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Heart Failure With Preserved Ejection Fraction (HFpEF)

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Heart Failure with Preserved Ejection Fraction (HFpEF)

Commonly known as a Diastolic Heart Failure — filling problem rather than a pumping problem

Also called

Diastolic Heart Failure

ICD-10

I50.30

Specialty

Cardiology

Onset

Acute & Chronic

Reviewed

June 2026

On This Page

Overview

Heart Failure with Preserved Ejection Fraction (HFpEF) is a heart failure type where the heart muscle is too thick and stiff to relax and fill with enough blood, even though it can still squeeze and pump blood out normally.

Etiology & Risk Factors

1. The Core Etiology (The “Why”)

The root cause of HFpEF boils down to two things: high pressure and chronic inflammation. Together, they cause the heart muscle cells to stiffen and fill with rigid scar tissue (fibrosis).

  • Chronic Hypertension (High Blood Pressure): This is the undisputed king of HFpEF. When blood pressure is constantly high, the heart has to pull overtime and push against massive resistance to move blood. To cope with the strain, the heart muscle grows thick and bulky (called left ventricular hypertrophy). Thick muscle cannot relax.

  • Microvascular Dysfunction: Chronic conditions trigger a state of constant, low-grade inflammation throughout the entire body. This inflammation damages the microscopic, tiny blood vessels (capillaries) inside the heart muscle itself. Without a healthy micro-blood supply, the heart tissue gets stiff, starved, and scarred.

2. The Major Risk Factors (The “Who”)

If you look at a typical HFpEF patient, they almost always check several of these boxes. These factors feed the inflammation and pressure that lock up the heart.

  • Age: The natural aging process makes both the blood vessels and the heart muscle lose their elasticity. HFpEF is heavily skewed toward older adults (usually 65+).

  • Biological Sex (Female): Interestingly, HFpEF is significantly more common in women than in men (unlike HFrEF/weak pump, which is more common in men due to heart attacks).

  • Obesity: Carrying excess weight forces the heart to work harder to pump blood further, while fat tissue constantly pumps inflammatory chemicals into the bloodstream.

  • Type 2 Diabetes: High blood sugar creates advanced glycation end-products (basically “sugar-coating” the heart tissue), making the muscle fibers physically rigid and less pliable.

  • Chronic Kidney Disease (CKD): When the kidneys fail to clear fluid and toxins, blood volume skyrockets. This creates a fluid overload that exerts massive, constant pressure on a heart that is already struggling to stretch open.

Pathophysiology

1. The Core Defect: Loss of “Suction”

A healthy heart acts like a vacuum pump during diastole—it actively relaxes and sucks blood into its main chamber. In HFpEF, the heart muscle loses this elasticity. It cannot relax quickly or stretch open, completely destroying its natural suction power.

2. Structural Changes: Thick Walls & Scar Tissue

Years of fighting high blood pressure forces the heart muscle to bulk up (concentric hypertrophy) to push against the resistance. At the same time, conditions like diabetes and obesity cause chronic inflammation that leaves behind rigid scar tissue (fibrosis). The result is a heart wall that is thick, crowded, and tough.

3. Hemodynamics: The Backward Pressure Wave

Because the main chamber is so rigid, blood trying to enter it hits a high-pressure wall. This pressure backs up into the left atrium and then flows backward into the lungs. This extreme backward pressure forces fluid out of the blood vessels and straight into the air sacs, causing the patient to feel like they are suffocating.

4. Exercise Intolerance: A Locked Output

A normal heart handles exercise by stretching out to hold and pump more blood (the Frank-Starling mechanism). A stiff heart cannot stretch, so its output stays locked in place. To make things worse, the heart’s electrical system fails to rev up the heart rate when the patient moves (chronotropic incompetence), leading to sudden, wiping-out fatigue.

Clinical Presentation

  1. The Key Symptoms (What the Patient Feels)

    • Exertional Dyspnea (Shortness of Breath): This is the hallmark. Patients feel fine sitting still, but walking to the mailbox feels like climbing Mount Everest. Because the stiff heart cannot stretch to accommodate increased blood flow during exercise, pressure spikes instantly and floods the lungs.

    • Orthopnea & PND: The patient cannot sleep flat without suffocating (orthopnea) and often wakes up gasping for air a few hours after falling asleep (Paroxysmal Nocturnal Dyspnea). When lying down, fluid from the legs redistributes to the chest, overloading the stiff heart.

    • Profound Fatigue: Because the heart cannot rev its engine or increase its stroke volume, muscles are chronically starved of oxygenated blood.

Heart Failure · NYHA Functional Classification

Class Functional Limitation Symptoms 5-Year Mortality ACC/AHA Stage
I No limitation
Ordinary physical activity causes no symptoms. No restriction on daily activities. Asymptomatic despite cardiac disease <10% Stage C
II Slight limitation
Comfortable at rest. Ordinary activity (climbing stairs, walking briskly) causes fatigue, dyspnea, or palpitations. Dyspnea on moderate exertion; orthopnea may be absent ~20% Stage C
III Marked limitation
Comfortable at rest. Less-than-ordinary activity (dressing, walking on flat) causes symptoms. Dyspnea on minimal exertion, fatigue, orthopnea, possible PND ~50% Stage C
IV Symptoms at rest
Unable to carry on any activity without discomfort. Symptoms present at rest. Bed-to-chair existence. Dyspnea at rest, severe orthopnea, PND, peripheral edema, ascites >50% Stage D

EF-based Classification

HFrEF
EF <40%
Heart Failure with reduced EF — systolic dysfunction. Responds to ACEi/ARB, BB, MRA, SGLT2i, ARNI.
HFmrEF
EF 40–49%
Heart Failure with mildly reduced EF — grey zone. Consider same therapies as HFrEF.
HFpEF
EF ≥50%
Heart Failure with preserved EF — diastolic dysfunction. SGLT2i (dapagliflozin) shown to reduce hospitalizations.

History Taking

Key Questions

“How many pillows do you need to sleep on at night to breathe comfortably?”

“Do you ever wake up suddenly in the middle of the night gasping for air?”

“Have your shoes, socks, or pants been feeling tighter due to swelling in your legs or belly?”

“What is a daily activity you used to do easily that completely wipes you out now?”

“Do you have to stop and catch your breath just walking to the mailbox or going up one flight of stairs?”

“Are you experiencing a constant, crushing fatigue that doesn’t go away with rest?”

“Do you have a history of high blood pressure, diabetes, or kidney disease?”

“Have you ever been told you have an irregular or fluttering heartbeat (AFib)?”

-Red Flags for Heart Failure with Preserved Ejection Fraction (HFpEF)

  • • Hemodynamic instability
  • • Acute pulmonary edema
  • • Tachyarrhythmias
  • • Bradyarrhythmia
  • • Cardiogenic shock

Physical Examination

-The Physical Signs (What You See on Examination)

  • Jugular Venous Distension (JVD): The neck veins look bulging and distended. This is a direct visual map of the high pressure backing up from the right side of the heart.

  • Pulmonary Crackles (Rales): Listening to the lungs with a stethoscope reveals a crisp, crackling sound at the bases—the literal sound of air bubbling through fluid in the alveoli.

  • Pitting Peripheral Edema: Significant fluid retention causes swollen ankles and legs. Pressing a thumb into the shin leaves a persistent indentation.

    -The Clinical Phenotype (The Typical Patient Profile)

    You can often spot a potential HFpEF patient before they even open their mouth. Unlike HFrEF patients (who are often younger men with a history of a massive heart attack), the classic HFpEF patient is typically:

    • An older female (often 70+).

    • Living with long-standing, poorly controlled hypertension.

    • Managing metabolic syndrome (obesity and Type 2 diabetes).

    • Frequently in Atrial Fibrillation (AFib)—because the high pressure stretches the left atrium until its electrical pathways become chaotic.

Investigations

1. Biomarker Assessment (Natriuretic Peptides)

Natriuretic peptides are the first laboratory tests used when HFpEF is suspected. Increased myocardial wall stress caused by elevated cardiac filling pressures stimulates the release of B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Elevated levels support the diagnosis of heart failure, whereas normal levels make HFpEF less likely. Because atrial fibrillation independently increases natriuretic peptide concentrations, higher diagnostic thresholds are required in patients with this arrhythmia.

2. Transthoracic Echocardiography

Transthoracic echocardiography is the most important non-invasive imaging test for diagnosing HFpEF. It confirms that the LVEF is preserved (≥50%) and evaluates both cardiac structure and diastolic function.

Key echocardiographic findings include:

  • Diastolic dysfunction: The E/e′ ratio estimates left ventricular filling pressure. A higher ratio indicates impaired ventricular relaxation and elevated filling pressures.
  • Left atrial enlargement: The left atrial volume index (LAVI) reflects chronic exposure to elevated filling pressures. Enlargement of the left atrium suggests long-standing diastolic dysfunction.
  • Left ventricular hypertrophy: The left ventricular mass index (LVMI) is used to detect increased ventricular wall thickness, which commonly results from chronic hypertension and contributes to ventricular stiffness.

3. Provocative Hemodynamic Testing

Some patients with HFpEF have normal filling pressures at rest but develop abnormal pressure increases during physical activity. When resting investigations are inconclusive but clinical suspicion remains high, additional testing is recommended.

    • Diastolic stress echocardiography: Echocardiographic measurements are obtained during exercise to identify exercise-induced elevations in left ventricular filling pressures that may not be present at rest.
    • Right heart catheterization: This is the gold standard for confirming HFpEF. It directly measures intracardiac and pulmonary capillary wedge pressures at rest or during exercise, providing definitive evidence of elevated left ventricular filling pressures when non-invasive tests are inconclusive.

Diagnosis

Diagnosis · HFrEF vs HFpEF

HFrEF
EF < 40%
HFpEF
EF ≥ 50%
Ejection fraction
EF < 40% — systolic dysfunction confirmed
EF ≥ 50% — systolic function preserved
EF 40–49% = HFmrEF (grey zone)
Key echocardiographic findings
• Dilated LV (LVEDV ↑)
• Reduced wall motion (global hypokinesia)
• Thin LV walls (eccentric remodelling)
• MR ± TR (secondary)
• Normal or small LV cavity
• LVH — concentric remodelling
• Impaired relaxation: E/e′ >14, e′ <7 cm/s
• LA dilation (LAVi >34 mL/m²)
BNP / NT-proBNP
Markedly elevated
BNP >100 pg/mL
NT-proBNP >300 pg/mL
Elevated but often lower than HFrEF
BNP >35 pg/mL
NT-proBNP >125 pg/mL
Typical patient
Younger males; post-MI; dilated cardiomyopathy; alcoholic CM; chemotherapy-induced
Older females; hypertension, obesity, diabetes, atrial fibrillation; metabolic syndrome
ECG clues
LBBB Q waves Poor R progression
LV dilation pattern; AF common
LVH criteria AF
May be normal; ST changes of LVH strain
Auscultation
S3 gallop (volume overload); displaced apex beat; pansystolic murmur (MR)
S4 gallop (stiff LV); non-displaced apex; signs of pulmonary hypertension
Haemodynamics
• Low CO / CI (<2.2 L/min/m²)
• High LVEDP
• High PCWP (>18 mmHg)
• Normal CO at rest
• High LVEDP (diastolic)
• PCWP rises steeply on exertion
Mortality-reducing therapy
ACEi/ARB/ARNI β-blocker MRA SGLT2i
ICD/CRT if indicated
SGLT2i (dapagliflozin / empagliflozin)
Diuretics for congestion
No proven mortality benefit for RAAS/BB
Prognosis
Worse; 5-yr mortality ~50% without optimal therapy. EF may recover with treatment (HFrecEF).
Similar overall mortality to HFrEF; harder to treat; driven by comorbidities.
ESC 2021 — Minimum diagnostic criteria for HFrEF
Required (all 3 must be present)
Symptoms of HF (dyspnea, orthopnea, fatigue, ankle swelling)
Signs of HF (elevated JVP, pulmonary crackles, peripheral edema)
LVEF < 40% on echocardiography
Supportive findings
Elevated BNP / NT-proBNP
Structural abnormality on echo (LV dilation, wall motion abnormality)
Response to diuretic therapy
Causative etiology identified (ischemic, valvular, idiopathic)
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Management of Heart Failure with Preserved Ejection Fraction (HFpEF)

1. The First-Line Breakthrough: SGLT2 Inhibitors

These are the undisputed cornerstone of modern HFpEF management. Originally designed for diabetes, drugs like Empagliflozin or Dapagliflozin are now prescribed to all HFpEF patients, regardless of whether they have diabetes.

  • How they work: They force the kidneys to dump excess sugar and sodium through the urine. This reduces blood volume, eases the pressure on the heart, and drastically lowers the risk of hospitalization.

2. Fluid and Pressure Control (Symptom Relief)

  • Loop Diuretics (Furosemide / Bumetanide): These are the “water pills.” While they don’t fix the stiff heart itself, they are critical for pulling excess fluid out of the lungs and swollen legs to relieve breathlessness.

  • Targeted Blood Pressure Control: Keeping blood pressure strictly controlled (typically <130/80 {mmHg} is mandatory. Lowering the pressure in the arteries gives the stiff heart less resistance to push against.

3. Second-Line Options (For Selected Patients)

If a patient is still struggling despite an SGLT2 inhibitor, guidelines allow for a few specific add-on therapies:

  • MRA (Spironolactone): A mild, potassium-sparing water pill that helps reduce the formation of rigid scar tissue (fibrosis) in the heart muscle.

  • ARNI (Sacubitril/Valsartan): A specialized blood pressure medication that helps dilate blood vessels and reduce heart strain, proven particularly beneficial in female HFpEF patients.

4. Aggressive Comorbidity Management

Because HFpEF is a systemic metabolic disease, you cannot fix the heart without fixing the rest of the body:

  • Obesity (GLP-1 Receptor Agonists): Medications like Semaglutide have shown massive success in HFpEF patients with obesity, rapidly reducing heart inflammation, improving exercise capacity, and shedding excess weight.

  • Atrial Fibrillation (AFib): If the patient lapses into AFib, the heart loses its coordinated rhythm, which a stiff ventricle cannot handle. Aggressive rhythm control (medications or ablation) is prioritized.

Complications of Heart Failure with Preserved Ejection Fraction (HFpEF)

    • 1. Fast, Chaotic Heartbeat (Atrial Fibrillation)

      Because the heart is stiff, blood backs up and stretches out the heart’s top chamber (the atrium). This stretching tears up the chamber’s electrical wiring, causing it to beat chaotically and way too fast. When this happens, the heart loses its ability to fill properly, which can cause the patient to suddenly crash.

      2. Right-Sided Heart Failure

      At first, the fluid backup only hurts the lungs. But over time, that constant high pressure backs up even further, damaging the blood vessels in the lungs and placing a massive strain on the right side of the heart. The right side eventually gives out, causing massive fluid buildup in the liver, belly, and legs.

      3. Kidney Damage (Cardiorenal Syndrome)

      The heart and kidneys work as a team. Because the heart is stiff and under high pressure, blood backs up into the kidneys and prevents them from draining properly. At the same time, the heart can’t pump enough fresh blood forward to feed them. Cut off from proper blood flow, the kidneys begin to fail.

      4. Blood Clots and Stroke

      When the top chamber of the heart stretches out and beats chaotically, blood stops moving smoothly and begins to pool. This stagnant, pooling blood can easily form a clot. If that clot breaks free and travels to the brain, it blocks blood flow and causes a stroke.

Prognosis of Heart Failure with Preserved Ejection Fraction (HFpEF)

    • The Survival Rate: Roughly 50% of patients die within 5 years of diagnosis, making it just as dangerous as a weak-pump heart failure.

    • The Causes: Half of the deaths are from the heart failing completely or a stroke, while the other half are caused by the patient’s other conditions, like kidney failure or diabetes.

    • The Bad Signs: The outlook gets much worse if the patient develops an irregular heartbeat (AFib), kidney damage, or requires repeated hospital visits.

    • The Good News: Modern lifestyle medications (like SGLT2 inhibitors and weight-loss drugs) are actively changing these statistics, keeping patients out of the hospital and living longer.

Key Points / Clinical Pearls of Heart Failure with Preserved Ejection Fraction (HFpEF)

  • Heart Failure with Preserved Ejection Fraction (HFpEF) stands for Heart Failure with Preserved Ejection Fraction. The heart squeezes normally, but it is too stiff to relax and fill up with enough blood.
  • This causes severe shortness of breath, especially when walking, moving, or lying flat in bed, along with extreme fatigue and fluid swelling in the ankles, legs, and belly.
  • To diagnose it, an echocardiogram must show the heart pumping out at least 50% of its blood while operating under high stiffness. A BNP or NT-proBNP blood test is also used to detect high stress levels in the heart muscle.
  • SGLT2 inhibitor medications are the primary treatment used to protect the heart and reduce hospital visits. Water pills are used alongside them to flush out excess fluid and keep the lungs dry.
  • Left untreated, the disease carries a tough 50% five-year survival rate, making early detection and treatment critical.
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