B.20 Chronic Heart Failure Treatment Flashcards
B.20 Chronic Heart Failure Treatment
What are the first line drugs for HF
ACE inhibitors
Beta-blockers
Diuretic
Aldosterone Antagonist/MRA
“ABCDE” of HFrEF
A – ACEi / ARNI B – Beta-blocker C – Correct congestion (loop diuretic) D – Dapagliflozin / Empagliflozin (SGLT2i) E – Eplerenone / Spironolactone (MRA)
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What are the general principals of pharmacotherapy
Titrate medications to the target dosage, even if symptoms improve at lower doses.
Dosages may be adjusted as frequently as every 1–2 weeks.
Most patients with HFimpEF should continue treatment, even if asymptomatic, to prevent relapse and worsening LV dysfunction.
Patients with HFmrEF may benefit from the agents recommended for HFrEF, especially SGLT2i.
Diuretics are recommended for all patients with congestion regardless of LVEF.
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Which of the first line drugs is not recommended for NYHA stage/Class I
aldosterone antagonists
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Drugs used in NYHA Class I
ACEi/ARNI
beta Blocker
MRA
SGLT2i - Dapagliflozin/Empagliflozin
Loop Diuretic For Fluid Retention
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MRA/Aldosterone Antagonist principles
“MRAs like spironolactone or eplerenone are key mortality-reducing agents in HFrEF, used in patients with EF <35% on standard therapy. They block aldosterone to reduce remodeling, but require careful monitoring of potassium and renal function.”
MRAs are a core, first-line therapy in heart failure with reduced ejection fraction (HFrEF, EF <40%), used to:
✅ Reduce mortality
✅ Decrease hospitalizations
✅ Prevent myocardial fibrosis and remodeling
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MRA/Aldosterone Antagonist what drugs are used
Spironolactone
Eplerenone
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MRA/Aldosterone Antagonist MOA
Mechanism of Action
Block aldosterone receptors in the distal nephron ↓ Sodium and water reabsorption ↑ Potassium retention Inhibit aldosterone-mediated myocardial fibrosis and vascular inflammation
🧠 Aldosterone contributes to cardiac remodeling, fibrosis, and potassium/magnesium loss – all of which worsen heart failure outcomes.
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Diuretics - principles
Initiate treatment using loop diuretics to address volume overload.
essential for symptom relief in HFrEF or HFpEF
DO NOT improve survivial
Thiazides can be included for a synergistic effect.
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MOA Diuretics
Furosemide, Bumetanide, Torsemide
Site of action: Thick ascending limb of Loop of Henle
Inhibits the Na⁺-K⁺-2Cl⁻ (NKCC2) transporter → Leads to massive natriuresis and diuresis → ↓ preload by reducing intravascular volume → Relieves pulmonary and peripheral congestion
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What are Thiazide Diuretics
A group of diuretic agents that act as Na⁺-Cl⁻ cotransporter inhibitors in the early distal renal tubule. Used mainly to treat hypertension
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MOA of Thiazide Diuretics
Hydrochlorothiazide, Metolazone
Site of action: Distal convoluted tubule
Inhibit Na⁺-Cl⁻ symporter → Modest diuresis → Used as add-on therapy in diuretic resistance to loop diuretics
Metolazone is especially potent when combined with loop diuretics.
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Do loop diuretics improve mortality in HF?
→ ❌ No – they improve symptoms only, not survival.
B.20 Chronic Heart Failure Treatment
Can thiazides be used as monotherapy in acute decompensated HF?
→ ❌ No – they are not potent enough; used with loop diuretics if needed.
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What electrolyte disturbances can loop diuretics cause?
→ Hypokalemia, hyponatremia, hypomagnesemia, metabolic alkalosis
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ACEi prinicples
Can improve prognosis and symptoms
Start treatment with ACE inhibitors to decrease preload, lessen afterload, and enhance cardiac output.
If the patient experiences intolerance to the medication (e.g., dry cough), consider switching to ARBs.
Monitor for hypokalemia, hypotension, and elevated creatinine levels (renal impairment).
All patients with ACC/AHA stage B HFrEF
Patients with ACC/AHA stages C and D HFrEF if ARNI is not tolerated or affordable
group of antihypertensive drugs that inhibit the enzyme responsible for the conversion of angiotensin I to angiotensin II.
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What ACEi are used to TX HR
Enalapril
Ramipril
Lisinopril
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MOA of ACEi
Inhibition of ACE enzyme
→ Prevents conversion of angiotensin I to angiotensin II
- ↓ Angiotensin II → multiple effects:↓ Vasoconstriction → ↓ afterload (↓ resistance the LV pumps against)↓ Aldosterone secretion → ↓ sodium and water retention → ↓ preload↓ Sympathetic activation↓ Myocardial remodeling & fibrosis↓ Ventricular hypertrophy and dilation
- ↓ Bradykinin breakdown (ACE also degrades bradykinin)
→ ↑ bradykinin → vasodilation → may cause dry cough and angioedema (side effects)
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Do ACE inhibitors improve mortality in HFpEF?
→ ❌ No – they do not improve survival in HFpEF (only HFrEF)
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Can ACE inhibitors be used during acute decompensated HF?
→ ❌ No – start after stabilization; may worsen hypotension or renal function if given too early
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Should ACEi be stopped if creatinine rises after starting?
→ ❌ Not necessarily – a rise up to 30% from baseline is acceptable and expected
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Are ACE inhibitors useful in asymptomatic LV dysfunction (EF <40%)?
→ ✅ Yes – they delay onset of symptoms and progression to symptomatic HF
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Beta Blockers general principles
Introduce a beta blocker once the patient is stable on ACE inhibitors. This is especially advantageous for patients with hypertension and those who have experienced a post-myocardial infarction. Note that beta blockers are contraindicated in acute decompensated heart failure (ADHF).
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What are the beta blockers used to tx HF
Bisoprolol – selective β₁-blocker
Carvedilol – blocks β₁, β₂, and α₁ (vasodilating)
Metoprolol succinate (extended-release, β₁-selective)
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MOA of beta blockers in HF
Beta-blockers inhibit β₁-adrenergic receptors (primarily in the heart), leading to:
1- ↓ Heart rate (negative chronotropy)
→ Increases diastolic filling time
→ Improves cardiac output and coronary perfusion
- ↓ Myocardial contractility (negative inotropy) (initially)
→ But long-term leads to improved LV function - ↓ Myocardial oxygen demand
→ Protects against ischemia and arrhythmias - ↓ Sympathetic overactivation
→ Which normally worsens HF by causing vasoconstriction, tachycardia, and remodeling
→ So beta-blockers reverse maladaptive remodeling, ↓ apoptosis, and ↓ fibrosis - ↑ β-receptor sensitivity and density over time
→ Improves heart’s long-term responsiveness to catecholamines