Pharm Ii, Inhaled Anesthetics, Part 2

Front 1

Uptake is directly proportional to what?

Back 1

cardiac output

Front 2

The higher the cardiac output, the ______ the uptake.

Back 2

greater

Front 3

Doubling cardiac output doubles the amount of?

Back 3

blood exposed to the anesthetic (more relevant for higher solubility agents)

Front 4

What does the alveolar-venous partial pressure gradient arise from?

Back 4

gas exchange into the tissues - tissue uptake

Front 5

Tissue uptake is governed by (3)?

Back 5

The same factors that apply to uptake from the lungs (solubility, tissue blood flow, arterial-tissue partial pressure gradient)

Front 6

Tissue solubility

Back 6

tissue-blood partition coefficients for lean tissue do not differ greatly, lean tissues do not have significantly different capacities for anesthetic per mL of blood

Front 7

What is the significance of this relative to the rate of uptake in the tissues?

Back 7

tissue blood flow

Front 8

Tissue blood flow is the main determinant of?

Back 8

tissue uptake

Front 9

Vessel rich group

Back 9

brain, heart, lungs, liver, kidneys
-10% of body mass, receives 75% of CO
-Rapidly equilibrates with anesthetic (4-8 min) due to high blood flow and small volume

Front 10

Muscle group

Back 10

Muscle and skin
-1-4hrs to reach equilibrium

Front 11

Fat group

Back 11

-High affinity for anesthetic
-Large fat:blood partition coefficients
-up to 30 hours for equilibrium

Front 12

Vessel poor group

Back 12

Insignificant uptake

Front 13

How do we compensate for anesthetic uptake?

Back 13

1. Increase alveolar ventilation
2. Increased inspired concentration (FI)

Front 14

The lowering of alveolar partial pressure by uptake can be countered by?

Back 14

increasing alveolar ventilation

Front 15

The higher the alveolar ventilation, the more?

Back 15

rapid the "wash in" of anesthetic

Front 16

How can you better maintain alveolar partial pressure?

Back 16

by constantly replacing anesthetic taken up by the pulmonary circulation (most pronounced with higher solubility agents)

Front 17

With the higher soluble anesthetics, is the anesthetic taken up more rapidly?

Back 17

Yes, uptake is higher

Front 18

Increasing the FI not only increases the _______ _______, it also increases the ____ __ ____.

Back 18

alveolar concentration, rate of rise (FA/FI)

Front 19

Overpressuring or concentration effect

Back 19

Increasing the FI to increase alveolar concentration and rate of rise

Front 20

What are 3 factors that govern FI?

Back 20

1. FGF rates
2. Volume of the system
3. Circuit uptake

Front 21

Do the inhaled anesthetics undergo uptake by the anesthesia breathing circuit?

Back 21

Yes (too small to appreciably influence the induction or recovery from anesthesia)

Front 22

What two things affect the amount of rebreathing that occurs?

Back 22

FGF and system volume

Front 23

Inspired gas consists of two gases?

Back 23

1. Gas delivered from the anesthesia machine
2. Gas previously exhaled by the patient

Front 24

Rebreathing occurs when?

Back 24

FGF is less than MV

Front 25

An increase in rebreathing will?

Back 25

lower the inspired concentration

Front 26

How do we eliminate or decrease rebreathing?

Back 26

increase FGF

Front 27

Second gas effect

Back 27

occurs with concomitant administration of N20 and potent inhaled agent

Front 28

The high volume uptake of a gas (N20) will?

Back 28

speed the rate of rise of the alveolar partial pressure of a second gas (potent agent)

Front 29

What is diffusion hypoxia?

Back 29

hypoxia that occurs due to discontinuation of the N2O if air is inhaled instead of 100% oxygen

Front 30

nitrous oxide is how many more times soluble than nitrogen?

Back 30

34x

Front 31

What is a consequence of nitrous oxide?

Back 31

will diffuse into air containing spaced much faster than air will diffuse out

Front 32

With N20, volume is increased in highly compliant spaces, what spaces?

Back 32

bowel, pneumothorax, ETT cuff

Front 33

With N20, pressure is increased in poorly compliant spaces, what spaces?

Back 33

intraocular, pneumocephalus, inner ear

Front 34

Recovery occurs how?

Back 34

reversing the partial pressure gradients present in the body

Front 35

List in order the partial pressures of induction

Back 35

PI>PA>Pa>PBr

Front 36

List in order the partial pressure in emergence

Back 36

PBr>Pa>PA>PI

Front 37

What factors determine the rate of recovery?

Back 37

1. Solubility
2. Alveolar ventilation
3. FGF

Front 38

What does the alveolar ventilation influence?

Back 38

the alveolar-venous partial pressure gradient (want alveolar to be zero)

Front 39

What does the FGF influence?

Back 39

The amount of rebreathing (increase FGF)

Front 40

All potent anesthetics are metabolized by?

Back 40

the liver

Front 41

Which anesthetics are more resistant to hepatic degradation

Back 41

Anesthetics halogenated with fluorine

Front 42

What is a breakdown product of inhaled anesthetics?

Back 42

inorganic fluoride

Front 43

Inorganic fluoride at high serum levels is?

Back 43

Nephrotoxic

Front 44

What anesthetics rarely cause hepatotoxicity? Why?

Back 44

Halothane, isoflurane, desflurane, via an immune-mediated reaction

Front 45

How do inhaled anesthetics (IA) affect myocardial contractility?

Back 45

Cause dose-dependent decreases in myocardial contractility

Front 46

Which agent may produce larger decreases?

Back 46

Halothane

Front 47

What is the proposed mechanism to the decreased myocardial contractility?

Back 47

direct myocardial depression, inhibition of calcium ion influx

Front 48

When does myocardial contractility become profound?

Back 48

at deep levels of anesthesia

Front 49

What increases vulnerability of the myocardium to depressant effects?

Back 49

Cardiomyopathy

Front 50

Myocardial protection and IAs

Back 50

Literature suggests that they exert some degree of myocardial protection during and after myocardial ischemia

Front 51

What 2 agents have been shown to enhance recovery of contractile function of postischemic, reperfused myocardium (stunned myocardium)?

Back 51

Isoflurane and halothane

Front 52

What occurred in the dog model when 1 MAC of des was administered before 60 minute occlusion of the LAD ?

Back 52

decreased infarct size by >15%

Front 53

What does this acceleration of functional recovery occur from?

Back 53

may occur through activation of sarcolemmal or mitochondrial ATP-sensitive potassium channels

Front 54

Ischemic preconditioning

Back 54

phenomenon by which transient myocardial ischemia protects the myocardium against future ischemic episodes
-IAs mimic this action
-probably results from action on ATP-dependant K channels

Front 55

Coronary Steal

Back 55

-areas of ischemia are maximally dilated
-IAs may dilate normal coronary vasculature, "stealing" blood away from ischemic areas

Front 56

SVR

Back 56

Des, Sevo, Iso reduce SVR in a dose-dependent manner
-result is a dose-dependant reduction in MAP

Front 57

HR

Back 57

All IAs attenuate the baroreceptor response to hypotension to some degree

Front 58

Which agent can transiently increase HR?

Back 58

Des, when FI is above 6%

Front 59

Arrythmogenicity

Back 59

Halothane predisposes the heart to ventricular dysrythmias in the presence of epi
-avoid epi doses greater than 1.5 mcg/kg

Front 60

Respiratory effects

Back 60

All IAs produce a dose-dependant depression of alveolar ventilation
- decreased tidal volume - increased dead-space contribution
-Increased RR
-Increased PCO2

Front 61

T or F. IAs cause a decreased response to hypercarbia and hypoxemia

Back 61

T

Front 62

IAs also have this effect on the respiratory system?

Back 62

Potent bronchodilation
-Des irritates the airway at concentrations greater than 6%

Front 63

Hypoxic pulmonary vasoconstriction

Back 63

process by which pulmonary blood flow is directed away from hypoxic alveoli, optimizing gas exchange

Front 64

T or F. There is conflicting literature to whether HPV is abolished by IAs.

Back 64

True

Front 65

IAs and analgesia

Back 65

extremely limited analgesic properties at clinical concentrations

Front 66

IAs and evoked potentials

Back 66

all inhaled agents depress somatosensory evoked potentials
-increased latency and decreased amplitude
Little to no effect on motor evoked potentials

Front 67

Cerebral blood flow

Back 67

all agents decrease cerebral vascular resistance, thereby increasing cerebral blood flow (CBF)

Front 68

IAs and ICP

Back 68

Increase ICP

Front 69

IAs and CMRO2

Back 69

decrease cerebral metabolic oxygen consumption (CMRO2)

Front 70

IAs and amnesia

Back 70

all agents produce amnesia at MAC levels approximating MAC awake (1/3 MAC)

Front 71

Seizures

Back 71

Sevoflurane-most often described with high-dose mask induction with concomitant alveolar hyperventilation
-literature describes both tonic-clonic and focal events
-described in patients with or without prior history of seizure disorder

Front 72

Neuromuscular

Back 72

all IAs produce some degree of skeletal muscle relaxation, potentiate the effects of neuromuscular blocking agents