The heart ejects blood in short, forceful bursts (systole) separated by refilling pauses (diastole). If arteries were rigid pipes, blood flow to the tissues would stop-start with every heartbeat. Instead, the aorta and large arteries are elastic — they bulge to store part of each stroke volume under pressure, then recoil to push that stored blood onward while the heart is resting. This is the Windkessel effect ("wind chamber", after the air-filled chambers old fire pumps used to smooth their pulsed output).
The two-element Windkessel model treats the arterial tree as one compliant chamber (compliance C) draining into the periphery through a resistance R:
C · dP/dt = Q_in(t) − P/R
Q_in(t) = Q_peak·sin(πt/T_s) during systole (duration T_s)
Q_in(t) = 0 during diastole
Q_out(t) = P(t) / R continuous peripheral runoff
- Heart rate / stroke volume — set the pulsatile input Q_in(t): how often and how much blood the heart injects each beat.
- Compliance C — how much the arterial wall stretches per mmHg. Low compliance (stiff, aged arteries) means small volume changes swing pressure widely — this is why systolic pressure rises with arterial stiffening.
- Resistance R — the peripheral (arteriolar) resistance draining the reservoir. Higher R raises mean pressure and slows the diastolic pressure decay.
- The chamber in the scene visibly swells during systole and slowly deflates during diastole; particles jet in bursts on the heart side but exit at a nearly steady rate on the periphery side — the Windkessel effect made visible.
This is a deliberately simplified 2-element model — real arterial trees add wave reflection and inertance — but it captures the core mechanism behind pulse pressure and why stiffening arteries (with age or disease) raise systolic blood pressure even when cardiac output is unchanged.