General Anesthetics Flashcards

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1
Q

Intravenous anesthetics?

A

Etomidate, ketamine, propofol, thiopental

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2
Q

Etomidate: Side Effects

A

Induction agent known for its
cardiovascular stability.
Contraindicated in septic shock.

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3
Q

Metabolism of IV general anesthetics?

A
Metabolism:
hepatic
Excretion:
renal
clearance
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4
Q

Ketamine: MOA

A

Antagonizes the NMDA receptor.
- Causes some areas of the brain to be
tonically excited → this central stimulation
of the sympathetic nervous system allows
for CV stability, maintained ventilation,
and increased cerebral blood flow,
intracranial pressure, and cardiac output.

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5
Q

Propofol: MOA

A
- Possesses high lipid solubility and a
redistribution phase with a short half-life
(t1/2α)
- Powerful respiratory depressant.
- Available for IV administration only.
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6
Q

Thiopental: MOA

A
  • Belongs to the barbiturate drug class.
  • Suppresses transmission of excitatory
    NTs (e.g., acetylcholine) and enhances
    inhibitory NTs (e.g., GABA).
  • Can create a loss of consciousness in
    30 seconds.
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7
Q

Ketamine: Indications

A
- Blocks polysynaptic reflexes in
spinal cord.
- Inhibits excitatory NT effects in parts
of the brain.
- Disassociates thalamus from limbic
cortex → “dissociative” anesthetic,
Pt appears conscious but can’t
process sensory input.
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8
Q

Propofol: Indications

A
  • Rapid onset and recovery
  • One of the most well-known and
    highly utilized general anesthetics.
  • Approved for mod-deep sedation
    and general anesthesia (induction +
    maint.).
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9
Q

Thiopental: Indications

A
Decreases ICP
- Acts as resp. and CV depressants.
Decreases both CBF and ICP →
reduces brain O2 consumption →
helpful in neurosurgical patients.
- Most used as induction agent.
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10
Q

Ketamine: Side Effects

A

Hallucinations,

nightmares

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11
Q

Propofol: Side Effects

A

Respiratory
depression,
bradycardia

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12
Q

Thiopental: Side Effects

A

Respiratory
depression,
bradycardia

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13
Q

Inhaled general anesthetics?

A

Desflurane, halothane, isoflurane, nitrous oxide, sevoflurane

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14
Q

Treatment for malignant hyperthermia?

A

Dantrolene

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15
Q

Dantrolene: MOA

A
Dantrolene is a muscle relaxant that
depresses excitation-contraction coupling
in skeletal muscle by binding to the
ryanodine receptor and decreasing
intracellular calcium concentration.
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16
Q

Inhaled general anesthetics: MOA

A
Although inhalation anesthetics are widely
used, their mechanism of action is
largely unknown. It is presumed that
their primary mechanism is through the
inhibition of glutamate receptors and
enhancement of GABA
neurotransmission. The site of action for
these drugs likely occurs at multiple
locations within the CNS. Specific brain
areas including the reticular activating
system (RAS), cerebral cortex,
hippocampus, and spinal cord are all
impacted by anesthetic agents,
contributing to these drugs’ various
physiologic effects.
17
Q

Inhaled anesthetics: Indications

A
Inhalation anesthetics are used for
the induction and maintenance
phase of general anesthesia. These
gases are administered by breathing
through an anesthesia mask or
endotracheal (ET) tube connected to
an anesthetic machine.
18
Q

What factors affect inhaled anesthetics?

A
The ultimate clinical effect of
inhalation anesthetics depends on
delivery of a therapeutic partial
pressure of an agent to the CNS. This
delivery is affected by properties of
the agents themselves and by
physiologic variables including
regional blood flow, cardiac output,
and ventilation.
19
Q

Side effects of inhaled anesthetics?

A
Myocardial
depression
- Decreased SVR
and SBP.
- Volatile anesthetics
create classic
respiratory pattern:
increased RR,
decreased TV, and
decreased
ventilatory response
to CO2
(hypercarbia). All
agents cause
reduced RBF and
GFR.
Malignant
hyperthermia (MH)
is a potential
complication shared
by all of the volatile
anesthetics (and
succinylcholine).
20
Q

Inhaled anesthetics: Metabolism

A
Inhalation
anesthetics
undergo
limited
metabolism.
The recovery
(emergence)
from these
drugs is
achieved by
lowering the
anesthetic’s
concentration
at the site of
action (the
brain). The
majority of
elimination
occurs at the
alveolus and is
dependent
upon same
principles that
facilitate
induction of
anesthesia.