Heart failure over time: acute, compensated, decompensated and high-output failure on the curves

Mechanism
Exam priority: medium

After the heart is damaged, nerves act at once and the kidneys add fluid over days. If the heart still cannot cope, fluid keeps building up.

Updated Nov 13, 2026

Also called: Graphical analysis of heart failure, Cardiac reserve, High-output failure

See it in 3D: Left ventricle · Right atrium · Pericardium

Key points

Acute failure: output falls and right atrial pressure rises; sympathetic reflexes partly restore output within ≈ 30 s.
No peripheral edema in the first hour or so: capillary pressure rises only a little at first, and edema needs days of renal fluid retention.
Compensated failure: retained fluid raises mean systemic filling pressure, so output returns to near normal at a higher atrial pressure; cardiac reserve stays low.
Decompensated failure: the heart cannot pump enough to bring renal output back to normal, so fluid keeps building; diuretics and inotropes reverse it by lowering volume or lifting the curve.
High-output failure (AV fistula, beriberi, thyrotoxicosis): low resistance raises venous return so much that a normal heart is eventually overloaded.
Higher intrapleural or pericardial pressure shifts the cardiac curve to the right: tamponade cuts output at any atrial pressure.

What it is

Heart failure is easiest to understand by crossing the cardiac-function curve with the venous-return curve. Damage flattens the cardiac curve; sympathetic drive lifts it within seconds, and renal fluid retention raises mean systemic filling pressure over days, restoring output at the cost of higher atrial pressure. If the heart is too weak, retention never stops (decompensation). Other states (high-output failure, tamponade, exercise) move the curves in their own typical ways.

Key facts

Plateau of the normal pumping heart ≈ 13 L/min; strong sympathetic drive and hypertrophy can raise it to ≈ 25–35 L/min (hypereffective heart).
Hypoeffective heart: low plateau from myocardial damage, valve disease, ischemia, high arterial pressure, or parasympathetic drive.
Cardiac reserve is the maximum rise of output above rest (≈ 300–400% in healthy young adults); an exercise test reveals its loss before symptoms at rest.
Low-output states: cardiac (MI, valve disease, arrhythmia) or peripheral (low volume, venous dilation, obstruction to venous return).
High-output states share low total peripheral resistance: AV fistula, beriberi, hyperthyroidism, anemia, pulmonary disease with low O₂.

How it works, step by step

Acute myocardial damage flattens the cardiac-function curve: output falls at every right atrial pressure.
Baroreflexes raise sympathetic drive: contractility rises (curve moves up) and veins constrict (mean filling pressure rises), so output recovers partly.
Low output lowers glomerular filtration and activates RAAS, ADH and sympathetic renal nerves: sodium and water are retained.
Over days, extra volume raises mean systemic filling pressure and venous return, so output rises toward normal (Frank–Starling) at a higher atrial pressure.
If the heart recovers or output is enough for renal excretion, retention stops: compensated failure.
If output stays below what the kidney needs, retention continues, the heart is overstretched, edema forms and the curve worsens: decompensation.
Treatment logic: diuresis lowers volume and filling pressure; an inotrope lifts the cardiac curve; both bring output back to the renal balance point.

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)

Heart failure with reduced ejection fraction: a larger, flatter loop. Try raising contractility or lowering preload.

How each situation moves the curves

Situation	Cardiac-function curve	Venous-return curve	Result
Acute heart damage	Down (flatter)	No change at first	Low output, high right atrial pressure
Sympathetic stimulation	Up (hypereffective)	Right shift (higher filling pressure)	Higher output
Transfusion / fluid retention	No change	Right shift, same slope	Higher output and atrial pressure
Large AV fistula	No change (or up with reflexes)	Steeper (low resistance to venous return)	Very high output
Tamponade / high pleural pressure	Right shift	No change	Low output, high atrial pressure
Heavy exercise	Up (sympathetic, hypertrophied in athletes)	Up and right (muscle pump, venoconstriction, low resistance)	Output up 4–7×, atrial pressure nearly unchanged

Clinical notes

Beriberi (thiamine deficiency) causes peripheral vasodilation and high venous return while weakening the heart: wet beriberi is a high-output failure.
Graves disease raises metabolic demand and lowers peripheral resistance, raising output; with heart disease it can tip into failure.
Cardiac tamponade lowers output because pericardial pressure limits filling at any venous pressure.

Test yourself

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

Why does a patient with an acute anterior MI usually not have leg edema in the first hour, even with low output?

Edema needs a sustained rise in capillary pressure and extra volume; renal retention of salt and water takes days to raise mean filling pressure enough.

On the Guyton graph, what happens to output and right atrial pressure during compensated heart failure?

The depressed cardiac curve meets a right-shifted venous-return curve (higher filling pressure from retained fluid): output is near normal, right atrial pressure is high.

Why does a large arteriovenous fistula raise cardiac output?

It lowers resistance to venous return, making the venous-return curve steeper; it crosses the cardiac curve at a higher output.

What separates decompensated from compensated heart failure?

In decompensation output never reaches the level the kidneys need to excrete normal salt and water, so retention, overstretch and edema keep worsening.

How does cardiac tamponade change the cardiac-function curve?

It shifts the curve to the right: a higher atrial pressure is needed for the same output, so output falls while atrial pressure rises.

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Connections

See it in 3D3

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

In Biochemistry1

Thiamine (vitamin B1)

In Pharmacology2

← 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: Heart Failure (Congestive Heart Failure) (StatPearls (NCBI Bookshelf), 2026); Cardiac Tamponade (StatPearls (NCBI Bookshelf), 2026); Beriberi: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Graves Disease (StatPearls (NCBI Bookshelf), 2024).

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