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Respiratory > Drugs > Flashcards

Drugs Flashcards

1
Q

Etomidate dose?

A

0.2-0.6mg/kg IV (cheat sheet cued to 0.3mg/kg). (mnemonic- E3/ The E looks like a 3 in reverse)

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2
Q

Age range for etomidate?

A

not approved for under 10 y.o.

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3
Q

How fast to administer Etomidate?

A

over 30-60 sec,

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4
Q

How long until etomidate takes action?

A

usually under a minute

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5
Q

How is the the duration of action correlated to the dose of etomidate?

A

each 0.1 mg/kg providing about 100 seconds of unconsciousness.

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6
Q

What is considered the most significant adverse effect of etomidate?

A

Transient inhibition of adrenal steroid synthesis is considered the most significant adverse effect of etomidate

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7
Q

How does transient inhibition of adrenal steroid synthesis effect a patient?

A

This poses at least a theoretical risk of impairing a patient’s ability to produce an adequate stress response

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8
Q

The most COMMON adverse reaction associated with the use of etomidate is?

A

transient intravenous pain on injection

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9
Q

32% of patients can experience this side effect from etomidate?

A

myoclonus

can increase aspiration risk and IOP (intraocular pressure)

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10
Q

What condition can increase the risk of adrenal suppression?

A

sepsis

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11
Q

How does etomidate effect BP?

A

It has a minimal effect on contractility and CO

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12
Q

What respiratory effects are seen with etomidate?

A

ventilation is not affected

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13
Q

What are etomidate’s effect on the brain? (3)

A
  1. decreases cerebral metabolic rate,
  2. decreased cerebral blood flow,
  3. and decreased intracranial pressure
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14
Q

How does etomidate affect ICP?

A

decreases ICP

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15
Q

How does succs work?

A

It blocks the action of acetylcholine (ACh); hence, it disrupts all nicotinic cholinergic receptors of the parasympathetic and sympathetic nervous systems

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16
Q

Is succs depolarizing or non-depolarizing?

A

depolarizing

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17
Q

Succs onset of action

A

60 seconds

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18
Q

Succs duration of action

A

up to 6 minutes

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19
Q

FDA approved dose for Succs

A

1.5mg/kg – A reasonably higher dose of the drug produces the same paralysis as an appropriate weight-based dose with little to no known dose associated with increased risk for the patient

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20
Q

Would it be better to under or overdose Succs administration

A

A reasonably higher dose of the drug produces the same paralysis as an appropriate weight-based dose with little to no known dose associated with increased risk for the patient

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21
Q

Most COMMON significant adverse effect of succs?

A

hyperkalemia increase by 0.5 - 1.0 mEq/L

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22
Q

Patients to use Succs cautiously in? (4)

A
  1. burns
  2. crush injury
  3. acute or chronic renal failure
  4. trauma
    due to increased risk of hyperkalemia
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23
Q

Most serious Succs adverse effect?

A

Malignant hyperthermia

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24
Q

Succs may have what cardio effect in children?

A

bradycardia in peds due to nicotinic receptor activation

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25
Q

How are succs cardio effects addressed?

A

pre-treatment with atropine

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26
Q

Nine conditions that succs should be used cautiously in or avoided

A
  1. Duchenne muscular dystrophy
  2. mastocytosis,
  3. myxedema,
  4. myasthenia gravis,
  5. muscular dystrophy,
  6. closed-angle glaucoma,
  7. severe liver and/or renal impairment or failure,
  8. cerebrovascular accident longer than 72 hours,
  9. and malignant hyperthermia.
  10. Those on aminoglycoside antibiotics or cholinesterase inhibitors should not be given succinylcholine chloride due to their ability to exacerbate paralysis or reduce the metabolism of the depolarizing neuromuscular blockade
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27
Q

List 6 non depolarizing neuro muscular blockers (NNMBs)

A

rocuronium, vecuronium, pancuronium, atracurium, cisatracurium, mivacurium

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28
Q

What are the 2 subcategories of nNMBs?

A

Steroidal and Benzylisoquinolinium

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29
Q

What are three Benzylisoquinolinium nNMBs ?

A

atracurium, cisatracurium, mivacurium

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30
Q

Steroidal nNMbs

A

Rocuronium, vecuronium, pancuronium

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31
Q

Reversal agent for steroidal nNMBs?

A

Sugammadex

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32
Q

Most common ASE of nNMBs

A

histamine release

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33
Q

The effects of histamine reaction include?

A

The effects of histamine reaction include hemodynamic instability (tachycardia, hypotension), bronchospasm, and urticaria

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34
Q

Train of four count as a % of receptors blocked?

A

TOFC of 1 = >95% of receptors blocked
TOFC of 2 = 85-90% of receptors blocked
TOFC of 3 = 80-85% of receptors blocked
TOFC of 4 = 70-75% of receptors blocked

35
Q

Name three nNMBs reversal agents?

A

Reversal of neuromuscular blockade is commonly achieved with neostigmine, an anticholinesterase, and glycopyrrolate. However, sugammadex can also be used as a reversal agent if a steroidal NMBA was used

36
Q

How should NMBA be dosed?

A

based on ideal body weight to avoid overdosing

37
Q

Propofol dose

A

0.5-2mg/kg IV
“P2”

38
Q

Rocuronium dose

A

1mg/kg IV

39
Q

Ketamine dose

A

2mg/kg IV (Mnemonic- People get “high” of ketamine or special K. How high? what is the highest mountain? Its “K2”, or Kilomonjaros second peak. So, “K2” Ketamine’s dose is 2mg/kg

40
Q

Lidocaine benefits in RSI?

A
  1. protects from increased ICP
41
Q

Lidocaine dose? (single dose not wt based)`

A

100mg IV

42
Q

Fentanyl dose?

A

2-3mcg/Kg IV

43
Q

How does Fentanyl assist with RSI?

A

decreases catecholamine discharge and decreases the risks of BP elevation

44
Q

Lidocaine criteria memory aid

A

“Tight lungs, tight brain”. Lidocaine is good for ^ICP and RAD. Think that is “relaxes” these tissues in much the same way it “relaxes” an irritable heart (ex. PVCs).

45
Q

How does Lidocaine effect the cough reflex?

A

decreases it

46
Q

How does Lidocaine effect airway resistance?

A

decreases it

47
Q

How does Lidocaine effect the potential for ^ICP

A

decreases it

48
Q

How does Lidocaine effect the cerebral metabolism and O2 demands?

A

decreases them

49
Q

How does Lidocaine effect the cerebral blood flow

A

decreases it

50
Q

What is the only real toxic effect of Lidocaine?

A

seizures at high doses p. 184

51
Q

What role does fentanyl play in premedication ?

A
  1. attenuates catecholamine release to largnoscopy
52
Q

ASE to opioids? (2)

A

1.

53
Q

Three conditions that could benefit from Fentanyl?

A
  1. ^ICP, ICH, aortic dissection. All need to avoid an increase in BP/HR from catecholamine releases r/t intubation.
54
Q

What general class are defasciculating agents?

A

your -roniums (Roc, Vec, Pan)

55
Q

What is the general defasciculating dose?

A

10% or the paralyzing dose, which is 50% of the intubating dose.

56
Q

What systemic function does Etomidate reversibly block?

A

11-beta-hydroxylase is blocked which reduces serum cortisol and aldosterone

57
Q

What drug class is ketamine in?

A

It is a phencyclidine derivative (PCP). If you think of someone being amped up on PCP you can remember that ketamine causes catecholamine release which in turn ^, HR, BP, CNS metabolism and ICP. However it does relax bronchial muscles

58
Q

Three respiratory effects of ketamine

A

relaxes bronchial muscles, increases bronchial secretions, increases laryngeal reflexes.

59
Q

Brocas index

A

used to estimate the weight of average built people based on height. Height in cm-100= KG for men
Height in cm-105=kg in women. estimates IBW

60
Q

Depolarizing NMBAs

A

Succs

61
Q

Non-depolarizing NMBAs

A

-roniums and -curiams

62
Q

What is the IM succs dose?

A

3-4mg/kg IM

63
Q

What could happen from overdosing a patient on Succs?

A

prolonged sedation

64
Q

If in doubt, should a larger or smaller dose of succs be given?

A

p. 201 “larger rather than smaller doses of SCh should be given in RSI”

65
Q

What is the max cumulative Succs dose

A

6mg/kg IV

66
Q

How is the dose of Succs adjusted in obese patients?

A

may need to be increased and use ABW

67
Q

How does the dose of succs change in children

A

use 2mg/kg d/t decreased vagal tone in kidsunder 10 y.o. but also give atropine to counter bradycardia.

68
Q

Defasciculating dose of Rocuronium in mg/kg

A

0.06mg/kg

69
Q

How can non-depolarizing NMBAs be reversed? (drug and dose)

A

with neostigmine 0.06-0.08mg/kg

70
Q

Depolarizing/defasculating mnemonic

A

DEEZnuts Roc, Vec and Pan can suck deeznuts

71
Q

Cardiac ASE of pancuronium?

A

tachycardia

72
Q

How can secretions be controlled pharmacologically in intubation?

A

glycopprolate (Robinul)

73
Q

How does Succs increase K+ ?

A

When the cell depolarizes, Na+ enters the cell and K+ exits moving from intracellular to extracellular.

74
Q

What receptor site does Succs bind to?

A

Nicotinic receptors.

75
Q

Pancuronium adverse side effect?

A

Increased heart rate

76
Q

Is Succs an agonist or antagonist of NAch receptors?

A

agonist , mimcs Ach

77
Q

What type of phase block does Succs cause?

A

Phase I block constant then fade reaction
may cause Phase II block with high or repated doses

78
Q

What is a phase II block

A

When Na+ channels become closed and prevent repolarization

79
Q

Ketamine binds to what kind of receptors?

A

NDMA receptor antagonist , which binds glutamate and glycine

80
Q

Rocuronium dose?

A

1.2 mg/kg IV

81
Q

Describe a Phase I block?

A

Succinylcholine is comprised of two acetylcholine molecules joined together and acts as a depolarizing neuromuscular blocker by binding acetylcholine receptors at the post-synaptic neuromuscular junction end plate. The resultant end plate depolarization initially stimulates muscle contraction; however, because succinylcholine is not degraded by acetylcholinesterase, it remains in the neuromuscular junction to cause continuous end plate depolarization and subsequent muscle relaxation. This is termed a phase I block

82
Q

Describe a Phase II Block?

A

The receptor does not respond appropriately to acetylcholine, and neuromuscular blockade is prolonged. Phase II block may be seen clinically with doses of succinylcholine >4mg/kg, but some characteristics of this blockade have been reported at 0.3mg/kg.

83
Q

Contrast the binding of depolarizing and non-depolarizing Ach receptor blockers?

A

Depolarizing (Succs) are resistant to and not metabolized by acetylcholinesterase, leading to persistent depolarization of the muscle fibers, resulting in the patient’s well-recognized muscle fasciculations and paralysis.
NON- Depolarizing drugs which act as competitive antagonists. They bind (ACh) receptors but do not produce an action potential. Thus, they prevent ACh from binding, and as a result, neural endplate potentials do not develop.

Respiratory (5 decks)

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