Inhalational Agents Chapter 9 Nagelhout

Front 1

What does end-tidal volatile inhalant concentration correlate to?

Back 1

Brain anesthetic partial pressures

Front 2

When cerebral vascular resistance decreases, what happens to to CBF, CBV and CSFP?

Back 2

They all increase.

Front 3

What is the normal Cerebrovascular response to CO2

Back 3

Vasoconstrict during hypocarbia

Vasodilate during hypercarbia.

Front 4

What PaCO2 range is desired when attempting to counteract drug induced cerebral vasodilation?

Back 4

30-35 mmHg

Front 5

Which of the three most commonly used inhalational agents produces the MOST reduction in cSSEP?

Back 5

Isofluorane

Front 6

What does end-tidal volatile inhalant concentration correlate to?

Back 6

Brain anesthetic partial pressures

Front 7

When cerebral vascular resistance decreases, what happens to to CBF, CBV and CSFP?

Back 7

They all increase.

Front 8

What is the normal Cerebrovascular response to CO2

Back 8

Vasoconstrict during hypocarbia

Vasodilate during hypercarbia.

Front 9

What PaCO2 range is desired when attempting to counteract drug induced cerebral vasodilation?

Back 9

30-35 mmHg

Front 10

Which of the three most commonly used inhalational agents produces the MOST reduction in cSSEP?

Back 10

Isofluorane

Front 11

What does end-tidal volatile inhalant concentration correlate to?

Back 11

Brain anesthetic partial pressures

Front 12

When cerebral vascular resistance decreases, what happens to to CBF, CBV and CSFP?

Back 12

They all increase.

Front 13

What is the normal Cerebrovascular response to CO2

Back 13

Vasoconstrict during hypocarbia

Vasodilate during hypercarbia.

Front 14

What PaCO2 range is desired when attempting to counteract drug induced cerebral vasodilation?

Back 14

30-35 mmHg

Front 15

Which of the three most commonly used inhalational agents produces the MOST reduction in cSSEP?

Back 15

Isofluorane

Front 16

Which of the 3 most commonly used inhalational agents is most likely to predispose ped and adult patients to epileptic activity?

Back 16

Sevofluorane (even though it suppresses drug-induced convulsive activity)

Front 17

Why can a slow emergence in a neuro patient be devastating?

Back 17

B/c it can make the post-op neuro assmt difficult, result in unnecc. diagnostic and therapeutic intervention and predispose patient to respiratory complications.

Front 18

T/F: All inhalational agents are capable of altering hemodynamics?

Back 18

True

Front 19

T/F: Sevo, Iso, and Des all reduce MAP and CO in a dose dependent fashion?

Back 19

True

MAP dropped by decreasing SVR (Sevo least of all).

Front 20

Does N2O affect MAP?

Back 20

Yes, nitrous actives the SNS and increases SVR--> increased MAP and CVP.

This still occurs even with co-administration of volatiles.

Front 21

Compare the vascular affects of N2O given with volatile inhalants vs opioids.

Back 21

N2O given with inhalants increases SVR and helps support MAP.

N2O given with opioids augments cardiac depression b/c N2O also causes direct negative inotropy.

Front 22

Why would you want to use caution in giving opioids AND N2O to patients with LV dysfx?

Back 22

B/C both these agents have a negative inoptropic effect and can cause cardiac depression.

Front 23

Dl volatile agents and N2O cause changes in HR?

Back 23

Yes.

Front 24

Which inhalant(s) cause the most profound change in HR?

Back 24

Des. But this change in HR can be modulated with fentanyl pretx. (This ^ in HR can be a problem in people with CAD-->myoc isch s/t ^ Myoc-O2 demand.

Iso and Sevo produce only minor increases in HR.

Front 25

What is the result of esmolol administration?

Back 25

Generally, a decrease in HR, but no sig change in MAP.

Front 26

What is coronary steal?

Back 26

reductino in perfusion of ischemic mycardium with simultaneous improvement of blood flow to nonischemic tissue.

Taking blood from the "poor" and "giving to the rich".

Isofluorane is most likely to cause this in hypotensive states. Normotension eases this occurence.

Front 27

When are volatile anesthetics more likely to produce reentry excitations?

Back 27

When fibers of heart are ischemic or injured. (So you would want to be cautious when maintaining a patient with known cardio conduction issues)

Front 28

Which volatile anesthetics are capable of producing bradycardia and disturbances in AV Node?

Back 28

All of them except isoflurane.

Des is not so bad, but still can.

Front 29

Do volatile inhalants cause Sensitazation?

Back 29

The ability of volatile anesthetics to reduce the quantity of catecholamines needed to produce dysrhythmias is often mistakenly called Sensitization.

It would be more accurate to call it an Adverse Drug Reaction.

Front 30

Do barbiturate and ketamine increase or decrease Sensitization?

Back 30

Increase it.

Front 31

What is the danger of patients who are on amiodarone getting a GA (opioid and inhalant)?

Back 31

They can develop sig dysrhythmias (including atropine resistant bradycardia) intra- and post-operatively. Some may even require AV pacing.

Front 32

What is the danger of administering N2O to a patient with pulmonary HTN?

Back 32

N2O causes further increase in PVR

Also, the HPV response to atelectasis is markedly attenuated by N2O

Front 33

How do volatile anesthetics affect the respiratory system?

Back 33

The effect is dose-dependent.

Primarily TV is impacted: responsiveness to CO2 is diminished and TV reduces as concentration of inhalant increases.

With des, iso and sevo & N2O, there is usually a compensatory increase in RR....BUT not sufficient enough to preventt elevations in arterial CO2 tension.

Front 34

What helps overcome respiritory depressant effects of volatiles?

Back 34

Surgical stimulation

Front 35

Why is des not the first choice for mask induction?

Back 35

It is a repiratory irritant - it stinks and makes people cough and gag.

Induce on sevo and change to des for maintenance. Then, if you have to...emerge on sevo.

Front 36

What is the impact of inhalants on renal fx?

Back 36

In general, renal circ remains intact.

SBP drop can lead to drop in GFR.

Des produces least alterations in indices of renal integrity.

Front 37

What variables increase compound A content?

Back 37

Low fresh gas flows

High concentrations of sevo

drying of soda-lime absorbent

Front 38

How do volatile anesthetics impact hepatic blood flow?

Back 38

All of them DECREASE total hepatic blood flow.

BUT iso, sevo and des increase/maintain hepatic artery flow which limits attenuation of hepatic portal vein blood flow.

So...no biggie in normal patients.

Of course, there always exists the rare chance that inhalational agents can cause hepatotoxicity...but what are you gonna do if you have no pre-op indicators it can happen?

Front 39

What is the impact of volatile inhalants on the neuromuscular system?

Back 39

Dose dependent relaxatin of the skeletal muscole & potentiaiton of the effects of NMBDs.

This can lead to some prolonged duration...titrate your inhalational agents carefully.

Front 40

MH???

Back 40

ALL volatile anesthetics can cause MH (Sux can too).

Front 41

What is the tx of MH?

Back 41

IV Dantrolene - 2.5 mg/kg q 5min up to 10 mg/kg.

Front 42

Would you use N2O with a potentially/pregnant pt?

Back 42

No - it is teratogenic.