Hemodynamic Homeostasis · §10 · MAP = CVP + CO × SVR (a different term fails per syndrome)

Hypotension as a node decomposition of the pressure loop

Hypotension is not one disease but a node decomposition of the same MAP = CVP + CO x SVR loop. Each low-pressure syndrome is a different node failing: the fast buffer (orthostatic), the renal reference (adrenal), the resistance effector (distributive), the volume substrate (hypovolemic), or the cardiac basin (cardiogenic). Direction reproduced [V], clinical anchors [L], absolute [O].

Where hypertension is a single reference reset upward, hypotension decomposes by which node of the defended-pressure loop fails. The fast buffer loss is orthostatic; a downward reference reset is adrenal; an SVR-effector collapse is distributive; a volume-substrate fold is hypovolemic; a cardiac-basin collapse is cardiogenic. Each is computed on the existing primitives. Direction [V], anchors [L], absolute [O].

One loop, five failure nodes

Hypertension is a single failure mode — the renal integral controller resets its reference upward. Low pressure is the symmetric but richer case, and it is a sharper test of the loop, because it probes every node independently. On the same relation MAP = CVP + CO × SVR, the failure is named by which node gives way, and the model derives each one from the primitives already established rather than positing a new mechanism per syndrome.

The decomposition (research targets RP6–RP9 + cardiogenic)

The fast buffer fails in orthostatic/autonomic hypotension: an intact baroreflex buffers a downward postural step (small residual), while autonomic failure or PIEZO knockout passes the full drop — the symmetric counterpart of the labile knockout in the fast-loop chapter (RP6). The renal reference resets DOWN in adrenal insufficiency (lost RAAS set-point, shift -20 mmHg): a fluid bolus is opposed back to the low reference, while restoring the reference with a mineralocorticoid is durable — the exact mirror of antihypertensive durability (RP7).

The resistance effector collapses in distributive/vasoplegic shock: as SVR falls, MAP drops below the perfusion floor even with doubled cardiac output, so a vasopressor that restores SVR (93 mmHg) beats an inotrope alone (57.4 mmHg) — a different therapeutic arm than heart failure (RP8). The volume substrate is depleted in hypovolemic shock: renal natriuresis is excrete-only, so a volume EXCESS self-corrects to 93 mmHg (the perfect adaptation of the slow loop) but a volume DEFICIT is a fold the kidney cannot self-correct (53 mmHg) — only external volume restores it (93 mmHg) (RP9). Cardiogenic shock is the heart-failure basin collapse taken to loss of perfusion; uniquely, its acute fix is temporary inotropic/mechanical support — the opposite of chronic heart failure, separated by timescale.

Therapy follows the failed node

The loop structure forbids a one-size-fits-all pressor: the corrective must match the node that failed, and applying the wrong one (fluids in adrenal reset, inotrope in vasoplegia) is rejected for the same reason the loop is defended. This is the practical payoff of the decomposition.