Cardiac output and what sets it !

Regulation
Exam priority: high

Cardiac output is how much blood the heart pumps each minute: beats per minute times the volume of each beat.

Updated 2026-11-01

Also called: Stroke volume, Cardiac index, Fick principle

See it in 3D: Left ventricle · Right ventricle

What it is

Cardiac output (CO) is the volume each ventricle pumps per minute, about 5 L/min in a resting adult. It equals heart rate times stroke volume; stroke volume depends on preload, afterload and contractility. Over minutes and hours, the heart pumps what returns to it, so venous return and tissue needs largely set CO.

Left-ventricular pressure–volume loop

EDV 120 mLESV 40 mLSV 81 mLEF 67%ESP 121 mmHg

↑ Contractility

↑ Contractility (sympathetic drive or an inotrope): the ESPVR gets steeper and the LV empties more: ESV falls, SV and EF rise.

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 stroke volume (loop width) with the normal, preload and afterload presets.

Equations

Cardiac outputCO = HR × SV

HR: heart rate
SV: stroke volume = EDV − ESV

Fick principleCO = V̇O₂ / (CaO₂ − CvO₂)

V̇O₂: O₂ consumption (≈ 250 mL/min at rest)
CaO₂ − CvO₂: arteriovenous O₂ content difference (≈ 50 mL/L)

250 ÷ 50 ≈ 5 L/min.

Hemodynamic Ohm's lawMAP − RAP = CO × SVR

MAP: mean arterial pressure
RAP: right atrial pressure
SVR: systemic vascular resistance

Reference values (resting adult)

Parameter	Value	Note
Cardiac output	≈ 4–8 L/min	≈ 5 L/min typical
Cardiac index	≈ 2.5–4 L/min/m²
Stroke volume	≈ 60–100 mL
Maximal CO in a trained athlete	up to ≈ 30–35 L/min

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

Regulation

+Sympathetic nerves (β1): Raise heart rate and contractility.
+Venous return / preload (Frank–Starling): More filling gives a larger stroke volume.
−Afterload (high arterial pressure, aortic stenosis): Lowers stroke volume.
−Vagus nerve: Lowers heart rate (little effect on ventricular contractility).
−Hypoxia, acidosis, ischemia: Reduce contractility.

Clinical notes

High-output states: anemia, sepsis (early), hyperthyroidism, pregnancy, arteriovenous fistula, beriberi.
Low output with high SVR and cold skin points to cardiogenic or hypovolemic shock.

Test yourself

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

A person consumes 300 mL O₂/min, with arterial O₂ content 200 mL/L and mixed venous 140 mL/L. What is the cardiac output?

5 L/min: 300 ÷ (200 − 140) = 300 ÷ 60 = 5 L/min (Fick principle).

Why does cardiac output fall when heart rate exceeds about 180/min in an adult?

Diastole shortens so much that the ventricle cannot fill; end-diastolic volume and stroke volume fall more than the rate rises.

Over the long term, what mainly sets cardiac output in a healthy person?

Venous return, which depends on the tissues' metabolic needs (local vasodilation); the heart, through Frank–Starling, pumps what returns.

Why does severe anemia raise cardiac output?

Low O₂ content causes tissue vasodilation and lower blood viscosity, so SVR falls and venous return rises; sympathetic activity also increases.

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See it in 3D

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

In Pharmacology

Beta blockers

← 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); Hypovolemia and Hypovolemic Shock (StatPearls (NCBI Bookshelf), 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 20). 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.