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Flashcards in general anesthetics Deck (38):

Nitrous oxide, N2O

Inhaled General Anesthetic (GA)
MAC = 105 %, by itself cannot achieve the desired depth of anesthesia
-analgesia at 20% conc. of inhaled air, sedation 30%-80%
-used in dentist's offices
-Blood : gas partition coefficient = 0.47--rapid induction and recovery or emergence


Isoflurane (Forane®)

Inhaled General Anesthetic (GA)
MAC = 1.2%, pungent
Blood:gas partition coefficient = 1.4
>99% eliminated unchanged via the lungs


Enflurane (Ethrane®)

Inhaled General Anesthetic (GA)
MAC = 1.6%, sweet
Blood:gas partition coefficient =1.8
2–8 % metabolized in liver


Desflurane (Suprane®)

Inhaled General Anesthetic (GA)
MAC = 6%
*Irritating gas – coughing, respiratory, secretions, must use IV GA to induce anesthesia
Blood : gas partition coefficient = 0.45
>99% eliminated unchanged via lungs
SEs: dec. in BP, CO is well preserved, dec. in vent. rate


Sevoflurane (Ultane®)

Inhaled General Anesthetic (GA)
MAC 2%
alone is non-irritating to airways and may be used to induce anesthesia
Blood : Gas partition coefficient = 0.65
*>99% eliminated unchanged via lungs


Propofol (Diprivan®)

IV General Anesthetic
Induction dose 1.5-2.5 mg/kg, duration of action 4-8 min
*Not water soluble (may be dissolved in vegetable oil) – very fatty, caution in pts with high TG levels*
*Most common induction agent of anesthesia in US
-Enhance effects of GABA at GABAA inhibitory receptors


Etomidate (Amidate®)

IV General Anesthetic
Induction dose 0.2-0.4 mg/kg, duration of action 4-8 min
-Not water soluble (35% propylene glycol), Used for pts at risk for hypotension
-Used for induction and maintenance of anesthesia
-Enhance effects of GABA at GABAa inhibitory receptor, Activate receptor without GABA present
-Metabolized in liver, metabolites eliminated in urine


Ketamine (Ketalar®)

IV General Anesthetic
Induction dose 0.5-1.5 mg/kg duration of action 10-15 min
-Water soluble (100 mg/ml preparation)
-Given IV also oral, rectal, IM
-*Produces profound analgesia* – no need for opioid co-administration
-Competitive antagonist of NMDA receptor
-Inhibition of voltage sensitive Na, K channels
-Metabolized in liver to norketamine (has further action on CNS), rapid clearance


Midazolam (Versed®)

GA Adjunct, benzo
water soluble, no pain on injection, rapid onset (2 min, IV), rapid recovery

-benzos used for *pre-op sedation* (Midazolam>> diazepam > lorazepam): dec. brain MR, BF, dec. BP, vent. rate


Fentanyl (Sublimaze®)

GA Adjunct, opioid
*Minimize vascular reflex to noxious, painful stimuli*, induction for later intubation
30 min duration of action; used in terrorist situations
-μ opioid receptor agonist
SEs: N/V, dec. vent rate, dec. HR, dec. BP


Dexmedetomidine (Precedex®)

GA Adjunct, α2 adrenergic agonist
dec. catecholamine release
-used for sedation in critically ill adults, off label use as GA
adjunct; IV use only, no amnesia
SEs: dec. BP, bradycardia, no change in vent rate, *Useful in non-intubated patients*


Dantrolene (Dantrium®)

Ryanodine receptor inhibitor
tx for malignant hyperthermia
Also used to treat spasms and spastic disorders


how are GAs dangerous

very narrow therapeutic index of 2 – 4 (LD50/ED50) and extremely fast acting


3 requirements for anesthetic state

Amnesia – occurs through depressing neuronal activity in the hippocampus -benzos
Immobility in response to noxious stimulation –NMJ blockers
Attenuation of autonomic response to noxious stimulus (^HR, ^BP); -analgesic opioids (fentanyl)
*inhaled and IV GAs enhance all three
-balanced implies use of multiple classes to get to desired depth of anesthesia


pre-op sx drugs
for sedation?
for slowing HR?
to prevent vomiting/acid reflux? regurgitation?

barbiturates, diazepam, midazolam for sedation
-Atropine to counteract bradyarrhythmia (blocks ACh)
-Serotonin receptor antagonist (Ondansetron) for vomiting
-Histamine R2 antagonist (Ranitidine) for acid reflux
-both these prevent regurgitation due to LES relaxes with musc. relaxers


?? are used to induce anesthesia because they faster acting (~1 min) than inhaled GAs

Intravenous GAs
-inhaled also tast bad


For maintenance of anesthesia, ?? are used.

inhaled GAs
-constantly monitored, can be fine tuned, N2O typically used, reduces amount GA used


other substances given during anesthesia

-fentanyl: reduce dose of GAs and blocks the noxious stimulus reflex in the ANS
-Succinylcholine or other NMJ blocking agents as needed (e.g. endotracheal intubation)


may have this effect post-op

“Emergence excitement” is a condition where the half conscious patient exhibits restlessness, crying, moaning, and in extreme cases thrashing
-may have rebound HTN and tachycardia


tx for post-op hypothermia/shivering

meperidine (12.5mg) to reduce the shivering threshold


tx for post-op pain

NSAIDS for pain, avoid narcotics until sx drugs wear off


real life example of balanced anesthesia

Oxygen + Desflurane
Propofol (induce anesthesia)
Fentanyl (narcotic pain)
Midazolam (tranquilizer sedative)
Rocuronium (muscle relaxer)


GA pharmacokinetics

-effect proportional to concentration in CNS
-GA diffusion from lung-->blood-->CNS determines rate of induction/recovery
-rate of induction for inhaled GAs not too important (IV GAs used for induction), rate of recovery is important (faster=better)
-High water (blood) solubility = slow induction


Blood/gas partition coefficient is a measure of ??

water solubility
[GA] in blood / [GA] in lung; when gas is in equilibrium


Compare speed of induction of N2O and halothane

N2O--- poorly soluble in blood (blood/gas partition coefficient = 0.47) ---
rapid induction
Halothane--- very soluble in blood (blood/gas partition coefficient = 2.3)----slow induction.


minimum alveolar concentration (MAC)

measure of potency;the concentration of inhaled GA needed for 50% of patients to NOT respond to pain.
-proportional to lipid solubility


GA mechanism: inhibit neuronal activity by causing ??

1) neuronal hyperpolarization
2) inhibition of excitatory synapses
3) enhancing inhibitory synapses


GA theories

Lipid theory: GAs swell lipid membranes causing a general alteration in ion channel conduction; Myer-Overton rule – potency correlates with its solubility in olive oil

Specific protein - GA interaction theory: GAs interact specifically with ion channels/receptors; isoflurane +/- sterioisomers (same lipid solubility) have diff. MAC values, but GABAa receptor point mutations abolish effects of isoflurane and enflurane (it's a receptor not solubility thing)

*GAs alter cell membranes and enhance inhibitory membrane- bound receptors (GABA) or inhibit excitatory membrane-bound receptors (e.g. NMDA)*


how to determine DoA (depth of anesthesia)

EEG; analyzed by Bispectral (BIS) index
-scale of 100 (awake) to 0 (deep coma)



Air pockets (e.g. middle ear) may expand
Can change blood pressure depending on what is co-administered
Depresses ventillary response to hypoxia
Does not trigger malignant hyperthermia


Enflurane SEs

-Dec. BP, cardiomyocyte contractility, peripheral vasodilation (cerebral vasculature), no change in HR
-*Produces electrical seizure activity, though no evidence, contraindicated for epileptics
-Muscle relaxation enhanced with NMJ blockers
-Decrease in vent. rate


Isoflurane SEs

-Dec. in BP, vasodilation only (cerebral vasculature),
CO maintained
-Mild tachycardia
-Decrease vent. response reflex to hypoxia/hypercapnia
-Modest vasodilation in cerebral vasculature, however metabolic rate of brain is decreased
-Preferred GA for neurosurgery
-Muscle relaxation enhanced with NMJ blockers
-Decreased renal blood flow


Sevoflurane SEs

-Decrease in blood pressure, systemic vasodilation
-No change in CO
-Preferred GA for patients prone to myocardial ischemia
-Renal effects
-Sevoflurane and soda lime combine to produce “Compound A” which may cause short term renal damage. Because of this, the FDA recommends sevoflurane administered with fresh gas at a rate of 2 L/min; semi closed or open gas administration.


Propofol SEs

Major decrease in BP, vasodilation and decrease myocardial contractility
-Pain of injection, reduced with local anesthetic or inject in large vessel
-*Decrease in vent rate* - (killed Michael Jackson)
-Anti-emetic properties – very useful property for people given opioids
-Does not cross placenta, safe for pregnant women


Etomidate SEs

-Pain of injection, reduced with local anesthetic or inject in large vessel
-Myoclonic movements, benzos co-admin to prevent
-Inhibition of adrenal gland synthetic enzymes
-No decrease in BP or CO


Ketamine SEs

-No pain of injection – no need for local anesthetics
-^cerebral blood flow, no change in brain metabolism
-Emergence delirium (1 hour post emergence)
-Hallucinations, vivid dreams, illusions (drug of abuse) -Benzos lessen the hallucinations
-only modest decrease in vent. rate and is potent bronchodilator
CV: ^BP, ^CO, ^HR- useful for pts at risk for hypotension
-severe deterioration of the urinary bladder (after only 2-3 years of abuse (~5 grams injected per day))


hypothermia as a sx complication

body temp is below 36°C
-cold OR, room-temp IV fluids, many GAs cause vasodilation-->heat loss
-^chance cardiac arrest, unstable angina, MI


malignant hyperthermia

-adverse reaction to inhaled GAs, high mort rate; core temp rapidly increases to over 42°C (108°F) due to uncontrolled muscle rigidity
-complication of most inhaled GAs; not N2O and not succinylcholine (NMJ blocker)
-ryanodine Ca2+ channels don't close-->uncontrolled muscle contraction-->heat generation.
-Fatigued myocytes eventually lyse releasing K+-->fatal cardiac events.
(KCl is the 3rd and final drug given in conventional lethal injection protocols)