General Anesthesia Flashcards

1
Q

What is anesthesia?

A
  • a combo of amnesia, analgesia and muscle relaxation to allow the performance of surgery or other procedures
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2
Q

3 phases of general anesthesia?

A
  • induction
  • maintenance
  • emergence
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3
Q

What are the agents used in induction?

A
  • “putting to sleep”
  • most commonly used induction agent is propofol
    which causes:
    drop in BP and CO, antiemetic properties
    other agents:
  • etomidate:
    doesn’t cause vasodilation, higher rate of post op nausea, inhibits the biosynthesis of cortisol, use is limited due to increase risk of death by 2.5x
  • ketamine:
    used in pts w/ hemodynamic instabilility, cardiac stimulant, significant analgesia, bronchodilation, hallucinations
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4
Q

What are the agents used in maintenance?

A
  • use inhaled (volatile) or IV
  • anesthetics inhalation anesthetic agents:
  • volatile anesthetic agents: sevoflurane and desflurane
  • nitrous oxide: can be used in combo w/ volatile gases
  • IV anesthetic agents: propofol and remifentanil
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5
Q

Emergence phase? What can this result in? What can blunt this autonomic response?

A
  • waking up
    can result in autonomic hyper-responsiveness:
  • tachycardia, HTN, bronchospasm, laryngospasm
  • short acting narcotics, BBs or lidocaine can blunt this autonomic response
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6
Q

What is propofol (Diprivan)?

When is it used? Onset of action? Duration? Effects?

A
  • non-barbiturate hypnotic agent
  • rapidly metabolized in liver and excreted in urine, so it can be used for long durations of anesthesia
  • used for general surgery, cardiac surgery, neurosurgery, and ped surgery
  • rapid onset of action (distribution 2-4 minutes), rapid clearance, and reversibility of effect once the drip is shut off
  • onset 40 sec
  • duration: 1-3 hrs
  • some anti-emetic effect so less nausea and vomiting assoc w/ use
  • weaker amnestic effect thanmidazolam (Versed)
  • no analgesic effect
  • milky looking soln (emulsion)
  • clear-headedness during recovery
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7
Q

Adverse effects of propofol?

A
  • can support rapid growth of microorganisms
  • hypotensive (administer slowly)
  • may cause hypertonia and movement
  • respiratory depression
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8
Q

Use of ketamine (ketalar)? affects what? Duration?

A
  • affects senses, produces a dissociative anesthesia (catatonia, amnesia, analgesia) in which the pt may appear awake and reactive, but can’t respond to sensory stimuli
  • frequently used in ped pts b/c anesthesia and analgesia can be achieved w/ an intramuscualr injection
  • also used in high-risk geri pts and in shock cases, b/c it also provides cardiac stimulation
  • rapid onset: 30sec
  • short duration: 5-10 min
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9
Q

What are the anesthestic gases used in surgery?

A
  • isolflurane (Forane)
  • desfluorane (Suprane)
  • sevofluorane (Ultane)
  • nitrous oxide
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10
Q

What is an impt property of anesthetics?

A
  • reversibility
  • once anesthetic gas is turned off, blood stream brings the gas back to lungs where it is eliminated: more soluble the gas is in blood, the longer it takes to eliminate
  • nitrous oxide and desflurane are the shortest acting anesthetic gases b/c they are the least soluble in blood
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11
Q

How do inhaled anesthetics work?

A
  • inhaled anesthetics act in different ways at level of CNS
  • disrupt normal synaptic transmission by:
    interfering w/ release of neurotransmitters from presynaptic nerve terminal (enhance or depress excitatory or inhibitory transmission).
    Alter re-uptake of neurotransmitters, and changes binding of NTs to post-synaptic receptor sites
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12
Q

MAC of inhaled agents?

A
- Minimum alveolar concentration:
inhaled anesthetic concentration (steady state) at which 50% of pts move in response to a std midline abdominal incision (37C, 30-55yo, 1 atm) 
- nitrous oxide: 105%
- isoflurane: 1.15%
- sevoflurane: 1.8%
- desflurane: 6.2%
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13
Q

Characteristics of isoflurane? What can it cause?

A
  • higher blood-gas solubility so takes longer for onset and longer for emergence
  • causes tachycardia
  • causes peripheral vasodilation
  • airway irritation, coughing
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14
Q

What does Desflurane require? What can it cause?

A
  • reqrs a heated-pressurized vaporizer for delivery
  • causes tachycardia
  • causes peripheral vasodilation
  • least well-tolerated on the airway - can cause coughing, bronchospasm
  • not used for mask induction
  • fastest onset and off-set of volatiles
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15
Q

What does sevoflurane cause? Onset?

A
  • doesn’t cause tachycardia
  • causes peripheral vasodilation
  • well-tolerated for mask induction
  • fast onset and quick awakening
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16
Q

Effects of nitrous oxide?

A
  • MAC is 105%: therefore alone, can’t provide anesthesia
  • nitrous oxide diffuses into air containing cavities 34x faster than nitrogen can leave that 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
17
Q

Advantages of Nitrous oxide?

A
  • inexpensive
  • readily available
  • odorless/slightly sweet
  • limited effect
  • no special equipment
  • sympathomimetic
  • will not cause malignant hyperthermia
18
Q

Disadvantages of nitrous oxide?

A
  • high MAC/FIO2
  • sympathomimetic
  • methionine synthetase inhibitor
  • expands air-filled spaces
19
Q

CI to potent inhaled anesthetic agents?

A
  • inability to tolerate the physiologic alterations produced

- malignant hyperthermia

20
Q

What are the NMBD drugs used?

A
  • succinylcholine (Anectine)
  • Rocuronium (Zemuron)
  • Vecuronium (Norcuron)
  • Pancuronium (Pavulon)
  • Cisatracurium (Nimbex)
21
Q

NMBDs produce what?

A

immobility needed for:

  • endotracheal intubation
  • surgical immobility/relaxation (Abdominal)
  • mechanical ventilation
22
Q

Action of ACh?

A
  • released into synaptic cleft and binds to nicotinic cholinergic receptors
  • then opens ion channel which causes depolarization along the muscle - and then contraction
23
Q

2 types of NMBDs?

A
  • depolarizing: succinylcholine (Anectine)
  • nondepolarizing:
    rocuronium
    vecuronium
    pancuronium
    cisatracurium
24
Q

MOA of depolarizing agents (NMBDs)?

A
  • causes 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 b/c the membrane is depolarized
25
Q

MOA of Succinylcholine (Anectine)? When is it used? Onset, duration?

A
  • causes depolarization at motor endplate
  • in contrast to ACh, succinylcholine slowly dissociates from ACh receptors, resultign in an inactive state
  • broken down by butyrylcholinesterase to choline and succinylmonocholine
  • often agent of choice when rapid control of airway is necessary
  • rapid onset: less than 1 min
  • short duration: 6-10 min
26
Q

Disadvantages of Succinylcholine?

A
  • cardiac dysrhythmias (tachyarrhythmias)
  • sinus bradycardia
  • myalgias
  • myoglobinuria
  • hyperkalemia
  • pt restrictions (kids)
  • masseter spasm (not good for intubation)
  • malignant hyperthermia trigger
  • possible increases in intraocular, gastric, and intracranial pressures
  • dependent upon normal (rare genotype that doesn’t metabolize properly)
27
Q

MOA of nondepolarizing NMBDs?

A
  • reversible competition b/t drug and ACh binding site
  • no fasciculations
  • nerve stimulation exhibits a fade in train-of four or tetany
  • best clinical marker of strength is sustained head-lift
28
Q

Nondepolarizing agents?

A
  • long acting: Pancurounium (onset: 1-1.5 min, duration 60 min, met: renal, SE: vagolytic)
  • intermediate acting:
    Vecuronium (1.5-2 min, duration: 40 min, hepatic, no SE)
    Rocuronium (1-1.5 min, 35 min, hepatic, none)
    Cisatracurium (2.5-3 min, 25 min, other metabolism, no SE)
  • short acting:
    Mivacurium
29
Q

What is the train of 4?

A

way you can measure concentration of NMBDs

  • when 4 twitches seen: 0-75% of receptors blocked
  • 3 twitches: at least 75% blocked
  • 2 twitches: 80% blocked
  • 1 twitch: 90% blocked
  • no twitches: 100% of receptors are blocked
30
Q

Reversal for NMBDs?

A

Acetylcholine esterase inhibitors:

  • neostigmine, edrophonium result in accumulation of Ach at neuromuscular jxn
  • sugammadex: no anticholinergic effects like those above, reverses vecuronium and rocuronium