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Spring Anesthesia Pharm > Inhaled Anesthetics - Part 2 > Flashcards

Inhaled Anesthetics - Part 2 Flashcards

1
Q

Components of general anesthesia

A

Amnesia, unconscious, imobility, relaxation

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2
Q

What do we want general anesthesia to do?

A
  1. Minimize deleterious direct and indirect effects of agents
  2. Sustain physiologic homeostasis during procedure
  3. improve postop outcomes
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3
Q

What is the drug doing to the body?

A

pharmacodynamics…MAC

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4
Q

1 MAC is ____% of patients have no response to noxious stimulus.

1.3 MAC prevents movement in ___%

A

50%

95%

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5
Q

T/F
MAC allows for comparison of potency and the values are additive.

A

True

0.5 MAC sevo + 0.5 MAC N2O = 1 MAC

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6
Q

By how much does MAC decrease per decade of age?

A

6%

Ex: 2.6% for 1 MAC at 20yo, 2.4% @ 30yo, 2.2% @ 40yo

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7
Q

What is MAC awake?

A

10% of MAC (0.2% for sevo)

End-tidal concentration of an anesthetic agent at which 50% of patients approptriately respond to verbal commands (open your eyes).

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8
Q

What is MAC bar?

A

Concentration required to block autonomic reflexes to nociceptive stimuli

1.3 MAC (if using inhalational agent only…not if using opioids)

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9
Q

If a patient is currently drunk, what affect will it have on MAC? (increase, decrease, stay the same)

A

Decrease MAC requirement

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10
Q

If a patient chronically abuses alcohol, what affect will it have on MAC? (increase, decrease, stay the same)

A

MAC is unchanged

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11
Q

Name three factors that will increase MAC requirements

A
  1. Hyperthermia
  2. Drug-induced increase in catecholamines
  3. Hypernatremia
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12
Q

An older patient who received preop meds and is hypothermic will require more/less/same amount of MAC?

A

Less MAC

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13
Q

History of inhaled anesthetics

A
  • 1840s
    • Nitrous Oxide
    • Ether
    • Chloroform
  • 1951
    • Fluroxene
    • Halothane
  • 1960
    • Methoxyflurane
  • 1973
    • Enflurane
  • 1981
    • Isoflurane
  • 1992
    • Desflurane
  • 1994
    • Sevoflurane
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14
Q

What do inhaled anesthetics do to cerebral blood flow?

Specifically to: Vasodilation, vascular resistance, CBF, and ICP

A

↑ Vasodilation

↓ vascular resistance

↑ CBF and ↑ ICP - can be opposed by hyperventilation (which vasoconstricts)

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15
Q

Compare halothane to isoflurane in the ways the affect CBF

A

Halothane increases CBF so much that it’s not used in neuro surgery

Isoflurane increases CBF the lease, and can be opposed by hyperventilation

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16
Q

How do inhaled anesthetics affect cerebral metabolic rate for oxygen (CMRO2)?

A

decreases CMRO2

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17
Q

Burst supression occurs at what MAC of Iso?

A

1.5 MAC

↓ systemic pressure, can impare cerebral perfusion pressure, sacrifice systolic

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18
Q

Inhaled anestheti effects on CNS physiology

19
Q

Cardiovascular Effects of inhaled anesthetics

on blood pressure

A
  • Halothane and enflurane decrease myocardial contractility
  • Other volatiles derease SVR, thus decrease BP
  • N2O has NO EFFECT, but slight increase
20
Q

Cardiovascular Effects of inhaled anesthetics

on heart rate

A
  • Des tachycardia due to stimulation of SNS (esp with rapid increase in vapor concentration)
  • Increase in HR from other volatiles or N2O usually baroreceptor mediated (halothane is exception) - relex tachycardia due to decrease in BP
21
Q

Cardiovascular Effects of inhaled anesthetics on Cardiac Output

A
  • Halothane and Enflurane decases CO because of decrease in contractility
  • Other volatiles decrease CO but to a lesser degree (almost negligible)
  • N2O is sypathomimetic, thus slight increase in CO (high doses may decrease)
22
Q

Cardiovascular Effects of inhaled anesthetics on SVR (systemic vascular resistance)

A

Iso, Des, and Sevo decrease SVR

23
Q

Cardiovascular Effects of inhaled anesthetics on pulmonary vascular resistance

A
  • All volatiles decrease PVR
  • BLUNT HYPOXIC PULMONARY VASOCONSTRICTION RESPONSE
  • N2O known to increase PVR with patients with pulmonary hypertension
24
Q

Cardiovascular Effects of inhaled anesthetics on coronary blood flow

A
  • Iso is a POTENT vasodilator - can cause coronary steal phenomenon, no increase in ischemia
    • Coronary steal = dilating good areas of heart, not areas of stenosis where already maximally dilated

volatile agents are weak coronary vaasodilators

25
Q

Cardiovascular Effects of inhaled anesthetics on cardiac arrythmias

A

Halothane is bad

Halothane + epi –> arrythmias

26
Q

Effects of inhaled anesthetics on cardiovascular physiology table

27
Q

What do volatile anesthetics do to Minute Ventilation (RR, Tidal Volume) and PaCO2

A

↑ RR (dose dependent)

↓ VT

This equals a net ↓ in minute ventilation (rapid, shallow breaths)

Causes ↑ PaCO2

28
Q

Des and sevo produce apnea at what MAC?

A

1.5 - 2 MAC (the anesthetics themselves, not including narcotics)

29
Q

True or false

Inhaled anesthetics decrease FRC

30
Q

T/F
All inhaled anesthetics decrease airway resistance

A

False (kind of)

All except Desflurane - do not use in asthmatic pts

31
Q

T/F

The drive to breathe for pts with COPD is hypercarbia

A

False, their drive to breat is hypoxemia

32
Q

Effects of inhaled anesthetics on respiratory physiology

33
Q

Renal effects

A

Decreases renal blood flow, GFR, urine output - due to the decrease in SVP (sideeffects of side effect, not the drug)

Nephrotoxicity

34
Q

Hepatic effect

A

Decreases hepatic blood flow, and hepatic clearance, hapatic toxicity

35
Q

T/F

Volatiles decrease uterine smooth muscle contractility and blood flow

A

True

Usefule in removing retained placenta

36
Q

T/F

Inhaled drugs do not cross the placenta

A

False, they do cross the placenta and can be delivered to the baby.
The baby breathes off and therefore no effect on baby.

37
Q

Effects on skeletal muscle

A

Ether derived drugs (sevo & des) produce muscle relaxation

N2O does not produce relaxation (may produce muscle rigidity)

38
Q

Effects on temp

A
  • Volatiles lower the core temp set point at which thermoregulatory vasoconstriction is activated
  • Vasodilation redistributes blood flow from central to peripheral compartments
  • Metabolic oxygen consumption is decreased—decreases heat generation
39
Q

What is compound A?

A

Caused by Sevo

Nephrotoxin

higher levels in baralyme than sodalime

Use higher than 2 L/min flows

40
Q

How many MAC hours are acceptable at low gas flows when using sevo to prevent Compound A?

A

2 MAC hours of low flows are ok

(< 1MAC sevo for 2 hrs @ low gas flows)

41
Q

T/F

Nephrotoxicity was due to an inactive fluoride metabolite

A

True, and it’s not seen much anymore

42
Q

Which agent is most potent when it come to MH?

A) Sevo

B) Des

C) Iso

D) Halothane

A

D) Halothane

43
Q

What is halothane hepatitis?

A

Two types:

  1. Mild, self-limited form (usually in kids)
  2. Rare, life-threatening hepatic necrosis (causes death or liver transplant)

Spring Anesthesia Pharm (2 decks)

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