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Anesthesia (Resp 314) > Induction Agents and Adjuvants (Mod 3) > Flashcards

Induction Agents and Adjuvants (Mod 3) Flashcards

1
Q

What is the MAC of Isoflurane?

A

0.0115 atm (low)

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2
Q

What is the B/G coefficient of Isoflurane

A

1.4 (Large)

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3
Q

What are common and adverse effects of Isoflurane?

A

Could depress CV (affects the myocardium) and the respiratory depression

  • could lead to arrhythmias
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4
Q

Is isoflurane dose dependant?

A

Yes; it has a high potency (low MAC) with low solubility (large b/G)

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5
Q

Contraindications for Isoflurane?

A

susceptibility to malignant hyperthermia

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6
Q

What is the relative potency and solubity of Sevoflurane?

A

High potency (low Mac) and low solubility (high b/g coefficient)

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7
Q

What can Sevoflurane be used as?

A

A potent bronchodilator; has been used in treatment of status asthmatics

  • Can be used for Asthma
  • Sweet smell and well tolerated for inhalation induction
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8
Q

Complications with Sevoflurane

A

Sevoflurane degrades into toxic compounds in the presence of a carbon dioxide absorber. Can cause nephrotoxitiy

  • causing CV and resp depression (and arrhythmias)
  • **Renal Toxicity)
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9
Q

Desflurane relative potency and solubility?

A

Moderate potency (MAC 0.06 atm mod) and low b/g coefficient (0.45)

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10
Q

Why is Desflruane a poor induction agent?

A

Pungency irritates the airway; increases risk of cough and laryngospasm

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11
Q

Which anesthetic gas has a similar induction time as nitrous oxide?

A

Desflurane; much more potent though (oil/gas partition coefficient is higher)

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12
Q

What occurs with increased/rapidly high concentration of anesthetics? -> think Desflurane

edit

A

Causes marked activation of the sympathetic nervous system

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13
Q

Relative potency and solubility of Nitrious Oxide?

A

Low potency (High MAC:1.04) and low b/g coefficient (b/g = 0.47)

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14
Q

Why is Nitrous oxide paired with other anesthetic agents?

A

Low potency means the need to maintain a acceptable partial pressure of O2 prevents the attainment of full anesthesia

  • Can provide a analgesic effect in combo with other agents
  • 2nd gas effect?
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15
Q

What are some adverse effects and considerations for Nitrous Oxide?

A

2nd gas effect; diffusion hypoxia aka cana displaces other gases

  • Can cause expansion of air collections (pneumothorax, bowel obstruction, obstructed middle ear, intracranial air)
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16
Q

Which anesthetic gas does not require a vaporizer?

A

Nitrous oxide, it mixes in with regular O2

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17
Q

What is Thiopental?

A

Barbiturate; ultra short acting; can induce anesthesia in seconds; BUT no reversal agent

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18
Q

Dose for Thiopental?

A

3-4 mg/kg IV

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19
Q

What are indications for Thiopental aside from

A

Reduction in elevated ICP (cerebral vasoconstriction) and seizures (increases the threshold for action potneitals in teh brain)

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20
Q

General doses for IV anesthetics?

A

3-4 mg/kg IV

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21
Q

Risk factor with Thiopental (barb)

A

Laryngospasm or Bronchospasm may occur with induction of light anesthesia and with airway manipulation (intubation).

  • potent short acting drug with no reversal agent. subbed out with propofol
  • indicated for elevated ICP or seizures, but benzos are preferred if available
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22
Q

Why is Propofol preferred to short acting barbiturates?

A

Ultra short acting; rapidly metabolized, meaning faster recovery than barbiturates

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23
Q

What is Propofol used for?

A

Induction and maintenance (sedation for mech. ventilation)

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24
Q

Why could Propofol be a source of infection?

A

It’s a intralipid preparation; side note, its also a large caloric source

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25
Q

Why is Propofol generally not used for patients with low BP?

A

Could cause shock or cardiac arrest

  1. Produces considerable decrease in BP w/reduction of up to 25-40% in systolic mean and diastolic pressures w/standard induction doses
  2. Both arterial and venous dilation results in reduction in SVR
  3. Inhibits baroreceptor response, limiting the normal increase in HR that occurs with decreased SVR
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26
Q

What does a inhibited or decreased baroreceptor response cause?

A

Inhibits the hypoxic respiratory drive and reduces the normal ventilatory response to hypercapnia

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27
Q

Induction dose of ketamine

A

0.5-2 mg/kg IV

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28
Q

Maintaince dose of Ketamine?

A

3-5 mg/kg IV

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29
Q

What are the desired affects of ketamine?

A
  • Analgesia
  • No effect on respiratory drive
  • Cardiovascular stability; Increases cardiac output by inhibiting norepinephrine reuptake
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30
Q

What are secondary affects of Ketamine?

A

Produces dissociative anesthesia

  • Patient may seem awake but is actually in an analgesic and amnesic state
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31
Q

Why could Ketamine increase CO?

A

Ketamine blocks receptors like norepinephrine from binding to synape sites

  • thus MORE norepinephrine will reside in the space between, prolonging the affects on CO
  • it inhibits norepinephrine reuptake
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32
Q

What are Adjuvants?

A

Provides additional effects that are desirable during surgery (help balanced anesthesia), but not necessarily provided by general anesthetics

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33
Q

3 classes of adjuvant drugs?

A
  1. Benzodiazepines and other sedatives
  2. Neuromuscular Blockades
  3. Opiates and Opioids
  • There are others tho
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34
Q

What is Glycopyrrolate (Robinul)?

A

Reduces secretion production and treat bradycardias

  • sometimes used to help increase BP
  • Adjuvant
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35
Q

How does Glycoprrolate indirectly help increase BP?

A

Helps with contractility (maintain CO)

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36
Q

What is Glycopyrrolate used with?

A

Used in conjunction w/neostigmine to mitigate the effect of bradycardias

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37
Q

What is Phenylephrine (neo synephrine)?

A

Alpha 1 agonist; which increases SVR via vasoconstriction

  • Very potent aka quick onset of action
  • Could cause reduction of organ perfusion
  • Adjuvant
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38
Q

When is Phenylephrine used?

A

when low perfusion/severe hypotension is present via bonus

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39
Q

What is Ephedrine ?

A

General adrenergic medication: Chronotrope, inotrope, and vasopressor

  • Stimulates both alpha and beta receptors
  • Stimulates norepinephrine release and reduces uptake
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40
Q

what is Dexmedetomidine (precedex)?

A

Sedative; Short acting alpha 2 adrenergic agonist; inhibits release of norepinephrine

  • Decreases activity of noradrenergic neurons in the brain and brain stem which leads to an increase in GABA (inhibitory) activity
  • Mimics sleep by promoting an endogenous sleep pathway (mimics natural sleep more than most sedatives)
  • Does not impact respiratory drive
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41
Q

When is Dexmedetomidine used?

A

Sedation of intubated patients; does not impact respiratory drive

42
Q

Dose of Demetomidine

A

0.2-0.7 ug/kg/hr continuous infusion

43
Q

What are Benzodiazpines?

A

Adjuvants used to modulate Gabanergic transmission aka inhibitory transmission (gaba agonist)

44
Q

Clinical applications of Benzos?

A
  • Anxiolytics
  • Sedatives
  • Anti-epileptics
  • Muscle Relaxants
  • Treatment of ethanol withdrawal symptoms
45
Q

What does anterograde amnesia?

A

Helps reduce PTSD with remembering operations

46
Q

What is midazolam?

A

Rapid onset and short acting (3-8 hours) anxiolytic/sedative/amnestic

  • Synergistic potentiation with opiates
  • Benzo
47
Q

When is Midazolam used?

A

Used as a preanesthetic to reduce the requirement of anesthetic, to induce anterograde amnesia

48
Q

Dose for Midazolam

A

Dose (Preanesthesia) 0.1 – 0.3 mg/kg every 2 mins as necessary for sedation

49
Q

How do NMBs work?

A

Produce skeletal muscle paralysis by interfering with Acetylcholine at the neuromuscular junction

50
Q

Onset for Pancuronium?

A

Quick onset, long acting NMB
Onset 60-90 seconds; Effects last 45-60 mins

51
Q

Dose for Pancuronium?

A

Dose: 0.08 mg/kg; anesthetic agents will potentiate the effect

52
Q

How are vitals affected by Pancuronium?

A

Modest increase (<15%) in HR and BP (due to inhibition of norepinephrine reuptake)

  • Does not result in histamine release?
  • risk of apnea tho
53
Q

How is Rocuronium reversed?

A

With Sugammadex (think the febreeze affect)

  • Acts as a chelating agent, encapsulating the free rocuronium to form a stable complex
54
Q

Onsent of Rocuronium

A

Quick onset; intermediate acting

  • 60-90 seconds; effects last 35-45mins
55
Q

Dose for Rocuronium

A

0.3-0.5 mg/kg IV

56
Q

What are the risks of using a NDMR like Rocuronium?

A

Hypertension;apnea -> need to confirm

57
Q

Why is hyperkalemia bad?

A

High potassium in the blood and therefore the heart will prevent the heart from contracting -> cardiac arrest

58
Q

Add slide 31 -> hinted to be tested material

A
59
Q

What are some drawbacks of Morphine and opioids?

  • general use?
A

Morphine and deriatives allow good hemodynamic stability but causes reduced ventilary drive

  • Analgesics are generally used to relieve pain with no loss of consciousness. (normal dosages)
60
Q

How do Opioids produce analgesia?

A

Analgesics are generally used to relieve pain with no loss of consciousness. (normal dosages)

  • Sometimes they can be used as the sole agent in anesthesia
  • Conspitation
61
Q

Affects of Opioids in the brain?

A

alter mood, produce sedation, and reduced the emotional reaction to pain

62
Q

Affect of Opioids in the brainstem?

A

opioids increase the activity of cells that provide descending inhibitory innervation to the spinal cord

63
Q

Mechanism of Action for Opiates and Opioids?

A

Slide 34

64
Q

Gold standard opiate/opioid used?

A

Morphine; used peripherally for long lasting analgesia

  • Available by PO, IV, IM, SC, epidural, spinal, and rectal
65
Q

Dose of Morphine?

A

2.5- 5mg IV slowly titrated to effect

66
Q

Most potent opioid in clinical use?

A

Sufentanil; 10-15 times more potent than fentanyl; which is 100 times more potent than morphine

67
Q

Induction dose of Sufentanil?

A

1.3-2.8 ug/kg

  • doses of 0.3-1 ug/kg can be used to blunt the hemodynamic response of intubation can be associated w/muscle rigidity, especially when admin’d
68
Q

Is Sufentanil dose dependent?

A
69
Q

Contraindications for Depolarizing Muscle Relaxants like Succ?

A
  • Burns (hyperkaliemia)
  • Traumatic paralysis
  • Myasthenia Gravis and NMB
70
Q

Why is Pungency a factor for inhaled anesthetics?

A

Pungency irritates the respiratory tract therefore not typically used to induce a patient (for some gasses such as Isoflurane)

71
Q

General contraindications for inhaled anesthetics?

A

Susceptible to malignant hyperthermia

72
Q

Why should Nitrous Oxide always be administered with oxygen?

A

Diffusion Hypoxia (second gas effect)

73
Q

Induction dose for Propofol?

A

1-2.5 mg/kg IV

74
Q

Maintenance dose for Propofol?

A

5-50 ug/kg/min IV infusion

75
Q

What do Alpha 1 agonists do?

A

Increase SVR via vasoconstriction

76
Q

When would Phenylephrine (neo syneprhine) be used

A

When low perfusion or severe hypotension is present

  • Typically given bolus
  • very potent
77
Q

What are neuromuscular blockades?

A

Introduction of a agent that produces skeletal muscle paralysis by interfering with Acetylcholine at the neuromuscular junction

78
Q

How does a non depolarizing muscle relaxant work?

A

NDMR compete with acetylcholine at the nicotinic receptor. Non depolarizing NMB antagonize (inhibit) the effect of acetylcholine, preventing the action of muscle movement.

  • Dose dependent; greater the dose the greater the intensity of muscle paralysis
79
Q

What is the reversal agent for Rocuronium?

A

There is 2!

  • Sugammadex
  • Neostigmine
  • Apparently anticholinesterase as well? 0->need to confirm
80
Q

How do Depolarizing Muscle relaxants work?

  • 3 steps
  • Succinylcholine
A
  1. Activate cholinergic receptors at the neuromuscular junction to produce depolarization of the cell membrane
  2. The result is a brief period of excitation, manifested by wide-spread fasciculations in muscle cells, followed by flaccid paralysis
  3. Paralysis occurs because the agent maintains the cells in a depolarized condition, preventing repolarization and activation of muscle sarcomeres
81
Q

What does Succinylcholine do?

A

Depolarizing muscle relaxant used for RSI

  • No effect on consciousness or pain threshold
  • Stimulates both nicotinic and muscarinic receptors; may cause bradycardia, dysrhythmias
  • short term drug for conscious sedation
82
Q

How does Succinylcholine affect ICP?

A

Succ can increase ICP up to 10mmhg

83
Q

Dose for Succinylcholine?

A

0.5-1.5mg/kg IV

84
Q

What risks are involved using Succinylcholine?

A

May cause bradycardia and dysrhythmias

  • don’t use on burns or trauma pts
  • Could increase ICP as well
85
Q

Why do patients with Myasthenia Gravis and NMB require a lower dosage for paralytics?

A

MG patients have fewer Ach receptors available due to destruction and down regulation by the body. MG patients have up to 80% fewer receptors available

86
Q

Why is dosage important to be mindful of when administering a paralytic (NMB) for patients with conditions like Myasthenia Gravis?

A

Under normal conditions approximately 20% of receptors are required to be activated for neuromuscular transmission. The remaining 80% of the receptors constitute a safety margin

  • In MG, there is a decrease in functional receptors with a subsequent decrease of the safety margin.
  • Because there are fewer receptors and a reduced safety margin, only a minimal amount required to be blocked to prevent neuromuscular transmission due to marked sensitivity to Non-depolarixing NMB
87
Q

Important consideration IV anesthetic

A

cannot easily be removed by ventilation, need to careful administration to avoid severe CNS depression. Hard to reverse

88
Q

Distribution order of IV anesthetics

A

Blood (venous) - VRG - MG - FG

89
Q

Depol NMBA in Myasthenia Gravis?

A

Increase dosage

90
Q

Nondepol NMBA in myasthenia gravis

A

Decrease dosage (due to decrease in number of receptors available)

91
Q

Succinylcholine contraindications?

A

Burns, Traumatic paralysis

  • May increase amount of potassium out of the muscle cells resulting in cardiac arrest
  • admin of succ will abnormally raise potassium out of the cells = cardiac arrest
92
Q

Depolarizing muscle relaxants

A

Activate cholinergic receptors
producing depolarization but prevent re-polarization

  • will see fasciculations during first seconds, demonstrating depolarizing. then muscles will relax
  • compete for receptor sites
93
Q

Non depolarizing muscle relaxants

A

compete with Ach at nicotinic receptors.

  • Inhibit the effect of depolarization. preventing any muscle movement
  • less receptors available
94
Q

Rocuronium use

A

Used alot in ICU and OR>
no effect on pain or consciousness

  • may result in apnea and HTN
95
Q

Isoflurane usage

A

used for maintenance, but to to high potency, respiratory tract irritations causes it not to be used much

96
Q

Contraindications to inhaled anesthetics (except N2O)

A

Malignant Hyperthermia

97
Q

Desflurane characteristics

A

Very low BG coefficient
Need special vapourizer due to boiling point
Better balance and induction agent

98
Q

Which inhaled anesthetics do NOT cause bronchospasm

A

Sevoflurane
N2O

99
Q

How is paralytic dosing controlled to reach therapeutic affect for myasthenia gravis and neurological muscles disorders?

A

For depolarizing blockages, you need more of the drug because the receptors are competing

  • competition for the receptors and how the drug works, trying to block it, few there and less of you need to
100
Q

How do motor vehicle collisions affect succinylcholine?

A

Increases number of extra junctional receptors

101
Q

Depolarizing vs non depolarizing

A
  • DP: nicotine, polarize and create the action vasculations but prevents repolarization. Anti cholinergic.
  • Non DP: Nicotinic; antagonist, prevent action potential of the neurons.
102
Q

Why would you use non depolarizing agents like roc or pancuronium over succ?

A

Pancuronium and rocuronium allows for cardiac stability by potentially increasing heart rate and blood pressure by preventing reuptake of norepi

  • heart keeps beating, but the skeletal muscles are impacted

Anesthesia (Resp 314) (9 decks)

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