Hemorrhage Compensation: MAP, Baroreflex & the Decompensation Cliff (2D)

Hemorrhage

Blood loss (% of volume) 30%

Bleed duration 20 s

Baroreceptor Reflex

Reflex gain (sensitivity) 4.0×

Response time-constant (τ) 6.0 s

Live Readout

Normal

MAP

93 mmHg

Heart rate

70 bpm

TPR

100%

Sympathetic drive

Blood volume

100%

Elapsed

0.0 s

How it works

Mean arterial pressure follows the standard hemodynamic identity MAP = CO × TPR (cardiac output times total peripheral resistance). Blood loss drops central venous filling (preload), so stroke volume — and therefore cardiac output — falls even before any reflex engages:

preload index = clamp[(BV − Vu) / 0.15, 0, 1]
SV = SV0 · preload index
CO = HR · SV
MAP = MAP0 · (CO / CO0) · (TPR / TPR0)

Falling MAP is sensed by carotid/aortic baroreceptors, which drive sympathetic outflow S up through a first-order lag (the response time-constant τ set above) toward a target proportional to the pressure error and the reflex gain:

error   = (MAP0 − MAP) / MAP0
S_target = clamp(gain · error, 0, 1)
dS/dt   = (S_target − S) / τ

Rising S raises heart rate toward ~180 bpm, raises TPR up to ~2.6×, and venoconstricts the venous reservoir (shrinking unstressed volume Vu), which recruits blood back into the "stressed" compartment and partly restores preload — the compensated phase, where MAP is held close to normal despite ongoing loss.

That compensation has a hard limit: once blood volume falls below what even maximal venoconstriction can keep in the stressed compartment, the preload index collapses to zero no matter how high S climbs. Cardiac output and MAP then fall steeply even though the reflex is already maxed out — the decompensation cliff, which this model places in the classic ~30–40% blood-loss range.

MAP (mmHg) Heart rate TPR Blood volume