_Nitrous Oxide:_ Blood/gas coefficient: Fat/blood coefficient: Mechanism of action: Flammable? CV effects (including effect on PVR): Changes to RR, Vt and MV: Changes in respiratory drive: Effects on ICP and CMRO2: Effect on renal and hepatic blood flow: Effect on muscle tone: Is it an MH trigger? Is it safe in pregnancy? One common side effect: Two adverse effects of prolonged exposure:

_Nitrous Oxide:_ Blood/gas coefficient: 0.47 Fat/blood coefficient: 2.3 (low) Mechanism of action: Inhibits NMDA receptors Flammable? : Nonflammable, but supports combustion like O2 CV effects (including effect on PVR): Direct myocardial depressant + increases sympathetic tone = Fairly unchanged HR, BP and CO, but may increase slightly. Unless pt has CAD or is hypovolemic. Increases PVR. Changes to RR, Vt and MV: RR increases, Vt decreases (rapid, shallow breathing) - result is minimal change in MV Changes in respiratory drive: Hypoxic drive is markedly reduced Effects on ICP and CMRO2: Mild increase in ICP and increases CMRO2 Effect on renal and hepatic blood flow: Decreases both Effect on muscle tone: No muscle relaxation per se, but potentiates. At high concentrations in hyperbaric chambers, can cause rigidity. Is it an MH trigger? Nope. Is it safe in pregnancy? It is possibly teratogenic so should be avoided before the 3rd trimester. One common side effect: N/V Two adverse effects of prolonged exposure: Inhibits Vitamin B12-dependent enzymes, so prolonged exposure can cause bone marrow depression (megaloblastic anemia) and peripheral neuropathies.

1. What is the site of inhibition of motor responses by volatile anesthetics? 2. Is MAC affected by the duration of anesthesia and how?

1. The spinal cord 2. No it is not.

_Halothane:_ Hemodynamic effects: Effect on coronary blood flow specifically? Effect on oxygen demand: Effect on renal and hepatic blood flow:

_Halothane:_ Hemodynamic effects: Direct myocardial depressant No effect on SVR Dose-dependent decrease in BP Increases right atrial pressure Blunts the baroreceptor reflex so the HR drops too Effect on coronary blood flow specifically? Decreases coronary blood flow because of the overall drop in BP, even though it is a coronary vasodilator Effect on oxygen demand: Oxygen demand decreases Effect on renal and hepatic blood flow: Decreases both.

Ch. 8: Inhalational Anesthetics Flashcards by Kristen Biefer

Methoxyflurane: Is metabolized to ___________ which can cause this adverse effect: ___________.

Solubility:

Vapour pressure:

Type of compound:

Methoxyflurane: Is metabolized to fluoride which can cause this adverse effect: renal failure.

Solubility: High

Vapour pressure: Low

Type of compound: Halogenated

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Induction and emergence with methoxyfluorane is ________ (fast or slow?)

Why? (2 reasons)

Induction and emergence with methoxyfluorane is slow.

Why?

Low vapour pressure
High solubility

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Discuss the solubility of Nitrous Oxide.

Relatively insoluble compared with other agents
But, compared to Nitrogen, nitrous oxide is 35x more soluble in blood. Therefore, it tends to diffuse into air-containing cavities such as bowel obstruction, pneumothorax, air emboli, tympanic membranes, and ETT cuffs.

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Nitrous Oxide:

Blood/gas coefficient:
Fat/blood coefficient:
Mechanism of action:
Flammable?
CV effects (including effect on PVR):
Changes to RR, Vt and MV:
Changes in respiratory drive:
Effects on ICP and CMRO2:
Effect on renal and hepatic blood flow:
Effect on muscle tone:
Is it an MH trigger?
Is it safe in pregnancy?
One common side effect:
Two adverse effects of prolonged exposure:

Nitrous Oxide:

Blood/gas coefficient: 0.47
Fat/blood coefficient: 2.3 (low)
Mechanism of action: Inhibits NMDA receptors
Flammable? : Nonflammable, but supports combustion like O2
CV effects (including effect on PVR): Direct myocardial depressant + increases sympathetic tone = Fairly unchanged HR, BP and CO, but may increase slightly. Unless pt has CAD or is hypovolemic. Increases PVR.
Changes to RR, Vt and MV: RR increases, Vt decreases (rapid, shallow breathing) - result is minimal change in MV
Changes in respiratory drive: Hypoxic drive is markedly reduced
Effects on ICP and CMRO2: Mild increase in ICP and increases CMRO2
Effect on renal and hepatic blood flow: Decreases both
Effect on muscle tone: No muscle relaxation per se, but potentiates. At high concentrations in hyperbaric chambers, can cause rigidity.
Is it an MH trigger? Nope.
Is it safe in pregnancy? It is possibly teratogenic so should be avoided before the 3rd trimester.
One common side effect: N/V
Two adverse effects of prolonged exposure: Inhibits Vitamin B12-dependent enzymes, so prolonged exposure can cause bone marrow depression (megaloblastic anemia) and peripheral neuropathies.

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Enflurane:

Type of compound:

Flammable?

Pungent?

CV effect:

Two unique things:

Enflurane:

Type of compound: Halogenated ether

Flammable? No

Pungent? No

CV effect: Myocardial depressant

Two unique things:

Risk of seizures
Decreases CSF production

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Xenon:

Mechanism of action:

Metabolism:

Toxicity level:

Blood solubility:

MH trigger?

2 other advantages:

2 disadvantages:

Xenon:

Mechanism of action: Inhibits NMDA receptors

Metabolism: Likely none (inert)

Toxicity level: Likely none (inert)

Blood solubility: Low

MH trigger? No.

2 other advantages: Environmentally friendly and has little effect on CV, hepatic or renal systems.

2 disadvantages: Expensive and low potency (MAC = 70%)

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In terms of MAC, what equals the ED₅₀ and the ED₉₅?

How much MAC equals MAC awake?

(What is the MAC awake?)

ED₅₀ = 1 MAC

ED₉₅ = 1.3 MAC

MAC awake = 0.3-0.4 MAC*

*when the only anesthetic agent onboard is the inhaled anesthetic

MAC awake = the MAC at which the pt awakens from anesthetic.

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MAC of common agents:

Nitrous Oxide:

Halothane:

Isoflurane:

Sevoflurane:

Desflurane:

MAC of common agents organized by potency going up:

Nitrous Oxide: 105%

Desflurane: 6.0%

Sevoflurane: 2.0%

Isoflurane: 1.2%

Halothane: 0.75%

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For each decade of age, MAC decreases by how much?

For each 1^oC drop in temperature below 37^oC, how much does MAC increase or decrease by?

6% decrease per decade of age

15% decrease per 1^oC drop below 37^oC

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What effect does hyperthermia have on MAC?

It decreases it, just like hypothermia.

Exception: if the temperature is over 42^oC, then the MAC actually increases.

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What is the site of inhibition of motor responses by volatile anesthetics?
Is MAC affected by the duration of anesthesia and how?

The spinal cord
No it is not.

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Effects of the following on MAC:

Hypoxemia:

Hypercarbia:

Thyroid disease:

Pregancy (And by how much? When does it return to normal?):

Hypercalcemia:

Hyponatremia:

Hypernatremia:

Effects of the following on MAC:

Hypoxemia: decreases

Hypercarbia: decreases

Thyroid disease: has no effect on MAC

Pregancy (and by how much?): Decreases. By 1/3 at 8 wk’s gestation. Back to normal by 72h postpartum.

Hypercalcemia: decreases

Hyponatremia: decreases

Hypernatremia: increases

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Halothane:

Hemodynamic effects:
Effect on coronary blood flow specifically?
Effect on oxygen demand:
Effect on renal and hepatic blood flow:

Halothane:

Hemodynamic effects:
- Direct myocardial depressant
- No effect on SVR
- Dose-dependent decrease in BP
- Increases right atrial pressure
- Blunts the baroreceptor reflex so the HR drops too
Effect on coronary blood flow specifically? Decreases coronary blood flow because of the overall drop in BP, even though it is a coronary vasodilator
Effect on oxygen demand: Oxygen demand decreases
Effect on renal and hepatic blood flow: Decreases both.

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Halothane:

Effect on RR, Vt and MV:

Effect on drive to breath:

Effect on resting PaCO2:

2 other effects on the pulmonary system:

Halothane:

Effect on RR, Vt and MV: Increases RR, decreases Vt and overall effect on MV: decreases it.

Effect on drive to breath: Decreases the hypoxic drive to breath severely, even at low doses. Increases the apneic threshold.

Effect on resting PaCO2: Increases it

2 other effects on the pulmonary system: Potent bronchodilator; not through B-agonism but through Ca++ inhibition. Secondly, depresses mucous clearance.

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Discuss using halothane for a pheochromocytoma.

Bad idea to use halothane for a pheo.

Reason: Halothane sensitises the myocardium to the arrythmogenic effects of epinephrine.

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Halothane Hepatitis

Incidence:

Pathophysiology:

Clinical characterized by:

Fatality rate:

Halothane Hepatitis

Incidence: 1 / 35,000

Pathophysiology: The 1^ometabolite of halothane is trifluoroacetic acid, produced through its usual oxidative metabolic pathway. This metabolite binds liver proteins, and in susceptible individuals, antibodies are formed to this metabolite-protein complex. This mediates Type II toxicity (fulminant hepatic necrosis).

Clinical characterized by: Fever, jaundice, and grossly elevated serum transaminase levels.

Fatality rate: 50%

Halothane Hepatitis:

Risk factors:

Can prophylax against with:

Not the same as this other type of hepatotoxicity:

Halothane Hepatitis:

Risk factors:

Multiple halothane anesthetics at short intervals
Middle age, obese females
Familial or PMHx of same

Can prophylax against with: Disulfiram (antabuse)

Not the same as this other type of hepatotoxicity: Type I hepatotoxicity, also associated with halothane. Relatively common (up to 25-30% of pts who receive halothane). Get mild, transient elevations in serum transaminases. Don’t get jaundice or clinically evident hepatocellular disease. Probably caused by reductive (anaerobic) biotransformation of halothane instead of the normal oxidative pathway.

Halothane

Effect on cerebral autoregulation:

Effect on CBF and CMRO2:

Does it trigger MH?

Effect on muscle tone:

Halothane:

Effect on cerebral autoregulation: Blunts it

Effect on CBF and CMRO2: Increases CBF and decreases CMRO2

Does it trigger MH? You bet! (think halothane contracture test)

Effect on muscle tone: Both relaxes skeletal muscle and potentiates nondepolarizing NMBDs

Halothane:

Soluble or not?

Blood/gas coefficient:

Fat/blood coefficient:

Discuss its elimination from the body as compared to iso:

Type of compound:

Flammable?

Halothane:

Soluble or not? Pretty soluble.

Blood/gas coefficient: 2.4

Fat/blood coefficient: 60

Discuss its elimination from the body as compared to iso: Halothane is eliminated faster than isoflurane even though isoflurane is less soluble because halothane undergos greater biotransformation.

Type of compound: Halogenated hydrocarbon

Flammable? No.

Desflurane:

Blood/gas coefficient:
Fat/blood coefficient:
Vapour pressure: ____ which is pretty _____ (high/low)
At high altitude, it:

Desflurane:

Blood/gas coefficient: 0.42
Fat/blood coefficient: 27
Vapour pressure: 681 mmHg which is pretty high (high/low)
At high altitude, it: boils, baby!

Desflurane:

Effects on hemodynamics:
Effects on RR and Vt:

Desflurane:

Effects on hemodynamics:
- HR, CVP and PA pressures all moderately increase
- Rapidly increasing concentrations increase catecholamines and HR
Effects on RR and Vt: RR increases, Vt decreases

Desflurane:

Effect on CBF, CMRO2 and ICP:
Effect on muscle tone:
How is it metabolized?

Desflurane:

Effect on CBF, CMRO2 and ICP:
- CBF increases
- CMRO2 decreases
- ICP increases
Effect on muscle tone: Potentiates NMBDs
How is it metabolized? Metabolism is minimal

Discuss two things about desflurane desiccation by CO₂ absorbent.

It gets degraded into carbon monoxide
Be sure to use calcium hydroxide as the CO₂ absorbent

In Pediatrics, desflurane has been associated with ____________ in some studies

Emergence delirium

_Sevoflurane_ * Blood/gas coefficient: * Fat/blood coefficient: * Type of compound: * Cerebral effects? * Neuromuscular effects? * Renal & hepatic effects?

_Sevoflurane_ * Blood/gas coefficient: **0.65** * Fat/blood coefficient: **48** * Type of compound: **Fluronated ether** * Cerebral effects? **Uncouples CBF and CMRO2 (increases CBF and decreases CMRO2)** * Neuromuscular effects? **Relaxes muscle and potentiates NMBDs** * Renal & hepatic effects? **Decreases blood flow**

_Sevoflurane_ * Hemodynamic effects?

* Moderate decrease in myocardial contractility * Decrease in SVR and BP but slightly less than iso and des * Can prolong the QT interval

Discuss the degree of metabolism that sevoflurane undergos compared to halothane, isoflurane and desflurane. Discuss its metabolism in general.

* Much less metabolism than halothane * But 10-25x more metabolism than iso/des * Increases in fluoride occurs in 7% of pts * But not associated with renal failure

Sevoflurane and Compound A; what's the deal? What things increase its production?

* Compound A is produced by sevoflurane interacting with CO₂ absorbents; EXCEPT Ca⁺⁺ hydroxide. In theory could lead to renal failure, but has not born out in practice. * Production increases with low-flows, dry barium hydroxide, long anesthetics and high concentrations.

_Isoflurane:_ * Blood/gas coefficient? * Fat/blood coefficient? * Type of compound? Related to? * Pungent? * Flammable?

_Isoflurane:_ * Blood/gas coefficient? **1.4** * Fat/blood coefficient? **45** * Type of compound? Related to? **Fluronated ether. And, isomer of enflurane.** * Pungent? **Yes!** * Flammable? **No**

_Isoflurane_ * Effect on muscle tone? * Effect on renal/hepatic blood flow? * Discuss its metabolism.

_Isoflurane_ * Effect on muscle tone? **Relaxes skeletal muscle like sevo & des** * Effect on renal/hepatic blood flow? **Decreases** * Discuss its metabolism. **Just like sevo, it's metabolized to _trifluroacetic acid_, and fluoride levels may increase. However, no evidence of renal damage.**

_Isoflurane_ * CV effects? * Effects on coronaries?

CV effects: * Minimal LV depression! (unique...) * Baroreceptor reflex remains intact and HR increases (unlike halothane) * Mild B1 stimulation * Rapid increases in concentration increase HR, BP and norepinephrine (similar to des) Effects on coronaries: * Coronary vasodilator but not as much as NTG or adenosine * In theory could cause coronary steal, but not so much in practice

_Isoflurane_ * Effects on the pulmonary system? * Effect on CBF and ICP?

_Isoflurane_ * Effects on the pulmonary system? * Irritating to the upper airways but bronchodilates * Causes less tachypnea than other volatiles and MV decreases * Effect on CBF and ICP? * When MAC \> 1, CBF increases and ICP increases. Reversed by hyperventilation.