGS

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Nitrous oxide

NMDA antagonist (methyl/aspartate)
prevents binding of glutamate(stimulate) (excite neurotransmitter)
to depress CNS
ketamine is similar*** level of anesthesia is not the same as other drugs

causes death via asphyxiation as it displaces oxygen

Fluranes

activate gaba receptors
gaba: agonist in cl- channel moves Cl- in CNS when active neuron is HYPER-POLARIZED=less activity

⇣opening of nicotinic receptor activated cation channel which

⇣ excite affect of acetylcholine

isoflurane

K+ channel activity to induce hyper polarization of neurons

Iso and Sevo

potentiate strychnine sensitive glycine receptor

what is MAC?

min alveolar anesthetic concentration
potency of inhaled anesthetics to compare drugs

⇡MAC , ⇣blood gas= ⇡potency (inverse)

effects of inhaled anesthetics: CNS

CNS: ⇣ cerebral mean arterial pressure

⇡cerebral blood flow

effects of inhaled anesthetics: uterine SM

uterine SM-relax

useful in OB for c-sec

effects of inhaled anesthetics: cardiovascular

Cardio:

⇣BP and myocardial function

effects of inhaled anesthetics: respiratory

ALL are respiratory depressants

effects of inhaled anesthetics: toxicity

fluoride released from methoxy, en, sevo may cause renal insufficiency as it can enter blood (not ideal)

malignant hypothermia

triggered by inhaled anesthetics and succs causes rapid onset of all bad things muscle biopsy and genetic test can predict use dantrolene to treat block Ca++ channels released from sarcoplasmic reticulum rare but causer of anesthetic mortality

IV anesthetics

- used for induction of general anesthesia - balanced anesthesia: inhaled and IV agents

Barbiturates(IV)

thiopental: ⇡lipid solubility; ⇡BBB penetration; loss of consciousness achieved \<1 min used to induced general anesthesia (skips step 2 the undesired step) MOA: activates GABA Cl- channels hyper-polarizes cause CNS depression

Benzodiazepines

MOA: inhibition of GABA receptors diazepam/lorazepam will help to sedate and decrease anxiety prior to procedure midazolam (general anesthetic) only benzo that goes straight to anesthesia stage so its used outpatient and induction flumazenil: benzo antagonist; used to reverse midazolam in emergencies

Opioids

MOA: **mu** opioid **agonist** **⇡**opioids dose w/ ⇡ benzo dose will achieve general anesthesia state good for cardiac surgery where primary goal is to minimize cardiac depression chest wall rigidity; impair ventilation abuse aware/alert after given just opioids

propofol

MOA: activates GABA receptors gold standard IV anesthetic induces anesthesia in \<1 min useful for prolonged surgeries rapid recovery anti emetic properties too!! causes hypotension during induction due to ⇣ peripheral resistance can cause dose dependent apnea

Etomidate

MOA: Inhibition of GABA GI surgeries minimal effect in cardiac and resp function ADR: PONV (must also dispense anti emetic)

ketamine

MOA: NMDA antagonist like nitrous oxide prevents glutamate binding produces dissociative anesthesia: conscious but still out of it cardiovascular stimulant high doses cause disorientation/hallucination low dose with other anesthetics used instead of opioids to minimize ventilatory depression used in vet clinics too stem from phencyclidine

typical anesthesia procedure

1. preop sedation (benzos like diazepam) 2. induction (IV propofol or IV thiopental); neuromuscular block w/ succs to intubate trachea 3. maintenance: inhaled anesthetics; IV anesthetics (USUALLY BOTH) 4. opioids for pain