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SURGERY EXAM II > GENERAL ANESTHESIA > Flashcards

GENERAL ANESTHESIA Flashcards

1
Q

anesthesia is the combination of

A

combo of amnesia + analgesia + muscle relaxation to allow the performance of surgery or other procedures

amnesia + analgesia + muscle relaxation

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2
Q

3 phases of general anesthesia

A

1) Induction
2) Maintenance
3) Emergence

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3
Q

most commonly used induction agent

A

Propofol (Diprivan)

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4
Q

Propofol causes a drop in

A

BP & CO

also has antiemetic properties

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5
Q

INDUCTION AGENTS

A

Propofol
etomidate
ketamine

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6
Q

Etomidate

A

⦁ Doesn’t cause vasodilation
⦁ higher rate of post-op nausea
⦁ inhibits the biosynthesis of cortisol
⦁ use is limited due to increased risk of death by 2.5x

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7
Q

higher rate of post op nausea

use is limited due to increased risk of death by 2.5x

A

ETOMIDATE

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8
Q

used in pts with hemodynamic instability
hallucinations
often used in kids
significant analgesic

A

ketamine

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9
Q

KETAMINE

A

⦁ Used in patients with hemodynamic instability
⦁ is a cardiac stimulant
⦁ significant analgesia, bronchodilation, and hallucinations
⦁ can cause severe hallucinations to where patient may not want to ever have surgery again…used more in children, pain management & treatment resistant depression

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10
Q

INDUCTION PHASE

A
  • “putting to sleep”
  • most commonly used induction agent = PROPOFOL

PROPOFOL CAUSES
- a drop in BP & cardiac output, antiemetic properties

OTHER AGENTS
o Etomidate
⦁	Doesn't cause vasodilation
⦁	higher rate of post-op nausea
⦁	inhibits the biosynthesis of cortisol
⦁	use is limited due to increased risk of death by 2.5x

o Ketamine
⦁ Used in patients with hemodynamic instability
⦁ is a cardiac stimulant
⦁ significant analgesia, bronchodilation, and hallucinations
⦁ can cause severe hallucinations to where patient may not want to ever have surgery again…used more in children, pain management & treatment resistant depression

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11
Q

MAINTENANCE PHASE

A
  • use of inhaled (volatile) or IV anesthetics
  • Inhalation Anesthetic Agents
    ⦁ Volatile Anesthetic Agents = Sevoflurane & Desflurane
    ⦁ Nitrous Oxide: can be used in combo with volatile gases
  • IV anesthetic agents
    ⦁ Propofol and Remifentanil
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12
Q

EMERGENCE

A

“WAKING UP”
last phase of general anesthesia

  • can result in autonomic hyper-responsiveness
    ⦁ tachycardia, hypertension, bronchospasm, laryngospasm

to blunt these responses = can give

  • short acting Narcotics
  • Beta blockers
  • Lidocaine
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13
Q

emergence autonomic hyper-responsiveness can cause

A
  • tachycardia
  • hypertension
  • bronchospasm
  • laryngospasm
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14
Q

to help blunt autonomic hyper-responsiveness in emergence

A
  • short acting narcotics
  • beta blockers
  • lidocaine
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15
Q

PROPOFOL (DIPRIVAN)

A
  • Non-barbiturate hypnotic agent
  • rapidly metabolized in liver & excreted in the urine - so can be used for long durations of anesthesia
  • used for general surgery, cardiac surgery, neurosurgery & pediatric surgery
  • rapid onset of action (distribution = 2-4 minutes)
  • rapid clearance
  • reversibility of effect once the drip is shut off
  • duration of action = 1-3 hours, onset = 40 seconds
  • Has some anti-emetic effect - so less Nausea / vomiting associated with use
  • weaker amnestic effect than Midazolam (versed)
  • no analgesic effect
  • milky looking solution (emulsion) - so called “milk of amnesia”
  • clear-headedness during recovery (rapidly clears, so don’t have much of a hangover during recovery period)
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16
Q

adverse effects of Propofol (diprivan)

A

⦁ can support rapid growth of microorganisms
⦁ hypotensive (so administer slowly)
⦁ may cause hypertonia & movement
⦁ respiratory depression

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17
Q

is a cardiac stimulant

A

KETAMINE (KETALAR)

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18
Q

KETAMINE

A
  • affects the senses
  • produces a dissociative anesthesia (catatonia, amnesia, analgesia) in which the patient may appear awake and reactive, but cannot respond to sensory stimuli
  • frequently used in pediatric patients because anesthesia and analgesia can be achieved with an IM injection
  • also used in high-risk geriatric patients and in shock cases - because it also provides cardiac stimulation
  • rapid onset (30 seconds)
  • short duration (5-10 minutes)
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19
Q

ANESTHETIC GASES

A

⦁ Isoflurane (Forane)
⦁ Desflurane (Suprane)
⦁ Sevoflurane (Ultane)
⦁ Nitrous Oxide

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20
Q

the more soluble the anesthetic gas is in the blood =

A

the longer it takes to eliminate

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21
Q

which anesthetic gases are the shortest acting

A

nitrous oxide
desflurane (suprane)

because they are the LEAST SOLUBLE in the blood

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22
Q

ANESTHETIC GASES

A
  • an important property of anesthetics = reversibility
  • once the anesthetic gas is turned off, the blood stream brings the gas back to the lungs, where it is eliminated; the more soluble the gas in the blood, the longer it takes to eliminate
  • Nitrous oxide & Desflurane = shortest acting anesthetic gases because they are the least soluble in the blood
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23
Q

how do inhaled anesthetics work

A
  • Inhaled anesthetics act in different ways at the level of the CNS
  • They disrupt normal synaptic transmission by:

⦁ interfering with the release of neurotransmitters from presynaptic nerve terminals (enhance or depress excitatory or inhibitory transmission)
⦁ alter the re-uptake of neurotransmitters
⦁ change the binding of neurotransmitters to the post-synaptic receptor sites

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24
Q

DOSING OF INHALED AGENTS

MAC

A

o MAC = Minimum Alveolar Concentration = the inhaled anesthetic concentration (steady state) at which 50% of patients move in response to a standard midline abdominal incision

⦁ Nitrous Oxide = 105%
⦁ Isoflurane = 1.15%
⦁ Sevoflurane = 1.8%
⦁ Desflurane = 6.2%

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25
Q

inhaled agent with highest MAC

A

nitrous oxide

then desflurane

(these are the shortest acting agents…are the least soluble in blood)

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26
Q

inhaled agent with the lowest MAC

A

isoflurane

then Sevoflurane

27
Q

MAC & AGE

A
  • the MAC required for adequate anesthesia decreases with age, due to alterations in metabolism (need lower dose with age)
28
Q

ISOFLURANE = inhaled agent

A
  • Higher blood-gas solubility => so it takes longer for onset, and longer for emergence
  • causes tachycardia
  • causes peripheral vasodilation (hypotension)
  • airway irritation & coughing (bronchospasm)
29
Q

fastest onset & offset inhaled agent

A

desflurane

30
Q

has highest airway irritation

least well tolerated on the airway (can cause coughing / bronchospasm)

A

desflurane

31
Q

DESFLURANE

A
  • requires a heated-pressurized vaporizer for delivery
  • causes tachycardia (just like isoflurane)
  • causes peripheral vasodilation (hypotension - just like isoflurane)
  • least well-tolerated on the airway - can cause coughing, bronchospasm
  • not used for mask induction
  • fastest onset & offset
32
Q

which inhaled agent does NOT cause tachycardia

A

sevoflurane

still causes peripheral vasodilation though

33
Q

not used for mask induction

well-tolerated for mask induction

A

desflurane

sevoflurane

34
Q

SEVOFLURANE

A
  • does NOT cause tachycardia
  • causes peripheral vasodilation
  • well tolerated for mask induction
  • fast onset & quick awakening
35
Q

NITROUS OXIDE

A

MAC = 104 - therefore, nitrous oxide alone cannot provide anesthesia

  • nitrous oxide diffuses into air-containing cavities 34x faster than nitrogen can leave the space
  • so bowel, middle ear, pneumothorax, pneumocranium, pneumo-peritoneum, or cuffs of endotracheal tubes can all increase in size when nitrous oxide is being used
  • Increases post-op nausea
  • has analgesic properties (nice for dental procedures)
36
Q

alone cannot provide anesthesia

A

nitrous oxide

37
Q

increased post op nausea (2)

decreased nausea (1)

A

etomidate & nitrous oxide

propofol

38
Q

no analgesic effect

analgesic effect

A

Propofol

nitrous oxide

39
Q

advantages of nitrous oxide

A 
Inexpensive
Readily available
Odorless/slightly sweet
Limited effect
No special equipment
Sympathomimetic
Will not cause malignant hyperthermia
40
Q

will not cause malignant hyperthermia

A

nitrous oxide

inexpensive & readily available

41
Q

disadvantages to nitrous oxide

A

High MAC/Limits FIO2
Sympathomimetic
Methionine synthetase inhibitor
Expands air-filled spaces

42
Q

expands air filled spaces

A

nitrous oxide

43
Q

PHARMACOKINETICS OF INHALED AGENTS

A

uptake time: Isoflurane > Sevoflurane > Desflurane > Nitrous Oxide

elimination time: Isoflurane > Sevoflurane > Desflurane > Nitrous Oxide

44
Q

physiologic responses to inhaled anesthetic agents

A
  • Tachycardia (except Sevoflurane)
  • Hypotension (vasodilation)
  • decreased cardiac output
  • respiratory depression (decreased ventilation)
45
Q

CONTRAINDICATIONS TO INHALED ANESTHETIC AGENTS

A

⦁ inability to tolerate the physiologic alterations produced (can pt tolerate decreased CO, hypotension, tachycardia, decreased ventilation?)

⦁ Malignant hyperthermia (does pt have a hx of MH?)

46
Q

NEUROMUSCULAR BLOCKING DRUGS (NMBDs)

A 
⦁	Succinylcholine (Anectine)
⦁	Rocuronium (Zemuron)
⦁	Vecuronium (Norcuron)
⦁	Pancuronium (Pavulon)
⦁	Cisatracurium (Nimbex)
47
Q

function of NMBDs

A
  • Produce the immobility that is needed for:
    ⦁ endotracheal intubation (if pt isn’t tolerating mechanical ventilation)
    ⦁ surgical immobility / relaxation (ex: abdominal)
    ⦁ mechanical ventilation
48
Q

depolarizing NMBD

A

succinylcholine (anectine)

49
Q

nondepolarizing NMBDs

A

⦁ Rocuronium (Zemuron)
⦁ Vecuronium (Norcuron)
⦁ Pancuronium (Pavulon)
⦁ Cisatracurium (Nimbex)

50
Q

ACh is rapidly inactivated by

A

acetylcholinesterase

51
Q

DEPOLARIZING AGENT MOA

A

Depolarizing agents cause brief twitches or fasciculations, followed by flaccid paralysis

  • Paralysis is due to depolarization of the nerve terminal, and the nerve being in a refractory state, because the membrane is depolarized; In a refractory state = cannot receive another impulse
    ex: Succinylcholine (Anectine)
52
Q

SUCCINYLCHOLINE (ANECTINE)

A
  • causes depolarization at the motor endplate
  • in contrast to ACh, succinylcholine SLOWLY dissociates from the ACh receptors, resulting in an inactive state. as it dissociates, the effects wear off
  • broken down by Butyrylcholinesterase to Choline + Succinylmonocholine
  • Succinylcholine is often the agent of choice when rapid control of the airway is necessary
  • rapid onset (< 1 minute) & short duration (6 - 10 minutes)
  • the go to paralytic for rapid sequence intubation
53
Q

SUCCINYLCHOLINE is broken down by

A

butyrylcholinesterase

into choline + succinylmonocholine

54
Q

go to paralytic for rapid sequence intubation

A

succinylcholine

because of rapid onset (< 1 minute) and short duration (6-10 minutes)

55
Q

DISADVANTAGES TO SUCCINYLCHOLINE

A

⦁ cardiac dysrhythmias
⦁ sinus bradycardia
⦁ myalgias (muscle pain = common complaint)
⦁ myoglobinuria
⦁ hyperkalemia
⦁ patient restrictions (ex: children)
⦁ masseter spasm = one of the first signs of malignant hyperthermia
⦁ malignant hyperthermia trigger
⦁ possible increases in intraocular, gastric and intracranial pressures
⦁ dependent upon normal butyrylcholinesterase (breaks down succinylcholine)
⦁ can have inappropriately prolonged response to medication with certain genotype (heterozygous or homozygous atypical)

56
Q

non-depolarizing NMBD

best clinical marker of strength

A

sustained head-lift

57
Q

non-reversible NMBDs

A
  • reversible competition between drug & ACh binding site
  • no fasciculations (unlike succinylcholine - depolarizing)
  • nerve stimulation exhibits a fade in train-of-four or tetany
  • best clinical marker of strength = sustained head-lift
58
Q

long acting non-depolarizing NMBD

intermediate acting

short acting

A

Pancuronium

Vecuronium, Rocuronium, Cisatracurium

Mivacurium

shortest onset, shortest duration = rocuronium
longer onset, longest duration = pancuronium
longest onset, shortest duration = cisatracurium

59
Q

which non-depolarizing NMBD has vagolytic side effects

A

PANCURONIUM

Vecuronium, Rocuronium, Cisatracurium = no SE

60
Q

metabolism of 4 non-depolarizing NMBD

A

pancuronium = renal

rocuronium & vecuronium = hepatic

cisatracurium = other…spontaneously degenerates

61
Q

TRAIN OF FOUR (non-depolarizing NMBDs)

A

⦁ When 4 twitches are seen, 0-75% of the receptors are blocked.
⦁ When 3 twitches are seen, at least 75% of the receptors are blocked.
⦁ When 2 twitches are seen, 80% of the receptors are blocked.
⦁ When 1 twitch is seen, 90% of the receptors are blocked.
⦁ When no twitches are seen, 100% of receptors are blocked.

62
Q

reverses vecuronium & rocuronium

A

Sugammadex

63
Q

REVERSAL OF NMBDs

A
  • Acetylcholinesterase Inhibitors*

⦁ Neostigmine, Edrophonium = result in the accumulation of ACh at NMJ

⦁ Sugammadex = no anticholinergic effects like the 2 above…reverses Vecuronium and Rocuronium

64
Q

MALIGNANT HYPERTHEMIA

A
  • An uncommon and sometimes life-threatening reaction to some anesthetic agents
  • autosomal dominant condition of skeletal muscle; disruption of intracellular calcium metabolism
  • the build up of calcium causes violent sustained muscle contraction & rigidity, heat production, acidosis, muscle necrosis & rhabdomyolysis (myoglobinuria)

TRIGGERS = Inhaled halogenated anesthetic agents & Succinylcholine

  • quick rise in CO2 (hypercarbia)
  • masseter muscle rigidity
  • increase in body temp (1-2 degrees q5 minutes)
  • tachycardia
  • cyanosis
  • muscle rigidity
  • compartment syndrome
  • rhabdomyolysis
  • Hyperkalemia

TREATMENT = IV Dantrolene - rapid IV push

  • can give oral dantrolene for 1-2 days prior to surgery, and up to 3 days after for prophylaxis
  • cooling blankets
  • Mannitol or Sodium Bicarb for renal support
  • Treat Hyperkalemia & Compartment Syndrome

SURGERY EXAM II (7 decks)

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