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Flashcards in Heart Failure Drugs Deck (24)

Compensatory Responses to Heart Failure Cycle

Compensatory responses lead to a cycle; start with decreased CO causing constriction from NE, AII, and ET-1 leading to increased afterload due to constriction leading to reduction in EF, which means more decreased CO then happens over and over again.


Loop Diuretics

Furosemide, bumetanide, torsemide

As sodium, K, and Cl move into the cell out of the urine and reabsorbing it; this causes a positive potential to recycle Mg and Ca2+

This causes fluid retention; the medication prevents fluid retention by inhibiting the NKCC2
25% of the Na and Cl is reabsorbed here – target will reduce absorption by 25%

High capacity diuretic = water pill


Thiazide Diuretics (DCT)

Hydrochlorothiazide (metolazone – action is the same)

Block Na/Cl channel and inhibits their reabsorption thus reducing water reabsorption
Often used in combination with loop diuretics
K+ wasting
5% of reabsorption occurs here



Controlling the symptoms without affecting the heart contractility

Decrease NaCl and KCl reabsorption

Increase H2O excretion

Decrease volume and cardiac preload and afterload

Decreases pulmonary and peripheral edema - suggested use only when these occur


Diuretic Side Effects

Water loss will decrease L ventricular filling so low as to decrease CO

Low K and Mg = arrhythmias


Diuretic Drug Interactions

Digitalis (increase loop diuretic and thiazide activity)

NSAIDs (decrease diuretic response)

Thiazide diuretics increase loop diuretic activity and vice versa

Quinidine + Thiazide = low K and risk of torsades de pointes


Aldosterone Antagonists

Sodium will not be reabsorbed by directly antagonizing mineralocorticoid receptors

Will not see much K loss = hyperkalemia is risk

Eplerenone- less activity on sex hormones and more selective for mineralocorticoids compared to Spironolactone

Significant reduction in morbidity and mortality when combined with a diuretic


Beta Blockers

Metoprolol and Atenolol

Counter intuitive because negative on inotropy and contractility, but are useful for tx of heart failure
Immediate effects: reduce systolic function, but recovers within a couple months
High NE increases apoptosis, so beta blockers may be blocking this
L ventricular geometry changes – decreases chamber size to increase EF
Increase expression of beta receptors
Lower HR
Need to be cautious due to negative inotropic effects


ACE Inhibitors and ARB

ACE Inhibitors: Captopril, Lisinopril
ARBs: Losartan, Valsartan

ACE: Prevent AI to AII resulting in reduced peripheral resistance to reduce afterload
Reduce water and salt retention
If reducing AII, it will decrease aldosterone thus reducing preload
Reducing sympathetic activity
Increase bradykinin levels to help with vasodilation

ARBs: work on AI receptor so same effects; reduced afterload and preload; reserved for those that cannot tolerate ACE inhibitors


Side Effects of ACE Inhibitors

Dry cough
Angioedema – potentially life threatening
Can impair auto-regulation of glomerular perfusion pressure in patients with decreased renal blood flow


Side Effects of ARBs

Renal dysfunction
Angioedema (rare; use caution if ACE inhibitor-associated angioedema in history)


Beta Agonists

Increase cAMP in the cell, and activate protein kinase A which phosphorylates the L type Ca channel to increase Ca influx into the cell; PKA also phosphorylate other substances like Ca channel on SR to cause Ca into cytoplasm; overall it causes an increase in contractility and CO

Beta agonists are IV only and used in acute heart failure while hospitalized; rapid development of tolerance within a few days


Beta Agonist Side Effects

Dobutamine –
mixed beta receptor agonist; cardiac effects through β1; β2 stimulation may decrease SVR and MAP
Supraventricular or ventricular arrhythmias



Inhibit PDE, which prevent hydrolysis of cAMP, and by preventing the breakdown it is increasing the time cAMP is present so it prolongs the actions of PKA and increases Ca2+ and contractility

Dilates resistance vessels to decrease preload and afterload

IV only in acutely ill hospitalized patients


Bipyridines Side Effects

Milrinone is the only PDE3 inhibitor used in acute heart failure in the US

Side effects:
Less bone marrow and liver toxicity than inamrinone


Inotropic Agents and Risk of Hospitalization and Death

Use of inotropic agents that increase cardiac cell cAMP are consistently associated with ↑ risk of hospitalization and death



Inhibit N/K exchange to increase Na in the cell which will decrease force for Na/Ca exchanger to keep Ca in, thus increasing free Ca2+ in the cell to increase contraction and EF, but decrease CO


Digoxin Side Effects

If you already have low K, low Mg, or high Ca = these effects will be increased as a side effect
Blurred or yellow vision
Disturbances in cognitive function


Drug Interactions with Digoxin

It will have interactions with other drugs like quinidine
Increased digitalis concentration can occur when using these drugs = cardio toxicity

Thiazide, furosemide, corticosteroids – decrease K in blood, so increase cardio toxicity

Increase PR interval and decrease QT interval on EKG


Isosorbide Dinitrate

Isosorbide dinitrate: direct vasodilator
Organic nitrate
Enzymatic biotransformation to NO
Short acting
Reduces preload by increasing peripheral venous capacitance


Sodium Nitroprusside

Sodium nitroprusside: direct vasodilator
Direct NO donor (quickly metabolized to generate NO)
IV only; effect occurs within 30 seconds and disappears within 3 minutes of discontinuation of drug



Hydralazine: direct vasodilator

Change in Ca2+ balance, membrane hyperpolarization from opening K channels but mechanism is not clear
Vasodilation of arterioles and reduces resistance
Reduces SVR and LV preload
Not used by itself (usually with nitrate), only in combination with isosorbide dinitrate especially for those that do not tolerate ACE/ARBs


Acute vs. Chronic HF Medications

Acute: diuretics are drug of choice especially if pulmonary or peripheral edema, vasodilators, beta agonists, bipyridines (PDE inhibitors), natriuretic peptide

Chronic: diuretics, aldosterone antagonists, ACE inhibitors, ARBs, beta blockers, cardiac glycosides, vasodilators


Effects of Multi Drug Therapy

Just a diuretic: reduce ventricular filling pressure from reduction of preload by reducing volume, but does nothing for SV

Inotropic agent: contractility increases as well as CO

Vasodilator: lower filling pressure and higher SV, but no where close to normal

Therefore, people need a combination to be maintained vs. just one drug alone