Signs of heart failure
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Signs and Symptoms of Heart Failure
Heart failure (HF) produces two main categories of findings: symptoms the patient reports, and physical signs found on examination. Neither HFpEF (preserved ejection fraction) nor HFrEF (reduced ejection fraction) has a unique clinical fingerprint - the findings below apply to both.
Symptoms (What the Patient Reports)
Respiratory
- Dyspnea - the cardinal symptom; worsening shortness of breath on exertion or at rest
- Orthopnea - dyspnea when lying flat; patients sleep with heads elevated
- Paroxysmal nocturnal dyspnea (PND) - one of the most reliable indicators of HF; sudden breathlessness waking the patient from sleep
- Trepopnea - dyspnea when lying on the left side
- Tachypnea
- Cough (often dry, may be frothy pink in acute pulmonary edema)
- Cheyne-Stokes respiration - periodic/cyclic breathing, often noticed by family rather than the patient
General & Activity
- Fatigue and markedly diminished exercise capacity
- Somnolence or diminished mental acuity (low cardiac output to brain)
Fluid Retention / Congestion
- Peripheral edema - ankles, legs, scrotum
- Increasing abdominal girth / bloating
- Weight gain (fluid) or weight loss (cardiac cachexia in advanced disease)
- Nocturia - nocturnal redistribution of fluid from dependent tissues
GI
- Right upper quadrant pain - hepatic congestion
- Loss of appetite / early satiety - gut edema, hepatomegaly
- Palpitations
- Chest discomfort
Physical Signs (Examination Findings)
These are from Table 48.3 of Braunwald's Heart Disease (starred items indicate more severe disease):
| System | Sign |
|---|---|
| Cardiovascular | Tachycardia; irregular rhythm or extra beats; narrow pulse pressure or thready pulse*; pulsus alternans* |
| Cardiac exam | Displaced apical impulse (leftward/inferiorly); sustained apical impulse; parasternal lift; S3 gallop and/or S4 (palpable or audible); tricuspid or mitral regurgitant murmur |
| Respiratory | Tachypnea; bilateral basilar rales/crackles; dullness and diminished breath sounds at lung bases (pleural effusion); rhonchi; wheezes ("cardiac asthma") |
| Venous | Elevated jugular venous pressure (JVP) - a key congestion marker |
| Extremities | Cool and/or mottled extremities*; pedal edema; pre-sacral edema; chronic venous stasis skin changes; anasarca* |
| Abdomen | Hepatomegaly; ascites |
Items marked indicate more severe/advanced disease.
Key Diagnostic Pearls
- JVP elevation + S3 + peripheral edema is the classic triad pointing strongly to HF
- S3 gallop (third heart sound) reflects a dilated, volume-overloaded ventricle and has high specificity for elevated filling pressures
- Absence of dyspnea does not exclude HF - patients often reduce activity to avoid symptoms, masking the diagnosis
- BNP (B-type natriuretic peptide) elevation supports the diagnosis when the clinical picture is ambiguous; a 2025 meta-analysis (PMID: 40641207) confirmed its high diagnostic utility for HF in patients presenting with acute dyspnea
NYHA Functional Classification (Symptom-Based)
| Class | Description |
|---|---|
| I | No symptoms with ordinary activity |
| II | Symptoms with moderate exertion |
| III | Symptoms with minimal exertion |
| IV | Symptoms at rest |
Sources:
- Braunwald's Heart Disease, Tables 48.2 & 48.3
- Goldman-Cecil Medicine, Chapter 221
How do I differentiate HFpEF from HFrEF clinically?
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Differentiating HFpEF from HFrEF
The definitive distinction requires echocardiography (LVEF ≥50% = HFpEF; LVEF <40% = HFrEF; LVEF 40-49% = HFmrEF). However, several clinical features point strongly toward one or the other before the echo result is available.
1. The LVEF Cut-offs (Formal Definitions)
| Category | LVEF | Old Terminology |
|---|---|---|
| HFrEF | < 40% | Systolic HF |
| HFmrEF | 40-49% | Mildly reduced EF |
| HFpEF | ≥ 50% | Diastolic HF |
2. Clinical Profile: Who Gets Each?
| Feature | HFpEF | HFrEF |
|---|---|---|
| Age | Older (typically >65) | Any age |
| Sex | More commonly female | More commonly male |
| Hypertension | Present in 60-80% | Less dominant |
| Prior MI / CAD | Less common | Frequent antecedent cause |
| Obesity / Diabetes | Strongly associated | Less strongly associated |
| Atrial fibrillation | Very common (often paroxysmal) | Common (often persistent) |
| CKD / COPD | High comorbidity burden | Less so |
| Cardiomyopathy history | Rare | Common (dilated, ischemic) |
Key pearl: An older, obese woman with longstanding hypertension and new dyspnea is HFpEF until proven otherwise. A middle-aged man with prior anterior MI and declining exercise capacity is HFrEF until proven otherwise.
3. Heart Sounds - the Most Useful Bedside Clue
| Finding | HFpEF | HFrEF |
|---|---|---|
| S4 gallop | Characteristic (stiff, non-compliant LV requires forceful atrial kick) | Less prominent |
| S3 gallop | Absent or rare | Classic - indicates dilated, volume-overloaded ventricle |
| Murmurs | Mitral regurgitation may occur | MR common (functional); TR may develop |
4. Chest X-Ray
| Finding | HFpEF | HFrEF |
|---|---|---|
| Cardiomegaly | Often absent - do not be fooled into excluding HF because the cardiac silhouette is normal | Almost always present |
| Pulmonary congestion | Present when decompensated | Present when decompensated |
5. Echocardiographic Features
| Finding | HFpEF | HFrEF |
|---|---|---|
| LVEF | ≥50% (normal/preserved contraction) | <40% (impaired contraction) |
| LV cavity size | Usually normal or small | Usually dilated |
| LV wall thickness | Often increased (concentric hypertrophy) | Thinned or normal |
| LV geometry | Concentric remodeling/hypertrophy | Eccentric dilation |
| Diastolic indices | Elevated E/e' ratio, reduced e' velocity (Grade II-III diastolic dysfunction) | Variable |
6. Pathophysiology Behind the Differences
-
HFrEF: The problem is systolic - the ventricle cannot contract adequately. Cardiac output falls, the ventricle dilates and remodels, and neurohormonal activation (RAAS, SNS) worsens the cycle.
-
HFpEF: The problem is diastolic - contraction is normal but the ventricle is stiff and cannot relax or fill properly. Resting hemodynamics may be near-normal, but during exercise or tachycardia (e.g., from AF), filling pressures spike dramatically, causing dyspnea. Because atrial contraction contributes disproportionately to filling of a stiff ventricle, loss of atrial kick in AF is particularly poorly tolerated. Patients also have a narrow "euvolemic window" - even modest fluid overload causes severe dyspnea, yet aggressive diuresis causes underfilling and hypotension.
7. BNP / NT-proBNP
Both forms elevate natriuretic peptides when decompensated. However, BNP levels are often lower in HFpEF than in HFrEF for the same degree of symptoms, because the smaller, stiffer LV generates less wall stress. Obesity (common in HFpEF) further suppresses BNP levels, which can mislead clinicians.
8. Response to Therapy - A Diagnostic Clue in Retrospect
| Drug class | HFrEF | HFpEF |
|---|---|---|
| ACE inhibitors / ARBs | Mortality benefit proven | No mortality benefit |
| Beta-blockers | Mortality benefit proven | No proven mortality benefit |
| Aldosterone antagonists | Strong benefit | Modest HF hospitalization reduction only |
| SGLT-2 inhibitors | Benefit (empagliflozin, dapagliflozin) | Benefit (empagliflozin in EMPEROR-Preserved) |
| Diuretics | Symptom control | Symptom control, but risk of over-diuresis |
Quick Summary Table
| HFpEF | HFrEF | |
|---|---|---|
| LVEF | ≥50% | <40% |
| Ventricle | Small, stiff, hypertrophied | Dilated, thin-walled |
| Typical patient | Old, female, hypertensive, obese | Male, post-MI or cardiomyopathy |
| S3 gallop | Absent | Present |
| S4 gallop | Present | Absent |
| Cardiomegaly on CXR | Often absent | Usually present |
| AF | Very common, paroxysmal | Common, persistent |
| Diuresis risk | Over-diuresis dangerous | Better tolerated |
Bottom line: echo is the arbiter. Clinically, the combination of patient demographics (older, female, hypertensive), preserved cardiac size on CXR, S4 (not S3), and preserved contraction on bedside assessment should raise strong suspicion for HFpEF - but you cannot reliably confirm it without measuring LVEF.
Sources: Swanson's Family Medicine Review, p. 127; Braunwald's Heart Disease, Chapter 51; Goldman-Cecil Medicine, Chapter 45; Harrison's Principles of Internal Medicine 22E, Chapter 28
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