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 · Right ventricle

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 mLESV 127 mLSV 53 mLEF 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 mmHgVenular NFP +6 mmHgFiltration 10.0Reabsorption 0.0Net 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	< 100 pg/mL makes acute heart failure unlikely	cut-offs vary with age and kidney function

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

HFrEF versus HFpEF

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	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.

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.

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See it in 3D

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

In Biochemistry

Aldosterone

In Pharmacology

← All of 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 (OpenStax (Rice University), 2022); Heart Failure (Congestive Heart Failure) (StatPearls (NCBI Bookshelf), 2025); Hypertensive Heart Disease (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.