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Anesthesia Pharm (Spring '24) - C > Anesthesia Adjuncts (Exam 4) > Flashcards

Anesthesia Adjuncts (Exam 4) 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

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

A

Receptor upregulation (aka ↑ # of receptors)

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6
Q

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

A

β-blockers

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7
Q

How do β blocker protect myocytes from perioperative ischemia?

A

By ↓O₂ demand on the heart

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8
Q

T/F. β blockers will potentiate renin release.

A

false. β blockers will inhibit renin release

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9
Q

How will β blockers affect the cardiac foci action potential?

A

Prolong Phase 4

↓ dysrhythmias during ischemia and reperfusion.

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10
Q

How will β blockers affect diastolic perfusion time?

A

β blockers will increase diastolic perfusion time.

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11
Q

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

A

Essential Hypertension

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12
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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13
Q

What were the three β1 selective agents discussed in lecture?

A
  • Atenolol
  • Metoprolol
  • Esmolol
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14
Q

What percentage of β receptors in the myocardium are β1 ?

A

75%

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15
Q

Do cardio-selective β-blockers cause vasodilation?

A

No

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16
Q

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

A

Propanolol

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17
Q

Differentiate the clearance mechanisms of metoprolol and esmolol.

A
  • Metoprolol = Hepatic
  • Esmolol = Plasma cholinesterases
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18
Q

Differentiate the E½ of metoprolol and esmolol.

A

Metoprolol E½ = 3-4 hours
Esmolol E½ = 0.15 hours (9 minutes)

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19
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.)

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20
Q

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

A
  • Opioids
  • Amide LA’s
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21
Q

What drug is the most selective β1 antagonist?

A

Atenolol

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22
Q

What are the three benefits of Atenolol?

A
  • Good for non-cardiac CAD patients (↓ complications for 2 years)
  • No insulin-induced hypoglycemia
  • Does not cross the BBB (no fatigue)
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23
Q

What is the dose for Atenolol?

A

5mg q10min IV

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24
Q

What is the dose of metoprolol?

A

1mg q5min until 5mg is given

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25
Q

What two formulation of metoprolol are there?

A
  • Metoprolol Tartate = multiple doses per day
  • Metoprolol Succinate = One dose per day
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26
Q

What β blocker would be used for treat intubation stimuli?

A

Esmolol

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27
Q

What are the onset and offset of esmolol?

A

Onset: 5 min
Offset: 10-30min

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28
Q

What is the dose for esmolol?

A

20-30mg IV

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29
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
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30
Q

Are the effects of CCBs and β-blockers additive?

A

No, synergistic

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31
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: β2 potentiates bronchospasm
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32
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
33
Q

What 2ⁿᵈ messengers are potentiated by α1 agonism?

A

IP₃ → Ca⁺⁺ release from SR

34
Q

What occurs with α2 agonism?

A

↓ release of NE in the brainstem

35
Q

Is phenylephrine primarily a venoconstrictor or an arterioconstrictor?

A

Venous constriction > arterial constriction

36
Q

Phenylephrine clinically mimics norepinephrine but is….

A

less potent and longer lasting

37
Q

What is the normal dosing of phenylephrine?

A

100mcg/mL

38
Q

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

A
  • Reflex bradycardia
  • Stopping the drug
39
Q

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

A

7:1

40
Q

Is Labetalol a selective β antagonist?

A

No: non-selective β and selective α1 antagonist

41
Q

What is the dose for labetalol?

A

2.5 - 5mg IV; 10mg max

42
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.

43
Q

Which drug is an indirect acting sympathomimetic?

A

Ephedrine

Releases NE

44
Q

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

A
  • 2-8mcg IVpush
  • 1-5 min
45
Q

What is the infusion dose of epinephrine for β2 effects?

A

1-2 mcg/min

46
Q

What is the infusion dose of epinephrine for β1 effects?

A

4 mcg/min

47
Q

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

A

10-20 mcg/min

48
Q

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

A

Epinephrine

49
Q

What catecholamine will have the greatest effect on SVR?

A

Phenylephrine

50
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.
51
Q

Why does tachyphylaxis occur with ephedrine?

A

Ephedrine depletes NE stores

52
Q

What is the preferred sympathomimetic for parturient patients?
Why?

A

Ephedrine (It doesn’t effect uterine blood flow)

53
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.

54
Q

What is the mechanism of action of vasopressin?

A

Stimulation of vascular V1 receptors → arterial vasoconstriction

55
Q

What drug would be utilized for catecholamine-resistant hypotension?

A

Vasopressin

56
Q

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

A

Vasopressin

Can occur with both ACEi and ARBs.

57
Q

How does Nitric Oxide cause vasodilation?

In broad terms.

A

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

58
Q

How can vasodilators alleviated pulmonary congestion?

A

By decreasing venous return via venodilation

59
Q

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

A

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

60
Q

What does nitroprusside vasodilate?

A

Arterial and venous vasculature

61
Q

What vasodilator absolutely requires arterial line monitoring?

A

Nitroprusside.

62
Q

What is the dose of Nitroprusside?

A

0.3 - 2 mcg/kg/min

63
Q

When is nitroprusside used?

A
  • Hypotensive necessary surgeries (aortic, spine, pheochromocytoma)
  • Hypertensive emergencies (post CEA’s)
64
Q

What drug is used to treat cyanide toxicity?

A

Methylene blue

65
Q

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

A
  • ↑ need for nitroprusside
  • ↑ SvO₂
  • Metabolic acidosis
  • LOC changes
66
Q

Where does nitroglycerin work?

A
  • Coronary arteries
  • Venous capacitance vessels
67
Q

Would nitroglycerin increase or decrease preload?

A

↓ preload

68
Q

Does nitroprusside or nitroglycerin exhibit tachyphylaxis?

A

Nitroglycerin

69
Q

What is the nitroglycerin dose?

A

5 - 10 mcg/min

70
Q

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

A
  • Glucagon
  • Nitroglycerin
71
Q

What are the indications for nitroglycerin?

A
  • Acute MI
  • Controlled Hypotension
  • Sphincter of Oddi spasm
  • Retained placenta
72
Q

How does hydralazine work?

A

↓ Ca⁺⁺ release and systemic arterial vasodilation

73
Q

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

A
  • Peak: 1 hour
  • ½-life: 3-7 hours
74
Q

What is the initial dose of hydralazine?

A

2.5mg

75
Q

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

A
  • AV Node (Phenylalkylamines & Benzothiazepines)
  • Vasculature (Dihydropyridines)
76
Q

How do CCBs generally work?

A

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

77
Q

CCBs will ______ blood pressure and ________ coronary blood flow.

A

decrease; increase

78
Q

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

A

Nicardipine

79
Q

What is the dose of nicardipine?

A

5mg/hr (2.5mg titration per hour) up to 15mg/hr (MAX)

Anesthesia Pharm (Spring '24) - C (20 decks)

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