Imagine this:

You have your final exams coming next week. Your project for the exams is due tomorrow. Your best friend’s birthday is in two days and you’re organizing it. You have to attend your classes too since the last few lectures usually help you for the exams and let’s face it, you need the attendance too.
There’s only so much you can take on right? You stretch beyond a point, you tend to just want to give up, and that seems like the most natural reaction to have too.

Something similar happens in our bodies too; in the organ that ironically works tirelessly from the womb to the tomb. Yes, I am talking about the heart.

Normally, blood from the peripheries are brought to the heart via the veins, a phenomenon called venous return, and the heart pumps it back to the peripheries via the arteries, called cardiac output.

Its logical to assume that at rest, the cardiac output is equal to the venous return, because well, the total volume of blood always remains constant, right? But what happens when we have a stress like surgery? Or if we are exercising? The cardiac output increases to match the increase in demand, and this occurs in a beautiful sequence of events.

Any stress activates the sympathetic system and the catecholamines released act at 2 places on the heart- one, on the cardiac muscle and increases its force of contraction, and two, at the cardiac pacemaker, which increases the heart rate and these two act together to increase the cardiac output.

But like the example at the start of the article, even the heart has a limit; this is described by what is called, The Frank-Starling’s Law.

This law states that within its limits, the force of contraction is directly related to the length of the muscle fibre before its contraction.

Let’s break it down.

When blood comes back to the heart via venous return, it stretches the heart muscle; this venous filling of the ventricles happens during the diastole (period of relaxation of the heart during the cardiac cycle), and there is maximum blood in the ventricles at the end of diastole. This is called the End Diastolic Volume, and since this End Diastolic Volume acts on the heart before it contracts, it is called Pre-Load. So here, the muscle length is essentially the pre-load, which is determined by the venous return.

After this stretch, the heart muscle contracts and the blood is ejected out via the great vessels- via the aorta to the peripheries, and via the pulmonary trunk to the lungs; this is called the Stroke Volume. As a stand-alone number, it doesn’t mean much,  but when described as a fraction of the EDV, it’s called the Ejection Fraction, and this is an important clinical marker of cardiac function.

Compare this phenomenon to an elastic band; the more we pull, the faster it contracts back to its original length. But beyond a certain limit, the elastic band snaps.

Which means that if the End Diastolic Volume is too high, the heart muscle cannot contract enough to push all the blood out; more and more blood stays back in the ventricles, which increases the EDV and hence the pre-load with every contraction, thus worsening the failure.

This is the exact pathophysiology behind the symptoms of congestive cardiac failure, where volume overload causes the heart’s pumping mechanism to fail; the treatment of which is primarily aimed at reducing this load on the heart.

Probably something we should try and extrapolate to our lives too, right?