heart failure medications

Question 1

What is heart failure?

Answer 1

Heart cannot pump enough blood to meet the body’s needs for blood and oxygen (i.e. supply ≠ demand)

Question 2

What is the goal of therapy?

Answer 2

Manage co-morbidities, lifestyle modifications, reduce mortality, reduce hospitalizations, symptom improvement, non-curative

Question 3

lowering afterload

Answer 3

use vasodilators
ACE inhibitors

Question 4

target MAP

Answer 4

50-60 mmhg

Question 5

treatment for preload and afterload reduction

Answer 5

ACE inhibitor
ARB
ARNI**
ISDN/Hydalazine

Question 6

sympathetic reduction

Answer 6

Beta blocker
Ivabradine

Question 7

beta blocker

Answer 7

very efficient way to lower the heart rate, can cause bradycardia if given high doses, can put them in cardiogenic shock, heart will stop

dont use beta blocker on ECMO patients

Question 8

Ivabradine

Answer 8

slows down heart rate without blocking beta receptors

Question 9

volume reduction

Answer 9

Loop diuretic

Mineralocorticoid receptor antagonists

SGLT-2 inhibitor

Question 10

Increase contractility

Answer 10

Digoxin –>has minor potential to act as a minor inotrope while slowing down your heart

Question 11

ACE inhibitors

Answer 11

Captopril
Enalapril
Lisinopril
Ramipril

side effect of ACE inhibitors is the COUGH

usually give ARBS instead of ACEi

Question 12

ARBS

Answer 12

Candesartan
Losartan
Valsartan

Mechanism of action:
Absorption:orally bioavailable​
Metabolism:hepatic​
Elimination:primarily feces​

Question 13

(ARNI) Angiotensin Receptor-Neprilysin Inhibitor

Mechanism of action

Answer 13

oral medication

Sacubitril/valsartan

Sacubitril: prodrug that inhibits neprilysin (neutral endopeptidase) leading to increased levels of peptides, including natriuretic peptides; induces vasodilation and natriuresis
Valsartan: direct antagonist of the angiotensin II (AT2) receptors; antagonizes AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses

two drugs that cause vasodilation through two different mechanisms

Question 14

BETA BLOCKERS

Answer 14

only three we use during heart failure

selective beta 1 blockers
Metoprolol –> ONLY SLOWS DOWN HEART RATE
Bisoprolol

nonselective beta-blockers
–> Carvedilol –> drops pressure and heart rate

labetalol is best used for aortic dissection –> NOT HEART FAILURE

Question 14

Sacubitril/Valsartan pharmacokinetics

Answer 14

Absorption:orally bioavailable​

Metabolism:converted to active metabolite by esterases (sacubitril); minimally metabolized (valsartan)​

Elimination:primarily urine (sacubitril); primarily feces (valsartan)

valsartan is VERY POTENT VASODILATOR

Question 15

beta blocker mechanism of action

Answer 15

Absorption:orally active; some are available IV (esmolol, metoprolol, propranolol, labetalol)

Onset: oral agents can take several weeks to see full effects

Metabolism:
Propranolol undergoes extensive and highly variable first-pass metabolism

Question 16

beta blocker pearls

Question 17

aldosterone antagonist

Answer 17

spironolactone (most common one we use)
Eplerenone

Absorption:orally active

Metabolism: rapid and extensive; hepatic to multiple metabolites

Elimination: urine (primarily as metabolites) and bile (secondary)

Question 17

SGLT inhibitors

Answer 17

Dapagliflozin
Empagliflozin

inhibition of proximal renal tubules –>
block reabsorption of filtered glucose –> increasing urinary glucose excretion (osmotic diuresis)

causes reduction in preload and afterload

“diuretic for your glucose”

pulls glucose from your blood and you pee it out

Question 18

SGLT-2 inhibitors Pearls

Answer 18

Contraindications:
Type 1 diabetes (increased risk of diabetes ketoacidosis)
Known hypersensitivity to drug
Pregnancy/lactation
Dialysis
Precautions
Dapagliflozin (eGFR < 25 mL/min/1.73 m2)
Empagliflozin (eGFR < 20 mL/min/1.73 m2)

Volume depletion:
Euglycemic ketoacidosis
Increased risk of mycotic genital infections, UTI, and necrotizing fasciitis of perineum

Question 19

Hydralazine and Isosorbide Dinitrate

Answer 19

African american pts have less renin

Hydralazine: direct arterial vasodilator  decreased SVR (afterload)
Nitrates: NO donor  venous vasodilation  decreased preload

dont use as commonly as other emds

Question 20

Ivabradine

Answer 20

use only for SINUS RHYTHM

Selectively inhibits If current (“funny current”) in SA node
↓ HR with no affect on blood pressure

It skews your action potential to go around and that slows down your action potential that slows down your heart rate

Use it for reduced heart failure EJ less than 55%

Question 21

Diuretics

Answer 21

LOOP DIURETICS are the most potent and remove the MOST VOLUME

Thiazide diuretics –> used for pts with high blood pressure –> BLOOD PRESSURE CONTROL

Question 22

Loop diuretics

Answer 22

Furosemide
Bumetanide
Torsemide

Question 23

thiazide diuretics

Answer 23

Chlorothiazide
Hydrochlorothiazide –> SHORTEST HALF LIFE
Metolazone –> LONGEST HALF LIFE

Question 24

digoxin

Answer 24

slows down heart rate and has a minor inotropic potential –> helps with patients that have AFIBB

Question 25

digoxin pearls

Answer 25

has a NARROW THERAPEUTIC INDEX

Question 26

meds to avoid in heart failure

Answer 26

NSAIDs
Nasal decongestants with pseudoephedrine/ephedrine
Alka-seltzer (sodium bicarbonate)

HFrEF
Thiazolidinedione (rosiglitazone, pioglitazone)
Most antiarrhythmic drugs (exceptions: dofetilide/amiodarone)
Calcium channel blockers (non-dihydropyridines  verapamil/diltiazem)