Cardiac Performance (CO, SV, Preload, and Afterload)
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Cardiac Output & Stroke Volume
Heart Rate
Baseline, aka, resting, heart rate is set by the sinoatrial node, and falls between 60-100 beats per minute.
Mechanical and electrical properties of the heart determine resting heart rate:
Strong, efficient hearts have lower resting heart rates (aka, sinus bradycardia) because they are able to pump sufficient blood to meet body tissue demands with fewer beats.
On the other hand, damages to the heart's electrical conducting system also alter the heart's baseline rhythm (arrhythmias).
The autonomic nervous system regulates the heart rate set by the SA node to ensure that cardiac output keeps up with changes in tissue demands.
Vagal stimulation decreases heart rate; for example, during sleep, when tissue demands for oxygen and other nutrients are decreased.
Conversely, sympathetic stimulation increases heart rate; for example, during exercise, when tissue demands rise. (for more on autonomic regulation of heart rate, specifically in response to changes in blood pressure, see our tutorial on the baroreceptor reflex).
Stroke Volume = EDV - ESV
Mathematically, stroke volume is equal to end diastolic volume (EDV) minus end systolic volume (ESV).
End diastolic volume represents the preload, which is defined as the tension on the muscle fibers at the beginning of contraction; in other words, the degree to which the muscle fibers are stretched.
End systolic volume is determined by:
a) Contractility, the ability of cardiac muscle cells to produce force, and,
b) Afterload, the force opposing muscle contraction.
Stroke volume is equal to the distance between the end systolic volume and end diastolic volume.
Changes in Preload, Contractility, or Afterload
Increased Preload Increases Stroke Volume
First, we show the normal pressure-volume loop. Then, we show another loop, this time with an increased end-diastolic volume.
We can see that, when preload, aka, end diastolic volume is increased, so, too, is stroke volume.
This makes sense, according to the Frank-Starling mechanism: there is more blood in the heart at the end of diastole, therefore, more blood is ejected in a heartbeat; we'll return to this concept.
Increase in Contractility increases Stroke Volume
We show the original loop plus a new pressure volume loop to illustrate that increased contractility shifts Points E and F to the left, which reduces end systolic volume.
We can see that, because contractility reduced end-systolic volume without altering end-diastolic volume, stroke volume is increased.
Increased Afterload decreases Stroke Volume
This occurs when aortic pressure rises, for example.
We show the original loop, then we show that changes in afterload increase the ventricular pressure needed to open the aortic valve and eject blood (Points D, E, and F).
Less blood can be ejected against the higher pressure, so end systolic volume is increased.
Recognize that if we also increased the contractility of the cardiac muscle, the heart could eject the same volume of blood, despite the increased afterload, to maintain stroke volume.
Interdependent Effects vs Independent Effects
This brings us to an important point about our diagrams: we've shown independent effects of preload, contractility, and afterload.
However, in real life, these variables are interdependent, so that the effects of one parameter are often partially offset by changes in another.
For example, an increase in preload can ultimately increase afterload.
Remember that higher stroke volume increases cardiac output; in turn, arterial pressure, aka, afterload, will rise (which means that the hypothetical increase in stroke volume will be partially offset by increase in afterload).
Or, consider that increased afterload lowers stroke volume; however, it also increases preload, which, thanks to the Frank-Starling mechanism, increases contractility.
The increased contractility can partially offset the initial decrease in stroke volume.
Increased contractility and stroke volume ultimately decreases end-systolic volume; decreased contractility ultimately increases end-systolic volume and decreases stroke volume.
Exercise is a good example of these interdependent mechanisms. When compensatory mechanisms fail, the heart cannot pump blood effectively.