The more the ventricle fills, the harder it contracts, within limits
Mnemonic
“The more you fill it, the harder it squeezes”: stroke volume increases with end diastolic volume, up to a point.
The mechanism is length-tension: stretching the sarcomere towards its optimum of about 2.2 micrometres improves actin-myosin overlap and increases calcium sensitivity of the myofilaments.
The curve, not the law, is what matters clinically:
- A healthy ventricle sits on the steep part, so extra preload increases output
- A failing ventricle has a flattened curve, so extra preload produces little extra output and simply raises filling pressure, causing pulmonary oedema
- Inotropes shift the curve up and left; negative inotropes shift it down and right
“Fluid helps a normal heart and floods a failing one”, which is the entire basis of fluid responsiveness testing, and why a passive leg raise is safer than a fluid bolus.
The law also explains why the two ventricles must match their outputs automatically over time, since any imbalance changes the filling of the other.
Expansion
Stroke volume rises as end-diastolic volume rises. The heart therefore pumps out whatever it receives, and the two ventricles automatically match their outputs.
The cellular basis has two parts:
- Stretch brings actin and myosin filaments to a more favourable overlap
- More importantly, stretch increases the calcium sensitivity of troponin C
The curve is not limitless. Beyond an optimal sarcomere length of about 2.2 micrometres the curve plateaus, and in the failing heart it flattens and shifts down and right, so a large rise in filling pressure produces little extra output; this is why fluid loading helps a hypovolaemic patient and causes pulmonary oedema in a failing one.
Positive inotropes shift the curve up and left; negative inotropes shift it down and right.