The Frank-Starling relationshipChanges in contractilityWhy this matters



The Frank-Starling relationship (named after its two discoverers) simply describes the phenomenon that if you increase the degree to which a cardiac myocyte is stretched, the more forcefully it will contract. This is a simple consequence of the effect of resting cell length on the overlap of contractile filaments. A myocyte that isn’t stretched very much can’t shorten very much. Thus, if central venous pressure – which causes stretch of the ventricles - falls, cardiac output will decrease.


The Frank-Starling relationship

The Frank-Starling relationship (AKA Frank-Starling mechanism or Starling’s law of the heart) simply recognises an important feature of the length-tension relationship of cardiac muscle. At a normal, resting venous pressure of about 5 mmHg, cardiac muscle still isn’t stretched to its optimal length. The degree to which striated muscle can shorten depends upon the degree to which the sliding filaments are stretched. So, if the cardiac muscle cells (myocytes) are stretched further, they are able to shorten to a greater extent:

myocyte stretch
Figure 1: Muscle contraction depends on the activity of myosin (black) interacting with actin filaments (red). Myosin “walks” down actin producing contraction. If myocytes are stretched, the degree of overlap increases, resulting in a greater amount of shortening per contraction. At normal central venous pressure, cardiac myocytes have what we might call “shortening reserve”. That is, they are not stretched optimally and will increase their capacity to shorten if they are further stretched. This is all the Frank-Starling relationship of the heart really involves: stretch the ventricles and they will contract more. Of course, if you overstretch cardiac myocytes, then their ability to contract becomes compromised.

The practical upshot of this is that the more you stretch the ventricles with blood returning to the heart, the more forcefully they contract. On the other hand, if central venous pressure (or pulmonary venous pressure, if we consider the other side of the heart) is lower, and doesn’t stretch the ventricular myocytes as much then stroke volume will be reduced:

frank starling law relationship
Figure 2:The relationship between the degree of stretch of cardiac muscle (here expressed as central venous pressure or CVP) and the stroke volume of the heart. The more blood you squeeze into the ventricles, the more will be pumped out with each contraction. Typical, resting CVP and stroke volume are indicated, showing that the heart has some reserve to cope with increased demand. Remember, this is just a property of cardiac muscle and nothing more: Starling demonstrated this relationship using a heart perfused outside the body.


Changes in contractility

In addition to the Frank-Starling relationship, the heart can increase contractility in response to adrenaline, for example. This is a different phenomenon that involves intracellular signalling that promotes and enhances the elevation of intracellular Ca2+ ions that are responsible for production of contraction of myocytes. Possibly the best way to think about this difference is to consider the “normal” Frank-Starling relationship has become amplified so that greater contraction is possible at each resting length of stretch. By contrast, when the heart fails (perhaps due to ischaemic heart disease) it is less able to contract at each degree of stretch:

frank starling law relationship
Figure 3:How changes in the contractility of cardiac muscle affect the Frank-Starling relationship and hence stroke volume. The normal relationship shows how increased stretch – in the form of increased central venous pressure – leads to increased stroke volume because stretched myocytes can shorten more (see above). If the contractile performance of the myocytes is increased (say by adrenaline; dotted line) then this relationship is simply amplified: for each degree of stretch a more powerful contraction ensues, emptying the ventricles more fully and increasing stroke volume. When contractility is compromised in heart failure – for whatever reason – the opposite effect is observed (dashed line). At each degree of stretch, only a lesser contraction is possible. This leads to a reduced cardiac performance, the all-encompassing definition of heart failure.


Why does all this matter?

Stroke volume is an important determinant of cardiac output, and hence blood pressure. If central venous pressure falls, as it does in sepsis, anaphylaxis or haemorrhage (for example), then blood pressure will fall too and organ perfusion will be compromised. Treatment strategies in such cases will be aimed at increasing venous return, for example by raising the leg end of the bed (assisting gravity) or fluid resuscitation to increase blood volume.



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