Inhalation Agents 2 Flashcards
1
Q
What factors influence absorption
A
Uptake
2
Q
What factors influence distribution
A
Biotransformation
Lipid Solubility, Tissue Factors, Metabolism (Small) CO
3
Q
What factors influence excretion
A
Elimination
4
Q
Depth of Anesthesia is measure by
A
Pbrain
5
Q
How is Fresh Gas Flow determined
A
vaporizer and flowmeter settings
6
Q
Fi Is and determined by
A
inspired gas concentration
it is determined by: FGF rate, breathing circuit volume and circuit/machine absorption
7
Q
FA is
A
alveolar gas concentration
8
Q
FA is determined by
A
uptake
ventilation
concentration effect and second gas effect
9
Q
Fa is
A
arterial gas concentration
10
Q
Fa is affected by
A
ventilation/perfusion mismatching
11
Q
3 A’s of anesthesia
A
Amnesia- Brain
Analgesia- Thalamus
Areflexia- Spinal Cord
12
Q
FA- factors affecting Alveolar Concentration
A
Blood Solubility of the agent
Alveolar Blood Flow
Partial Pressure between alveoli and venous blood
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
14
Q
Ventilation/Perfusion MisMatch is due to
A
Right Bronchial Intubation or PFO
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)
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
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
18
Q
Stage 3 of Anesthesia
A
Surgical Anesthesia
Initial cessation of spontaneous respirations, absence of eyelash response and swallowing reflexes
19
Q
Stage IV of Anesthesia
A
Anesthetic Overdose
Cardiovascular collapse requiring provider intervention (yes, thats you)
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
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
22
Q
What does N2O do to CMRO and CBF?
A
Increases CMRO2 and CBF
23
Q
When does burst suppression occur?
A
1.5 MAC of Des
2 MAC w/ Iso and Sevo
24
Q
What effect do inhalation agents have on evoked potentials
A
decrease amplitude and increase latency
25
Developmental Neurotoxicity
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
26
Post-Operative Cognitive Dysfunction
POCD
Greater concern in Elderly
No clinical significant association b/t major surgery and anesthesia w/ long term POCD
27
Emergence Delirium in Children
common with SEvo and Des
| Medication adjunct: Precedex
28
In a dose dependent fashion, all inhalation agents reduce
cardiac output and cardiac index. They reduce the free intracellular Ca2+ contractile state.
As MAC increases, slight increase in Cl and HR
29
With inhalation agent administration, you can witness reduce MAP secondary to
SVR reduction. N2O in combination with anesthetic will reduce this phenomenon
30
Volatile agents and N2O induce
HR changes via the sinoatrial node antagonism
Modulation of baroreflex activity
Sympathetic nervous system activity
31
All inhalation agents produce some
vasodilation (SVR)
32
Isoflurane can induce
reverse Robin-Hood syndrome in hypotensive patients
33
Preconditioning
phenomenon in which the heart is exposed to a cascade of intracellular events that protect it from ischemic and re-perfusion insult
34
Sensitization
volatile agents reduce the quantity of catecholamines necessary to evoke arrhythmias
35
Safe Epinephrine Dosing
10 ml in 1:100,000 epi in a 10 min period or up to 30ml/hour
36
Nitrous Oxide causes a slight decrease in
PVR
| Worsens pulmHTN
37
Volatile agents decrease
pulmonary artery pressure
38
Hypoxic Pulmonary vasoconstriction is
mildly depressed.
| Iso has the greatest effect
39
Cardiovascular Effects of Iso
decreases CO
Decreases SVR
Decreases MAP
increases HR
40
Cardiovascular effects of Des
no change CO
decrease SVR
Decrease MAP
increase HR
41
Cardiovascular Effects of Sevo
No change CO
Decrease SVR
Decrease MAP
No change HR
42
Cardiovascular Effects of N2O
Decrease CO
Increase SVR
No change MAP
Increase HR
43
Cardiovascular Effects of Xenon
No Change CO
No change SVR
No change MAP
Decrease HR
44
Volatile agents cause dose dependent decreases in
Tidal volume
Responsiveness in CO2
- increase apneic threshold
- exacerbated by co-administration of an opioid
45
Halothane Hepatitis
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
Transient increase in ALTs will occur with what inhalation agent
Des
47
What inhalation agent is most associated with risk in patients with renal compromised
Sevo
48
What inhalation agents has the LEAST impact on renal function
Des
49
Sevoflurane has the greatest metabolism where and how much
liver
| 5-8%
50
All volatile agents produce a dose-dependent relaxation on what muscle
Skeletal muscle
Additive effect with NMBDs
Can be reduced 25-50% of dose when compared to TIVA
Delay recovery from nondeplorizing NMBD
51
The IDEAL anesthetic Agent
```
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
Four Properties of how agents work
Vapor Pressure
Boiling Point
Partial Pressure
Solubility
53
Vapor Pressure
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
Boiling Point
Temperature at which VP exceeds Atm Pressure in an open container
55
Partial Pressure
fraction of pressure within a mixture (Dalton's Laws)
56
Solubility
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
The concentration of an anesthetic in the tissues is depenedent on (2)
partial pressure and solubility
| inspired concentrations or fractional volumes are typically used instead of partial pressures
58
MAC
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
MAC Awake
50% of the population opens their eyes to command
60
Mac BAR
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
MAC's additive Effect
0.5 MAC of N2O + 0.5 MAC of iso= 1 MAC Sevo
62
Factors that increase MAC
hyperthermia
drug induced increases in CNS activity
Hypernatremia
Chronic Alcohol Abuse
63
Factors that Decrease MAC
```
hypothermia
increasing age
alpha 2 agonist
acute alcohol ingestion
pregnancy
hyponatremia
```
64
Vaporizers
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
Isoflurane
Halogenated Methyl Ethyl Ether
Most POTENET
Slower onset and recovery from anesthesia
66
Isoflurane's Cardiovascular Effects
minimal cardiac depression, preserves carotid baroreceptors
| dilated coronary arteries, concerns for reverse robin hood
67
Iso Respiratory Effects
Pungent NOT used for inhalation induction
| tachypnea less pronounced
68
Desflurane
Least Potent
Quicker induction and emergency
Potential to boil at Room temperature
69
Desflurane Cardiovascular Effects
Rapid increase in Des = increase in HR and BO
| Attenuated with fentanyl, Esmolol, and clonidine
70
Desflurane Respiratory Effects
VERY PUNGENT
cause cause airway irritation
increased salivation, breath holding coughing and laryngospasm
avoid in patient with airway disease
71
Sevoflurane
Moderate Potency
| Rapid induction and emergence
72
Sevo Cardiovascular Effects
May prolong QT interval
Cardiac Output is less maintained than other agents
HR NOT increased
73
Sevo Respiratory Effects
Non pungent
| preferred for inhalation
74
Sevo Metabolism and Renal Effects
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
Nitrous Oxide
```
Not a volatile Anesthetic
colorless odorless
gas at room temp
nonexplosive and nonflammable (but can contribute to combustion)
NMDA receptor antagonist
```
76
N20 Systemic Effects
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
absolute Contraindications of N20
methionine synthase pathway deficiency
| expansion of gas-filled space
78
Relative N20 Contraindications
```
PONV
First Trimester of Pregnancy
Increased ICP
Pulm HTN
Prolonged surgery (>6hr)
```
79
Xenon
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
Malignant Hyperthermia
Pharmacogentic disordered triggered by volatile agents succinylcholine and stress
Ryanodine receptor gene mutation
81
MH signs and symptoms
```
Increase in Co2 production
muscle rigidity
metabolic acidosis
high temperature (late sign)
urine color darkness
tachycardia, tachypnea
```
82
MH is caused by what gases
all inhalation agents except N20
83
MH treatment
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
Anesthesia in Pregnancy
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
