Anesthesia Adjuncts (Exam IV) Flashcards

(84 cards)

1
Q

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

A

Adenylyl Cyclase (AC)

cAMP

S2

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2
Q

Does Ca⁺⁺ influx or efflux during β agonism?

A

Influx

S2

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3
Q

What type of receptors are β receptors?

A

GPCR

S2

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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

S3

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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

S4

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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

S5

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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.

S7

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15
Q

What were the three β1 selective agents discussed in lecture?

A
  • Metoprolol
  • Atenolol
  • Esmolol

not cause vasodilation

S9

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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

S10

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20
Q

Differentiate the E½ of metoprolol and esmolol.

A

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

S10

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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

S11

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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
What are the three benefits of Atenolol?
- Good for non-cardiac sx CAD patients (↓ complications for 2 years) - No insulin-induced hypoglycemia - Does not cross the BBB (no fatigue)
26
What is the dose for Atenolol?
5mg q10min IV
27
What is the dose of metoprolol?
1mg q5min (Given in 5mg "blocks")
28
What two PO formulations of metoprolol are there?
- Metoprolol Tartate = multiple doses per day - Metoprolol Succinate = One dose per day ## Footnote S13
29
What β blocker would be used for treat intubation stimuli?
Esmolol ## Footnote S14
30
What are the onset and offset of esmolol?
Onset: 5 min Offset: 10-30min ## Footnote S14
31
What is the initial dose for esmolol?
20-30mg IV ## Footnote S14
32
Caution should be taken when giving esmolol with which two conditions? Why?
- Cocaine and/or epinephrine - Can cause pulmonary edema and cardiac collapse ## Footnote S14
33
Are the effects of CCBs and β-blockers additive?
No, synergistic ## Footnote S14
34
What two scenarios were given in class for a β1 indication over a non-selective β blocker?
- DM: β2 can cause hypoglycemia by insulin potentiation - Airway: blocking β2 potentiates bronchospasm
35
What volatile anesthetic will cause the greatest additive depression when combined with a β blocker? The least? Why does this not matter?
- Enflurane = greatest additive depression - Isoflurane = least additive depression - Not significant between 1-2 MAC
36
What 2ⁿᵈ messengers are potentiated by **α1 agonism**?
IP₃ → Ca⁺⁺ release from SR ## Footnote S
37
What occurs with **α2 agonism**?
↓ release of NE in the brainstem
38
Is phenylephrine primarily a venoconstrictor or an arterioconstrictor?
Venous constriction > arterial constriction ## Footnote S20
39
Phenylephrine clinically mimics norepinephrine but is....
less potent and longer lasting ## Footnote S20
40
What is the normal dosing of phenylephrine?
100mcg/mL IV push | can be IV gtt that is on roller clamp ## Footnote S21 extra
41
What adverse effect results from phenylephrine? How is it resolved?
- Reflex bradycardia - Stopping the drug ## Footnote S20
42
What is the ratio of β to α blockade for Labetalol?
7:1 ## Footnote S22
43
Is Labetalol a selective β antagonist?
No: non-selective β and selective α1 antagonist ## Footnote S22
44
Which of the following receptors does Labetalol antagonize? A. α1 B. α2 C. β1 D. β2
A, C, and D ## Footnote S22
45
What is the dose for labetalol?
2.5 - 5mg IV; 10mg max ## Footnote S23
46
Which of the following drugs would you utilize for a post-carotid endarterectomy with a BP of 214/62 ? Labetalol Esmolol
Esmolol *Labetolol could drop the dBP too much*. ## Footnote S25
47
Which drug is an *indirect* acting sympathomimetic?
Ephedrine *Releases NE* ## Footnote S29
48
What is the IV push dose of epinephrine? How long does it last?
- 2-8mcg IVpush - 1-5 min ## Footnote S30
49
What is the infusion dose of epinephrine for β2 effects?
1-2 mcg/min ## Footnote S30
50
What is the infusion dose of epinephrine for β1 effects?
4 mcg/min ## Footnote S30
51
What is the infusion dose of epinephrine for predominantly α effects?
10-20 mcg/min ## Footnote 30
52
What catecholamine will have the greatest effect on heart rate and cardiac output?
Epinephrine ## Footnote S31
53
What catecholamine will have the greatest effect on PVR?
Phenylephrine ## Footnote S31
54
Which SNS agonist can be given IM? Why would this be done?
- Ephedrine IM 50mg - Long lasting increase in BP for *OB patients.* ## Footnote S32
55
Why does tachyphylaxis occur with ephedrine?
Ephedrine depletes NE stores ## Footnote S32
56
What is the preferred sympathomimetic for parturient patients? Why?
Ephedrine (It doesn't effect uterine blood flow) ## Footnote s33
57
How does phenylephrine compare to ephedrine in parturient patients?
Phenylephrine has similar effects but has the additional benefit of a higher umbilical pH in neonates. ## Footnote S33
58
What is the mechanism of action of vasopressin?
Stimulation of vascular V1 receptors → arterial vasoconstriction ## Footnote S34
59
What drug would be utilized for catecholamine-resistant hypotension?
Vasopressin ## Footnote S34
60
What drug would be used for ACE-Inhibitor induced resistant hypotension?
Vasopressin *Resistant hypotension can occur with both ACEi and ARBs*. ## Footnote S34
61
MAP formula per Dr. Kane
(DBP x2 + SBP) / 3 ## Footnote S37
62
How does Nitric Oxide cause vasodilation? *In broad terms*.
NO → GC → cGMP → Ca⁺⁺ inhibition and increased uptake. ## Footnote S42
63
How can vasodilators alleviate pulmonary congestion?
By decreasing venous return via venodilation ## Footnote S42
64
What does Nitroprusside dissociate on contact with? What is the result?
Dissociates on contact with oxyhemoglobin → methemoglobin, NO, and cyanide released. ## Footnote S44
65
What does nitroprusside vasodilate?
Arterial **and** venous vasculature but MORE ARTERIAL ## Footnote S44
66
What vasodilator absolutely requires arterial line monitoring?
Nitroprusside. ## Footnote S44
67
What is the dose of Nitroprusside?
**0.3** - 2 mcg/kg/min ## Footnote S44
68
When is nitroprusside used?
- Hypotensive necessary surgeries (aortic, spine, etc.) - Hypertensive emergencies (post CEA's) ## Footnote S45
69
What drug is used to treat cyanide toxicity?
Methylene blue ## Footnote S46 extra
70
What signs would tip you off to possible cyanide toxicity secondary to nitroprusside administration?
- ↑ need for nitroprusside dose - ↑ SvO₂ - Metabolic acidosis - LOC changes ## Footnote S47
71
Where does nitroglycerin work?
- Coronary arteries - Venous capacitance vessels | by far more venous vasodilator ## Footnote S47
72
Would nitroglycerin increase or decrease preload?
↓ preload
73
Does nitroprusside or nitroglycerin exhibit tachyphylaxis? How do you treat it?
Nitroglycerin have a drug-free interval of 12-15 hrs ## Footnote S47
74
What is the nitroglycerin dose?
5 - 10 mcg/min ## Footnote S47
75
What is the firstline treatment for sphincter of Oddi spasm? What is second?
1. Glucagon 2. Nitroglycerin ## Footnote S48
76
What are the indications for nitroglycerin?
- Acute MI - Controlled Hypotension - Sphincter of Oddi spasm - Retained placenta
77
How does hydralazine work?
↓ Ca⁺⁺ release and systemic arterial vasodilation ## Footnote S49
78
When does hydralazine peak? What is it's half-life?
- Peak: 1 hour - ½-life: 3-7 hours ## Footnote S49
79
What is the initial dose of hydralazine?
2.5mg ## Footnote S49
80
What are the three categories of CCBs? Where do each interact?
- AV Node (**Phenylalkylamines & Benzothiazepines**) - Vasculature (**Dihydropyridines**) ## Footnote S50
81
How do CCBs generally work?
Bind and block VG-Ca⁺⁺ channels thus ↓ Ca⁺⁺ influx. ## Footnote S50
82
CCBs will ___ blood pressure and ___ coronary blood flow.
decrease; increase ## Footnote S51
83
Which CCB has the greatest coronary artery dilation and least myocardial depression?
Nicardipine ## Footnote S52
84
What is the dose of nicardipine?
5mg/hr (2.5mg titration) ## Footnote S53