Cardiac Output and Its Regulation

Part 3 · Cardiovascular System · Chapter 12 of 47

Learning objectives

By the end of this page you should be able to:

• Define cardiac output, cardiac index and their typical resting values.
• Explain how heart rate and stroke volume are controlled.
• Describe the Frank–Starling mechanism and the effects of preload, contractility and afterload.
• Explain venous return and the muscle and respiratory pumps.
• Calculate cardiac output with the Fick principle.
• Describe the cardiovascular response to exercise and training, and use heart rate to guide intensity.

Why it matters

When you walk a patient after surgery, cycle a patient in cardiac rehabilitation, or watch an athlete’s heart rate climb, you are watching cardiac output respond to demand.

In heart failure, cardiac output cannot rise enough, and exercise tolerance falls. Training raises the maximum. Knowing the levers that set cardiac output tells you what is limiting a patient and what you can change.

Cardiac output and its components

Cardiac output is heart rate multiplied by stroke volume. At rest, about 70 beats a minute times about 70 mL gives roughly 5 litres per minute in an adult. Because body size varies, output is sometimes divided by body surface area to give the cardiac index, about 3 L/min per square metre.

Figure 1 · What sets cardiac output

Controlling heart rate

Heart rate is set by the SA node and adjusted by the autonomic nervous system, as described in Chapter 11. Vagal activity slows the heart; sympathetic activity and circulating adrenaline speed it up. At the start of exercise, heart rate rises first because vagal tone is withdrawn.

Controlling stroke volume

The Frank–Starling mechanism

In 1914 Patterson and Starling showed in the isolated heart that the more the ventricle was filled, the more forcefully it contracted and the more it ejected [1]. Stretching the muscle brings its filaments towards a more effective overlap, and the heart pumps out whatever it receives.

Figure 2 · The Frank–Starling relationship

This mechanism keeps the two sides of the heart in step beat by beat. If the right ventricle ejects slightly more, the left ventricle fills slightly more on the next beat and ejects more to match.

Contractility shifts the whole curve. Sympathetic stimulation lifts it; heart failure lowers and flattens it, so extra filling produces little extra output and instead backs up as congestion.

Venous return

Over time the heart can pump only what returns to it. Most blood volume sits in the veins, and several things help it back.

Measuring cardiac output: the Fick principle

Figure 3 · The Fick principle

The Fick principle states that the oxygen the body takes up must equal the blood flow through the lungs times the oxygen each litre picks up. Rearranged, it gives cardiac output from oxygen uptake and the difference in oxygen content between arterial and mixed venous blood.

It also shows that oxygen uptake can rise in two ways: more cardiac output, or more oxygen extracted by the tissues. Exercise uses both.

Cardiac output in exercise

In heavy exercise, cardiac output can rise four- to fivefold in a healthy young adult. Heart rate rises roughly in step with intensity. Stroke volume rises early, helped by the muscle pump and sympathetic drive, and then levels off.

In 1968 Ekblom and Hermansen measured cardiac output in endurance athletes and found very high maximal values [2]. Much of the difference from untrained people lies in a larger stroke volume.

Figure 4 · Where the cardiac output goes

Output is redistributed as well as increased. Working muscle receives most of it, while flow to gut and kidneys falls and flow to the brain stays about the same. Joyner and Casey describe how very high muscle blood flow competes with the heart’s maximum output. The sympathetic system therefore restrains muscle vasodilation just enough to keep blood pressure up [3].

Training adaptations

Endurance training enlarges the ventricles and increases blood volume, so stroke volume rises. The same cardiac output at rest is then produced at a lower heart rate, which is why trained people often have resting rates in the 50s or lower. Maximal heart rate is not raised by training; maximal cardiac output rises through stroke volume.

Using heart rate to guide exercise

Because heart rate tracks cardiac output, it is a practical guide to intensity. Maximal heart rate falls with age. The common formula 220 − age was never properly validated in older adults.

Figure 5 · Predicting maximal heart rate

Tanaka and colleagues pooled data from 18,712 people and validated the equation 208 − 0.7 × age [4]. It does not differ between men and women or with habitual activity, and it gives higher values than 220 − age in older adults [4]. Both are population averages; an individual may differ by 10 beats or more either way.

Clinical relevance for the physiotherapist

• Heart failure. A flat Starling curve means cardiac output rises little with exercise; progress gradually and watch for breathlessness and fatigue.
• Post-operative mobilisation. Calf pumping and deep breathing aid venous return, supporting cardiac output when patients first stand.
• Dehydration and blood loss. Reduced preload lowers stroke volume, so heart rate rises to compensate.
• Beta-blockers. They blunt heart rate and contractility responses; use perceived exertion.
• Hypertension and aortic stenosis. High afterload limits stroke volume; avoid heavy straining and breath-holding.
• Exercise prescription. Use 208 − 0.7 × age rather than 220 − age for older adults [4].

Assessment and application

Common mistakes

• Adding heart rate and stroke volume instead of multiplying.
• Confusing preload (filling) with afterload (resistance to ejection).
• Thinking the Frank–Starling mechanism is a nervous reflex. It is a property of the muscle itself [1].
• Assuming training raises maximal heart rate. It raises maximal stroke volume.
• Relying on 220 − age for older patients [4].

Exam preparation

Long answer

Define cardiac output. Describe the factors that regulate it, and its changes during exercise.

• Definition, normal values, cardiac index (Figure 1).
• Heart rate control by the autonomic system.
• Stroke volume: preload, contractility, afterload; Frank–Starling (Figure 2) [1].
• Venous return and its aids.
• Measurement: Fick principle (Figure 3).
• Exercise: rise and redistribution of output (Figure 4) [2, 3]; training adaptations.

Short notes

• Frank–Starling law of the heart [1].
• Fick principle.
• Venous return.
• Predicting maximal heart rate [4].

Viva and practical

• “Why does a fit person have a slow resting heart rate?” — larger stroke volume delivers the same output at a lower rate.
• “What did Patterson and Starling show?” — ventricular output increases with filling [1].
• “What equation do you use for maximal heart rate in a 70-year-old?” — 208 − 0.7 × age, about 159 [4].
• Practical: measure resting and post-exercise heart rate and calculate a training range.

Current evidence

Exam and traditional teaching

Maximal heart rate is taught as 220 − age, and exercise blood flow as a simple matter of muscles dilating.

What the evidence adds

208 − 0.7 × age predicts maximal heart rate more accurately across the age range [4].

Exercise blood flow reflects a balance between muscle demand and the need to maintain blood pressure, with no single dominant dilator mechanism identified [3].

What the student should understand

Use heart rate as a guide but not a rule, especially in older and medicated patients. The underlying question is always whether cardiac output can meet the demand you are placing on it.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Quick review

Further reading

References

1. Patterson SW, Starling EH. On the mechanical factors which determine the output of the ventricles. Journal of Physiology. 1914 Sep 8;48(5):357–379. doi:10.1113/jphysiol.1914.sp001669 PMID 16993262 Original study
2. Ekblom B, Hermansen L. Cardiac output in athletes. Journal of Applied Physiology. 1968 Nov;25(5):619–625. doi:10.1152/jappl.1968.25.5.619 PMID 4879852 Experimental study
3. Joyner MJ, Casey DP. Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiological Reviews. 2015 Apr;95(2):549–601. doi:10.1152/physrev.00035.2013 PMID 25834232 Review
4. Tanaka H, Monahan KD, Seals DR. Age-predicted maximal heart rate revisited. Journal of the American College of Cardiology. 2001 Jan;37(1):153–156. doi:10.1016/s0735-1097(00)01054-8 PMID 11153730 Meta-analysis and validation study

Related topics

• Previous: Chapter 11 — Cardiac Electrophysiology and the ECG
• Next: Chapter 13 — Haemodynamics and Blood Pressure
• Exercise dose
• Cardiac rehabilitation

Reviewed by the Physiotherapist India Team. · Human Physiology contents