What is the Frank-Starling mechanism of the heart?

How does the body know how much blood to send to each of the various tissues in the body? Well, if their metabolic needs stayed constant, the body could be pre-programmed to distribute blood accordingly in a set fashion. But what if they changed? What if (as happens, of course) our skeletal muscles required lots more blood flow during exercise, and our guts required far less blood flow during the same period? How would the body know how to adjust its pattern of blood distribution?

The answer is: it leaves this decision largely up to the tissues themselves. On the whole, the byproducts of metabolism (low oxygen, high carbon dioxide, adenosine [from the hydrolysis of ATP], etc.) will build up whenever the cells in a particular area increase their rate of metabolism. The local vessels sense these substances, and dilate - thus increasing blood flow to the tissues that need it! Clever, no?

This does pose a little problem for the heart though. The amount of blood it receives by the end of each diastole (i.e. the "end diastolic volume") is obviously dependent on how much blood flows through the tissues and back to the heart - a factor which we've just noted the tissues determine for themselves. Thus the heart can't "know" in advance how much blood it's going to receive, and thus have to pump out, each time.

To cope with this problem, it is equipped with the Frank-Starling mechanism. Fundamentally, this is the heart's ability to match its stroke volume to the end diastolic volume it receives; in other words, it is the ability to pump out more (or less) blood if it receives more (or less) blood.

How is this possible? Well, let's say that the venous return is abnormally high. By definition this means that the heart is sitting with quite a lot of blood in its ventricles when the time comes for it to contract. Compared with normal, that is, the end diastolic volume is high. This extra volume of blood distends the ventricle more than normal, stretching the cardiac muscle cells and causing them to contract with extra strength. And this extra strength forces the extra blood out during systole. Thus, the heart adjusts its stroke volume (i.e. the amount of blood it ejects with each contraction) to cater for increased or decreased amounts of venous return.

(At a molecular level, what is happening is that the extra stretch increases troponin C's affinity for calcium, facilitating the formation of a greater than normal amount of crossbridges. If this is Greek to you, fear not, for we shall cover muscle contraction in a separate post.)

There are limits to the Frank-Starling mechanism; you can't just keep filling the heart with more and more blood and expect it to cope! Eventually, the heart's muscle cells are stretched to capacity and any further increase in venous return can't be expelled. With a healthy heart and body, this almost never happens, but the limits of the Frank-Starling mechanism begin to be noticeable when patients have cardiac failure.