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general anesthetics Flashcards

1
Q

Nitrous oxide, N2O

A

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

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2
Q

Isoflurane (Forane®)

A

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

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3
Q

Enflurane (Ethrane®)

A

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

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4
Q

Desflurane (Suprane®)

A

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

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5
Q

Sevoflurane (Ultane®)

A 
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
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6
Q

Propofol (Diprivan®)

A

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

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7
Q

Etomidate (Amidate®)

A

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

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8
Q

Ketamine (Ketalar®)

A

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

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9
Q

Midazolam (Versed®)

A

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

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10
Q

Fentanyl (Sublimaze®)

A

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

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11
Q

Dexmedetomidine (Precedex®)

A

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

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12
Q

Dantrolene (Dantrium®)

A

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

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13
Q

how are GAs dangerous

A

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

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14
Q

3 requirements for anesthetic state

A

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

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15
Q

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

A

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
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16
Q

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

A

Intravenous GAs

-inhaled also tast bad

17
Q

For maintenance of anesthesia, ?? are used.

A

inhaled GAs

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

18
Q

other substances given during anesthesia

A
  • 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)
19
Q

may have this effect post-op

A

“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

20
Q

tx for post-op hypothermia/shivering

A

meperidine (12.5mg) to reduce the shivering threshold

21
Q

tx for post-op pain

A

NSAIDS for pain, avoid narcotics until sx drugs wear off

22
Q

real life example of balanced anesthesia

A 
Oxygen + Desflurane
Propofol (induce anesthesia) 
Fentanyl (narcotic pain) 
Midazolam (tranquilizer sedative) 
Rocuronium (muscle relaxer)
23
Q

GA pharmacokinetics

A
  • 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
24
Q

Blood/gas partition coefficient is a measure of ??

A

water solubility

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

25
Q

Compare speed of induction of N2O and halothane

A

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.

26
Q

minimum alveolar concentration (MAC)

A

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

27
Q

GA mechanism: inhibit neuronal activity by causing ??

A

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

28
Q

GA theories

A

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)

29
Q

how to determine DoA (depth of anesthesia)

A

EEG; analyzed by Bispectral (BIS) index

-scale of 100 (awake) to 0 (deep coma)

30
Q

N2O SEs

A

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

31
Q

Enflurane SEs

A
  • 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
32
Q

Isoflurane SEs

A

-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

33
Q

Sevoflurane SEs

A
  • 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.
34
Q

Propofol SEs

A

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
35
Q

Etomidate SEs

A
  • Pain of injection, reduced with local anesthetic or inject in large vessel
  • Myoclonic movements, benzos co-admin to prevent
  • N/V
  • Inhibition of adrenal gland synthetic enzymes
  • No decrease in BP or CO
36
Q

Ketamine SEs

A

-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))

37
Q

hypothermia as a sx complication

A

body temp is below 36°C

  • cold OR, room-temp IV fluids, many GAs cause vasodilation–>heat loss
  • ^chance cardiac arrest, unstable angina, MI
38
Q

malignant hyperthermia

A

-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)

Pharm (45 decks)

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