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[Physiology](https://durgical.com/en/physiology/) · [Cardiovascular](https://durgical.com/en/physiology/#s-cardio)

# Heart failure physiology

- Mechanism
- Exam priority: medium

In heart failure the heart cannot pump enough at normal filling pressures; the body's rescue hormones help at first, then make things worse.

Updated 2026-11-01

Also called: HFrEF and HFpEF, Neurohormonal activation

**See it in 3D:** [Left ventricle](https://durgical.com/en/anatomy/left-ventricle/) · [Right ventricle](https://durgical.com/en/anatomy/right-ventricle/)

## Key points

- HFrEF (EF ≤ 40%): weak contraction, dilated ventricle, flat Starling curve. HFpEF (EF ≥ 50%): stiff ventricle, steep diastolic P–V curve, high pressure at normal volume.
- Low output → baroreceptor unloading and low renal perfusion → sympathetic + RAAS + ADH → Na⁺ and water retention, vasoconstriction (more afterload).
- Chronic angiotensin II, aldosterone and catecholamines cause fibrosis, myocyte loss and remodelling: the basis for RAAS and β blockade improving survival.
- Left failure → pulmonary congestion: dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, crackles. Right failure → raised JVP, hepatomegaly, leg edema, ascites.
- Natriuretic peptides (BNP, NT-proBNP) rise with ventricular wall stretch: useful to support the diagnosis.

## What it is

Heart failure is a syndrome in which the heart cannot deliver enough output, or only does so at high filling pressures. It can be mainly systolic (reduced ejection fraction, a weak dilated ventricle) or mainly diastolic (preserved ejection fraction, a stiff ventricle). Sympathetic, RAAS and ADH activation retain fluid and constrict vessels, which helps briefly but drives congestion and remodelling.

## How it works, step by step

- Injury (infarction, pressure or volume overload, cardiomyopathy such as Chagas) lowers stroke volume or raises filling pressures.
- Arterial baroreceptors and the kidney sense low effective volume.
- Sympathetic activity raises heart rate, contractility and vascular tone.
- RAAS and ADH retain Na⁺ and water; preload rises and, via Frank–Starling, output is partly restored.
- On a flat curve, more preload mostly raises atrial and capillary pressure: congestion and edema.
- Vasoconstriction raises afterload, which a weak ventricle tolerates poorly; output falls further.
- Sustained neurohormones remodel the heart (dilation, fibrosis, arrhythmias), closing a vicious cycle.

### Left-ventricular pressure–volume loop

**EDV** 180 mL **ESV** 127 mL **SV** 53 mL **EF** 30% **ESP** 85 mmHg

#### HF with reduced EF

Heart failure with reduced EF: a flat ESPVR (↓ contractility) and a dilated LV: high EDV and ESV, low SV and EF, and a raised end-diastolic pressure.

Tap a corner of the loop (MC, AO, AC, MO) to see the valve event.

- Current loop
- Normal loop
- ESPVR (contractility, Ees)
- EDPVR (passive filling)
- Ea (arterial afterload)
- Stroke volume (SV)

Compare the HFrEF and HFpEF presets: one moves the end-systolic line, the other the diastolic curve.

### Starling forces along a capillary

**Arteriolar NFP** +14 mmHg **Venular NFP** +6 mmHg **Filtration** 10.0 **Reabsorption** 0.0 **Net filtration** 10.0 a.u. (lymph capacity 7.5)

Heart failure: high venous pressure raises Pc along the whole capillary; there is almost no reabsorption and filtration outruns the lymph (peripheral edema in right-sided failure, pulmonary edema in left-sided).

Edema: net filtration (10.0 a.u.) is more than the lymph can return (7.5 a.u.), so fluid collects in the interstitium.

Tap a force (Pc, πc, Pif, πif), the lymph or the net pressure value.

- Filtration (fluid out)
- Absorption (fluid in)
- Net filtration pressure
- Normal net pressure
- Lymphatic (returns the excess)
- Edema

Illustrative Durgical schematic of the classic Starling model; values are approximate and flow units arbitrary. The revised Starling principle (glycocalyx) shows that most capillaries at steady state absorb very little: the lymph returns almost all that is filtered.

## Reference values

| Parameter | Value | Note |
| --- | --- | --- |
| Ejection fraction (normal) | ≈ 55–70% | |
| Pulmonary capillary wedge pressure | ≈ 6–12 mmHg normal | > 18 mmHg with pulmonary congestion |
| BNP |

| Feature | HFrEF | HFpEF |
| --- | --- | --- |
| Ejection fraction | ≤ 40% | ≥ 50% |
| Main problem | Contraction (systolic) | Relaxation and filling (diastolic) |
| Ventricle | Dilated, eccentric | Normal size, often concentric hypertrophy |
| [Typical causes](https://durgical.com/en/conditions/chagas-cardiomyopathy/) | Myocardial infarction, dilated or Chagas cardiomyopathy | Hypertension, older age, obesity, diabetes |
| Extra heart sound | S3 | S4 |

## Clinical notes

- Orthopnoea: lying flat shifts blood from the legs to the chest, raising preload on a failing left ventricle and pulmonary capillary pressure.
- Chagas cardiomyopathy, a leading cause of heart failure in parts of Colombia, combines dilated HFrEF with conduction disease and apical aneurysm.

## Memory aid

In heart failure the body thinks it is bleeding: it squeezes the vessels and hoards salt, which the weak heart can least afford.

## Test yourself

Think of the answer, then tap the question to see it.

## Why does activation of the RAAS, helpful after acute blood loss, become harmful in chronic heart failure?

Retained volume mostly raises filling pressures on a flat Starling curve, vasoconstriction raises afterload on a weak ventricle, and angiotensin II and aldosterone promote fibrosis and remodelling.

## How does the pressure–volume loop of HFpEF differ from that of HFrEF?

HFpEF keeps a normal end-systolic line but has a steep end-diastolic curve (high pressure at normal volume); HFrEF has a flatter end-systolic line and the loop shifts right.

## Why does lying flat worsen breathlessness in left heart failure?

Blood from the legs and abdomen moves into the chest, raising preload; the failing left ventricle cannot handle it, so pulmonary capillary pressure and lung water rise.

## Why do natriuretic peptides rise in heart failure?

Ventricular and atrial myocytes release them in response to wall stretch from raised volume and pressure; they promote Na⁺ excretion and vasodilation.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/heart-failure-physiology/)

## See it in 3D

The structures of Durgical's 3D anatomy where it happens.

- [Left ventricle](https://durgical.com/en/anatomy/left-ventricle/)
- [Right ventricle](https://durgical.com/en/anatomy/right-ventricle/)

## Related topics

- [The Frank–Starling mechanism](https://durgical.com/en/physiology/the-frank-starling-mechanism/)
- [The ventricular pressure–volume loop](https://durgical.com/en/physiology/the-ventricular-pressure-volume-loop/)
- [The renin–angiotensin–aldosterone system](https://durgical.com/en/physiology/the-renin-angiotensin-aldosterone-system/)
- [How edema forms](https://durgical.com/en/physiology/how-edema-forms/)
- [Preload, afterload and contractility](https://durgical.com/en/physiology/preload-afterload-and-contractility/)
- [Heart sounds and where they come from](https://durgical.com/en/physiology/heart-sounds-and-where-they-come-from/)

## Related conditions

- [Heart failure](https://durgical.com/en/conditions/heart-failure/)
- [Hypertensive heart disease](https://durgical.com/en/conditions/hypertensive-heart-disease/)
- [Chagas cardiomyopathy](https://durgical.com/en/conditions/chagas-cardiomyopathy/)
- [Myocardial Infarction (Heart Attack)](https://durgical.com/en/conditions/myocardial-infarction/)

## In Biochemistry

- [Aldosterone](https://durgical.com/en/biochemistry/molecules/aldosterone/)

## In Pharmacology

- [ACE inhibitors](https://durgical.com/en/pharmacology/classes/ace-inhibitors/)
- [Angiotensin II receptor blockers (ARBs)](https://durgical.com/en/pharmacology/classes/angiotensin-ii-receptor-blockers/)
- [Beta blockers](https://durgical.com/en/pharmacology/classes/beta-blockers/)
- [Digoxin](https://durgical.com/en/pharmacology/digoxin/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [19.4 Cardiac Physiology](https://openstax.org/books/anatomy-and-physiology-2e/pages/19-4-cardiac-physiology) (OpenStax (Rice University), 2022); [Heart Failure (Congestive Heart Failure)](https://www.ncbi.nlm.nih.gov/books/NBK430873/) (StatPearls (NCBI Bookshelf), 2025); [Hypertensive Heart Disease](https://www.ncbi.nlm.nih.gov/books/NBK539800/) (StatPearls (NCBI Bookshelf), 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 22). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/physiology/heart-failure-physiology/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/heart-failure-physiology/