3. Intrinsic Regulation (Autoregulation)

i) Heterometric Autoregulation - the Frank-Starling law of the heart.

The Frank-Starling law of the heart states that, within physiological limits, the heart's output is determined by the volume of blood in the ventricles immediately before contraction (the end-diastolic volume). This can be explained by the length-tension relationship of cardiac muscle fibres.

Increasing venous return increases the end-diastolic volume and stretches the myocardial muscle fibres. Stretch increases the tension developed when the ventricles next contract ( the next heartbeat ) and the stroke volume increases. This relationship holds until the fibres are overstretched when the tension decreases.

Additional Information

Frank-Starling Law of the Heart
In the late nineteenth century two eminent physiologists Otto Frank and Ernest Starling studied cardiac physiology in an isolated dog heart preparation. They found that under certain conditions the heart was able to regulate its own output and that this regulation was independent of nervous and hormonal influences. Their findings are neatly summarised in the following poem.

What goes in, must come out.
The great Dr. Starling, in his Law of the Heart
Said the output was greater, if, right at the start,
The cardiac fibres were stretched a bit more,
So their force of contraction would be more than before.
Thus the larger the volume in diastole
The greater the output was likely to be.
But when the heart reaches a much larger size,
This leads to Heart Failure, and often, Demise.

The relevant law is not Starling's, alas,
But the classical law of Lecompte de Laplace.
Your patient is dying in Decompensation,
So reduce his Blood Volume, or call his relation.
If the right heart keeps pumping more blood than the left,
The lung circuit's congested; the systemic-bereft.
Since no one is healthy with pulmo-congestion,
The law of Doc Starling's a spendid suggestion.
The balance of outputs is made automatic
And blood-volume partition becomes steady-static.

Length-Tension Relationship
The length-tension relationship describes the increase in muscle fibre contractility which occurs when a muscle fibre is stretched shortly before contraction. Stretching the fibres achieves a more optimal overlap of actin myosin filaments.

If we apply this relationship to myocardial fibres in the walls of the ventricles, then increasing venous return (increase end-diastolic volume) will stretch the fibres. When they contract they develop more tension and more blood will be ejected (the ventricular stroke work increases).

Thus increasing venous return results in increased stroke volume.

If the fibres are overstretched the degree of overlap of actin and myosin filaments is decreased and the tension developed is reduced (decompensation).