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Pharmacology > Inhalation Agents 2 > Flashcards

Inhalation Agents 2 Flashcards

1
Q

What factors influence absorption

A

Uptake

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2
Q

What factors influence distribution

A

Biotransformation

Lipid Solubility, Tissue Factors, Metabolism (Small) CO

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3
Q

What factors influence excretion

A

Elimination

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4
Q

Depth of Anesthesia is measure by

A

Pbrain

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5
Q

How is Fresh Gas Flow determined

A

vaporizer and flowmeter settings

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6
Q

Fi Is and determined by

A

inspired gas concentration

it is determined by: FGF rate, breathing circuit volume and circuit/machine absorption

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7
Q

FA is

A

alveolar gas concentration

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8
Q

FA is determined by

A

uptake
ventilation
concentration effect and second gas effect

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9
Q

Fa is

A

arterial gas concentration

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10
Q

Fa is affected by

A

ventilation/perfusion mismatching

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11
Q

3 A’s of anesthesia

A

Amnesia- Brain
Analgesia- Thalamus
Areflexia- Spinal Cord

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12
Q

FA- factors affecting Alveolar Concentration

A

Blood Solubility of the agent
Alveolar Blood Flow
Partial Pressure between alveoli and venous blood

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13
Q

Fa- Factors affecting Arterial Concentration

A

Alveolar and arterial anesthetic partial pressure are considered equal
Fa is less than the end tidel level will predict. Due to venous admixture, alveolar dead space and non-uniform distribution

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14
Q

Ventilation/Perfusion MisMatch is due to

A

Right Bronchial Intubation or PFO

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15
Q

V/Q mismatch effect is

A

to increase the alveolar partial pressure (highly soluble agents) and decrease in arterial partial pressure (low solubility agents)

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16
Q

Stage 1 of Anesthesia

A

Amnesia & Anesthesia
Initiation of Anesthesia, LOC, patient able to follow simple commands, protective reflexes remain intact, eyelid reflex intact

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17
Q

Stage 2 of Anesthesia

A 
Delirium & Excitation
LOC and eyelid reflex
Irregular Breathing pattern
Dilated pupils
Neurons that inhibit excitation are not functional and can lead to vomiting, laryngospasm, cardiac arrest and emergence delirium.
More exaggerated in pediatrics
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18
Q

Stage 3 of Anesthesia

A

Surgical Anesthesia

Initial cessation of spontaneous respirations, absence of eyelash response and swallowing reflexes

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19
Q

Stage IV of Anesthesia

A

Anesthetic Overdose

Cardiovascular collapse requiring provider intervention (yes, thats you)

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20
Q

MOA of Inhalation Agents

A 
Unknown, but thought to work on these targets:
NMDA Receptors
tandem pore potassium channels
Voltage-gated sodium channels
Glycine Receptors
GABA Receptors
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21
Q

CNS Effects of Inhalation Agents

A

CMRO2 is decreased
Cerebral BF is increased (dose dependent)
This effect is called uncoupling.
Greater with Sevo

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22
Q

What does N2O do to CMRO and CBF?

A

Increases CMRO2 and CBF

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23
Q

When does burst suppression occur?

A

1.5 MAC of Des

2 MAC w/ Iso and Sevo

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24
Q

What effect do inhalation agents have on evoked potentials

A

decrease amplitude and increase latency

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25
Q

Developmental Neurotoxicity

A

Evidence that in rodents and non-human primates that anesthetic agents are toxic to human brain
Three major studies look at it, and found no evidence to support claims. Take aways where: keep surgery as short as possible and use short acting medications and multimodal approaches

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26
Q

Post-Operative Cognitive Dysfunction

A

POCD
Greater concern in Elderly
No clinical significant association b/t major surgery and anesthesia w/ long term POCD

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27
Q

Emergence Delirium in Children

A

common with SEvo and Des

Medication adjunct: Precedex

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28
Q

In a dose dependent fashion, all inhalation agents reduce

A

cardiac output and cardiac index. They reduce the free intracellular Ca2+ contractile state.
As MAC increases, slight increase in Cl and HR

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29
Q

With inhalation agent administration, you can witness reduce MAP secondary to

A

SVR reduction. N2O in combination with anesthetic will reduce this phenomenon

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30
Q

Volatile agents and N2O induce

A

HR changes via the sinoatrial node antagonism
Modulation of baroreflex activity
Sympathetic nervous system activity

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31
Q

All inhalation agents produce some

A

vasodilation (SVR)

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32
Q

Isoflurane can induce

A

reverse Robin-Hood syndrome in hypotensive patients

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33
Q

Preconditioning

A

phenomenon in which the heart is exposed to a cascade of intracellular events that protect it from ischemic and re-perfusion insult

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34
Q

Sensitization

A

volatile agents reduce the quantity of catecholamines necessary to evoke arrhythmias

35
Q

Safe Epinephrine Dosing

A

10 ml in 1:100,000 epi in a 10 min period or up to 30ml/hour

36
Q

Nitrous Oxide causes a slight decrease in

A

PVR

Worsens pulmHTN

37
Q

Volatile agents decrease

A

pulmonary artery pressure

38
Q

Hypoxic Pulmonary vasoconstriction is

A

mildly depressed.

Iso has the greatest effect

39
Q

Cardiovascular Effects of Iso

A

decreases CO
Decreases SVR
Decreases MAP
increases HR

40
Q

Cardiovascular effects of Des

A

no change CO
decrease SVR
Decrease MAP
increase HR

41
Q

Cardiovascular Effects of Sevo

A

No change CO
Decrease SVR
Decrease MAP
No change HR

42
Q

Cardiovascular Effects of N2O

A

Decrease CO
Increase SVR
No change MAP
Increase HR

43
Q

Cardiovascular Effects of Xenon

A

No Change CO
No change SVR
No change MAP
Decrease HR

44
Q

Volatile agents cause dose dependent decreases in

A

Tidal volume
Responsiveness in CO2
- increase apneic threshold
- exacerbated by co-administration of an opioid

45
Q

Halothane Hepatitis

A

Occurs in b/t 6k-35,000 cases
mostly like from the trifluoracetyl-contained metabolites binding to proteins and forming anti-trifluroacetyl protein antibodies
Re-exposure of the patient to halothane these antibodies will mediate massive hepatic necrosis that can result in death

46
Q

Transient increase in ALTs will occur with what inhalation agent

A

Des

47
Q

What inhalation agent is most associated with risk in patients with renal compromised

A

Sevo

48
Q

What inhalation agents has the LEAST impact on renal function

A

Des

49
Q

Sevoflurane has the greatest metabolism where and how much

A

liver

5-8%

50
Q

All volatile agents produce a dose-dependent relaxation on what muscle

A

Skeletal muscle
Additive effect with NMBDs
Can be reduced 25-50% of dose when compared to TIVA
Delay recovery from nondeplorizing NMBD

51
Q

The IDEAL anesthetic Agent

A 
non-irritating to respiratory tract
rapid induction and emergence
Chemical stable (non flammable)
produce amnesia, analgesia and areflexia
potent
not metabolized and excreted by respiratory tract
free of toxicity and allergic reactions
minimal systemic changes
uses a standardized vaporizer
affordable
52
Q

Four Properties of how agents work

A

Vapor Pressure
Boiling Point
Partial Pressure
Solubility

53
Q

Vapor Pressure

A

Pressure exerted inside a container between liquid and vapor
at Room temp, most volatile agents have a VP below atm pressure
As long as liquid is present, VP is independent of volume
Directly proportional with temperature

54
Q

Boiling Point

A

Temperature at which VP exceeds Atm Pressure in an open container

55
Q

Partial Pressure

A

fraction of pressure within a mixture (Dalton’s Laws)

56
Q

Solubility

A

tendency of gas to equilibrate with a solution (Henry’s Law)
Anesthetic gases administered to the lungs diffuse into the blood until their partial pressures to the alveoli and blood are equal
equalizing of blood and target tissues occurs simultaneously, however there is not gas phase

57
Q

The concentration of an anesthetic in the tissues is depenedent on (2)

A

partial pressure and solubility

inspired concentrations or fractional volumes are typically used instead of partial pressures

58
Q

MAC

A

Minimun Alveolar Concentration
The definition of MAC is the minimum alveolar concentration (%) required to produce anesthesia (lack of movement) in 50% of the population (ED50)

59
Q

MAC Awake

A

50% of the population opens their eyes to command

60
Q

Mac BAR

A

MAC necessary to block adrenergeric response to stimulation
Usually 1.3 of MAC value
Can be reduced by administering a narcotic prior to incision

61
Q

MAC’s additive Effect

A

0.5 MAC of N2O + 0.5 MAC of iso= 1 MAC Sevo

62
Q

Factors that increase MAC

A

hyperthermia
drug induced increases in CNS activity
Hypernatremia
Chronic Alcohol Abuse

63
Q

Factors that Decrease MAC

A 
hypothermia
increasing age
alpha 2 agonist
acute alcohol ingestion
pregnancy 
hyponatremia
64
Q

Vaporizers

A

the delivery device for volatile agents
Facilitate the movement of anesthetic from the machine to the patient through
-Fresh gas flows
-pressure
-temperature
Vaporizers are calibrated for specific agents

65
Q

Isoflurane

A

Halogenated Methyl Ethyl Ether
Most POTENET
Slower onset and recovery from anesthesia

66
Q

Isoflurane’s Cardiovascular Effects

A

minimal cardiac depression, preserves carotid baroreceptors

dilated coronary arteries, concerns for reverse robin hood

67
Q

Iso Respiratory Effects

A

Pungent NOT used for inhalation induction

tachypnea less pronounced

68
Q

Desflurane

A

Least Potent
Quicker induction and emergency
Potential to boil at Room temperature

69
Q

Desflurane Cardiovascular Effects

A

Rapid increase in Des = increase in HR and BO

Attenuated with fentanyl, Esmolol, and clonidine

70
Q

Desflurane Respiratory Effects

A

VERY PUNGENT
cause cause airway irritation
increased salivation, breath holding coughing and laryngospasm
avoid in patient with airway disease

71
Q

Sevoflurane

A

Moderate Potency

Rapid induction and emergence

72
Q

Sevo Cardiovascular Effects

A

May prolong QT interval
Cardiac Output is less maintained than other agents
HR NOT increased

73
Q

Sevo Respiratory Effects

A

Non pungent

preferred for inhalation

74
Q

Sevo Metabolism and Renal Effects

A

Metabolized in CYP 450 2E1
- increases inorganic fluoride ions, but has not resulted in nephrotoxicity
Soda Lime can degrade Sevo into Compound A
For safety, calcium hydroxide absorbent, flows 2 lpm, avoid in patients with renal dysfunction

75
Q

Nitrous Oxide

A 
Not a volatile Anesthetic
colorless odorless
gas at room temp
nonexplosive and nonflammable (but can contribute to combustion)
NMDA receptor antagonist
76
Q

N20 Systemic Effects

A

Cardiovascular- stimulates Sympathetic nervous system (BP HR CO unchanged or slightly elevated)
RR- increases Respiratory Rate; decreases hypoxic drive
Cerebral- increases CMRO2 and CBF
GI- increases risk of PONV

77
Q

absolute Contraindications of N20

A

methionine synthase pathway deficiency

expansion of gas-filled space

78
Q

Relative N20 Contraindications

A 
PONV
First Trimester of Pregnancy
Increased ICP
Pulm HTN
Prolonged surgery (>6hr)
79
Q

Xenon

A

Noble gas with known anesthetic properties
odorless colorless nonexplosive naturally occurring
inert, dose not form chemical bonds
Actions via NMDA and glycine receptor binding sites
minimal cardiovascular, hepatic and renal effects
no effect to ozone layer
cost and limited availability have prevented widespread use

80
Q

Malignant Hyperthermia

A

Pharmacogentic disordered triggered by volatile agents succinylcholine and stress
Ryanodine receptor gene mutation

81
Q

MH signs and symptoms

A 
Increase in Co2 production
muscle rigidity
metabolic acidosis
high temperature (late sign)
urine color darkness
tachycardia, tachypnea
82
Q

MH is caused by what gases

A

all inhalation agents except N20

83
Q

MH treatment

A

Dantrolene Sodium- muscle relaxant
1mg/kg administer til symtpoms subside, up to 10mg/kg
Ryanodex- new IV formulation of dantrolene for prevention and treatment of MH
- requires fewer vials and less reconstitution
-shorter half-life
-requires supplementation of mannitol

84
Q

Anesthesia in Pregnancy

A

0.2-0.75% of pregnant patients require general anesthesia (appendectomy, cholecystectomy, ovarian, trauma)
some clinicians avoid N2O due to teratogenic effects
-elective surgery should be delayed until after delivery
- non-urgent surgery should be performed in 2nd trimester

Pharmacology (14 decks)

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