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E3 Flashcards

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1
Q

Boyles Law

A

Pressure and volume are inversely proportional

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2
Q

Ficks diffusion law

A 
Diffusion depends on:
Partial pressure gas gradient
Solubility of gas
Membrane thickness
Size of molecule
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3
Q

How does molecule size, membrane thickness, gas solubility, and pressure gradient affect gas effusion.

A

Molecule size
Big= slow
Small = fast

Solubility
High=
Low=

Pressure gradient
High=fast
Low=slow

Membrane thickness
Thick=Slow
Thin=Fast

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4
Q

What is a blood:gas partition coefficient?

What is it dependent on?

A

Equilibration ratio of pressure of volatile between gas in alveoli and blood

Dependent on:
CO
A-V pressure gradient

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5
Q

What is a blood:brain partition coefficent? What is it dependent on?

A

Equilibration ratio of pressure of gases between blood and brain.

Dependent on:
CBF
a-v pressure gradient

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6
Q

Influence of age on PK/metabolism of volatile.

A

<30 yo = INC met by 6% per decade

> 55 yo = DEC by 6% per decade

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7
Q

4 factors that alter volatile PK/metabolism

A

Age
DEC Lean body mass
INC fat
DEC hepatic fxn

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8
Q

What is the goal of volatile anesthetic

A

PA = Pa = PBr

End tidal PA = PBr

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9
Q

What does alveolar pressure indicate?

A

Depth of anesthesia
Recovery of anesthesia
Potency

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10
Q

What occurs to PA & PBr during anesthesia recovery

A

PA starts to INC

PBr DEC

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11
Q

What is concentration effect?

A
  • Impact of INSPIRED pressure (Pi) on rate of rise of PA

- Higher the Pi FASTER PA = Pi b/c HIGH delta-P

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12
Q

How does Pi r/t end tidal?

A

Picking up gas:
Pi > end tidal

Balance:
Pi = end tidal

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13
Q

How does Pi affect uptake & PA?

A

Low Pi = longer uptake and equilibration w/ PA

Higher Pi = more rapid uptake and equilibration w/ PA

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14
Q

8) What are some disadvantages of methoxyflurane

A

Disadvantage = dose related nephrotoxicity d/t fluroide

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15
Q

9) What are some advantages and disadvantages of enflurane?

A

Advantage= doesn’t sensitize myocardium to catechols
Not associated w/ hepatotoxicity
Disadvantage = Metabolism could lead to Sz in high concentration

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16
Q

10) What are some advantages and disadvantages of isoflurane?

A

Advantages= lack of cardiac dysrhythmias
lack of organ toxicity
rapid induction and emergence
Disadvantages = longer than sevo and des

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17
Q

11) What are some advantages and disadvantages of sevoflurane and desflurane?

A

Advantages = wholly fluorinated, low blood solubility

rapid induction

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18
Q

12) What characterizes the anesthetic state?

A

Characteristics of the anesthetic state include immobility, amnesia, analgesia and skeletal muscle relaxation

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19
Q

13) Which characteristics of the anesthetic state are achieved by the administration of inhaled volatile anesthetics?

A

Immobility
amnesia
skeletal muscle relaxation

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20
Q

14) Which characteristics of the anesthetic state are achieved by the administration of nitrous oxide?

A

Immobility, but not as sole anesthetic
Amnestic effects
No skeletal muscle relaxation

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21
Q

15) What is the mechanism of action of inhaled anesthetics in the central nervous system?

A

CNS depression by enhancing inhibitory ion channels and block excitatory ion channels
Affect release of NTs

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22
Q

16) Why are vaporizers required for the inhaled administration of volatile anesthetics?
How does this apply to N2O

A

Volatiles are liquid @ room temp and P_atm
They accurately deliver specified concentration of anesthetic
N2O is a gas at room temp so it doesn’t require vaporizer for delivery

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23
Q

4 purposes of anesthesia circuit

A

Deliver O2
Deliver inhaled drugs
Maintains temp and humidity
Removes CO2 and exhaled gases

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24
Q

3 Types of gas delivery systems

A

Rebreathing (Bain)
Non-rebreathing (self-inflating BVM)
Circle system

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25
Set-up of Bain system, what it has and doesn't have and its use?
``` Set-up Has APL valve, circuit tubing No scavenger, CO2 absorver or HME Use Rebreathing circuit for transport ```
26
7 Component parts of circle system
``` Fresh gas inlet inspiratory and expiratory limbs resevoir bag CO2 absorbent one-way valves (insp/exp) Y piece Scavenger system ```
27
Definition, advantages and disadvantages of high flow (HGF) anesthesia
Definition: Gas flow exceeds Vm in L/min Advantages: Prevents rebreathing Rapid change in anesthetic delivery, can INC anesthetic delivery Disadvantages: Wasteful (removes exhaled gas; no rebreathing) Higher cost Cools/Dries delivered volume (alters solubility and pressures)
28
How does HGF affect solubility, pressure and rebreathing?
Flow is cooled and dried which alters solubility and pressure INC flow removes exhaled gas leading to NO rebreathing
29
Definition, advantages and disadvantages of low gas flow (LGF) anesthesia
Definition: FGF < Vm Advantages: Allows for rebreathing Low cost Less cooling/drying Disadvantages: VERY slow anesthetic uptake
30
Non-anesthetic effects of volatiles
Bronchodilation | Muscle relaxation
31
How do anesthetics affect the airway? Descending order of most beneficial anesthetic?
Bronchodilation Relax smooth muscle (that are already constricted) Via VG Ca++ depletion in SR DEC SM constractility Sevo > Iso > Des
32
Conditions for anesthetics to bronchodilate
Already constricted airway | Intact epithelium w/o inflammatory process
33
Which anesthetic should be avoided in pts w/ asthma, COPD, and reactive airway and at what concentrations?
Desflurane | >2 MACs (according to Eger videos)
34
Volatile gas effects on neuromuscular system? Relate to NMBD
Dose-dependent skeletal muscle relaxation Potentiate depolarizing and ND-NMBDs Enhances glycine at SC
35
How do volatile gases mediate MR at the SC
Enhance glycine Inhibit AMPA Block glutamate release
36
Anesthetic effects on CMRO2 and cerebral activity. MAC burst suppression MAC electrical silence
DEC in both 1.5 MAC = burst suppression 2 MAC = electrical silenc
37
Which gas has no muscle relaxant properties and why?
N2O | B/c you can't ever administer 1 MAC
38
Anesthetic effects on sz
Anticonvulsant At high concentration AND DEC CO2 LOWER CO2 in combination lowers Sz threshold Proconvulsant Enflurane not used in pts w/ h/o Sz Esp >2MAC or PaCO2<30 mmHg
39
Anesthetic effect on evoked potentials of SSEP and MEP.
Dose related @0.5-1.5 MAC DEC amplitude INC latency/freq
40
What is SSEP and MEP and monitoring purposes
SSEP = somatosensory evoke potential Monitors sensory/brain response MEP = motor evoked potential monitors motor response
41
Anesthetic effects on CBF and ICP. Onset/dose of effects.
Dose dependent INC CBF d/t DEC cerebral vascular resistance May INC ICP Onset >0.6 MAC w/in minutes
42
Dose at which autoregulation ability is altered
``` Halothane = lost @0.5 MAC Sevo = lost>1 MAC Iso/Des = lost @0.5-1.5 ```
43
How do anesthetics affect ICP and why? What pts are most at risk for INC and MAC onset
Parallel INC w/ CBF b/c INC BF d/t vasodilation At risk pts w/ space occupying lesions or brain injury Onset > 0.8 MAC
44
Respiratory effects of anesthetics
Dose-Dependent INC rate and DEC Vt Iso up to 1 MAC (celing) Rate change is insufficient to maintain/counter DEC Vm or PaCO2 INC Direct depression of medullary ventilatory centers
45
MAC dose for apnea
1.5-2.0 MAC | except Iso
46
Anesthesias effect on hypoxic response and at what dose
Blunts hypoxic response normally mediated by carotid bodies T/F DEC drive to breathe 0. 1 MAC = 50-70% depress initiated 1. 1 MAC = 100% depression
47
Anesthesia's effect on hypercarbic response and at what doses
All anesthetics INC PaCO2 (according to Eger) N2O doesn't INC PaCO2 Substitution for part of MAC will provide less depression
48
Anesthetic effect on HPV response. At what dose? Biggest concern?
Dose-dependent DEC in HPV response (no vasoconstriction to hypoventilated alveoli) 2 MAC = 50% depression Most concerning = 1 lung ventilation and hypoxemia
49
5 CV effects of anesthetics
``` Direct myocardial depression Peripheral autonomic ganglion blockade Attenuation of carotid sinus reflexes DEC formation of cAMP DEC Ca++ influx ```
50
Anesthetic effects on MAP and when is it worse?
MAP: Direct myocardial depression alters CA++ into SR DEC contractility, SV, CO DEC MAP d/t DEC SVR Worse: w/ Iso in diseased hearts
51
Anesthetic effects on HR. Difference in anesthetics.
Dose dependent INC To compensate for DEC SV/CO Sevo only >1.5 MAC Des VERY tachy w/ overpressurization
52
Confounding variables to HR variability and anesthesia
INC: Anxiety Vagolytic admi DEC: Opioids beta blockers
53
Anesthetic effects on CO
DEC CO is offset by INC HR | N2O has mild sympathomimetic INC in CO
54
Principle behind coronary steal and effects on heart
D/T coronary vasodilation Coronary blood is rerouted from poorly perfused, sclerotic vessel collateral supply Worsens injury to poorly perfused myocardium
55
1. Describe the physiologic effect of neuromuscular blocking drugs (NMBDs).
Interrupt the transmission of nerve impulses to the NMJ causing paralysis
56
2.What are some clinical situations in which NMBDs are used to produce skeletal muscle relaxation?
ET intubation | Surgery
57
What analgesic effects do NMBDs have
None
58
4.How does the clinician evaluate the intensity of the neuromuscular blockade?
Monitoring twitch response from electrical stimulation of peripheral nerve from a nerve stimulator
59
What are 5 characteristics of NMBDs that may influence the choice of which drug is administered to a given patient?
MOA, onset, duration, route of elimination and side effects
60
7.Which NMBDs are the common offenders to triggering life-threatening anesthetic-related hypersensitivity reactions?
NMBDs Quaternary ammonium groups | Rocuronium and SCh are most common?
61
8.What is component that is common to all NMBDs, resulting in possible allergic cross-reactivity of these drugs?
Quaternary ammonium group leads to possible allergic cross-sensitivity
62
9.What is the most common side effects reaction to sugammadex?
N/V Pruritis and urticaria Anaphylaxis Marked bradycardia
63
Which NMBD class is associated w/ histamine release and which is not?
Benzylisoquinolinium = histamine release Atracurium, mivacurium (Cisatracurium doesn't in normal doses) Aminosteroid = no histamine release Pancuronium, Vecuronium, Rocuronium
64
What is the neuromuscular junction (NMJ) and it's components
Location where the transmission of neural impulses at motor nerve translate into skeletal muscle contraction Consists of prejunctional MN ending, synaptic cleft and postjunctional membrane.
65
11.What events lead to the release of neurotransmitter at the NMJ? What is the neurotransmitter that is released?
Events to release: Impulse down MN fiber to axonal end of prejunctional nerve. Stimulation causes Ca++ influx into prejxn and stimulates the release of NT ACh into synaptic cleft. NT ACh is synthesized and stored in presynaptic terminal until released by CA++ influx
66
12.What class of receptors is located at prejunctional and postjunctional sites?
nACh receptors are on both
67
13.What clinical effect results from the stimulation of postjunctional receptors?
ACh binds to ligand-gated ion channels allowing influx of Na+ into postunctional membrane. Results in potentiation of

Pharm (4 decks)

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