General anesthesia Dr. Pond Flashcards

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1
Q

What are the factors that need to be fulfilled for anesthesia?

A

-hypnosis - sleep state
-analgesia - pain relief
-amnesia - no memory
-muscle relaxation - no muscle response to pain
-homeostasis - still intact (breathing, heartbeat, life supporting functions)
-> Usually IV or inhalation as a mixture of these

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2
Q

What are the stages of anesthesia?

A
  1. analgesia: pain relief and patient has memory
  2. excitement/delirium: respiration might be irregular, vomitting may occur if the patient is stimulated
  3. surgical anesthesia: respiration gets back to normal, all 5 factors of anesthesia are met
  4. medullary depression: too much -> severe depression of vasomotor center and respiratory center -> can cause death
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3
Q

Examples of complete anesthetics

A

Halothane
Enflurane
Isoflurane
Sevoflurane
Desflurane

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4
Q

What is the Minimal Alveolar Concentration MAC?

A

the alveolar concentration that prevents purposeful movement in 50% of subjects in response to pain stimulus (surgery)

-> need to give 1.2 or 1.3x the MAC

MACs can be additive between drugs -> so if a patient is using an opioid we will need a lower concentration of an anesthetic

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5
Q

What is the MAC of newborns?

A

1.2x the MAC of an adult (30y)

6 month old baby: 1.5x the MAC

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6
Q

What affects the uptake and distribution of inhaled anesthetics in the brain?

A

-Solubility of anesthetic
-Its concentration in inspired air
-The volume of pulmonary ventilation

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7
Q

Which agent will equilibrate the fastest?
EXAM Q

A

the one with the lower blood gas partition coefficient -> less soluble in blood and able to move to the brain, the ones with higher blood/gas coefficient will stay longer in the blood (quicker onset with the lower coefficient)
-infervsley related

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8
Q

How does elimination work compared to uptake and distribution?

A

blood/gas coefficient and elimination are proportional
-> the lower the blood/gas coefficient the slower the elimination???

-mainly eliminated through exhalation

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9
Q

What is the theory about anesthestics introduced by Meyer and Overton?

A

relationship between lipidsolubility (hydrophobicity) and anesthetic potency

in general: the more hydrophobic the more potent

-> theory: anesthetics incorporate into the plasmamembran (lipid bilayer) and stabilize ion fluxes across the membrane (less ion flux -> less action potential firing)

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10
Q

How is Isoflurane thought to affect neuronal activity?

A

in a frequency-dependent manner
-neurons that fire at a higher frequency are more affected by anesthetic action

-cognition and movement require high-frequency action potential neurons

-life supporting functions tend to require low-frequency action potential neurons

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11
Q

How does Isoflurane cause the decrease in neuronal activity?
MOA

A

decrease activation in voltage-gated Ca2+channels on neuron terminals
-> decreased vesicle docking and NT release

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12
Q

How do anesthetics affect mean arterial pressure (MAP)?

A

all anesthtis (except N2O, incomplete anesthetic) decrease the mean arterial pressure

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13
Q

Which chamber of the heart is affected by anesthetics?

A

-inhaled anesthetics increase right atrial pressure bc the heart is not able to pump out blood as much
-> greatest increase with halothane

arryhtmias can occur in patients with cardiac disease

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14
Q

How do anesthetics affect respiratory function?

A

-all (except N2O) decrease tidal volume (amount of intake per breath)
-increase in respiratory rate
-overall decrease in minute ventilation (Tidal volume x respiratory rate)
-> increase in pCO2

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15
Q

How does the body respond to hypoxia that is induced by anesthetics?

A

0.1 MAC: 50-70% decrease in response to hypoxia

at 1.1 MAC: no response to hypoxia

-> we usually use 1.2-1.3x

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16
Q

How do anesthetics affect the pressure in the brain?

A

increase in intercranial pressure

-blood flow is driven by metabolic activity of the brain -> in the case of CNS depression the brain is not as active but the blood supply is still high -> causing an increase in intracranial blood pressure
-> also seen with opioids

-some agents have a risk for seizure:
Enflurane
Sevoflurane

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17
Q

Which anesthetics have a risk for seizure?

A

Enflurane
Sevoflurane

18
Q

Which anesthetic drugs are converted to trifluoroacetate causing hepatoxicity?

A

-Halothane
-desflurane
-isoflurane

19
Q

Which anesthetic drug can cause Nephrotoxicity?

A

Methoxyflurane
-> produces flouride ions when metabolized

Sevoflurane
-> reacts with CO2 absorbents to form “compound
A” -> nephrotoxic

20
Q

Which drug can cause malignant hyperthermia?

A

succinylcholine (muscle relaxant), also anesthetic drugs
-> due to a genetic disorder (regulating Ca2+ release in muscle cells)

-prolonged muscle contraction -> RIGIDITY

-increase in metabolic activity -> Hyperthermia and acidosis

21
Q

What are the symptoms of malignant hyperthermia?

A

-rapid onset of tachycardia and hypertension
-muscle rigidity
-hyperthermia
-acidosis

22
Q

How to treat malignant hyperthermia

A

-dantrolene

-reduce body temp
-restore acid-base balance

23
Q

How does dantrolene work?
MOA

A

it blocks the Ryanodine receptor
-> ryanodine receptor is responsible for Ca2+ influx in muscle cells from the sarcoplasmic reticulum

24
Q

Anesthetic function of Barbiturates

A

-Rapid onset
-sedation, anxiolytic

-With continuous infusion,
decrease MAP and CO (cardiac output)

25
Q

ADE - Barbiturates and respiratory depressants

A

-transient apnea
-lowered sensitivity to pCO2

26
Q

Anesthetic function of Benzos

A

-sedation
-anxiolytic
-amnestic properties

-No analgesia
-insufficient muscle relaxation

27
Q

Which drug can be used to cause sedation, and reduce anxiety and amnesia?

A

Benzos

Diazepam (t1/2 = 43 hr)
midazolam (t1/2= 2 hr)

No analgesia, insufficient muscle relaxation

28
Q

Which drug is used to accelerate recovery from Benzodiazepines?

A

Flumazenil
-> Benzodiazepine antagonist

29
Q

Which drug is used to produce an analgesic effect in anesthesia?

A

opioids
-Morphine
-fentanyl
-sufentanil

-No muscle relaxation
-No amnesia

mu receptor agonists

30
Q

Role of Etomidate

A

-Non-barb. hypnotic

-rapid action

-> sedation
-> No analgesia

-Minimal cardiovascular and respiratory depression
-> beneficial in patients with CV disease

31
Q

Which receptor is targeted by Etomidate?

A

acts on GABA(A) receptor -> increases frequency of Cl(-) channel opening -> INHIBITORY

32
Q

ADE Etomidate

A

-myoclonic activity (muscle jerks)
-nausea after surgery
-avoid prolonged sedation due to adrenal steroidogenesis inhibition

33
Q

Which receptor is targeted by Propofol/Fospropofol?

A

-act on GABA(A) receptor

-Rapid action with more rapid recovery

34
Q

How does Propofol affect BP and respiratory function?

A

-reduces BP by dcreasing vascular resistance

-causes respiratory depression

35
Q

How does Propofol affect cerebral blood flow and intracranial pressure?

A

-reduces cerebral blood flow

-reduces metabolic rate

-decrease intracranial pressure

36
Q

Which drug can cause Adrenal steroidogenesis inhibition with prolonged use?

A

Etomidate

37
Q

Which receptor is targeted by Ketamine?

A

NMDA receptor -> acts as an agonits

may also target opioid receptors

38
Q

How does Ketamine affect cardiac function?

A

-increases HR, MAP, and CO
(stimulation of the sympathetic nervous system)

39
Q

How does Ketamine affect cerebral blood flow and intracranial pressure?

A

increase in cerebral blood flow

increase in intracranial pressure

40
Q

How does Ketamine affect respiratory function?

A

decrease in respiratory rate