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Heart Failure Management

Name: Heart Failure Management
Creator: Veli Bakalov, MD

Four pillars that save lives, and the diuretics that only ease symptoms

Cardiology·Heart Failure & Cardiomyopathy·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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HFrEF is EF ≤40%, HFmrEF 41–49%, HFpEF ≥50%; the mortality-proven drugs apply to HFrEF.
HFrEF four pillars, each lowering mortality: ARNI (sacubitril-valsartan) or ACEi/ARB, beta-blocker, MRA, SGLT2 inhibitor.
Only carvedilol, metoprolol succinate, and bisoprolol reduce HFrEF mortality; do not start or up-titrate them during acute decompensation.
Stop an ACE inhibitor 36 hours before starting an ARNI to avoid angioedema.
MRAs (spironolactone, eplerenone) cause hyperkalemia; avoid if K >5 mEq/L or creatinine is elevated; switch to eplerenone for gynecomastia.
SGLT2 inhibitors (dapagliflozin, empagliflozin) reduce HF hospitalization with or without diabetes and are recommended in both HFrEF and HFpEF.
Loop diuretics relieve congestion but do not improve survival; digoxin reduces hospitalizations only.
ICD for EF ≤35% on GDMT; add CRT (CRT-D) for EF ≤35% with LBBB and QRS ≥150 ms.
Low BNP/NT-proBNP rules out HF in acute dyspnea; acute pulmonary edema = LMNOP (loop diuretic, morphine rarely, nitrates, oxygen/NIPPV, upright), inotropes if cold and wet.

Classification and diagnosis

Sort by ejection fraction. HFrEF is EF ≤40%, HFmrEF (mildly reduced) is 41–49%, and HFpEF is EF ≥50%. All present with dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema, and fatigue, but the therapies proven to lower mortality differ sharply, so the echocardiographic EF drives management.

Stages and classes. ACC/AHA stages describe progression and never move backward; NYHA classes describe current symptoms and can improve with treatment.

Stage AAt risk (hypertension, diabetes) with no structural disease or symptoms.
Stage BStructural disease without symptoms.
Stage CStructural disease with current or prior symptoms (NYHA I–IV).
Stage DRefractory, advanced HF needing transplant, an LVAD, or palliation.

NYHA classes. I, no limitation; II, symptoms with ordinary activity; III, symptoms with less than ordinary activity; IV, symptoms at rest.

BNP rules heart failure out. BNP and NT-proBNP are released with ventricular wall stretch and have a strong negative predictive value: a low level in an acutely dyspneic patient makes HF unlikely (roughly BNP under 100 pg/mL or NT-proBNP under 300 pg/mL). Levels also rise with renal failure, older age, and AFib, and run lower in obesity. Sacubitril raises BNP itself by blocking its breakdown, so follow NT-proBNP in patients on an ARNI.

GDMT for HFrEF: the four pillars

Four classes, each independently lowering mortality. Together they cut HFrEF mortality dramatically, so the goal is to get all four on board and up-titrated, not to perfect one before starting the next.

The four pillars

Class	Agents	Evidence	Cautions
ARNI (or ACEi/ARB)	Sacubitril-valsartan	Superior to enalapril (PARADIGM-HF); ACEi/ARBs also reduce mortality	Never with an ACEi: 36-hour washout (angioedema); hypotension, hyperkalemia, renal function
Beta-blocker	Carvedilol, metoprolol succinate (extended-release), bisoprolol only	Mortality benefit limited to these three	Start low and up-titrate; do not start or up-titrate during acute decompensation
MRA	Spironolactone, eplerenone	RALES, EPHESUS	Hyperkalemia; avoid if K >5 mEq/L or creatinine elevated (eGFR under 30); spironolactone gynecomastia
SGLT2 inhibitor	Dapagliflozin, empagliflozin	DAPA-HF, EMPEROR; benefit with or without diabetes	Genital mycotic infection, volume depletion, euglycemic DKA

Practical points. Eplerenone is more selective, so switch to it if spironolactone causes gynecomastia. SGLT2 inhibitors act through glucosuria and natriuresis and help regardless of diabetes status. A beta-blocker the patient already takes is usually continued through a mild decompensation rather than stopped.

Diuretics, add-ons, and devices

Diuretics ease symptoms, not mortality. Loop diuretics such as furosemide relieve congestion but do not reduce mortality. Titrate them to euvolemia: they are for the congested patient, not for prognosis.

Add-on and substitute agents.

Hydralazine plus isosorbide dinitrate: lowers mortality in self-identified Black patients with persistent NYHA III–IV symptoms on GDMT, and substitutes when ACEi, ARB, and ARNI cannot be used.
Ivabradine: EF ≤35% in sinus rhythm with resting heart rate ≥70 despite a maximally tolerated beta-blocker.
Digoxin: fewer hospitalizations, no mortality benefit.

Avoid drugs that worsen HFrEF: non-dihydropyridine calcium channel blockers (verapamil, diltiazem), NSAIDs, and thiazolidinediones.

ICD vs CRT

Feature	ICD	CRT (biventricular pacing)
Criteria	EF ≤35% on GDMT (primary prevention)	EF ≤35% with LBBB and QRS ≥150 ms on GDMT
Purpose	Shocks lethal ventricular arrhythmias to prevent sudden death	Resynchronizes ventricular contraction; improves symptoms and survival
Timing	After about 3 months of GDMT and at least 40 days after an MI	After optimized GDMT

A patient who meets both sets of criteria receives a combined CRT-defibrillator (CRT-D).

HFpEF: control the drivers

Fewer mortality-proven drugs. In HFpEF (EF ≥50%) the stiff ventricle depends on adequate filling time and pressure, and outcomes hinge on the conditions that drive it:

Control blood pressure, the main driver of diastolic dysfunction.
Use diuretics for volume overload.
Treat comorbidities: AFib (rate control lengthens filling time), obesity, and ischemia.
SGLT2 inhibitors are now guideline-recommended; their benefit here is mainly fewer HF hospitalizations.

An MRA or ARNI may be considered in selected patients, particularly toward the lower end of the preserved EF range, but a beta-blocker aimed at "raising the EF" has no role.

Acute decompensated heart failure

LMNOP. Acute cardiogenic pulmonary edema with volume overload is managed with:

Loop diuretic: IV furosemide is the first-line drug to offload volume.
Morphine: rarely used now.
Nitrates: lower preload and afterload when blood pressure allows.
Oxygen, including non-invasive positive pressure ventilation for respiratory distress.
Position: sit the patient upright.

Hypoperfusion. A patient who is congested and poorly perfused (the cold-and-wet profile: cool extremities, low blood pressure, worsening renal function) needs inotropes such as dobutamine or milrinone to restore output before diuresis can work.

A fluid bolus is never part of treating acute pulmonary edema; it worsens congestion.