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Pharmacology Test 2 Material > General Anesthesia > Flashcards

General Anesthesia Flashcards

(32 cards)

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1
Q

What is general anesthesia?

A

A pharmacologically induced state of amnesia, unconsciousness, skeletal muscle relaxation, and reduction of autonomic responses

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2
Q

What is altered with medically induced loss of consciousness?

A

Medically induced loss of consciousness (mLOC) causes a breakdown in the signaling between brain regions (macro scale) and altered signaling between neurons (microscale)

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3
Q

What are the five phases of an anesthesia?

A 
Preoperative: eval, H&P, anxiolysis
Induction
Maintenance: during procedure
Emergence: reverse or let medications wear off
Postoperative: PACU
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4
Q

What is the goal preoperatively? What types of meds are used for this?

A

Anxiolysis; Benzodiazepines

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5
Q

Diazepam

  1. Use
  2. Mechanism of action
  3. Half life
A
  1. Sedation, anxiolysis, muscle relaxation, ANTEROgrade amnesia **No analgesic properties
  2. facilitates the action of GABA at the a subunit –> enhanced opening of Cl- channels causing hyper polarization of the membrane–> resistant to excitation
  3. 21-37 hrs
    * *least potent
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6
Q

Midazolam

  1. Use
  2. Mechanism of action
  3. Half life
A
  1. Sedation, anxiolysis, muscle relaxation, ANTEROgrade amnesia **No analgesic properties
  2. facilitates the action of GABA at the a subunit –> enhanced opening of Cl- channels causing hyper polarization of the membrane–> resistant to excitation
  3. 1-4 hrs
    * *medium potent
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7
Q

Lorazepam

  1. Use
  2. Mechanism of action
  3. Half life
A
  1. Sedation, anxiolysis, muscle relaxation, ANTEROgrade amnesia **No analgesic properties
  2. facilitates the action of GABA at the a subunit –> enhanced opening of Cl- channels causing hyper polarization of the membrane–> resistant to excitation
  3. 10-20 hrs
    * *most potent
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8
Q

Propofol

  1. Use
  2. Mechanism of action
  3. Termination of action
A
  1. Induction of anesthesia and general anesthesia
  2. Presumed interaction with GABA; delays the dissociation of GABA from receptors –> hyperpolarization of cell membranes
  3. Tissue uptake and redistribution causes termination of action, not metabolism
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9
Q

Propofol

  1. CV effects
  2. Pulmonary effects
  3. CNS effects
A
  1. Decreased SBP, MAP, SVR (no change HR)
  2. RR depression is dose dependent
  3. Decreased CBF, ICP and CMRO2
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10
Q

Etomidate

  1. Use
  2. Mechanism of action
A
  1. Induction of anesthesia
  2. Rapid onset of sleep and awakening from assumed enhanced GABA effects

**Myoclonus and adrenal suppression; increased PONV

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11
Q

Etomidate

  1. CV effects
  2. Pulmonary effects
  3. CNS effects
A
  1. If low volume or pain/anxiety causing higher blood pressure or HR, can caused decreased BP and HR, otherwise no change. No change or decreased SVR
  2. Minimal respiratory depression
  3. Decreased CBF, ICP, CMRO2
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12
Q

Ketamine

  1. Use
  2. Mechanism of action
A
  1. Induction of anesthesia, adjunct analgesic
  2. NMDA, interaction with opiod, monoaminergic, muscarinic receptors and voltage gated Ca++ channels

**Emergence delirium

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13
Q

Ketamine

  1. CV effects
  2. Pulmonary effects
  3. CNS effects
A
  1. Increased BP, HR and SVR
  2. No respiratory depression
  3. Increased CBF, ICP, CMRO2 **don’t give for neuro surgery
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14
Q

Barbiturates

  1. Use
  2. Mechanism of action
A
  1. Induction of anesthesia
  2. Interacts with GABAa receptor

**contraindicated in patients with Acute Intermittent Porphyria

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15
Q

Barbiturates

  1. CV effects
  2. Pulmonary effects
  3. CNS effects
A
  1. Decreased BP, Increased HR, Decreased SVR
  2. Rapid and profound respiratory depression, apnea
  3. Decreased CBF, ICP, CMRO2
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16
Q

Dexmedetomidine

  1. Use
  2. Mechanism of action
Study These Flashcards
A
  1. Premedication, MAC, Maintenance of GA

2. Nonselective a2 agonist causing sedation and analgesia

17
Q

Dexmedetomidine

  1. CV effects
  2. Pulmonary effects
  3. CNS effects
Study These Flashcards
A
  1. Decreased HR and SVR (indirectly CO, SBP and contractility as well)
  2. Similar to natural sleep (decreased minute ventilation but maintains CO2 response)
  3. Unknown, maybe some neuroprotection
18
Q

Volatile Anesthetics

  1. General properties
  2. Mechanism of action
Study These Flashcards
A
  1. Absence of flammability, vapors at room temperature, potent, low solubility in blood with minimal tissue metabolism
  2. Inhibiting glutamate (excitatory NT) and enhancing GABA (inhibitory NT) produces amnesia, sedation, hypnosis and muscle relaxation
19
Q

Why are volatile anesthetics fluorinated?

Study These Flashcards
A
  1. Reduce or eliminate toxicity
  2. Reduce or eliminate flammability
  3. Increased speed of induction and recovery from anesthesia
20
Q
  1. What is solubility?
  2. What molecules cause anesthesia?
  3. How does solubility effect wake up?
Study These Flashcards
A
  1. Solubility is how much of the anesthetic agent soaks into bodily tissues
  2. Only free, gaseous anesthetic molecules cause anesthesia
  3. The more soluble an anesthetic, the slower the onset and the slower the wake up

**Smaller coefficients (low solubility) move in and out of tissues faster and make for faster induction and wakeup

21
Q
  1. What is Dalton’s law of Partial Pressure?

2. How does this relate to inhaled anesthesia?

Study These Flashcards
A
  1. The total pressure in a mixture of gasses is the sum of the partial pressures of each gas
  2. The partial pressure of anesthesia in the lungs (PAlveoli) equilibrates with the partial pressure in the blood (Parterial) which equilibrates with the partial pressure in the brain (Pb)–> causes anesthetic level
22
Q

What is MAC? How is this number used?

Study These Flashcards
A

MAC is the partial pressure (Vol%) of an anesthetic that must be present in the brain to result in general anesthesia (hypnosis)
It is used to compare anesthetics to each other

23
Q
  1. What is MAC incision?
  2. What is MAC awake?
  3. What is MAC BAR?
Study These Flashcards
A
  1. Level of anesthesia at which 50% of the patients will not move to a surgical stimulus = 1MAC
  2. Proportion of MAC at which patients will wake up and follow commands = .4MAC
  3. Blunting of autonomic responses: very deep level of anesthesia at which patients show no CV response (BP or HR) in response to stimulation = 1.3MAC
24
Q

Are MACs additive?

25
Isoflurane 1. MAC 2. Blood/gas coefficient 3. Side effects
1. 1.15 2. 1.4 --> slower onset/wakeup 3. Myocardial depression, dose dependent hypotension, mild negative cardia chronotrope *BUT may elicit tachycardia due to baroreceptor response **somewhat irritating to breath
26
Desflurane 1. MAC 2. Blood/gas coefficient 3. Side effects
1. 6 (less potent, need more) 2. .42 --> very fast onset/wakeup 3. Direct SNS stimulant: tachycardia and HTN, with minimal myocardial depression **VERY irritating to breath
27
Sevoflurane 1. MAC 2. Blood/gas coefficient 3. Side effects
1. 2.0 2. .69 --> fast onset/wakeup 3. Minimal myocardial depression **Non-irritating to breath
28
Nitrous Oxide 1. MAC 2. Blood/gas coefficient 3. Side effects
1. 105 (can't be sole anesthetic) 2. .47 3. Minimal side effects; Expands rapidly in closed air spaces: SBO and tension pneumas expand **Non-irritating to breath
29
What are the pulmonary effects of all potent inhaled anesthetics?
Decreased tidal volume, increased RR, decreased residual oxygen in the lungs at the end of expiration and bronchodilate **Depress ventilatory response to hypercapnia at .2MAC and attenuate the ventilatory response to hypoxia at .1MAC
30
What are the cardiovascular effects of all potent inhaled anesthetics?
Decreased myocardial contractility, SBP, SVR and chronotropy potentially resulting in hypotension... This hypotension then commonly causes tachycardia due to the baroreceptor response
31
What are the neurological effects of all potent inhaled anesthetics?
Increase cerebral blood flow and ICP while decreasing the CMRO2 (cerebral rate of oxygen metabolism)
32
Malignant Hyperthermia 1. What is it? 2. What can trigger it? 3. How is it treated?
1. Genetically inherited disease that trigger hyper metabolism in skeletal muscles. This causes overproduction of CO2, a critical rise in body temperature and fatality if not immediately treated 2. Succinylcholine, volatile anesthetics 3. Dantrolene sodium

Pharmacology Test 2 Material (10 decks)

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