Lecture 19 (Exam 4) - Anesthesia Pharmacology Adjuncts Flashcards

1
Q

What type of receptors are Alpha Agonists?

What are the two subtypes and give a brief description on what happens when an agonists binds to them.

A

G-protein coupled receptors

Two subtypes:
1. Occupancy by agonists at alpha-1
- ⬆ synthesis of 2nd messengers: IP3 …⬆ Ca++ release from SR
- Affects vascular smooth muscle
- Determine arteriolar resistance, venous capacity and BP

  1. Occupancy by agonists at alpha-2
    - Decrease release of NE from presynaptic nerve terminals (brainstem) and locus coeruleus.
    - ⬆ sleepiness, ⬇️ sympathetic outflow.

(Slide 19)

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2
Q

Is Metoprolol selective or Non-selective Beta antagonist?

Which effects would we expect with Metoprolol?

A

Selective Beta-1 Antagonist

Leaves B2 functions intact: Bronchodilation, Vasodilation, and metabolic effects

(slide 13)

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3
Q
  1. What are the doses for Phenylephrine (Neosynephrine)?
  2. What two forms does it usually come in?
A
  1. IVP: 100 mcg per push (can give 50 mcg). Can give 200 - 300 mcg if needed in 100 increments that are spread out.
  2. Can come in a 100 mcg/mL syringe (Expensive but safer) Can come in 1000 mg/mL vials (Make the math math)

Fun Fact: It is Corndog’s favorite drug <3!

(Slide 20)

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4
Q

What should you worry about when giving Phenylephrine?!

What can you do to fix it?!

A

Reflex bradycardia with high doses!

You can wait for it to resolve or you can give propofol or VA to counteract the bradycardia!

(Slide 20 )

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5
Q

Is Phenylephrine (Neosynephrine) an alpha or beta agonist?

Is it used in the OR?

Does it do more venous or arterial constriction?

A

Alpha 1 Agonist!
Clinically mimics NE but less potent and longer-lasting
- Indirectly releases small amount of norepinephrine.

Given everyday in the OR

Venous constriction > arterial constriction

(Slide 20)

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6
Q

Phenylephrine is used to treat hypotension from?

Why do we like it for CAD and aortic stenosis?

A
  • SNS blockade by regional anesthesia and spinal
  • Inhaled/injected anesthetics
  • Patients not responding to fluids, or you are giving them fluids
  • Very useful in CAD and AS –> no tachycardia.
  • Commonly used both IVP & IV drip

(Slide 20)

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7
Q

Metoprolol (Lopressor) has 2 PO formulations, what are they and what are their individual elimination 1/2 times?

Metoprolol IV is usually dosed ___mg q___mins in blocks of ___mgs.

A

Tartrate - E1/2 time of 2-3 hours
Succinate - E1/2 time of 5-7 hours

Metoprolol IV is usually dosed 1 mg q 5 mins in blocks of 5 mgs.

(slide13)

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8
Q
  1. What drug class is Labetalol?!
  2. What should you watch out for when giving Labetalol?
  3. How does Labetalol work?
  4. Typical doses?
A
  1. Selective alpha1, non-selective B1 and B2 antagonist effect
    - Beta to alpha blocking ratio is 7:1 for IV form (More HR change than vasodilation)
  2. High incidence of tachyphylaxis
  3. Lowers systemic BP by ↓ SVR
    - Reflex tachycardia attenuated by beta blockade
    Maximum effect of IV dose 5-10 minutes
  4. Usual dose 2.5-5 mg IV; may increase to 10mg IV

(Slide 22)

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9
Q

Is Nitric Oxide a vasodilator or constrictor? And what is its MOA?

A

Vasodilator
It is a chemical messenger that activate cGMP in the cell to inhibit Ca++ entry into smooth muscle and increases uptake by the ER

(slide 42)

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10
Q

With Nitric Oxide, what effects does it have in the body? (6)

A

Cardiovascular tone relaxation
Platelet regulation
CNS neurotransmitter
GI smooth muscle relaxation
Immune modulation
Pulmonary artery vasodilation

(slide 42)

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11
Q

Mr. Spencer is in your preoperative holding room, scheduled for a CABG x 4 this am. You realize that he has not had his beta blocker this am. Which beta-blocker will you administer???

A. Labetalol
B. Metoprolol
C. Carvedilol
D. Esmolol
E. Propranolol

A

A or B!

A. Labetalol: It is shorter which will cause a small swing. We do not need a lot of drugs in his system because he will be on bypass and pulseless.

B. Metoprolol: Because CABG will be a long procedure.

C. Carvedilol: For CHF

D. Esmolol: Too short

E. Propranolol: Not Beta specific

(Slide 24)

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12
Q

What are 2 Nitro-Vasodilator drugs we use and what do they do in the body?

A

Sodium Nitroprusside, Nitroglycerin

↓ SVR….arterial vasodilators…treat effects of vasoconstriction
↓ venous return…venous vasodilators…alleviate pulmonary/systemic congestion

(slide 43)

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13
Q

You are in the process of extubating a patient immediately following a left carotid endarterectomy. His blood pressure is 210/64. Which of the following drugs would be most desirable?

A. Labatolol
B. Metoprolol
C. Esmolol
D. Propranolol

A

C!
B is also correct if depending on the situation.

A. Labetalol: No because of the alpha component.
B. Metoprolol: DOA too long for this case. Given only if he skipped his BB dose in the AM and is constantly hypertensive!
C. Esmolol: It is short acting, once neck stimulation is over BP will drop back to normal.
D. Propranolol

(Slide 25)

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14
Q

Sodium Nitroprusside (SNP) does what in the body? and does it work on the arteries or veins?

A

Vasodilator that causes relaxation of arterial and venous vascular smooth muscle
(arterial >venous)

(slide 44)

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15
Q

What is Sodium Nitroprusside (SNP) dose?
What is the onset, duration and special considerations?

A

Initial dose: 0.3 mcg/kg/min…titrated to 2 mcg/kg/min
Immediate onset, transient duration (hard to titrate, use small amounts)
Requires continuous administration
Requires invasive arterial monitoring
Sensitive to sunlight

(slide 44)

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16
Q

What is a side effect with Sodium Nitroprusside (SNP) that could be dangerous?

A

Dissociates immediately upon contacting oxyhemoglobin to methemoglobin: releasing cyanide and NO –> cyanide poisoning!

(slide 44)

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17
Q

Why and when do we use Sodium Nitroprusside (SNP)?

A

Production of controlled hypotension:
- Aortic surgery
- Pheochromocytoma
- Spine surgery

Hypertensive emergencies:
- Carotid surgery
(in instances that need immediate decreases in BP)

(slide 45)

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18
Q

In what instances could Cyanide Toxicity be seen with SNP admin? and What causes it?

A

With higher IV doses
Cyanide radical accumulate d/t sulfur donors/methemoglobin exhaustion

(slide 46)

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19
Q

What is a treatment for Cyanide toxicity with SNP admin?
How does it treat?

A

Give Methylene blue – to convert methemoglobin back to oxyhemoglobin

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20
Q

When do we suspect we have a Cyanide toxicity? And what are some indications?

A
  • When Increasing doses SNP needed
  • Increased mixed-venous sats….tissues aren’t using/extracting oxygen - will see: SVO2 increasing
  • Metabolic acidosis….same
  • CNS dysfunction/change in LOC occurs

Use labs to help diagnose!

(slide 46)

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21
Q

What is Nitroglycerin and does it work on arteries or veins?

A

Vasodilator - Acts on venous capacitance vessels and large coronary arteries
(more venous > than arterial)

(Slide 47)

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22
Q

What is the dose of Nitroglycerin, and what does it do in the body? Also, what can happen in a short period of time with this drug?

A

Initial dose: 5-10 mcq/min infusion and titrate

Vasodilation:
- Decreases preload to right heart.
(Can cause Venous pooling)
- Relaxation of arterial vascular smooth muscle (high doses)

Can develop Tachyphylaxis very quickly.

(slide 47)

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23
Q

The tachyphylaxis that can happen with Nitroglycerine is due to:
And what can we do to fix it?

A
  • Dose dependent and duration dependent (within 24 hours)
  • Limits vasodilation

to fix: Drug free interval for 12-15hrs reverses tolerance (to help reset the receptor) BUT ….rebound ischemia risk (will need to find something to replace or t fix in the mean time)

(slide 47)

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24
Q

When/Why do we use Nitroglycerin?

A
  • Acute MI- Relieves pulmonary congestion, ↓ O2 requirements, limits MI size
  • Controlled Hypotension- Less potent than SNP
  • Sphincter of Oddi Spasm- During cholecystectomy/opioid induced Glucogon is the first line drug for this)
  • Retained placenta- to relax uterus.

(slide 48)

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25
Q

What does SCIP stand for?

A

Surgical Care Improvement Protocol.

Slide 8

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26
Q

Under SCIP, Beta blockers have to be given within _____ hours of the procedure for what kind of patients?

A

24 hours
Patients at risk for myocardial ischemia and those already on beta-blockade therapy.
(Pts at risk for MI are; unstable angina, MI in the past, pt who had stent before due to MI, pt’s non-compliant to their statin drug. It’s a guesswork!)

Slide 8

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27
Q

If your patient forgot to take beta-blocker and its almost 24 hours to surgery but your pt’s HR is 63 and BP is 100/65. Would you give beta-blocker to your patient?

A

Yes, you would, according to the SCIP. But you would give just a small dose. (Play the game. CMS does not know what beta-blocker and how much beta-blocker you gave. Check the box.)

Slide 8

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28
Q

What are three ß1 selective agents that we use most in OR?

A

Atenolol
Metoprolol
Esmolol

(They do not cause vasodilation, so they are not involved in decreasing afterload.)

Slide 9

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29
Q

About ___% of beta receptors are ß1 in the myocardium.

A

75%

Slide 9

(25% are not ß1, so ß1 selective drugs are mostly specific.)

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30
Q

Which beta blocker that we do not use in anesthesia but we compare all the other beta blockers with?

A

Propranolol (Inderal)

Slide 10

(It is not cardio-selective, has an active metabolite and elimination half-time is 2-3 hrs)

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31
Q

What’s the elimination half-time of Esmolol?

A

0.15 hours (9 mins)

Slide 10

(Very short half-life)

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32
Q

What are the common characteristics of metoprolol, atenolol, and Esmolol?

A

All of them are cardio-selective, do not have active metabolite, and have low protein binding.

Slide 10

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33
Q

Propranolol (Inderal) are prototypical ________ and it has activity on both ____ and _____ receptors.

A

Prototypical antagonist
ß1 and ß2 receptors in equally.

Slide 11

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34
Q

Propranolol has a negative ionotropic effect and chronotropic effect. Which effect lasts longer?

A

The negative chronotropic effect (slow HR) lasts longer than the negative ionotropic effect.

(This is thought to be due to subdivisions of ß1 receptors, like ß1A and ß1B. This is just a proposed idea, nobody knows🤷‍♀️ )

Slide 11

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35
Q

Propranolol (Inderal) decreases clearance of what two classes of drugs?

A

Opioids and Amine LA’s.
(Propranolol decreases clearance of amide local anesthetics by decreasing hepatic blood flow and inhibiting metabolism in the liver. Pulmonary first-pass uptake of fentanyl is substantially decreased in patients being treated chronically
with propranolol.)

Slide 11

This is what I found in the book. She did not elaborate on it.

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36
Q

Which is THE most ß1 selective agent that anesthesia do not use very often?

A

Atenolol (Tenormin)
(Important when ß2 agonist receptor activity is important.)

Slide 12

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37
Q

What is the usual dose of Atenolol?

A

5mg q 10 minutes IV.

Slide 12

38
Q

Why do we choose Atenolol vs. other ß1 selective agents?

A
  1. Useful pre/post non-cardiac surgery in CAD pts. (↓ complications of CAD/MI for 2 years. Only dosed 1xday)
  2. Does not potentiate insulin-induced hypoglycemia. (It is a side effect of ß2 selective agents. So, safe for insulin-dependent diabetic patients.)
  3. Does not enter CNS in large amounts. ( Pt’s are less fatigue.)

Slide 12

39
Q

Esmolol is most known and used for its _______ onset of therapeutic effect in ___ mins.

Offset is in how many mins? (range)

Esmolol is broken down by what?

Initial dose is usually __ - __ mg IV. (range)

A

RAPID; reaches therapeutic effect in 5 mins

Offset in 10-30 mins

broken down by plasma esterases in cytosol (just the “liquid stuff” inside the cell)

Initial dose usually 20-30 mg IV

(slide 14)

40
Q

What 2 instances should Esmolol’s use be avoided?

Why?

A

Esmolol C/I in the pts who sniff-snuff the ruff stuff - cocaine; also if they have had Epinephrine

Can cause Pulmonary Edema and/or CV collapse which can lead to cardiac arrest

(slide 14)

41
Q

What is Esmolol useful in treating?

What other 2 drugs are used similarly?

A

Useful in treating intraoperative noxious stimuli (i.e. N-too-bay-shun)

Fentanyl or Lidocaine can be used for similar purposes

(slide 14)

42
Q

According to the graph:
Which drugs are most and least effective in treating HR?

Which drugs are most and least effective in treating SBP?

A

HR: most effective = Esmolol; least effective = Lidocaine

SBP: most effective = Fentanyl; least effective = Placebo

(slide 15)

43
Q

What are vasopressors/sympathomimetics used most often for?

A

⬆ myocardial contractility (CO)
⬆ SBP

Slide 27

44
Q

What class of drugs do beta-blockers interact with?

What type of interaction?

A

Calcium Channel blockers

Synergistic

(slide 16)

45
Q

T/F: We administer nonselective beta-blockers to insulin-dependent diabetics and asthmatics/COPD.

A

False

(slide 16)

46
Q

Sympathomimetics that lack B1 specificity can cause:

A. intense vasodilation
B. intense vasoconstriction
C. reflex bradycardia
D. reflex tachycardia
E. Who cares, ill just fix whatever happens…

A

B. intense vasoconstriction
C. reflex bradycardia (from increased after load…)

Slide 27

47
Q

MOA for Sympathomimetics:

Activate directly/indirectly _____ or ____ adrenergic receptors.

What type of adrenergic receptors are these?
(HINT: do they include second messenger?)

A

Both direct and indirectly acting…alpha and beta adrenergic receptors.

GCPR!

Slide 28

48
Q

Why wouldn’t we use B-2 blockers on an insulin-dependent diabetic?

Why wouldn’t we use B-2 blockers on an asthmatic/COPD?

A

nonselective beta-blockers would interfere with glycogenolysis and potentiates insulin

nonselective beta-blockers potentiate bronchospasm and ventilatory depression

(slide 16)

49
Q

MOA for Sympathomimetics:

GPCR –> What is ⬆ to enhance Ca++ into the cytosol?

What does this ⬆ Ca++ do to help our cells out?

A

cAMP! –> leads to ⬆ Ca++ influx which then aids Actin and Myosin to interact more forcefully –> ⬆ heart contraction!

Slide 28

50
Q

What does a direct vs indirect adrenergic drug mean?

A

Direct: drug that directly activates the receptor

Indirect: drug that evokes the release of NE release from POSTganglionic sympathetic nerve endings.

Slide 29

51
Q

What are 3 examples of selective B-1 blockers?

A

Metoprolol
Atenolol
Esmolol

(Kane)

52
Q

List the Direct Acting sympathomimetics. (4)

List the Indirect Acting. (2)

A

Direct: Epi, NE, phenylephrine, dopamine

Indirect: Ephedrine (we use this the most), phenylephrine (a lil bit…)

Slide 29

53
Q

What is the GOLD STANDARD/Prototype catecholamine?

A

Epinephrine!

(will most likely use in vascular cases only…not predominately used day-day)

Slide 30

54
Q

Beta-blockers have additive __________ depression.

Seen most with __________ and least with __________. (volatile anesthetics)

T/F: mostly significant between 1-2 MAC

A

myocardial depression (i.e. negative chrono-, ino-, and dromotropic effects)

seen most with Enflurane, least with Isoflurane

False: Not significant within 1-2 MAC (i.e. prolly not much of a concern for us since we use 1-1.3 MAC)

(slide 17)

55
Q

So your BP is in the trash - you give another Ephedrine bolus - BP is still in the toilet - you must now resort to Epi.

What is your bolus dose?
How long can you expect this to work?

A

Bolus dose Epi 2-8mcg
Works for ~1-5 mins…

Slide 30

56
Q

Your patient is septic and you must start an Epi gtt.

Which doses correspond with which receptors?

B2, B1, Alpha

1-2mcg/min
10-20mcg/min
4mcg/min

Which is the least desired?

A

1-2mcg/min = B2 :)
4mcg/min = B1 :)
10-20mcg/min = mostly Alpha :(

We want Beta > Alpha
(Dare to dream…)

Slide 30

57
Q

Kane’s favorite charts - KNOW THE EXTREMES (one that always does this - or never does this…)

A

Epi - does everything (lil dose)

Ephedrine - Alpha, ⬆ CO & HR

Phenylephrine - ALPHADADDY (⬆ PVR) - NO beta!

Vaso - CO & PVR, in units…

Slide 31

58
Q

The most popular indirect acting sympathomimetic?

A

Ephedrine!

(Slide 32)

59
Q

Increased BP effects of ephedrine lasts how much longer than EPI?

A

10x longer! However the effect may not be as intense as it would be with EPI.

(Slide 32)

60
Q

Tachyphylaxis with ephedrine is due to what?

A

Indirect acting ephedrine causes NE to be released, eventually the NE runs out.

(Slide 32)

61
Q

Ephedrine IV dose and IM dose?

A

IV = 5 - 10 mg.

IM = 50 mg

(Slide 32)

62
Q

Vasopressin is a stronger vasoconstrictor in the veins or arteries? What other organ does vasopressin affect?

A

Stimulates V1 receptors that lead to arterial vasoconstriction.

Remember vasopressin aka ADH stimulates ADH receptors in the kidneys to reabsorb water. (V2)

(Slide 34)

63
Q

Vasopressin is especially useful for treating hypotension that is related to what 2 things?

A

ACE-I induced hypotension & catecholamine resistant hypotension.

(Slide 34)

64
Q

Vasopressin side effects?

CV:
GI:
PLT/Antibody:

A

CV —> coronary vasoconstriction.

GI —> stimulates GI smooth muscle, leads to abd pain and N/V.

Decreases PLT counts and antibody formation.

(Slide 35)

65
Q

You have epinephrine, phenylephrine, ephedrine, and vasopressin. Your patient was just induced and they’re hypotensive. Which hypotensive drug will you try first? If that doesn’t work, what will you try next?

A

Try a milder sympathomimetic first, like ephedrine, then phenylephrine. If pt continues to remain hypoTN, you might need more powerful sympathomimetics like vasopressin, then EPI.
(Slide 37, 38)

66
Q

Your patient has received a fluid bolus for low BP, but their BP remains low and HR is high. Which drug in your anesthesia Pyxis is most appropriate to treat this patient’s BP?

A

Phenylephrine! This Alpha 1 agonist will have great vasoconstricting effects with no effect on HR (except for some reflex bradycardia if your BP gets too high). (Slide 39)

67
Q

Your patient is on enalapril. They’re in the OR and BP is low. You’ve given 3 doses of ephedrine and it’s not working. What sort of scenarios would make any of the following a good idea for your patient?

IVF bolus
Albumin bolus
PRBCs
Vasopressin

A

IVF bolus - pt may be dehydrated from being NPO for procedure. They might just need a little fluid.

Albumin bolus - pt may have fluid but it’s third spaced, so this will help to bring that fluid back into the vascular space. Maybe you don’t want to give crystalloids, so give a colloid like albumin to help provide volume to raise BP.

PRBCs - pt may be hypovolemic if they lost a lot of blood in surgery. PRBCs would then be the more appropriate fluid to give back volume to pt and raise BP.

Vasopressin - if it’s not a fluid issue, maybe you need to give a sympathomimetic, especially since pt is on enalapril. Vasopressin would be a good drug to give for ACE-I induced hypotension.

(Slide 40)

68
Q

Which very potent arterial vasodilator decreases ITP (Inositol Triphosphate) and calcium release, leading to extreme hypotension and rebound tachycardia?

A

Hydralazine
Slide 49

69
Q

Hydralazine
Initial Dose?
Peak?
1/2 Life?

A

Initial Dose - 2.5 mg IV
Peak - 1 hour
1/2 Life - 3-7 hours
Slide 49

70
Q

What are the three types of calcium channel blockers and what are they selective for?

A

Phenylalkylamines - selective for AV node
Benzothiazepines - selective for AV node
Dihydropyrimidines - selective for arteriolar beds
Slide 50

71
Q

This classification of drug binds to receptors on voltage-gated calcium ion channels (L-Type) and decreases calcium influx, inhibiting excitation-contraction coupling

A

Calcium Channel Blockers
Slide 50

72
Q

Calcium channel blockers decrease vascular ____________ contractility, causing peripheral vasodilation.

A

Smooth muscle
Slide 51

73
Q

The peripheral vasodilation associated with calcium channel blockers decrease SVR and systemic blood pressure which leads to an increase in what?

A

Coronary blood flow
Slide 51

74
Q

Calcium channel blockers decrease speed of conduction through the _____________

A

AV node
Slide 51

75
Q

Which CCB has the greatest effect on coronary artery dilation and a slight effect on myocardial depression?

A

Nicardipine
Slide 52

76
Q

Which two calcium channel blockers will most likely decrease HR?

A

Verapamil and Diltiazem
Slide 52

77
Q

Verapamil has a marked effect on ___________ conduction

A

AV node
Slide 52

78
Q

Which IV infusion is for short-term control of hypertension?

A

Nicardipine (Cardene)
Slide 53

79
Q

What is the starting dose of Cardene? How much can you increase?

A

Initial dose is 5 mg/hr
Increase 2.5 mg/hr x4 to a max dose of 15 mg/hr
Slide 53

80
Q

30 minutes after Nicardipine has been discontinued, by what percentage does the drug decrease?

A

50%
Slide 53

81
Q

Which antihypertensive works primarily through altering venous capacitance?

A. Hydralazine
B. Sodium nitroprusside
C. Nitroglycerin
D. Nicardipine

A

C. Nitroglycerin
Slide 55

82
Q

Your end-stage COPD patient needs emergent blood pressure control in the ICU. Which of the following medications might worsen his PaO2 the most?

A. Nitroglycerin
B. Sodium nitroprusside
C. Hydralazine
D. Labetalol

A

B. Sodium Nitroprusside
Slide 56

83
Q

Your physician is closing the neck incision following an uneventful right carotid endarterectomy. You have reversed the muscle relaxant and the patient is spontaneously breathing at 20/min; BP 140/90 and climbing, HR 84 and climbing. Your 1st intervention is:

A

Probably start a Cardene drip so there is no stress on the suture lines
Also, maybe give a narcotic to help with pain.
Slide 57

84
Q

How many subtypes of β receptors are there? What area of the body does each mostly effect?

A

β1 - mostly the heart
β2 - mostly the lungs
β3 - lipolysis

(Slide 2)

85
Q

A β receptor is occupied by an agonist. What happens at the cellular level? A review :)

A

Activation of adenylyl cyclase to produce cAMP.

Enhancement of Ca++ influx

Producing chronotropic, inotropic, and dromotropic effects.

(Slide 2)

86
Q

Dr. Kane mentioned in lecture what side effect of chronic β blockade.

A

Up-regulation of β receptors

(slide 4)

87
Q

What are the 4 effects of Beta Antagonists mentioned in this lecture?

A

May restore receptor responsiveness if tachyphylaxis exists.

Protect myocytes from perioperative ischemia and infarction

May decrease arterial vascular tone and reduce afterload

Decrease CO and inhibit renin release.

(slide 5)

88
Q

How does beta antagonism effect the slope of phase 4?
What is the result of this change?

A

Decreased slope

Decreases the rate of spontaneous depolarization

(Slide 6)

89
Q

T/F: Beta antagonism increases diastolic perfusion time.

A

True

(slide 6)

90
Q

What are some indications for beta antagonism mentioned in lecture?

A

Excessive SNS stimulation (drugs, thyroid, a Pheo, etc)

Cardiac dysrhythmias

Essential hypertension (in some patients)

SCIP protocol

(Slide 7)

91
Q

Preferred sympathomimetic for pregnant or laboring patients and why?

A

Ephedrine! Ideal for treating hypotension related to the spinal/epidural anesthesia that mom is getting.

Does not affect uterine blood flow = better for baby.

Some research suggests that phenylephrine might be better though!

(Slide 33)