Module B-2 Flashcards

1
Q

Induces the least cerebral vasodilation of inhaled anesthetics making it preferred agent for neurosurgical patients with elevated ICP

A

Sevoflurane

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2
Q

Coronary steal

A

Blood flow distal to a fixed, atherosclerotic lesion would decrease when the surrounding, normal vasculature dilated in response to Isoflurane, triggering ischemia

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3
Q

Inhalation consideration with pregnancy

A

Nitrous oxide is teratogenic

Volatile agents decrease smooth muscle tone-maintaining uterine tone is critical for postpartum hemostasis so volatile agents are minimized0 less than 0.5 MAC Sevoflurane and 1.0 Desflurane

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4
Q

Relationship between CMRO2 and CBF and impact of inhaled anesthetics

A

Cerebral metabolic rate of oxygen consumption and cerebral blood flow are typically coupled, as one increases the other increases.

However, IAs induced a dose dependent cerebral vasodilation (increase CBF) and a decrease in the CMRO2- we call this an uncoupling

-nitrous increases CMRO2 and CBF

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5
Q

Cerebral hypocapnia

A

Vasoconstrict

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6
Q

Cerebral vasculature hypercarbia

A

Vasodilate

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7
Q

Calcium and Inhaled anesthetics

A

Reduce intracellular free calcium in cardiac and vascular smooth muscle!!

End result is depression of contractile state of the myocardium and peripheral vasodilation

This is probably why giving calcium is cardio protective

Mechanism pg 88 Nagelhout

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8
Q

Explain increase in HR with inhaled anesthetics

A
  1. Trigger sympathetic response
  2. Baroreceptor reflex
  3. Antagonism of SA node automaticity
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9
Q

Arrhythmias and Inhaled Anesthetics

A

All three can lead to Bradycardia(Sevoflurane) and prolonged QTc, which can lead to torsades which is a polymorphic ventricular tachycardia

Bonus: Likely due to interruption of cardiomyocyte repolarization via inhibition of K+ through hERG channels

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10
Q

Cardiovascular effect of Nitrous oxide

A

Increase in SVR and HR but a decrease in CO

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11
Q

IA impact on Respiratory system

A

Lower tidal volumes
Higher Respiratory Rate

not enough to prevent elevations in CO2 but surgical stimulation aids with this

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12
Q

IA biotransformation rates:

A

Sevoflurane 5-8% —initially caused concern for
Everything else in trace amounts

Primarily hepatic etabolism via P450 oxidation

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13
Q

Problems with Nitrous

A

Inactivation of B12 cofactor for methionine synthase which may inhibit DNA synthesis and have teratogenic & immunosuppressive effects

Watch for cobalamin deficiency!!

DO NOT USE IN PULM HTN

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14
Q

Number of fluorine atoms on modern IA’s

A

Isoflurane- 5
Desflurane- 6
Sevoflurane- 7

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15
Q

Impact of Halogenation

A

-Flammability-reduced
-Chemical Stability-enhanced
-Arrhythmogenic potential- increased
-Potency- increased
-Biotransformation

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16
Q

Vapor Pressure, which has the highest?

A

Desflurane
The pressure were your liquid is in equilibrium with the surrounding gas in a given volume at an established pressure.
Molecules that want to evaporate with have a higher vapor pressure- due to low molecular weight/high kinetic energy/low intermolecular forces

17
Q

Modern “MOA” for Inhaled Anesthetics

A

Multiple and diverse targets that contribute to unconsciousness, amnesia, analgesia, and immobility,
-impact brain and spinal cord in a dose dependent manner

18
Q

Area of action and impact of IA’s in general

A

Immobility- spinal cord
Analgesia- spinothalamic tract
Unconsciousness- Cortex, thalamus, brainstem
Amnesia- Amygdala, hippocampus

19
Q

Common values for MAC-Awake and MAC-BAR

A

0.3
1.6

20
Q

What increases MAC??

A

High CNS Metabolic activity
Neurotransmission
Red hair lol

21
Q

What decreases MAC

A

CNS metabolic activity and neurotransmission
Concurrent administration of other drugs
Age

22
Q

Advantages/concerns of Nitrous

A

Rapid uptake/elimination
Odorless
Mild analgesic-NMDA

Air filled spaces
Toxic effects
PONV/environmental effects

23
Q

Why is NItrous a problem in air filled spaces

A

More soluble than N2- both attracted to gas phase and accumulate in cavities but N2O diffuses in faster than N2can be displaced out (34xfaster)

24
Q

N2O problematic air spaces:

A

Pneumothorax
Air emboli
Bowel
Pneumoperitoneum
Intraocular air bubbles
Equipment cuffs

25
Q

Why do we avoid IA’s while monitoring evoke potentials

A

They decrease amplitude and increase latency

Amplitude-strength of nerve response
Latency- speed of conduction

26
Q

Nitrous cardiovascular impact

A

Increase in SVR and HR due to SNS activation
-can be given with other agents to support MAP

27
Q

Preconditioning (cardiovascular)

A

Mimics myocardial injury which triggers cascade of intracellular events that ends up being cardio protective for future events

28
Q

Goal of HPV

A

Hypoxia pulmonary vasoconstriction diverts blood flow to areas of lung with greater ventilation in order to improve arterial oxygenation

-inhibited by volatile agents

29
Q

What do we avoid in Pulmonary hypertension?

A

Nitrous Oxide- it increases pulmonary vascular resistance

30
Q

Inhaled Anesthetics impact on Ventilation

A

Decrease Tidal Volume
Increase Respiratory rate
Impairs hypercarbia ventilatory response
Impairs hypoxic ventilatory drive

31
Q

What contributes to Formation of compound A??

A

Low flow of Sevoflurane (less than 2L)
Older/early generation CO2 absorbents
Desiccated CO2 Absorbents

32
Q

What is safe for Malignant Hyperthermia?

A

Nitrous Oxide and complete IV anesthetic

Minus Succ?

33
Q

Neuromuscular considerations

A

-Additive effect with muscle relaxants
-Dosages of muscle relaxants are decreased by 25-50%
-Prolonged recovered compared to TIVA (Total IV anesthetic)

34
Q

Why do we not run low flow sevo (<1-2L/min)

A

Compound A- nephrotoxicity