CorpusHuman Anatomy
CardiovascularPhysiological process

Cardiac output

Also known as: CO, stroke volume, ejection fraction, preload, afterload, contractility, Fick principle, venous return

Cardiac output is the volume of blood each ventricle pumps per minute. It equals heart rate multiplied by stroke volume, about 70 beats/min × 70 mL ≈ 5 L/min at rest, and can rise four- to sevenfold during exercise.

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Overview

Resting CO≈5 L/min
Cardiac index2.5–4.0 L/min/m²
Stroke volume≈60–100 mL
Ejection fraction≈55–70%
Maximal CO≈20–25 L/min (untrained); 35–40 L/min (elite)

Basic relationships. Cardiac output = HR × SV. Stroke volume = end-diastolic volume − end-systolic volume. Ejection fraction = SV ÷ EDV. Cardiac index is cardiac output divided by body surface area, normally 2.5–4.0 L/min/m².

What sets stroke volume. Preload is the end-diastolic stretch of the ventricle. It depends on venous return, filling time, the atrial contribution and how compliant the ventricle is. Afterload is the wall stress the ventricle must develop during ejection. It depends on aortic pressure, systemic vascular resistance and aortic valve area, and by Laplace's law wall stress ≈ P × r ÷ 2h. Contractility (inotropy) is the strength of contraction independent of loading. It is increased by β1 stimulation (through cAMP and PKA, which act on L-type Ca²⁺ channels, phospholamban and troponin I), digoxin and Ca²⁺. It is reduced by β-blockers, non-dihydropyridine calcium channel blockers, acidosis, hypoxia and ischaemia.

Heart rate. Raising the heart rate increases cardiac output until about 150–180 beats/min. Above this, filling time becomes too short and stroke volume falls.

Venous return. In the steady state, cardiac output equals venous return. Venous return = (mean systemic filling pressure − right atrial pressure) ÷ resistance to venous return. On Guyton's diagram, the steady-state cardiac output is where the cardiac function curve crosses the venous return curve.

Measurement. The Fick principle states that cardiac output = O₂ consumption ÷ (arterial − mixed venous O₂ content). For example, 250 mL/min ÷ 50 mL/L = 5 L/min. Cardiac output can also be measured by thermodilution with a pulmonary artery catheter, by echocardiography and by pulse-contour analysis.

Parts & subdivisions

  1. Heart rate
    About 60–100/min at rest. It is set by the SA node and modified by the autonomic nervous system (chronotropy).
  2. Stroke volume
    About 60–100 mL (typically 70 mL), equal to EDV minus ESV.
  3. Preload
    End-diastolic fibre length or volume. It is the basis of the Frank–Starling mechanism.
  4. Afterload
    Wall stress during ejection, set mainly by arterial pressure and systemic vascular resistance.
  5. Contractility
    Inotropic state, which shifts the Frank–Starling curve up or down.

Function

  • Matches blood delivery to the body's metabolic demand.
  • Together with total peripheral resistance, determines mean arterial pressure.
Physiology

At rest, cardiac output is shared roughly as follows: liver and gut about 25%, kidneys about 20%, skeletal muscle about 15–20%, brain about 15%, skin about 5–10% and heart about 4–5%. During maximal exercise, output reaches about 20–25 L/min in untrained adults and 35–40 L/min in elite endurance athletes. Most of the increase goes to working skeletal muscle.

Clinical significance

Shock types by haemodynamics

Each type of shock has a characteristic haemodynamic pattern. Hypovolaemic shock has low preload and low cardiac output, with high SVR. Cardiogenic shock has low cardiac output with high filling pressures and high SVR. Obstructive shock (tamponade, massive PE) has low cardiac output and high SVR. Distributive shock (sepsis) usually has a high cardiac output with very low SVR.

Athlete's heart

Endurance training enlarges the ventricles and raises stroke volume, so the resting heart rate can fall to 40–50/min while resting cardiac output stays normal.

Test yourself

The Frank–Starling mechanism explains why stroke volume rises when:
  1. Sympathetic stimulation increases heart rate
  2. End-diastolic volume (preload) increases
  3. Aortic pressure (afterload) increases
  4. Vagal tone increases

Answer: End-diastolic volume (preload) increases

Greater filling stretches the sarcomeres toward their optimal length and increases the Ca²⁺ sensitivity of troponin C. Contraction is therefore stronger. This is intrinsic to the heart and needs no nerves.

Using the Fick principle: O₂ consumption is 250 mL/min, arterial O₂ content is 200 mL/L and mixed venous O₂ content is 150 mL/L. What is the cardiac output?
  1. 2.5 L/min
  2. 5 L/min
  3. 7.5 L/min
  4. 12.5 L/min

Answer: 5 L/min

CO = VO₂ ÷ (CaO₂ − CvO₂) = 250 ÷ (200 − 150) = 250 ÷ 50 = 5 L/min.

More cardiovascular system questions

Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.