Cumulative Final (Exam 3) Flashcards
(119 cards)
1
Q
What are the brand names for sevo, des, iso, and enfulrane?
A
Sevo - Ultane
Des - Suprane
Iso - Forane
Enfurane - Ethrane
2
Q
What is Boyle’s Law?
Example?
A
- At a constant temperature, pressure and volume of a gas in inversely related
- Anesthetic machine bellows contract increasing pressure in the ventilator and circuit causing gases to move from high pressure (vent) to low pressure (lungs)
3
Q
What is Fick’s law of diffusion?
Example?
A
- It describes the rate at which molecules move from an area of high concentration to an area of low concentration.
- Once the molecules get to the alveoli, they move around randomly and begin to diffuse into the pulmonary capillary.
4
Q
What three things does diffusion of a gas depend on?
A
- Partial pressure gradient of the gas
- Solubility of the gas (diffusion)
- Thickness of the membrane
5
Q
What is Graham’s law of diffusion?
Example?
A
- Proccess in which molecules diffuse through pores and channels without colliding
- Smaller molecules effuse faster (leave their container) depending on solubility (diffusion)
- EX: CO2 is 20x more diffusable than O2 despite having a larger molecular weight
6
Q
What is the concentration effect and how does it affect induction times?
A
- The higher the inspired gas concentration (PI) the faster alveolar concentration (PA) will reach the inspired gas concentration
- Higher inspired gas pressure with decrease breaths to unconciousness
- 8 % desflurane will cause unconciousness in less breaths than 1%
7
Q
Describe over pressurization?
Example?
A
- Increasing PI by a large amount will result in a rapid loss of conciousness
- Left at these high levels will result in overdose
- 1 vital capacity breath of 7% sevo will result in loss of eyelash reflex
8
Q
What is the second gas effect?
A
- Uptake of a high volume gas (N2O) accelerates a concurrently administered companion gas
- A high volume of N2O is highly diffusable and is taken up quickly into the pulmonary capillary
→ this leaves a high concentration of the second gas in the alveoli → second gas will be uptaken more rapidly now due to the gradient created
9
Q
What effects the magnitude of pressure exerted by nitrous administration?
A
- Compliant vs non-compliant walls
- Partial pressure of nitrous oxide
- Blood flow to the cavity
- Duration of administration
10
Q
What 2 specific pathologies are contraindicated for nitrous administration?
A
- Pneumothorax - will greatly increase size
- Intraocular procedures - will cause retinal artery compression and vision loss
11
Q
Rannk the volatiles from least soluble in blood to most soluble?
A
- Desflurane (most rapid induction/emergence)
- Nitrous
- Sevoflurane
- Isoflurane
- Enflurane
- Halothane (slowest induction/emergence)
12
Q
Blood:Gas partition coefficient of Halothane?
A
2.54 - More blood soluble, slower induction and emergence
13
Q
Blood:Gas partition coefficient of Enflurane?
A
1.90 - More blood soluble, slower induction/emergence
14
Q
Blood:Gas partition coefficent of Nitrous?
A
0.46 - poorly blood soluble, quick induction and emergence
15
Q
Blood:Gas partition coefficient of Isoflurane?
A
1.46 - More blood soluble, slower induction/emergence
16
Q
Blood:Gas partition coefficent of Desflurane?
A
0.42 - poorly blood soluble, quick induction and emergence
17
Q
Blood:Gas partition coefficent of Sevoflurane?
A
0.69 - poorly blood soluble, quick induction and emergence
18
Q
Which gas would be better for a morbidly obese patient, sevoflurane or desflurane?
A
Desflurane- Sevoflurane has a almost 2x the fat:blood partition coeffient, meaning emergence will take longer due to resedation from gas stored in fats
19
Q
MAC % is based upon what constants?
A
- 30-55 y/o
- 37 ℃
- 760 mmHg
20
Q
What is 1 MAC of nitrous oxide?
A
104 %
21
Q
What is 1 MAC of Halothane?
A
0.75 %
22
Q
What is 1 MAC of Enflurane?
A
1.63 %
23
Q
What is 1 MAC of Isoflurane?
A
1.17 %
24
Q
What is 1 MAC of Desflurane?
A
6.6 %
25
What is 1 MAC of Sevoflurane?
1.8 %
26
What is the most important factor that alters MAC?
Body temperature
27
How does age alter MAC?
* MAC peaks at 1 y/o
* For **every** decade below constant range (30-55) **increase** by 6 %
* For **every** decade after constant range (30-55) **decrease** by 6 %
28
List the 4 things that increase MAC?
- Hyperthermia
- Excess pheomelanin production (redheads)
- Drug induced increase in catecholamines (cocaine, meth)
- Hypernatremia (membranes depolarize faster)
29
Factors that decrease MAC? (there are lots)
**Hypothermia**
Pre-op Meds (BZD), intraop opioids (synergism)
Alpha-2 agonist (decreases SNS)
Acute EtOH ingestion
Pregnancy
Post partum (12-72 hours)
Lidocaine
**PaO2 < 38 mmHg**
**Mean BP < 40 mmHg**
Cardiopulmonary Bypass
**Hyponatremia**
Age
Renal failure
30
Factors that do not affect MAC.
Chronic EtOH abuse
**Gender**
**Duration of anesthesia**
PaCO2 15-95 mmHg
**PaO2 > 38 mmHg**
Hyper/hypokalemia
Thyroid gland dysfunction
31
How do volatiles cause spinal immobility?
- Depress excitatory AMPA and NMDA (glutatmate receptors)
- Enhance inhibitory glycine receptors (strychnine - glycine antagonist)
- Blocks presynaptic release of glutamate via sodium channels
32
How do volatiles cause loss of conciousness?
- Inhibtory transmission of GABA - especially in RAS
- Potentiates activation of glycine in the brainstem
- Does not affect AMPA, NMDA, or kainate receptors
33
What is Dalton's Law?
The total pressure exerted by a gas mixture is equal to the sum of the individual gas partial pressures
34
What is the vapor pressure of Enflurane?
175 torr
35
What is the vapor pressure of Isoflurane?
238 torr
36
What is the vapor pressure of Desflurane?
669 torr
| Means will evaporate readily at sea level
37
What is the vapor pressure of Sevoflurane?
157 torr
38
What is the vapor pressure of Halothane?
243 torr
39
How can you calculate volume percent of an anesthetic?
partial pressure / total pressure
40
How does a flow over vaporizer work?
- Increases efficency of vaporization by increasing the gas-liquid interface (allows fresh gas to mix more with the anesthetic)
41
What is high-flow inhalation anesthesia? Uses?
What are some downsides to high-flow anesthesia?
* Fresh gas flow (FGF) exceeds minute ventilation.
* High flow allows providers to make rapid changes in anesthetics (induction) and prevents rebreathing (washes out gases in the circuit).
* Used for preoxygenation/denitrogenation during induction
* Wasteful (not all gas is inhaled, some washed downstream) and cools/dries delivered volume.
42
What is low-flow inhalation anesthesia? Benefits?
What are some downsides to low-flow anesthesia?
* Fresh gas flow (FGF) less than minute ventilation.
* Low cost, conserves gas, less/cooling and drying.
* A **very** slow change in anesthestic depth - may be good for slow emergence
* Compound A production (*not clinically relevant*)
43
How do volatile anesthetics cause bronchodilation?
* Relax airway smooth muscle by blocking VG Ca2+ channels.
* For bronchodilation to occur, there needs to be an intact epithelium. Inflammatory processes and epithelial damage will alter responses.
44
For a patient with bronchospasm which volatile gas will be most beneficial for bronchodilation?
Which gas will worsen bronchospasm for smokers?
Sevoflurane (best bronchodilator)
Desflurane
45
What is ischemic preconditioning?
Brief periods of ischemia and exposure to volatile anesthetics can enhance tolerance to subsequent ischemia, enhance cardiac function, and reduce infarction size.
## Footnote
Stoelting p. 2744
46
What are the benefits of ischemic preconditioning?
Clinically, when can ischemic preconditioning be useful?
Prevents "reperfusion injury"
Do not see as many cardiac dysrhythmias.
Less contractile dysfunction.
Clinically apparent in delaying MI for PTCA or CABG.
47
At ______ MAC, wakefulness changes to unconsciousness.
What MAC will there be burst suppression?
What MAC will there be electrical silence?
0.4
1.5
2.0
48
Which volatiles have anticonvulsant activity?
Which volatiles have pro-convulsant activity?
* Des, Iso, and Sevo (at high concentrations and with hypocarbia)
* Enflurane (no longer used) - especially above 2 MAC or PaCO2< 30 mmHg
49
How do you prevent the negative effects on SSEP and MEP monitoring when using volatiles?
* Do not use more than 0.5 MAC if you are monitoring SSEP or MEP for spinal cases.
* Instead, use 0.5 MAC of volatile with 60% of N2O or IV anesthetic/opioid.
50
How do volatile anesthetics affect CBF?
Increase CBF d/t decrease cerebral vascular resistance. This can result in an increase in ICP.
51
What is the best volatile anesthetic to use for a patient with a known increased ICP?
Which volatile will have the greatest vasodilatory effect?
* Sevoflurane has the least vasodilatory effect. (*not shown in graph*)
* Halothane will have the greatest increase in CBF.
* Nitrous is okay at less than 1 MAC
52
Which gasses will blunt the hypoxic response? How long will the effects?
* All volatiles including nitrous
* Several hours post-op
53
How do volatile anesthetics affect heart rate?
A dose-dependent **increase** in HR.
54
Sevoflurane will see a HR increase at a MAC greater than ____ .
What about Iso and Des?
1.5 MAC
*Iso and Des at lower concentrations*
55
What happens to HR with desflurane overpressurization?
* A significant increase in HR (60 bpm to 140 bpm)
* Can be catastophic in pts with aortic stenosis or bad hearts
## Footnote
Per the Eger vidoes this response is very transient (couple of mins)
56
What is the effect of the volatile anesthetic on cardiac output?
What drug is the exception?
* A dose-dependent decrease in CO (offset by a mild increase in HR for most volatiles).
* Nitrous - mild ↑ in CO
57
Which volatile anesthetic will have the largest decrease in the cardiac index?
Least decrease?
* Halothane
* Desflurane
58
How do volatile anesthetics affect hepatic blood flow?
Which volatiles effect it the most?
Total hepatic blood flow and hepatic artery flow are maintained.
Volatiles dilate the portal vein which will increase blood flow at 1-1.5 MAC.
*Iso, Des, and Sevo have the same effects*
**Halothane decreases hepatic flow**
59
Which anesthetic is not capable of stimulating hepatic antibodies?
Sevoflurane
Metabolized to vinyl halide, not acetyl halide
60
Nephrotoxicity is caused by ?
Fluoride metabolites.
*Volatile anesthetics have fluoride in them*
61
Which volatile anesthetic causes the worst nephrotoxicity?
Methoxyflurane
*70% metabolized, removed from the market*
62
What is compound A?
How is it formed?
- Fluromethyl-2,2-difluro-1-vinylether
- Nephrotoxin formed from reactions between sevoflurane and CO2 absorbents ( KOH and NaOH) *at low flow rates*
63
Why is compound A not considered a problem today?
- Most absorbents are composed of CaOH
- Levels of compound A formation at low flow rates are well below the level that causes ATN
64
How is MH diagnosed?
Caffeine contracture test
65
Sx of MH
* Increase body temp
* Increase CO2 production
* Increase O2 consumption
66
How does dantrolene treat MH?
Blocks intracellular Ca++ release
67
What are the effects of volatile anesthetics on obstetrics?
* A dose-dependent decrease in uterine smooth muscle contractility (0.5-1.0 MAC)
* This can be useful for a retained placenta stuck in the patient.
* Worsen blood loss in uterine atony (need uternine contraction to decrease bleeding)
68
Over-pressurizing desflurane will cause ____ stimulation.
SNS
69
List the volatiles from most to least likely to degrade to CO if the absorbent is dehydrated?
Desflurane > Enflurane > Isoflurane > Sevoflurane
70
3 purposes of NMBD for anesthesia?
1. Decrease airway trauma
2. Facilitate surgical exposure
3. Minimize injury from patient movement
71
Give the generic name for these drugs:
Anectine
Pavulon
Tracrium
Norcuron
Zemuron
Nimbex
Mivacron
Anectine = Succinylcholine
Pavulon = Pancuronium
Tracrium = Atracurium
Norcuron = Vecuronium
Zemuron = Rocuronium
Nimbex = Cisatracurium
Mivacron = Mivacurium
72
What are the 3 long acting NDMB and their chemical classification?
- Pancruonium (Pavulon); Aminosteroid
- Doxacurium; aminosteroid
- Pipecuronium; aminosteroid
73
What are the 4 intermediate acting NDMB and their chemical classification?
74
What is the short-acting NDMB and its chemical classification?
75
What nerve is stimulated so that the adductor pollicis muscle will produce a single twitch at 1 Hz (thumb adduction)?
Ulnar nerve
76
What is the order of muscular blockade with NMBD?
- Small moving muscles block faster than large (eyes before diaphragm)
- Central muscles block faster but a lesser intensity (laryngeal before adductor pollicis)
77
What does this graph show?
Both Muscles experience a dramatic decrease in twitch percent height, but the adductor pollicis is completley blocked while the larynx got down to a twitch height of 20%.
Both muscles recovered at the same rate. Almost 100% twitch response returned by minute 40.
## Footnote
Central muscles have less intense block than peripheral
78
Checking a twitch in which muscle will assess the diaphragm and laryngeal muscle blockade?
Orbicularis Oculi
*If there are no twitches to the facial nerve, the diaphragm and laryngeal muscles are adequately blocked. Best indicator of intubating conditions.*
79
The orbicularis oculi underestimates _____________.
residual paralysis.
80
Where should you check twitches to determine recovery from NMBD?
Adductor pollicis (Ulnar Nerve)
## Footnote
Gold standard for recovery
81
Double burst stimulator is ____ short burst followed by ____ short burst.
The double burst stimulator uses ________ Hz
2-3, 2-3
50 Hz (supramaximal current)
82
Why was the double burst stimulator developed?
To improve detection of residual block (fade).
Fade in 2nd response vs 1st response.
Qualitatively better than TOF.
83
If a ____ NMBD is given, a tetanic stimulation will result in a sustained muscle response.
Depolarizing NMBD (Succinylcholine)
84
If a _____ NMBD is given, a tetanic stimulation will result in a a non-sustained muscle response (fade).
Nondepolarizing NMBD (Roc/Vec)
*The fade is a result of presynaptic depletion of ACh or inhibition of release*
85
What is post-tetanic stimulation?
Difference with phase I and phase II block?
Single twitch 3 seconds after tetanic stimulation.
*The post-tetanic stimulation will occur **d/t accumulation of calcium during tetany, the excess calcium will stimulate ACh release.***
Phase I = equal amplitude
Phase II = increase amplitude
86
What kind of NMBD are used in column A, B, and C?
What kind of nerve stimulation is performed in row 1 through 4?
87
The presynaptic motor neuron is large and ____ which helps with transmission of nerve impulses.
myelinated
88
The motor nerve ending is ____ and innervates single muscle fibers.
unmyelinated
89
ACh release is dependent on what electrolyte?
Calcium
90
What does Acetylcholinesterase do to ACh?
Hydrolyze ACh to acetic acid and choline
91
How many subunits are in a nACh receptor?
How does ACh open the receptor?
5
There must be an ACh bound to each ⍺ subunit
92
How does succ affect the nACh receptor?
How does succ cause fasiculations?
- Only requires binding to 1 of the ⍺ subunits
- Succ "jumps" from one binding site to another causing frequent and non-consistent depolarizations
93
Succ releases ____ and can cause allergic type reactions?
Histamine
94
SCh will cause how much increase in serum K+?
0.5 mEq/L
95
What is another name given to depolarizing muscle relaxants?
Phase I block
96
Twitch characteristics of phase 1 blocks?
- Decrease in amplutude and contraction, no fade
- TOFR > 0.7
- No post-tetanic increase
- Fasiculations
97
Phase II Block are typical of ___________ NMBD.
non-depolarizing
98
How can a Phase I block transition to a Phase II block?
* Large dose of SCh (2-4 mg/kg)
* Lack of/ poorly functioning pseudocholinesterase
* Relative "overdose".... become desensitized → receptors antagonized but channels are closed (not depolarized)
99
Succinylcholine is hydrolyzed by ____ which is made in the ____
* Butyrylcholinesterase (plasma cholinesterase)
* Liver
100
What increases pseudocholinesterase activity?
Obesity
101
What does dibucaine number mean?
The percentage of plasma cholinesterase enzyme inhibitied by dibucaine.
Reflects quality of cholinesterase enzyme (ability to hydrolyze succinylcholine) and not the quantity of the enzyme that is circulating in the plasma - Stoelting p. 1036
102
What is a normal and abnormal dibucaine number?
80% = normal
20% = abnormal (normal succ dose will last 3 hours)
103
What is the pre-treatment to the side effects of SCh?
* Pre-treatment with a small dose of non-depolarizing NMBD.
* The defasciculating dose either decreases, prevents, or masks the side effects of SCh.
104
What causes aspiration sometimes seen with succ?
Increased intragastic and lower esophageal sphincter pressure
105
What is an absolute contratindicatino to succ?
Open anterior eye injury
106
MH is caused by mutations in what receptor to have excessive calcium release from the SR?
Ryanodine Receptor (RyR1)
107
What ethnicity of patients are susceptible to MH?
Native Americans
108
What is the dose of dantrolene?
2mg/kg IV
Repeat doses until symptoms subside or 10mg/kg IV
109
How does dantrolene work?
Inhibits the Ca2+ release from the SR and produces a muscle relaxant effect.
110
Twitch characteristics with NDNMB?
- Fade w/ continuous stimulus
- Post-tetanic potentiation
- Decreased twitch response with singlw stimulus
111
The cardiovascular effects of non-depolarizing NMBD are due to what factors?
Release of histamine
Effects on cardiac muscarinic receptors
Effects on nAChRs at autonomic ganglia
112
What non-depolarizing NMBD has the same dose for ED95 and autonomic nervous system stimulation?
Pancuronium (sympathomimetic) will result in tachycardia at the ED95 dose
113
Which non-depolarizing NMBD is not metabolized by the liver but is pH and temperature dependent?
What is the MOA?
Atracurium and Cisatracurium
MOA: temperature-dependent elimination process through Hoffman elimination (need normal temperature and pH) and ester hydrolysis
114
Non-Depolarizing NMBD on stroke patients.
Paretic Arm
Unaffected Side
MOA
Paretic Arm: Resistance compared to the unaffected side
Unaffected Side: Resistance compared to normal patients
MOA: Proliferation of extrajunctional nAChRs
115
Which NMBD is more prone to allergic reactions?
Succinylcholine
116
What are the cardiovascular effects of pancuronium?
* Increase HR, MAP, and CO from vagal blockade
* Release NE presynaptically and blocks the reuptake of NE.
* No histamine release.
117
Where is Vec metabolized and excreted?
Metabolized in the liver primarily (70%), excreted in the kidneys.
## Footnote
Avoid in liver failure
118
Cardiovascular effect of Atracurium
Histamine release
119
How is mivacurium broken down?
Plasma cholinesterases
