Systolic heart failure (HFrEF) is a ventricle that cannot squeeze, so the ejection fraction falls to 40% or below and the heart dilates. Diastolic heart failure (HFpEF) is a ventricle that cannot relax and fill, so the ejection fraction stays at 50% or above while the walls thicken and filling pressures climb. On a board question, the fastest separators are the ejection fraction on echo, an S3 versus an S4, and the cause in the history. The drug list follows from the type, because only HFrEF has a long list of medications proven to reduce mortality.
Why do HFrEF and HFpEF look the same in a question stem?
Both types end in the same place: high pressure in the left atrium that backs up into the lungs. That is why both patients have dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, crackles, jugular venous distension, and pitting edema. Both have an elevated BNP. Both can show pulmonary edema on chest x-ray. If you try to sort them by symptoms, you will guess.
The difference is the mechanism. In HFrEF, the problem is contraction. The ventricle cannot push blood forward, so it dilates to hold more volume and stretch its fibers. In HFpEF, the problem is filling. The ventricle squeezes normally, but the stiff, thick walls need a high pressure to accept a normal volume of blood. One heart is big and weak. The other is small, thick, and stiff.
Once you see that, the board clues line up. Echo measures the squeeze directly. The extra heart sound tells you which wall the blood is hitting. The history tells you why the heart got that way.
What ejection fraction cutoffs define each type?
The 2022 AHA/ACC/HFSA heart failure guideline sorts heart failure by left ventricular ejection fraction (LVEF). HFrEF is an LVEF of 40% or less. HFpEF is an LVEF of 50% or more with evidence of high filling pressures. The range in between, 41% to 49%, is heart failure with mildly reduced ejection fraction (HFmrEF). A patient whose LVEF was 40% or less and has since improved above 40% has heart failure with improved ejection fraction (HFimpEF).
| Category | LVEF | What it means on a question |
|---|---|---|
| HFrEF | 40% or less | Systolic dysfunction, dilated ventricle, full mortality-reducing regimen |
| HFmrEF | 41% to 49% | Gray zone, treated much like HFrEF in current guidelines |
| HFpEF | 50% or more | Diastolic dysfunction, normal or small cavity, thick walls |
| HFimpEF | Was 40% or less, now above 40% | Keep the HFrEF drugs going, because stopping them can drop the EF again |
A normal LVEF sits around 55% to 70%. An "ejection fraction of 25%" in a stem is HFrEF before you read another word. An "ejection fraction of 60% with concentric left ventricular hypertrophy" is HFpEF.
The HFrEF pattern: a big, weak ventricle
What causes it
Ischemic heart disease is the most common cause of HFrEF. A prior myocardial infarction kills muscle, the scar does not contract, and the rest of the ventricle remodels around it. After coronary disease, the board-favorite causes are the dilated cardiomyopathies.
| Cause | Classic stem | Board clue |
|---|---|---|
| Ischemic cardiomyopathy | Older patient with prior MI, diabetes, smoking history | Q waves on ECG, regional wall motion abnormality on echo |
| Alcohol | Long history of heavy drinking | Dilated cardiomyopathy that can improve with abstinence |
| Doxorubicin | Patient treated for breast cancer or lymphoma | Dose-dependent dilated cardiomyopathy, dexrazoxane is protective |
| Trastuzumab | HER2-positive breast cancer on therapy | Drop in EF that is usually reversible when the drug stops |
| Viral myocarditis | Young adult with heart failure weeks after a viral illness | Coxsackie B, lymphocytic infiltrate |
| Peripartum cardiomyopathy | Woman in the last month of pregnancy or the first 5 months after delivery | New heart failure with no other cause |
| Chagas disease | Patient from rural Central or South America | Trypanosoma cruzi, dilated heart, megacolon, megaesophagus |
| Wet beriberi | Chronic alcohol use or malnutrition | Thiamine deficiency, high-output failure that dilates the heart |
| Tachycardia-induced | Weeks of uncontrolled atrial fibrillation or flutter | EF recovers once the rate is controlled |
| Hemochromatosis | Bronze skin, diabetes, high ferritin | Iron overload, dilated or restrictive pattern |
What the exam and tests show
A dilated left ventricle pushes the point of maximal impulse down and to the left, so a stem may describe a displaced, diffuse apical impulse. The S3 is the signature sound. It comes in early diastole, right after S2, when blood rushes into an overfilled, dilated ventricle. It sounds like "Ken-tuck-y," and in an adult over 40 it means volume overload.
Echo shows a large left ventricular cavity, thin walls, and a low ejection fraction. The hypertrophy is eccentric, which means new sarcomeres are added in series and the chamber gets longer and wider. An ECG may show Q waves from an old infarct or a left bundle branch block. The EKG interpretation pearls guide covers how to spot both. A dilated ventricle also stretches the mitral annulus, so a holosystolic murmur of functional mitral regurgitation at the apex is common.
The HFpEF pattern: a thick, stiff ventricle
What causes it
Long-standing hypertension is the classic cause of HFpEF. The ventricle pumps against high pressure for years, adds sarcomeres in parallel, and the walls thicken inward. That is concentric hypertrophy. The cavity stays normal or gets smaller, and the thick wall resists filling. The typical patient is an older woman with hypertension, obesity, diabetes, or atrial fibrillation.
| Cause | Classic stem | Board clue |
|---|---|---|
| Hypertensive heart disease | Older patient with years of poorly controlled blood pressure | Concentric LVH, LVH voltage on ECG |
| Aortic stenosis | Older patient with exertional syncope, angina, and dyspnea | Crescendo-decrescendo murmur at the right upper sternal border radiating to the carotids |
| Hypertrophic cardiomyopathy | Young athlete with syncope or sudden death, family history | Asymmetric septal hypertrophy, murmur louder with Valsalva |
| Cardiac amyloidosis | Older man with carpal tunnel syndrome or a patient with multiple myeloma | Thick walls on echo with low voltage on ECG |
| Sarcoidosis | Young Black woman with hilar adenopathy and heart block | Noncaseating granulomas in the myocardium |
| Constrictive pericarditis | History of radiation, cardiac surgery, or tuberculosis | Pericardial knock, Kussmaul sign, pericardial calcification |
Constrictive pericarditis is not a disease of the muscle, but it limits filling the same way and lands on the same side of the comparison.
What the exam and tests show
The S4 is the signature sound. It comes in late diastole, right before S1, when the atrium contracts hard against a stiff ventricle. It sounds like "Ten-nes-see." A stiff ventricle depends on that atrial kick, which is why an S4 can never be heard in atrial fibrillation. The atrium is not contracting. The apical impulse in LVH is sustained and forceful but not displaced.
Echo shows thick walls, a normal or small cavity, a normal ejection fraction, and an enlarged left atrium from years of high filling pressure. Doppler shows the abnormal relaxation: an E/A ratio below 1 in early diastolic dysfunction and a high E/e' ratio as filling pressure rises. The ECG often shows LVH voltage criteria. Cardiac amyloidosis is the exception to that rule, and the mismatch between thick walls on echo and low voltage on ECG is the clue that names it.
Side-by-side comparison table
| Feature | HFrEF (systolic) | HFpEF (diastolic) |
|---|---|---|
| Core problem | Cannot squeeze | Cannot relax and fill |
| LVEF | 40% or less | 50% or more |
| LV cavity | Dilated | Normal or small |
| Wall thickness | Thin | Thick |
| Hypertrophy type | Eccentric (sarcomeres in series) | Concentric (sarcomeres in parallel) |
| Extra heart sound | S3 | S4 |
| Apical impulse | Displaced down and left | Sustained, not displaced |
| Most common cause | Ischemic heart disease | Hypertension |
| Typical patient | Man with prior MI | Older woman with hypertension, obesity, or diabetes |
| BNP | Elevated, often higher | Elevated, often lower |
| Drugs proven to reduce mortality | ARNI, ACE inhibitor, or ARB, beta blocker, MRA, SGLT2 inhibitor | No drug class has the same mortality evidence |
How do pressure-volume loops show systolic vs diastolic dysfunction?
A pressure-volume loop traces one heartbeat, with left ventricular volume on the x-axis and pressure on the y-axis. Systolic dysfunction flattens the end-systolic pressure-volume line, so the loop shifts to the right with a larger end-diastolic volume, a larger end-systolic volume, and a smaller stroke volume. Diastolic dysfunction steepens the end-diastolic pressure-volume curve, so filling pressure rises sharply while end-diastolic volume stays normal or falls.
This is the Level 1 and Step 1 version of the question. The stem draws two loops and asks which change happened. Ask yourself which line moved. If the upper left corner of the loop moved, contractility changed, and that is HFrEF. If the bottom edge of the loop got steeper, compliance changed, and that is HFpEF.
The Frank-Starling curve tells the same story. In HFrEF the whole curve shifts down, so a higher preload buys less stroke volume. In HFpEF the curve is closer to normal, but the ventricle reaches a dangerous filling pressure at a much smaller volume.
What drugs treat HFrEF, and which ones lower mortality?
Four drug classes lower mortality in HFrEF, and the 2022 guideline recommends all four together. Diuretics help symptoms but do not change survival.
| Drug class | Examples | Board points |
|---|---|---|
| ARNI, ACE inhibitor, or ARB | Sacubitril-valsartan, lisinopril, losartan | ARNI is preferred. Stop an ACE inhibitor 36 hours before starting sacubitril-valsartan because of angioedema risk |
| Evidence-based beta blocker | Carvedilol, metoprolol succinate, bisoprolol | Only these three. Do not start one in a patient in cardiogenic shock |
| Mineralocorticoid receptor antagonist | Spironolactone, eplerenone | Watch potassium and kidney function. Spironolactone causes gynecomastia, eplerenone does not |
| SGLT2 inhibitor | Dapagliflozin, empagliflozin | Benefit is seen with or without diabetes |
Several other drugs show up on boards with narrower roles. Hydralazine plus isosorbide dinitrate lowers mortality in self-identified Black patients who are already on optimal therapy, and it is the substitute when a patient cannot take an ACE inhibitor, ARB, or ARNI. Ivabradine reduces hospitalization in patients in sinus rhythm with an LVEF of 35% or less and a resting heart rate of 70 or higher on a maximal beta blocker dose. Digoxin reduces hospitalizations but not mortality. Loop diuretics such as furosemide treat congestion and are the first move in a volume-overloaded patient.
Devices are part of the HFrEF answer too. An implantable cardioverter-defibrillator is indicated for an LVEF of 35% or less with NYHA class II or III symptoms after at least 3 months of guideline-directed therapy, and at least 40 days after an MI. Cardiac resynchronization therapy is added when the LVEF is 35% or less with a left bundle branch block and a QRS of 150 ms or longer.
Know what makes HFrEF worse. Verapamil and diltiazem depress contractility. Pioglitazone and rosiglitazone cause fluid retention. NSAIDs cause sodium retention and blunt diuretics. Cilostazol is contraindicated in heart failure of any severity. If an answer choice adds one of these to a patient with an EF of 30%, it is wrong.
What treats HFpEF?
HFpEF has a much shorter list. SGLT2 inhibitors are the one class with strong trial evidence, because empagliflozin and dapagliflozin both reduced the combined outcome of cardiovascular death or heart failure hospitalization. The 2022 guideline gives them a 2a recommendation. Spironolactone, sacubitril-valsartan, and ARBs carry weaker 2b recommendations in selected patients.
The rest of HFpEF management is treating what caused it. Control the blood pressure. Use diuretics for congestion, but carefully, because a stiff ventricle needs a high filling pressure and over-diuresis drops cardiac output. Control the heart rate in atrial fibrillation. A fast rate shortens diastole, and a stiff ventricle needs that time to fill. Treat obesity, diabetes, and sleep apnea.
Hypertrophic cardiomyopathy has its own rule. Beta blockers or non-dihydropyridine calcium channel blockers slow the heart and lengthen filling time. Drugs that drop preload, such as nitrates or aggressive diuresis, make the outflow obstruction worse.
How should you approach an acutely decompensated patient?
For a patient who shows up in acute heart failure, both types are managed by the same first steps: oxygen if hypoxic, an IV loop diuretic for congestion, and noninvasive ventilation for respiratory distress. Boards like the "warm and wet" versus "cold and wet" split. A warm, wet patient has good perfusion and fluid overload, so the answer is an IV diuretic plus vasodilators if the blood pressure allows. A cold, wet patient has poor perfusion with cool extremities, low urine output, or rising lactate, so the answer adds an inotrope such as dobutamine or milrinone.
A chest x-ray in decompensation shows cephalization of the pulmonary vessels, Kerley B lines, perihilar "bat-wing" opacities, and pleural effusions. Cardiomegaly is more common in HFrEF, because a thick-walled HFpEF heart may have a normal silhouette. The high-yield chest x-ray guide shows how each of these findings looks on film.
Stem clues that sort heart failure questions fast
The clues I look for in every question are age, acuity, unusual findings, matching timelines, laterality, labs and imaging, and the question part. Here is how they apply to heart failure stems.
- Age. A 28-year-old with new heart failure two weeks after a flu-like illness points to viral myocarditis. When a 22-year-old basketball player collapses, think hypertrophic cardiomyopathy. Heart failure with an EF of 60% in a 74-year-old woman with hypertension is HFpEF.
- Acuity. Flash pulmonary edema in a patient with crushing chest pain is an acute MI or acute mitral regurgitation from papillary muscle rupture. Months of slowly worsening exertional dyspnea is chronic heart failure.
- Unusual findings. Carpal tunnel syndrome, macroglossia, or periorbital purpura next to thick ventricular walls points to amyloidosis. Bronze skin and diabetes points to hemochromatosis.
- Matching timelines. Peripartum cardiomyopathy lives in the last month of pregnancy and the 5 months after delivery. Doxorubicin toxicity tracks the cumulative dose. Myocarditis follows a viral illness by days to weeks.
- Laterality. Left-sided failure backs up into the lungs and causes crackles, orthopnea, and paroxysmal nocturnal dyspnea. Right-sided failure backs up into the body and causes jugular venous distension, hepatomegaly, nutmeg liver, and peripheral edema. The most common cause of right heart failure is left heart failure. Isolated right heart failure should make you think of the lungs, and the pulmonary embolism guide covers the acute version.
- Labs and imaging are king. The echo ejection fraction decides the category. Low voltage on ECG with thick walls names amyloid. A BNP below 100 pg/mL makes acute heart failure an unlikely cause of dyspnea.
- The question part. "Most likely heart sound," "drug that reduces mortality," and "most likely cause" are three different questions about the same patient. Read the last sentence slowly, and read it twice if the stem is confusing you.
Common board pitfalls and how to avoid them
Pitfall 1: Assuming a normal ejection fraction means a normal heart. HFpEF patients have an EF of 50% or more and are still in heart failure. The question is filling, not squeeze.
Pitfall 2: Picking an S4 in a patient with atrial fibrillation. The S4 needs an atrial contraction. No organized atrial contraction means no S4.
Pitfall 3: Calling an S3 abnormal in a young athlete or a pregnant patient. An S3 can be normal in children, young adults, and pregnancy. In an adult over 40 it points to volume overload.
Pitfall 4: Picking digoxin or furosemide for "reduces mortality." Both help symptoms or hospitalizations. Neither lowers mortality in HFrEF.
Pitfall 5: Picking any beta blocker. Only carvedilol, metoprolol succinate, and bisoprolol carry HFrEF mortality data. Metoprolol tartrate and atenolol do not.
Pitfall 6: Using BNP after starting sacubitril-valsartan. Sacubitril blocks neprilysin, the enzyme that breaks down BNP, so BNP rises on the drug. NT-proBNP is not a neprilysin substrate and remains the better marker. If you want to see more cardiology stems like these worked out on video, the free Skool community has a large library of question breakdowns.
Frequently asked questions about HFrEF vs HFpEF
What ejection fraction separates HFrEF from HFpEF?
The 2022 AHA/ACC/HFSA guideline defines HFrEF as a left ventricular ejection fraction of 40% or less and HFpEF as an ejection fraction of 50% or more with signs of high filling pressure. The range from 41% to 49% is heart failure with mildly reduced ejection fraction. A patient who was at 40% or less and improved above 40% has heart failure with improved ejection fraction and should stay on the HFrEF medications.
Is an S3 or an S4 a sign of systolic or diastolic heart failure?
An S3 points to systolic heart failure. It is an early diastolic sound made when blood rushes into a dilated, volume-overloaded ventricle. An S4 points to diastolic heart failure. It is a late diastolic sound made when the atrium contracts against a stiff, thick ventricle, as in hypertensive LVH or aortic stenosis. An S4 cannot occur in atrial fibrillation, and an S3 can be normal in children, young adults, and pregnancy.
Which drugs lower mortality in HFrEF?
Four classes lower mortality in HFrEF: an ARNI (sacubitril-valsartan) or an ACE inhibitor or ARB, an evidence-based beta blocker (carvedilol, metoprolol succinate, or bisoprolol), a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and an SGLT2 inhibitor (dapagliflozin or empagliflozin). Hydralazine plus isosorbide dinitrate also lowers mortality in self-identified Black patients on optimal therapy. Loop diuretics and digoxin improve symptoms and hospitalizations but do not lower mortality.
How is HFpEF treated?
SGLT2 inhibitors are the one drug class with strong trial evidence in HFpEF, since empagliflozin and dapagliflozin both reduced cardiovascular death or heart failure hospitalization. Diuretics treat congestion, but over-diuresis can drop cardiac output in a stiff ventricle. The rest of management targets the cause: blood pressure control, rate control in atrial fibrillation so the ventricle has time to fill, and treatment of obesity, diabetes, and sleep apnea.
What does BNP tell you in heart failure?
BNP is released when the ventricular walls are stretched, so it rises in both HFrEF and HFpEF. A BNP below 100 pg/mL makes acute heart failure an unlikely cause of shortness of breath. BNP alone does not tell you which type the patient has, and it often runs lower in HFpEF and in obesity. Sacubitril raises BNP by blocking its breakdown, so NT-proBNP is the marker to follow on that drug.
How does COMLEX or USMLE test heart failure?
Both exams test heart failure from several angles. Level 1 and Step 1 questions lean on mechanism: pressure-volume loops, eccentric versus concentric hypertrophy, S3 versus S4, and drug mechanisms and side effects. Level 2 and Step 2 CK questions lean on management: which drug lowers mortality, when to add an ICD or CRT, and which medication to stop in a patient with a low ejection fraction. The comparison tables above cover each of those question types.
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