Heart failure questions love to test one thing over and over: is the ventricle too weak to squeeze (HFrEF) or too stiff to fill (HFpEF)? If you can identify that quickly, you can predict the echo findings, typical patient profile, and first-line management.
The 5-Second Mnemonic: “FAT vs THICK”
Think of the left ventricle (LV) as either FAT and floppy or THICK and stiff:
HFrEF = “FAT Failure”
- FAT ventricle → dilated, thin-walled, weak squeeze
- One-liner: “Can’t pump.” (systolic dysfunction)
- Key echo: ↓ EF (classically < 40%) + ↑ EDV (dilated LV)
HFpEF = “THICK Failure”
- THICK ventricle → concentric hypertrophy, stiff filling
- One-liner: “Can’t fill.” (diastolic dysfunction)
- Key echo: Preserved EF (≥ 50%) with ↓ compliance + often normal/↓ EDV
Visual: What the LV “Looks Like” on Test Day
| Feature | HFrEF (Systolic) | HFpEF (Diastolic) |
|---|---|---|
| Mnemonic | FAT | THICK |
| LV size | Dilated | Normal or small |
| LV wall | Thin | Concentric hypertrophy |
| Primary problem | ↓ contractility | ↓ relaxation/compliance |
| EF | ↓ | Normal (preserved) |
| Common trigger words | MI, dilated cardiomyopathy | Long-standing HTN, aging, restrictive CM |
High-Yield USMLE Hooks (Classic Associations)
HFrEF: “FAT” causes = damaged myocytes
Common causes you’ll see in stems:
- Ischemic heart disease / MI (most common)
- Dilated cardiomyopathy (alcohol, doxorubicin, viral myocarditis, peripartum, hemochromatosis)
- Chronic volume overload (e.g., regurgitant valves)
Typical clue: displaced PMI, S3, cardiomegaly, pulmonary edema.
HFpEF: “THICK” causes = stiff ventricle
Common causes:
- Long-standing hypertension → concentric LVH
- Aortic stenosis → pressure overload hypertrophy
- Restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis, radiation)
- Hypertrophic cardiomyopathy (diastolic dysfunction prominent)
Typical clue: older patient with HTN, S4, “normal EF but still in CHF.”
One More Micro-Mnemonic: S3 vs S4
- HFrEF (FAT, dilated) → S3 (volume overload into a dilated ventricle)
- HFpEF (THICK, stiff) → S4 (atrial kick into a stiff ventricle)
Hemodynamics You Can Predict in 1 Line
Both syndromes cause congestion, so filling pressures rise even though EF differs:
- HFrEF: ↑ LVEDV + ↑ LVEDP (big, overfilled, weak LV)
- HFpEF: normal/↓ LVEDV but ↑ LVEDP (small-ish, stiff LV)
If you remember only one: HFpEF has preserved EF but elevated filling pressures.
Treatment Pearls (Step-Friendly)
HFrEF: mortality benefit matters
Core disease-modifying meds (think “block neurohormones”):
- ARNI (sacubitril/valsartan) or ACEi/ARB
- Evidence-based beta-blocker (metoprolol succinate, carvedilol, bisoprolol)
- Mineralocorticoid receptor antagonist (spironolactone/eplerenone)
- SGLT2 inhibitor (dapagliflozin/empagliflozin)
Symptom relief:
- Loop diuretics for congestion (don’t confuse symptom improvement with mortality benefit)
HFpEF: treat BP/ischemia and decongest
- Diuretics for volume overload
- Aggressive management of HTN, AF, ischemia
- SGLT2 inhibitors have benefit in HFpEF outcomes (commonly tested conceptually as “helps HF across EF ranges”)
Test tip: HFpEF management is often described as risk factor control + diuresis, whereas HFrEF has multiple medications with proven mortality benefit.
Quick Share Summary (Screenshot-Ready)
- HFrEF = FAT (dilated, thin, weak) → can’t pump → ↓ EF
- HFpEF = THICK (concentric, stiff) → can’t fill → preserved EF
- Sounds: S3 = HFrEF, S4 = HFpEF
- Causes: MI/DCM → HFrEF; HTN/AS/restrictive → HFpEF