Pathophysiology
II-22. Phases of hypovolemic shock
循環血液量減少性ショックの病期
Phases of Hypovolemic Shock
- Phases are defined by the changes in CO and arterial pressure after hemorrhage
- 10% loss (~0.5 L): no change → further loss → CO falls first, BP later
1. Compensated stage
- From the start of CO decrease until BP begins to drop
- Blood loss compensated by physiological negative feedback; fully reversible without intervention
- Goal: maintain BP despite falling CO
Counter-Regulatory Processes by Time Scale
- Seconds–minutes (maintainable only minutes–hours):
- Baroreceptor reflex
- ↑adrenaline (adrenal medulla)
- Reverse stress relaxation
- 10 min–1 h (restore blood volume):
- RAAS activation
- ↑ADH secretion
- ↓ANP secretion
- Thirst & salt appetite
- 1 h–2 days: fluid auto-infusion + plasma protein replacement
- 3–4 days: RBC production (EPO)
Mechanism of Activation
- ↓venous return → ↓CO → ↓BP detected by high-pressure baroreceptors (aortic arch/carotid) & low-pressure baroreceptors (atria/large veins) → ↑SYM outflow
- Heart: ↑HR + ↑contractility → ↑CO
- Arteries: constriction → ↑TPR (good for BP, bad for tissue perfusion later)
- Veins: constriction → mobilize stored blood → ↑venous return
- Kidney: renin → ANGII (strong vasoconstrictor)
- Reverse stress relaxation: ↓volume → wall stress pushes blood out (esp. veins)
- Redistribution of CO: brain vessels do not constrict (perfusion preserved); GI strongly constricts
- Fluid conservation: ANGII → ↓GFR + aldosterone → Na⁺/water retention; ADH V2 (water) + V1 (vasoconstriction); ↓ANP
- Fluid replacement: auto-infusion from interstitium (↓colloid osmotic pressure), plasma protein from liver, ↑RBC via EPO
2. Progressive stage (depletion of counter-regulation)
- ~20% loss → CO and BP fall together; negative feedback exhausted:
- ↓renal medullary osmotic gradient → ↓urine concentration → less fluid retained
- ADH depletion, catecholamine depletion + adrenoceptor desensitization
- Vasodilator mediators/toxins from tissues
- Auto-infusion failure (altered Starling forces)
- CNS ischemic (Cushing) response at ~50 mmHg → SYM burst → transient BP plateau
3. Irreversible stage
- Positive feedback dominates; death despite intervention
一問一答
▶How are the phases of hypovolemic shock defined?
By the changes in cardiac output and arterial pressure after hemorrhage.
▶What marks the boundaries of the compensated stage of hypovolemic shock?
It runs from the start of the CO decrease until BP begins to drop, is compensated by physiological negative feedback, and is fully reversible without intervention.
▶What is the goal of compensation in the compensated stage?
To maintain blood pressure despite a falling cardiac output.
▶Which fast counter-regulatory processes can be maintained only for minutes to hours?
The baroreceptor reflex, increased adrenaline (adrenal medulla), and reverse stress relaxation.
▶Which counter-regulatory processes (10 min–1 h) restore blood volume?
RAAS activation, increased ADH secretion, decreased ANP secretion, and thirst & salt appetite.
▶What restores blood volume over 1 h–2 days and over 3–4 days?
1 h–2 days: fluid auto-infusion + plasma protein replacement; 3–4 days: RBC production via EPO.
▶What triggers the increase in sympathetic outflow during hemorrhage?
↓Venous return → ↓CO → ↓BP detected by high-pressure baroreceptors (aortic arch/carotid) and low-pressure baroreceptors (atria/large veins) → ↑SYM outflow.
▶How does the sympathetic response act on the heart, arteries, and veins?
Heart: ↑HR + ↑contractility → ↑CO; arteries: constriction → ↑TPR; veins: constriction → mobilize stored blood → ↑venous return.
▶What is the role of the kidney's renin response during shock?
Renin → ANGII, a strong vasoconstrictor that also drives ↓GFR and aldosterone-mediated Na⁺/water retention.
▶Why is brain perfusion preserved while GI perfusion is sacrificed in shock?
Brain vessels do not constrict under sympathetic drive (autoregulation), whereas GI vessels strongly constrict, redistributing CO to vital organs.
▶How do ADH V1 and V2 receptors contribute differently during shock?
V2 promotes renal water retention, while V1 causes vasoconstriction.
▶What drives fluid auto-infusion from the interstitium during shock?
Reduced capillary hydrostatic pressure and decreased colloid osmotic pressure pull interstitial fluid into the vasculature.
▶At what blood loss does the progressive stage start, and what happens?
~20% loss → CO and BP fall together as the negative feedback systems become exhausted.
▶Why does the renal medullary osmotic gradient failure worsen progressive shock?
A reduced medullary gradient impairs urine concentration, so less fluid is retained, accelerating volume depletion.
▶Why does catecholamine depletion and adrenoceptor desensitization worsen shock?
They blunt the sympathetic vasoconstrictor response, so BP and CO can no longer be supported.
▶What causes the transient BP plateau in the progressive stage?
The CNS ischemic (Cushing) response at ~50 mmHg triggers a sympathetic burst that briefly raises BP.
▶Why does auto-infusion fail in the progressive stage?
Altered Starling forces (e.g., increased capillary permeability and changed pressures) prevent further interstitial fluid recruitment.
▶What defines the irreversible stage of hypovolemic shock?
Positive feedback dominates and death occurs despite intervention.
▶Why is reverse stress relaxation only a short-term compensation?
It is one of the seconds-to-minutes mechanisms that can be maintained only for minutes to hours before being exhausted.
▶Why does arterial constriction help BP but harm tissues during shock?
It raises TPR to support blood pressure but reduces peripheral tissue perfusion, which becomes harmful later.