Heart Failure Pharmacotherapy Flashcards

1
Q

What are the 4 medication classes included in GDMT for HFrEF?

A

ARNI/ACE/ARB (aka RAAS inhibitors)
Beta blockers
Aldosterone antagonists (diuretics, usually K+ sparing or thiazide like)
SGLT2 inhibitors

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2
Q

What is the most common cause of HFrEF?

A

Ischemia (CAD, ACS, HTN, etc.)

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3
Q

What are some non-ischemic causes of HFrEF?

A

Idiopathic/congenital
Amyloid, sarcoid, genetic
Drug or toxin induced (chemotherapy)

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4
Q

What are the two classifications of medications in HF?

A

Symptom management medications

Meds that reduce mortality/have a mortality benefit

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5
Q

Does GDMT focus more on symptom management or mortality benefits?

A

Mortality benefits

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6
Q

Which cornerstone medication of GDMT also has evidence to be effective in HFpEF?

A

SGLT2 inhibitors

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7
Q

Examples of HFrEF meds that focus on symptom management

A

Diuretics
Digoxin
Inotropes (in end of life patients)
Vericiguat

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8
Q

Which medications should you use in patients with low renin instead of ACE/ARB/ARNI?

A

Hydralazine + nitrate therapy

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9
Q

Where do ACEs work on the RAAS system?

A

Prevent conversion of angiotensin I to angiotensin II AND prevent conversion of bradykinin into inactive kinins

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10
Q

Where do ARBs work on the RAAS system?

A

Prevent angiotensin II from binding to its receptor

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11
Q

Where do ARNIs work on the RAAS system?

A

Prevent angiotensin II from binding to its receptor (like ARBs)

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12
Q

What is the overall result of ACE and ARB use?

A

Decreased cardiac remodeling and decreased morbidity/mortality

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13
Q

What effect do ACEs and ARBs have on preload and afterload?

A

Decreases both

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14
Q

ADRs of ACEs and ARBs

A

Acute kidney injury (HOWEVER an up to 30% increase in serum creatinine is normal)
Hypotension
Hyperkalemia
Angioedema (much less common with ARBs)

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15
Q

Specific ADRs of ACEs

A

Angioedema and cough (d/t increased bradykinin)

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16
Q

Contraindications of ACEs and ARBs

A

Pregnancy
Bilateral renal artery stenosis
Patients with low renin

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17
Q

What should you do if a patient on an ACE develops a cough?

A

Switch to an ARB

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18
Q

Is there a washout period when switching between ACEs and ARBs?

A

No because they have a similar MOA –> can start next dose of new class when the other one is due

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19
Q

Suffix for ACEs and suffix for ARBs

A

ACEs - pril
ARBs -sartan

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20
Q

Entresto is a combination of…

A

Sacubitril (neprilysin inhibitor) and valsartan (ARB)

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21
Q

What is the overall result of ARNI use?

A

Prevent breakdown of natriuretic peptides (somewhat of a diuretic effect)

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22
Q

ADRS of ARNIs

A

Cough
Angioedema
Hyperkalemia
Hypotension (MC, even more common than in ACEs or ARBS)

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23
Q

ARNI contraindications

A

Pregnancy
Bilateral renal artery stenosis
Potential hx of angioedema with an ACE

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24
Q

ARNI dosing

A

Always BID (can cut tablets in half if unable to tolerate higher doses)

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25
Is there a washout period when switching between ARNIs and ACEs? ARBs?
ARNI + ACE = 36 hour washout ARNI + ARB = no washout (b/c ARNI/Entresto already has an ARB component)
26
T or F: You start patients on the target dose of Entresto when initiating therapy
FALSE
27
Beta blockers used for HFrEF
Bisoprolol, carvedilol, metoprolol succinate
28
ADRs of BBs
Fatigue/exercise intolerance Bradycardia Hypotension (minimal) Sexual dysfunction
29
Contraindications for BBs
Sinus bradycardia 2nd or 3rd degree heart block (unless pt has pacemaker) Active asthma with bronchospasms
30
Which is better for mortality in HFrEF, metoprolol tartrate or succinate?
Succinate (50 mg daily) -- tartrate has NO MORTALITY BENEFIT
31
What is the overall result of aldosterone antagonist/diuretics/MRA use?
Decreased sodium/water retention Fibrosis (cardiac remodeling) Decreased morbidity/mortality
32
Examples of MRAs
Spironolactone (non-selective antagonist) Eplerenone (selective antagonist)
33
ADRs of spironolactone
Gynecomastia (b/c it is non selective, it also binds androgen pathways) Hyperkalemia Hypotension
34
ADRs of eplerenone
Hyperkalemia Hypotension NO GYNECOMASTIA (b/c this is selective)
35
MRA contraindications
Hyperkalemia Poor kidney function (SCr > 2 in females, SCr > 2.5 in males)
36
Where do SGLT2 inhibitors work in the nephron?
Proximal tubule
37
Examples of SGLT2 inhibitors
Dapagliflozin (Farxiga) Empagliflozin (Jardiance)
38
ADRS of SGLT2 inhibitors
Euglycemic DKA (blood sugar not high) Dyslipidemia Increased urination UTIs
39
SGLT2 inhibitor contraindications
Pregnancy (2nd and 3rd trimesters) eGFR < 20 for Jadiance eGFR < 25 for Farxiga
40
True or false: SGLT2i dosing for HF is fixed
TRUE -- changes when dosing for diabetes
41
What is the result of using hydralazine?
Direct ARTERIAL vasodilator --> decreases afterload
42
What is the result of using nitrate therapy (isosorbide dinitrate)?
Direct VENOUS vasodilator --> decreases preload
43
When should you use hydralazine/nitrate therapy?
Patients who cannot tolerate ACE/ARB/ARNI (d/t renal function, hyperkalemia, or presence of ADRs) Patients with low renin (AA) Pregnancy
44
ADRs of hydralazine/nitrate therapy
Headache, dizziness Hypotension with reflex tachycardia Lupus like syndrome @ high doses
45
Hydralazine/nitrate contraindications
PDE-5 inhibitors (sildenafil, tadalafil) --> decreases BP TOO much
46
Do loop diuretics reduce mortality or manage symptoms?
Manage symptoms
47
Where do loop diuretics work?
Loop of Henle of the nephron
48
What symptoms do loop diuretics address?
Relieve pulmonary congestion ("wet" patients) and peripheral edema
49
Examples of loop diuretics
Furosemide (lasix) Torsemide (Demadex) Bumetanide (Bumex)
50
Loop diuretics ADRs
Electrolyte disturbances: - Hypokalemia - Hypomagnesemia - Hyperuricemia Ototoxicity @ high doses
51
Should you take loop diuretics in the morning or at night?
In the morning to avoid peeing during the middle of the night
52
Which is more potent, furosemide or bumetanide?
Furosemide (IV, more potent than oral)
53
Digoxin MOA?
Inhibits Na/K/ATPase pump --> increase calcium concentration intracellularly --> positive inotropic effect --> increased contractility and CO
54
Does digoxin have a mortality benefit?
NO - strictly sx management
55
Digoxin has a narrow therapeutic index. What are some signs of digoxin toxicity?
N/V Anorexia Bradycardia Visual disturbances
56
At what dose do you common see digoxin toxicity?
> 2 ng/mL
57
How is digoxin eliminated?
Renally, so consider kidney function when dosing and dose based on ideal body weight
58
When do SGLT2 inhibitors have the most benefit in HFpEF?
When the EF is closer to 50% (b/c it's more like HFrEF at that point)
59
Mainstay of HFpEF treatment?
Symptom management and lowering of BP
60
BP goal for managing HFpEF?
<130/80 mmHg
61
When can ARNI be useful in HFpEF?
If BP is very uncontrolled
62
What are some medications to avoid in HF?
Non DHP CCBs NSAIDs (increase fluid retention and therefore increase risk of AKI) Arrhythmia meds COX 2 inhibitors Estrogens and androgens Cardiotoxic agents