Anesthesia Adjuncts (Exam IV) Flashcards

1
Q

β agonism results in activation of _____ which then produces _______.

A

Adenylyl Cyclase (AC)

cAMP

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2
Q

Does Ca⁺⁺ influx or efflux during β agonism?

A

Influx

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3
Q

What type of receptors are β receptors?

A

GPCR

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4
Q

What types of β receptors are there and where are they primarily located?

A
  • β1 - Heart
  • β2 - Lungs
  • β3 - Fat/Muscle

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5
Q

What type of affinity are Beta-blockers and what happens at high doses?

A

Selective affinity

Selectivity is lost at high doses of Beta Blockers

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6
Q

Chronic administration of β blockers results in what effect on receptors?

A

Receptor upregulation (aka ↑ # of receptors)

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7
Q

After β receptor desensitization from prolonged catecholamine exposure, what drug class can restore receptor responsiveness?

A

β-blockers

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8
Q

How do β blockers protect myocytes from perioperative ischemia?

A

By ↓O₂ demand on the heart

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9
Q

What do some Beta blockers do to arterial vascular tone and afterload?

A

reduce arterial vascular tone and decrease afterload

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10
Q

T/F. β blockers will potentiate renin release.

A

false. β blockers will inhibit renin release

decreases C.O.

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11
Q

How will β blockers affect the cardiac foci action potential?

A

Prolong Phase 4

↓ dysrhythmias during ischemia and reperfusion.

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12
Q

How will β blockers affect diastolic perfusion time?

A

β blockers will increase diastolic perfusion time.

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13
Q

What type of HTN is a possible indication for β blocker therapy?

A

Essential Hypertension

Sy

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14
Q

What is SCIP?
Describe the protocol and its goals.

A
  • Surgical Care Improvement Protocol
  • β-blockers must be given within 24 hrs of surgery for patients at risk for cardiac ischemia and ones already on β-blocker therapy.

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15
Q

What were the three β1 selective agents discussed in lecture?

A
  • Metoprolol
  • Atenolol
  • Esmolol

not cause vasodilation

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16
Q

What percentage of β receptors in the myocardium are β1 ?

A

75%

S9

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17
Q

Do cardio-selective β-blockers cause vasodilation?

A

No

S9

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18
Q

What non-selective β-blocker has active metabolites and is generally shitty for anesthesia?

A

Propanolol

S10

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19
Q

Differentiate the clearance mechanisms of metoprolol and esmolol.

A
  • Metoprolol = Hepatic
  • Esmolol = Plasma cholinesterases

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20
Q

Differentiate the E½ of metoprolol and esmolol.

A

Metoprolol E½ = 3-4 hours
Esmolol E½ = 9 minutes

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21
Q

When propanolol is given, what effect lasts longer, negative inotropy or negative chronotropy?

A

Negative chronotropy (bradycardia) lasts longer

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22
Q

What is a possible reason why the heart rate slowing effects of propanolol last longer than the negative inotropic effects?

A

Possible β1 sub-receptor types (ex. β1A, β1B, etc.)

S11

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23
Q

Propanolol will decrease the clearance of which two important anesthetic drug classes?

A
  • Opioids
  • Amide LA’s

d/t lower C.O. /HR

S11

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24
Q

What drug is the most selective β1 antagonist?

A

Atenolol

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25
Q

What are the three benefits of Atenolol?

A
  • Good for non-cardiac sx CAD patients (↓ complications for 2 years)
  • No insulin-induced hypoglycemia
  • Does not cross the BBB (no fatigue)
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26
Q

What is the dose for Atenolol?

A

5mg q10min IV

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27
Q

What is the dose of metoprolol?

A

1mg q5min
(Given in 5mg “blocks”)

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28
Q

What two PO formulations of metoprolol are there?

A
  • Metoprolol Tartate = multiple doses per day
  • Metoprolol Succinate = One dose per day

S13

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29
Q

What β blocker would be used for treat intubation stimuli?

A

Esmolol

S14

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30
Q

What are the onset and offset of esmolol?

A

Onset: 5 min
Offset: 10-30min

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31
Q

What is the initial dose for esmolol?

A

20-30mg IV

S14

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32
Q

Caution should be taken when giving esmolol with which two conditions?
Why?

A
  • Cocaine and/or epinephrine
  • Can cause pulmonary edema and cardiac collapse

S14

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33
Q

Are the effects of CCBs and β-blockers additive?

A

No, synergistic

S14

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34
Q

What two scenarios were given in class for a β1 indication over a non-selective β blocker?

A
  • DM: β2 can cause hypoglycemia by insulin potentiation
  • Airway: blocking β2 potentiates bronchospasm
35
Q

What volatile anesthetic will cause the greatest additive depression when combined with a β blocker?
The least?
Why does this not matter?

A
  • Enflurane = greatest additive depression
  • Isoflurane = least additive depression
  • Not significant between 1-2 MAC
36
Q

What 2ⁿᵈ messengers are potentiated by α1 agonism?

A

IP₃ → Ca⁺⁺ release from SR

S

37
Q

What occurs with α2 agonism?

A

↓ release of NE in the brainstem

38
Q

Is phenylephrine primarily a venoconstrictor or an arterioconstrictor?

A

Venous constriction > arterial constriction

S20

39
Q

Phenylephrine clinically mimics norepinephrine but is….

A

less potent and longer lasting

S20

40
Q

What is the normal dosing of phenylephrine?

A

100mcg/mL IV push

can be IV gtt that is on roller clamp

S21 extra

41
Q

What adverse effect results from phenylephrine?
How is it resolved?

A
  • Reflex bradycardia
  • Stopping the drug

S20

42
Q

What is the ratio of β to α blockade for Labetalol?

A

7:1

S22

43
Q

Is Labetalol a selective β antagonist?

A

No: non-selective β and selective α1 antagonist

S22

44
Q

Which of the following receptors does Labetalol antagonize?

A. α1
B. α2
C. β1
D. β2

A

A, C, and D

S22

45
Q

What is the dose for labetalol?

A

2.5 - 5mg IV; 10mg max

S23

46
Q

Which of the following drugs would you utilize for a post-carotid endarterectomy with a BP of 214/62 ?

Labetalol
Esmolol

A

Esmolol

Labetolol could drop the dBP too much.

S25

47
Q

Which drug is an indirect acting sympathomimetic?

A

Ephedrine

Releases NE

S29

48
Q

What is the IV push dose of epinephrine?
How long does it last?

A
  • 2-8mcg IVpush
  • 1-5 min

S30

49
Q

What is the infusion dose of epinephrine for β2 effects?

A

1-2 mcg/min

S30

50
Q

What is the infusion dose of epinephrine for β1 effects?

A

4 mcg/min

S30

51
Q

What is the infusion dose of epinephrine for predominantly α effects?

A

10-20 mcg/min

30

52
Q

What catecholamine will have the greatest effect on heart rate and cardiac output?

A

Epinephrine

S31

53
Q

What catecholamine will have the greatest effect on PVR?

A

Phenylephrine

S31

54
Q

Which SNS agonist can be given IM?
Why would this be done?

A
  • Ephedrine IM 50mg
  • Long lasting increase in BP for OB patients.

S32

55
Q

Why does tachyphylaxis occur with ephedrine?

A

Ephedrine depletes NE stores

S32

56
Q

What is the preferred sympathomimetic for parturient patients?
Why?

A

Ephedrine (It doesn’t effect uterine blood flow)

s33

57
Q

How does phenylephrine compare to ephedrine in parturient patients?

A

Phenylephrine has similar effects but has the additional benefit of a higher umbilical pH in neonates.

S33

58
Q

What is the mechanism of action of vasopressin?

A

Stimulation of vascular V1 receptors → arterial vasoconstriction

S34

59
Q

What drug would be utilized for catecholamine-resistant hypotension?

A

Vasopressin

S34

60
Q

What drug would be used for ACE-Inhibitor induced resistant hypotension?

A

Vasopressin

Resistant hypotension can occur with both ACEi and ARBs.

S34

61
Q

MAP formula per Dr. Kane

A

(DBP x2 + SBP) / 3

S37

62
Q

How does Nitric Oxide cause vasodilation?

In broad terms.

A

NO → GC → cGMP → Ca⁺⁺ inhibition and increased uptake.

S42

63
Q

How can vasodilators alleviate pulmonary congestion?

A

By decreasing venous return via venodilation

S42

64
Q

What does Nitroprusside dissociate on contact with?
What is the result?

A

Dissociates on contact with oxyhemoglobin → methemoglobin, NO, and cyanide released.

S44

65
Q

What does nitroprusside vasodilate?

A

Arterial and venous vasculature
but MORE ARTERIAL

S44

66
Q

What vasodilator absolutely requires arterial line monitoring?

A

Nitroprusside.

S44

67
Q

What is the dose of Nitroprusside?

A

0.3 - 2 mcg/kg/min

S44

68
Q

When is nitroprusside used?

A
  • Hypotensive necessary surgeries (aortic, spine, etc.)
  • Hypertensive emergencies (post CEA’s)

S45

69
Q

What drug is used to treat cyanide toxicity?

A

Methylene blue

S46 extra

70
Q

What signs would tip you off to possible cyanide toxicity secondary to nitroprusside administration?

A
  • ↑ need for nitroprusside dose
  • ↑ SvO₂
  • Metabolic acidosis
  • LOC changes

S47

71
Q

Where does nitroglycerin work?

A
  • Coronary arteries
  • Venous capacitance vessels

by far more venous vasodilator

S47

72
Q

Would nitroglycerin increase or decrease preload?

A

↓ preload

73
Q

Does nitroprusside or nitroglycerin exhibit tachyphylaxis?

How do you treat it?

A

Nitroglycerin

have a drug-free interval of 12-15 hrs

S47

74
Q

What is the nitroglycerin dose?

A

5 - 10 mcg/min

S47

75
Q

What is the firstline treatment for sphincter of Oddi spasm?
What is second?

A
  1. Glucagon
  2. Nitroglycerin

S48

76
Q

What are the indications for nitroglycerin?

A
  • Acute MI
  • Controlled Hypotension
  • Sphincter of Oddi spasm
  • Retained placenta
77
Q

How does hydralazine work?

A

↓ Ca⁺⁺ release and systemic arterial vasodilation

S49

78
Q

When does hydralazine peak?
What is it’s half-life?

A
  • Peak: 1 hour
  • ½-life: 3-7 hours

S49

79
Q

What is the initial dose of hydralazine?

A

2.5mg

S49

80
Q

What are the three categories of CCBs?
Where do each interact?

A
  • AV Node (Phenylalkylamines & Benzothiazepines)
  • Vasculature (Dihydropyridines)

S50

81
Q

How do CCBs generally work?

A

Bind and block VG-Ca⁺⁺ channels thus ↓ Ca⁺⁺ influx.

S50

82
Q

CCBs will ___ blood pressure and ___ coronary blood flow.

A

decrease; increase

S51

83
Q

Which CCB has the greatest coronary artery dilation and least myocardial depression?

A

Nicardipine

S52

84
Q

What is the dose of nicardipine?

A

5mg/hr (2.5mg titration)

S53