Cardiovascular System
Frank-Starling law, venous return and stroke volume
The Frank-Starling law says that, within the physiological (normal) range, a ventricle that fills more is stretched more and contracts harder, so it pumps out a larger stroke volume.
Remember
Within the physiological range, more filling means more stretch, and more stretch gives a stronger next beat, so stroke volume follows venous return (the flow of blood back to the heart) without any nerve or hormone signal.
A healthy heart can match its output to the blood that returns to it. Venous return (the flow of blood back to the heart) fills the ventricle during diastole (the relaxation phase, when the ventricles fill). More filling gives a larger end-diastolic volume (EDV), the volume in the ventricle at the end of filling, which is also called the preload. The heart muscle is then stretched further before it contracts.
Stretched sarcomeres (the repeating contractile units inside each muscle cell) become more responsive to calcium, which is part of length-dependent activation, the way greater length raises force within the physiological range. The next systole (the contraction phase) is therefore more forceful, and it pumps out a larger stroke volume, the blood pumped out by one ventricle per beat. Because cardiac output is stroke volume multiplied by heart rate, the output rises even if the heart rate stays the same.
The effect is intrinsic, which means that nerves and hormones are not needed, and it works beat by beat. It also has a limit: a failing ventricle may gain little extra stroke volume from further filling. Force can also fall with excessive experimental stretch of muscle, but that result does not show how stroke volume changes with filling in a ventricle.
Sympathetic stimulation raises contractility (the strength of contraction at a given filling), so stroke volume is higher at the same EDV. Afterload (the force the ventricle must overcome to pump blood out) also affects stroke volume. At a given contractility and afterload, a larger EDV usually gives a larger stroke volume within the physiological range. A change in heart rate alters how often the heart beats, not the strength of a beat after greater filling.
Memory aid
like an elastic band, the more it is stretched, the harder it snaps back, up to a limit.
The ventricle is the band: more filling stretches it and the next beat is stronger, up to a limit.
Key facts
- Trigger
- a rise in venous return enlarges the end-diastolic volume and stretches the heart muscle.
- Mechanism
- stretched sarcomeres become more responsive to calcium, which is part of length-dependent activation, so the next contraction is stronger.
- Result
- stroke volume rises, so cardiac output (stroke volume multiplied by heart rate) rises even if the heart rate stays the same.
- Nature
- intrinsic to the heart muscle, so no nerve or hormone signal is needed.
- Limit
- a failing ventricle may gain little extra stroke volume from further filling, and force can fall with excessive experimental stretch of muscle, but that result does not show how stroke volume changes with filling in a ventricle.
- Separate influence
- sympathetic stimulation raises stroke volume at any given filling, so it shifts the relationship between filling and stroke volume rather than explaining it.
Exam traps
- A reduction in afterload can raise stroke volume by making it easier to pump blood out, but it acts through the resistance met by the ventricle and not through stretch during filling, so it is not the Frank-Starling mechanism.
- Contractility is the force of the beat at a given filling and is raised by sympathetic stimulation, whereas the Frank-Starling mechanism is the change in force that follows a change in filling.
- A much faster heart rate leaves less time for filling and can lower the end-diastolic volume, which would weaken the Frank-Starling effect rather than produce it.
- A fall in force with stretch can be seen with excessive experimental stretch beyond the physiological range, but within the normal range greater length increases force, so this describes the opposite of the law.
- The coronary arteries supply the heart muscle itself, so greater coronary flow concerns oxygen delivery and not the response of the muscle to stretch, and it gives no reason for a fuller ventricle pumping out more blood on the next beat.
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