IV Anesthetics Flashcards

1
Q

How does anesthesia work?

A

No idea. Macroscopic: transmission disrupted throughout CNS, decerebration does not alter requirements. Microscopic: Axonal disruption needs higher concentration than synaptic disruption, blockage of excitatory and enhancement of inhibitory transmission, intracellular calcium alters pre and other ions alter post synaptic. Molecular: potency of an anesthetic is proportional to its lipid solubility (Meyer-Overton rule), suggests lipophilic site of action though both lipid and protein involved.

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2
Q

GABA receptor

A

Inhibitory, has 2 alpha, 2 beta and 1 gamma binding site with specific sites to bind benzodiazepines, barbiturates

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3
Q

Central Drug Distribution in the body

A

Liver, brain, heart and kidneys - the plasma & vessel-rich group of tissues. Elimination of IV medication occurs through the central compartment (area of action for sedatives & narcotics)

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4
Q

Peripheral Drug Distribution in the body

A

Muscle, bone, skin & fat - the vessel-poor group

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5
Q

Distribution of Cardiac Output in the body

A

vessel rich group is only 10% body mass - gets 75%, vessel poor group is 20% body mass - gets only 0.5%, muscle 50% body mass - gets 19%, fat 30% body mass - gets 6%

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6
Q

How drug binding affects distribution

A

Protein binding decreases available drug. Albumin binds acidic drugs (barbiturates), A1AG binds basic drugs (locals)

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7
Q

Factors affecting distribution

A

Protein binding, protein availability, lipid solubility, ionization

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8
Q

How protein availability affects distribution

A

Decrease albumin = decreased acidic drug binding, usually with liver, kidney or heart failure or cancer. Increased A1AG increased binding basic drugs - from trauma, infection, MI or chronic pain

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9
Q

Initial volume of distribution

A

describes distribution of a drug throughout the body after dosing and prior to reaching steady state equilibrium

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10
Q

Benzodiazepine Use

A

Sedation, anxiolysis, anticonvulsant effects, spinal-cord mediated muscle relaxation, anterograde amnesia, high doses - unconsciousness & respiratory depression. (NOT ANALGESIC)

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11
Q

Benzodiazepine Therapeutic Indexes

A

Above 100, when used with narcotic decreases to <10

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12
Q

Benzodiazepine site on GABA A receptor

A

Facilitates action of GABA at alpha subunit, enhances opening of chloride channels, hyperpolarization of postsynaptic membrane, postsynaptic neurons resistance to excitation

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13
Q

Flumazenil

A

Specific & exclusive BZD competitive antagonist with high affinity for BZD receptor, reverses all BZD effects in dose dependent manner without abrupt reversal (wake up a little, not acutely anxious

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14
Q

Flumazenil onset of action

A

30 seconds to 2 minutes

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15
Q

Flumazenil redistribution

A

7-15 minutes, may need re-dosing

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16
Q

Flumazenil dosing

A

0.2 mg IV over 15 seconds, wait 45 seconds, redoce 0.2 mg increments over 15 seconds.. do not exceed 3.0 mg/hour. If no response after 1 mg consider other options

17
Q

Other BZD reversals

A

Nonspecific, unpredictable & inconsistent– physostigmine causes Ach buildup, aminophylline may antagonize sedative effects of adenosine in CNS

18
Q

Alpha 2 adrenoreceptors

A

Membrane spanning G proteins, cause inhibition of adenylate cyclase, modulation of ion channels, alpha 2B & alpha 2C receptors in the brain & spinal cord - stimulation leads to sympatholysis, sedation & antinociception

19
Q

Albumin binds what kind of drugs?

A

Acidic (Barbiturates)

20
Q

A1AG binds what kind of drugs?

A

Basic (Locals)

21
Q

Low albumin results from?

A

CHF, liver disease, kidney disease, cancer

22
Q

High A1AG results from?

A

MI, trauma, infection, chronic pain