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Pharm Block 11 > Cardiovascular Pharm II > Flashcards

Cardiovascular Pharm II Flashcards

1
Q

What is heart failure associated with?

A

Decreased contractility

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2
Q

What does the decreased contractility in heart failure ultimately do

A

Tissues cant get enough O2 bc blood not pumping enough, this causing a sympathetic compensation

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3
Q

What things does the sympathetic system do to compensate for heart failure?

A

Increase arteriolar constriction (afterload)
Increase blood volume (preload)
Increase heart rate

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4
Q

Sympathetic compensation of heart failure: arteriolar constriction

A

Increases TPR-vascular resistance-increased afterload

  • now heart has to constrict even harder against arterioles
  • TX: want to decrease afterload so heart wont have to work as hard
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5
Q

Sympathetic compensation of heart failure: increased blood volume

A
  • increased blood pressure
  • this is a problem because the heart is already failing and now has to pump extra fluid around
  • problem at the level of the veins
  • preload increased (increased, end diastolic and increased venous return, all mean the same things)
  • TX: want to decrease preload with diuretics or venodilate
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6
Q

Sympathetic compensation for Heart failure: increased HR

A
  • leads to arrhythmia
  • control this by decreasing HR
  • do this with B1 blocker in low dose, because B1 blockers reduce HR AND contractility, and you do not want to decrease contractility in an already failing heart
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7
Q

Why do we use low does beta blocker in heart failure

A

Because it will Lower the heart rate without affecting contractility. If you give a higher does of B blocker, it could lower contractility, and we dont want that in an already failing heart

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8
Q

How does the heart compensate during failure?

A
  • increased SANS activity
  • myocardial hypertrophy
  • increased RAAS
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9
Q

What do all of the compensatory actions of the heart during heart failure lead to

A

Cardiac remodeling

-fibrosis

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10
Q

What is the main target when trying to combat cardiac remodeling in cardiac failure

A

Aldosterone

-epi and NE are potential targets too, but aldosterone main one

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11
Q

If you something decreases remodeling, what else does it do

A

Increases survival

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12
Q

If something increases survival, what else does it do

A

Decreases remodeling

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13
Q

What is the main goal when treating someone with heart failure

A

Improve survival

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14
Q

Why is there an increase in heart failure today

A

Because more people are surviving heart attacks and are left with failing hearts instead of dying right away

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15
Q

///./.][]\\

A

A Note Card- by Champ

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16
Q

What are the drugs used to treat CHF

A
  1. RAAS inhibitors
  2. B blockers
  3. Diuretics
  4. Inotripic drugs
  5. Other vasodilators
  6. If channel blocker

1-3 are the first line drugs, the others are back up

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17
Q

What are the type 3 drugs we use to treat CHF

A
  1. RAAS inhibitor (ACEI or ARB, ACEI first)
  2. B blocker (metoprolol)
  3. Diuretics (loops and thiazides)
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18
Q

What is the very first drug usually given in CHF

A

ACEI

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19
Q

What is the second drug usuallygiven for CHF

A

Metoprolol

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20
Q

Why do we not give inotropic drug first for CHF?

A

Digoxin is very dangerous, and it’s the best option of them all. Don’t want to risk this with patients

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21
Q

What do diuretics do in CHF

A

Decrease fluid

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22
Q

What do ionotropic drugs do for CHF

A

Increase contractility

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23
Q

What is the only inotropic drug that is ok for chronic use

A

Digoxin

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24
Q

What are the two inotropic drugs that are for acute only when treating CHF?

A 
B agonists 
Phosphodiesterase inhibitors (inamrinone)
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25
Q

What are some other vasodilator that can be used for CHF treatment but are not first choice

A
  • Neprilysin inhibitor (sacubitril)

- amlodipine (CCB)

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26
Q

What is considered first line therapy for CHF?

A

ACEI (and ARB but mostly ACEI)

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27
Q

Mechanism of ACEI in treating CHF

A
  • inhibit the vasoconstriction effects of ANGII
  • inhibit the retention of sodium and water by inhibiting aldosterone
  • prevent aldosterone-mediated cardiac remodeling
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28
Q

Cardiovascular actions of ACEI in CHF

A

Preload is reduced
Afterload is reduced
Reduce the long term remodeling and therefore INCREASES SURVIVAL

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29
Q

What is the B blocker that is most commonly used for CHF

A

Metoprolol

30
Q

Clinical use of metoprolol for CHF

A
  • In combination with ACEI (+/- diuretics, +/- digoxin)
  • decreasing mortality (INCREASED SURVIVIAL)
  • decreased remodeling
31
Q

Dosage of B blockers for CHF

A

Dosing is critical

  • start with low dose and titration upwards
  • high doses could be lethal
  • if low does is not enough, you must supplement with another drug as opposed to increasing the dose
32
Q

Other than decreasing HR, what other way can a low does B blocker be beneficial to a patient with CHF?

A

Blocks B1 on the kidneys, reducing renin

  • decreases RAAS
  • decreases aldosterone
33
Q

MOA of diuretics in CHF

A

Reduce preload!!!

Good at lowering fluid

34
Q

What diuretics are good at decreasing fluid for CHF?

A

Loops: furosemide
Thiazides: HCTZ

35
Q

What do furosemide and HCTZ do for cardiac remodeling in CHF?

A

NOTHING!

These only work to decrease fluid

36
Q

What diuretics are good at reducing adolsterone in CHF?

A

Spironolactone and eplerenone

37
Q

What is the primary use of spironolactone and eplerenone?

A

Decrease aldosterone to decrease remodeling to increase survival

They are not very good diuretics when it comes to decreasing fluid and decreasing preload

38
Q

What is the difference in the diuretics: furosemide and HCTZ vs spironolactone and eplerenone?

A

Furosemide and HCTZ are good diuretics at decreasing fluid and therefore decreasing preload

spironolactone and eplerenone are good at decreasing aldosterone to decrease remodeling to increase survival! They are not good diuretics when it comes to decreased fluid

39
Q

What is the neprilysin inhibitor used for CHF

A

Sacubitril

40
Q

An enzyme that degrades atrial and brain natriuretic peptide, two blood pressure-lowering peptides that worl mainly by reducing blood volume

A

Neprilysin

41
Q

What does sacubitril (a neprilysin inhibitor) do

A
  • Inhibits neprilysin (increase ANP and BNP levels)

- increases levels of bradykinin

42
Q

What is an ARNI

A

Sacubitril + Valsartan

Angiotensin II receptor blocker neprilysin inhibitor

43
Q

How do you take sacubitril?

A

You take it in combination with valsartan, called ARNI together

44
Q

Adverse effects of sacubitrol

A

Cough and angioedema, due to the increased bradykinin

45
Q

What is ivabradine

A

If (funny) sodium channel blocker

46
Q

What is the If channel responsible for

A

The automaticity of the SA node; these channels are unregulated in heart failure patients

47
Q

How does ivabradine (If channel blocker) work

A
  • Decreasing the diastolic depolarization slope in the SA node, decreasing heart rate without direct effects on contractility
  • used for patients in sinus rhythm with resting HR >70bpm and also taking B blockers at their highest tolerable dose
48
Q

Ivabradine is used with what other drug

A

B blockers

49
Q

If sodium channel blockers on HR and contractility

A

Decreases HR and does nothing to contractility

50
Q

Does ivabradine replace B blockers?

A

No

Use WITH B blockers

51
Q

CCB for heart failure

A

Pretty much don’t use them much but it is a last resort option

  • amlodipine
  • provide no mortality benefit
52
Q

Digitalis

A
  • Derived from the plant digitalis (foxglove)
  • increase contractility of heart (positive inotropic effect)
  • digoxin
53
Q

Therapeutic index of digoxin

A

<2

Very toxic

54
Q

MOA of digoxin (inotropic drug)

A

Reversible binds to the Na+-K+ ATPase of cardiac cells

55
Q

How does digoxin cause increased contractiltiy ?

A
  • Digoxin binds and inhibits Na+-K+ ATPase
  • increases intracellular Na+
  • increased intracellular Na leads to a greater Ca++ incflux
  • Ca++ stored in SR
  • more Ca++ now released when heart contracts, causing stronger contractility
56
Q

When is digoxin contraindicated?

A

In patients with hypokalemia

57
Q

Why is digoxin contraindicated in patients with hypokalemia?

A

Digoxin binds to the same site as the K+ on the Na+-K+ ATPase, competing.

  • hypokalemia leads to more digoxin being able to bind
  • huge problem leading to digoxin toxicity
58
Q

When do you use digoxin?

A

When you cant control heart failure with the first three choice drugs

59
Q

What are the adverse effects of digoxin?

A

Severe arrhhhmias

Nausea, vomiting, confusion, and blurred vision (CNS EFFECTS!)

60
Q

What drug is someone proanbably on if they complain of yellowish halos and blurred vision?

A

Digoxin

61
Q

Factors predisposing to digitalis toxicity

A

Hypokalemia

62
Q

What drugs should be avoided when taking digoxin

A

Diuretics, they can be potassium wasting and cause digoxin toxicity

63
Q

What drugs are only used for acute settings of heart failure, such as in the hospital

A

B agonists

Phosphodiesterase inhibitors

64
Q

B agonists and congestive heart failure

A

Positive inotropic effects, but used only short term due to tachypylaxis (rapid tolerance)

65
Q

What is the B agonist we use for acutely for heart failure

A

Dobutamine

-actions on B1 receptors and enhances cardiac contractiltiy

66
Q

Phosphodiesterase inhibitors and heart failure

A
  • Only in hospital (acute)
  • short term
  • mortality with long term use
67
Q

How does phosphodiesterase inhibitor work?

A

B receptors stimulation causes production of cAMP, which causes protein kinase A increase, which phosphorylation the Ca2+ channel to open it

Phosphodiesterase inhibitors stop the PDEIII from breaking down cAMP, so that it can open more Ca2+ channels

Only want to do this short term
Opposite of a B blocker

68
Q

How does a B agonist increase contractility?

A

Increase of Ca++ into the cell, goes to SR, more Ca++ released for contraction

69
Q

What is the phosphodiesterase inhibitor we use for heart failure

A

Inamrinone

70
Q

What drug increases cAMP?

A

Phosphodiesterase inhibitor (inamrinone)

Pharm Block 11 (7 decks)

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