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Pharmacology > Cardio: Heart Failure Drugs > Flashcards

Cardio: Heart Failure Drugs Flashcards

1
Q

What are some drugs used for heart failure?

A 
ACEi
ARBs
Carvedilol
Diuretics (both loop and K+ sparing)
Nitrates
Digoxin
Dobutamine/Dopamine
Milrinone
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2
Q

What is the difference between systolic and diastolic heart failure?

A

Systolic=pump issue
-loss of contractility, usually due to volume overload and eccentric hypertrophy

Diastolic=relaxing issue
-hypertrophic and stiff ventricle leads to decrease in filling, contractility is fine though

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3
Q

Which of the two, systolic or diastolic, has a preserved ejection fraction?

A

Diastolic

-like I said, systolic is a bad pump so you cannot get the fluid out

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4
Q

What can make Diastolic HF worse?

A

A fib leads to less filling, making it worse

Tachycardiac means less filling

Increase in MAP

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5
Q

MOA of ACEi/ARBs

A

Blocks formation of/effect of Angiotensin II

  • decrease afterload (vasodilation)
  • blocks aldosterone (less Na+/water retention)
  • -lowers BP
  • decreasing remodeling
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6
Q

Clinical applications for Captopril (or other -prils)?

A

HTN, Systolic HF, diabetic nephropathy

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7
Q

What are some common toxicities of all ACEi?

A

Cough, angioedema, Teratogenic!!
-do not use w pregnancy

Also hyperkalemia, hyponatrema

Altered taste (mainly captopril)

Embryotoxic!

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8
Q

Which ACEi’s have longer half life, permitting once/day dosing and are more widely used today?

A

Benazepril and lisonopril

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9
Q

Clinical applications for losaratan (or other sartans)

A

HTN,
diabetic nephropathy,
CKD,
HF resistent to ACEis

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10
Q

What are some common toxicities of all ARBs?

A

Hypotension, hypoglycemia, hyperkalemia

Embryotoxic!

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11
Q

What make valsartan unique to the other ARBs?

A

It is not a prodrug, therefore does not need activation and is eliminated primarily in the feces
-works if poor renal function

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12
Q

What makes candesartan unique to other ARBs?

A

It has irreversible binding to AT1

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13
Q

Effects of Valsartan/Sacubitril?

A

Leads to increased secretion of BNP and ANP
-increases fluid loss, lowers BP

Valsartan is an ARB, so blocks Angiotensin II

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14
Q

Clinical applications of Valsartan/Sacubitril?

A

Heart failure w Reduced EF

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15
Q

How does Sacubitril work?

A

Inhibits neprilysin NEP through its active metabolite, LBQ657

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16
Q

Adverse effects of Valsartan/Sacubitril?

A

Hypotension, hyperkalemia, increased serum Creatinine

Angioedema**

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17
Q

MOA of carvedilol?

A

nonselective (inverse agonist) Beta- and alpha-adrenergic blocker
-B>a activity

Slows HR (less O2 use), protects from arrhythmias, reduces Renin

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18
Q

Clinical applications for carvedilol?

A

If stable:

  • recent MI with rEF
  • HFrEF (systolic HF)
  • HTN (not first choice)
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19
Q

Toxicities of carvedilol?

A

Chest pain, discomfort, dizziness, lightheaded, swelling of LE, pain, SOB, bradycardia

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20
Q

Which B-blocker is good for HTN emergencies?

A

Labetalol

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21
Q

If a patient has had a recent MI and now has reduced ejection fraction, what should be given along with B-blockers?

A

ACEi

-this has been proven to reduce mortality

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22
Q

Would you use B-blockers in someone with COPD, Asthma, or heart blocks?

A

Nope

-can make all worse

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23
Q

What should you do when taking someone off a B-blocker?

A

Taper them off!

-abrupt removal can cause acute tachycardia, HTN and ischemia

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24
Q

MOA of Ivabradine?

A 
blocks If (funny) channels
-prolongs diastole and slows HR
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25
Q

Clinical applications of Ivabradine?

A

Treatment of HR>70 with systolic HF

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26
Q

can you use B-blockers with ivabradine?

A

Yes, but only maximally tolerated doses of B-blockers, or if they are contraindicated

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27
Q

Toxicities of Ivabradine?

A 
Bradycardia, 
HTN (reflex), 
increase A-fib risk, 
heart block, 
SA arrest
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28
Q

Contraindications of Ivabradine?

A

Decompensated HF
-meaning regulation isn’t working

Hypotension, AV block, hepatic impairment

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29
Q

MOA of spironolactone

A

Competitive aldosterone antagonist

  • decreases reabsorption of Na and water
  • -lowers BP

Also antagonizes pro-fibrotic effect of aldosterone

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30
Q

Clinical applications of spironolactone

A

Tx of:

  • HF without loss of K+**
  • reduces fibrosis in HFrEF post MI**
  • Primary hyperaldosteronism
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31
Q

What is interesting about spironolactones pharmacokinetics?

A

it is a steroid, so it is slow on, slow off

-single dose lasts for a few days

32
Q

Adverse effects of spironolactone?

A

Hyperkalemia

Amenorrhea, hirsuitism, gynecomastia, impotence

Tumorigen

33
Q

What can happen if you mix loop diuretics with digoxin?

A

Increases toxic effects!

-hypokalemia increases the effect of digoxin

34
Q

MOA of loop diuretics?

A

NKCC blocker, so water will follow

  • lowers fluid, therefore lowers preload and BP
  • removes fluid congestion to bring heart to optimal stretch length
35
Q

Where do loop diuretics work?

A

Thick ascending loop of Henle

36
Q

Clinical applications of Furosemide

A

Loop diuretic for edema in:
-HF, cirrhosis, renal issues**

Lowers preload and BP

37
Q

Toxicities in furosemide?

A

Loss of electrolytes (K, Na, Ca, Mg)

Hyperglycemia, Hyperuricemia

Ototoxic!*
-vertigo, tinnitus

Sulfa drug*

38
Q

What loop diuretics have better oral absorption, so work better in HF?

A

Torsemide and butemide

39
Q

What can be given as a loop diuretic in those w a sulfa allergy?

A

Ethacrynic acid

40
Q

What drug drug interactions do you need to watch for with loop diuretics?

A

Digoxin
-less K+ can increase toxicity of digoxin

Ototoxic drugs
-mycin Abs!

41
Q

What can be given with loop diuretics to prevent hypokalemia?

A

K+ sparing diuretics

-spironolactone

42
Q

What class of diuretics loses the least amount of bicarb?

A

Loop diuretics

43
Q

Hydrochlorothiazide MOA

A

Blocks NaCl cotransporter at distal tubule

-decreases Na and Water absorbed to lower BP

44
Q

What is an off label use of Hydrochlorothiazide

A

Calcium nephrolithiasis

-counters loss of Ca+

45
Q

Toxicities of Hydrochlorothiazide

A

Loss of electrolytes (K, Na, Mg)

Hyperglycemia, Hyperuricemia

Sulfa drug*

46
Q

Which thiazide diuretic is a favorite of cardiologists?

A

Metolazone

47
Q

Which thiazide diuretic is longest acting?

A

Chlorthalidone

48
Q

What are some common causes of diuretic failure?

A

Nonadherance, excess salty diet
Decreased GFR
NSAID use

49
Q

Isosorbide dinitrate decreases ___load while hydralazine decreases ___load

A

Isosorbide dinitrate decreases preload while hydralazine decreases afterload

50
Q

What does hydralazine require to become activated?

A

COX activation, mediated by PGI

51
Q

Clinical applications of hydralazine?

A

HTN and HF (especially African Americans, or if ACEi contra)

52
Q

When is hydralazine used in HTN emergency?

A

In pregnancy!

53
Q

Does hydralazine dilate arterioles or veins?

A

Arterioles

-decrease afterload

54
Q

Does nitroglycerin dilate arterioles or veins?

A

Veins

-decrease preload

55
Q

Adverse effects of hydralazine

A

angina pectoris, flushing, tachycardia, edema
pruritis**
drug-induced lupus**

56
Q

MOA of digoxin

A

Inhibits Na/K ATPase

  • increases Na and Ca in heart, increasing contractility (positive inotrope)
  • directly suppresses AV node
57
Q

Clinical applications of Digoxin

A

To..

  • control RVR in a-fib
  • Treat HF by increasing contractility of heart
58
Q

How is digoxin administered?

A

Orally

-increases as CO and renal function decrease so needs loading dose!

59
Q

Is digoxin safe in pregnancy?

A

Yup, safe to use in SVTs during pregnancy

60
Q

Adverse effects of digoxin

A

Cholinergic effects (N/V, diarrhea), blurry yellow vision, arrythmias (PVC), AV block

these are the ones in FA

61
Q

How does digoxin affect ANS activity?

A

Increases Vagus firing rate, so more response to SA node to ACh

62
Q

How do you treat digoxin overload?

A

KCl
Lidocaine, Phenytoin (Class IB antiarrythmic)
Anti-digitalis Abs

63
Q

First line Tx of Systolic HF?

A

ACEi or ARBs or ARNI in conjuction with B-blockers/aldosterone antagonists

64
Q

Tx of Diastolic HF?

A

Control BP

-treat symptoms with diuretics

65
Q

Do nitrates, PDE5 inhibitors, or digoxin have efficacy for treating HFpEF?

A

No, so dont use

66
Q

If a patient is hyper/normotensive with Acute Decompensated HF, how should you treat?

A

Loop Diuretic + Vasodilator (nitrates/nitroprusside)

67
Q

If a patient is hypotensive with Acute Decompensated HF, how should you treat?

A

Just a loop diuretic

68
Q

If a patient has Decompesated HF and signs of symptomatic hypotension with end-organ dysfunction what should be given?

A

Dobutamine or Dopamine

and

Discontinue B-blockers if pt has moderate-severe end organ damage

69
Q

MOA of milrinone

A

Selective PDE-3 inhibitor

-used as inotropic agent increasing cAMP

70
Q

Clinical use of milrinone?

A

Used for unresponsive HF

71
Q

Adverse effects of milrinone?

A

Ventricular arrythmias, SVTs, headache

72
Q

MOA of Dobutamine

A

Increase B1/B2 activity (+) enantiomer
-increase HR and Contractility for cardiac shock

Block a-receptors (-) enantiomer

73
Q

MOA of dopamine

A

Low doses=activates B1

-increase HR and contractility for shock and cardiac decompensation

74
Q

What drugs should you avoid in decompensated HF?

A

Class I antiarrythmics (consider amiodarone instead),
CCBs,
NSAIDs

75
Q

How do you know if digitalis is therapeutic or toxic based on ECG?

A

Therapeutic
-ice cream scoop

Toxic
-decoupled Atria and ventricular contraction or even PVCs

Pharmacology (50 decks)

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