General Anesthetic Flashcards

1
Q

What leads to higher potency in inhalatioal aneshtetics?

A

Lipid solublity determines potency

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2
Q

What do inhalational anesthetics work on for its effects?

A

GABAa receptors which are Cl- channesl to produce an IPSP

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3
Q

Is there an antidote for inhaled anesthetics?

A

No

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4
Q

What influences potency and the MAC level for inhaled anesthetic?

A

Age, Temperature, Medicine

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5
Q

What happens with increased cardiac output with inhaled anesthetics?

A

Slower induction of effects

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6
Q

What is Fa/Fi?

A

End Tidal Partial Pressure (aka brain partial pressure)/Inspired concentration

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7
Q

What do we measure to get the measurement of the inhaled drug in the pt?

A

Measure hte expiratory concentration of anesthetic

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8
Q

What determines the anestheic uptake into blood after delivery to alveoli?

A

Solubility
Partial Pressure Difference
Cardiac Output

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9
Q

Whichis imore soluble in blood halothane or NO?

A

Halothane is very soluble in blood

NO is not soluble

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10
Q

Why does halothane take a long time to reach equilibrium?

A

Halothane likes to be in blood- > blood can thus hold halothane as it diffuses throuhg -> longer time to reach eqiulibrium

Thus it takes longer to spill over into brain as well than NO

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11
Q

What a does a lamda value indicate?

A

Blood/Gas Partition coefficient

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12
Q

What is solubility?

A

How much a gas diffuses from alveoli into arterial blood

More soluble gas will take longer to equlibriate due to rapid solubilization into blood

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13
Q

Which organs do the inhaled anesthetics reach first?

A

BHLK: Brain Heart Lung Kidneys which are vessel rich organs

Then skin and muscle

Last: Fat

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14
Q

How does increased C.O decrease induction?

A

Increased blood flow near alveolus slows equilibrium due to increased uptake of anesthetics -> brain concentration takes longer time to reach equilibrium now if heart rate is higher

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15
Q

How do pts emerge from the anesthetics?

A

Turn off gas and give 100% oxygen or extubate to protect airway

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16
Q

What are hte side effects of general anesthetics?

A

Decreases Cardiact output and O2 consumption
Decreased vascular resistance (vasodilations)
Increased blood flow to brain but decreased CMRO2 (cerebral metabolic rate of O2 ) => uncoupling

17
Q

Which anesthetic has hte most rapid onset and recovery?

A

Sevoflurane

18
Q

Which anesthetics have a medium rate of onset and recovery?

A

Isoflurane
Enflurane
Halothane

19
Q

Which anestheic is an incomplete anesthetic?

A

NO

20
Q

What is propofol?

A

IV anesthetic agent

Can be used to maintain anesthetic to keep pts asleep

21
Q

How does propofol work?

A

IPSP via gaba receptor

22
Q

What are the effects of propofol?

A

Decreased CMRO2 and ICP in brain
Veno/Vasodilation
Respiratory Depression

23
Q

What is thiopental?

A

Barbiturate using GABA

Not avilable in US

24
Q

What are the effects of thiopental?

A

Decreased CMRO2 and Vasoconstriction

25
Q

What is ketamine?

A

NMDA receptor antagonist for dissociative anesthesia (Pt looks awake despite being asleep)

26
Q

What is ketamine used for?

A
Induction and short procedures
Pain Control
Keep breathing (Bronchodilator) and does not decrease respiratory drive
27
Q

What are the effects of ketamine?

A

Increased CMRO2, Cerebral blood flow and ICP

Inc BP and HR

28
Q

What are hte indications for ketamine?

A

Trauma

Asthma

29
Q

What is Etomidate?

A

GABA receptor agonist anesthetic with the least CV side effects

30
Q

What are the effects of Etomidate?

A

Vasoconstrictor and dec CMRO2

Decreased adrenal -> dec NE -> body response to stress ddecreased