Pathophysiology
II-21. Forms of hypovolemic shock
循環血液量減少性ショックの病型
Stages of Hemorrhagic (Hypovolemic) Shock
- 10% loss (~0.5 L, blood-donation volume): no change in CO or arterial pressure
- Further loss → CO falls first, then BP → BP alone is misleading (falls later than CO)
1. Compensated stage
- CO ↓ without BP change — fully reversible even without intervention
- Negative-feedback processes (by time scale):
- Seconds–minutes: baroreceptor reflex, ↑adrenaline, reverse stress relaxation
- 10 min–1 h: RAAS activation, ↑ADH, ↓ANP, thirst & salt appetite
- 1 h–2 days: fluid auto-infusion + plasma protein replacement
- 3–4 days: RBC production (EPO)
- Baro/chemoreflex: ↓venous return → ↓CO → ↓BP sensed by high-pressure (aortic arch, carotid) & low-pressure (atria, large veins) baroreceptors → ↑SYM outflow → ↑HR/contractility (↑CO), arterial constriction (↑TPR), venous constriction (mobilizes stored blood), renal renin → ANGII
- Redistribution of CO: brain vessels do not constrict (perfusion preserved), while GI vessels strongly vasoconstrict
- Fluid conservation: renal Na⁺/water retention (RAAS, ADH V2), ADH V1 vasoconstriction, ↓ANP
- Fluid replacement: auto-infusion from interstitium (↓colloid osmotic pressure), plasma protein from liver (space of Disse + de novo albumin), ↑RBC via EPO
2. Progressive stage
- ~20% loss → CO and BP fall together, with negative feedback exhausted (↓medullary osmotic gradient, ADH & catecholamine depletion, adrenoceptor desensitization, vasodilator toxins, auto-infusion failure from altered Starling forces)
- CNS ischemic (Cushing) response at ~50 mmHg → strong SYM burst → transient BP plateau (↑ICP → ↓HR + ↑BP)
- Positive-feedback vicious cycles: ↓coronary perfusion → ↓CO, ↓brain perfusion → ↓SYM output, tissue hypoxia → vasodilator mediators → venous pooling, and vessel-wall hypoxia → vasodilation + ↑permeability → edema → ↓blood volume/venous return
- Metabolic: lactic acidosis (anaerobic metabolism) + hypercapnia. Mitochondrial depression → ↓ATP → ↓Na⁺/K⁺ ATPase → cell swelling → necrosis
3. Irreversible stage
- Positive feedback dominates (vicious circles), with death despite intervention → MOF/MODS
Therapeutic Options
- Replace volume where it is missing: colloids (albumin, gelatins, dextrans) for intravascular deficit, isotonic saline/Ringer for ECF deficit, 5% glucose for total-body-water deficit
- Treat the underlying cause, and monitor perfusion parameters (not BP alone)
一問一答
▶How much blood loss occurs without change in CO or arterial pressure?
About 10% (~0.5 L, a blood-donation volume); beyond this, CO falls first and BP later.
▶What defines the compensated stage of hemorrhagic shock?
CO decreases without a change in BP, and it is fully reversible even without intervention.
▶What are the seconds-to-minutes compensatory mechanisms in hemorrhagic shock?
Baroreceptor reflex, increased adrenaline, and reverse stress relaxation.
▶What compensatory processes act over 10 minutes to 1 hour in hemorrhagic shock?
RAAS activation, increased ADH, decreased ANP, and thirst & salt appetite.
▶What compensatory processes act over 1 hour to 4 days in hemorrhagic shock?
1 h–2 days: fluid auto-infusion + plasma protein replacement; 3–4 days: RBC production via EPO.
▶How does the sympathetic response support circulation in the compensated stage?
↑SYM outflow raises HR/contractility (↑CO), constricts arteries (↑TPR), constricts veins (mobilizes stored blood), and triggers renal renin → ANGII.
▶How does fluid auto-infusion replace volume after hemorrhage?
Reduced capillary pressure (and ↓colloid osmotic pressure) draws interstitial fluid into vessels, while the liver replaces plasma proteins (space of Disse + de novo albumin) and EPO increases RBC.
▶How is cardiac output redistributed during hemorrhagic shock?
Brain vessels do NOT constrict (perfusion preserved), while GI vessels strongly vasoconstrict.
▶At what blood loss does the progressive stage begin, and what happens to CO and BP?
At ~20% loss, CO and BP fall together as negative feedback becomes exhausted.
▶Why does negative feedback become exhausted in the progressive stage?
↓Medullary osmotic gradient, ADH & catecholamine depletion, adrenoceptor desensitization, vasodilator toxins, and auto-infusion failure from altered Starling forces.
▶What is the CNS ischemic (Cushing) response in shock?
At ~50 mmHg, a strong sympathetic burst causes a transient BP plateau (↑ICP → ↓HR + ↑BP).
▶Give examples of positive-feedback vicious cycles in the progressive stage of shock.
↓Coronary perfusion → ↓CO; ↓brain perfusion → ↓SYM output; tissue hypoxia → vasodilator mediators → venous pooling; vessel-wall hypoxia → vasodilation + ↑permeability → edema → ↓blood volume.
▶What metabolic disturbances occur in the progressive stage of shock?
Lactic acidosis (anaerobic metabolism) and hypercapnia; mitochondrial depression → ↓ATP → ↓Na⁺/K⁺ ATPase → cell swelling → necrosis.
▶What defines the irreversible stage of hypovolemic shock?
Positive feedback (vicious circles) dominates, leading to death despite intervention → MOF/MODS.
▶How is fluid replaced according to the site of the deficit in hypovolemic shock?
Colloids (albumin, gelatins, dextrans) for intravascular deficit, isotonic saline/Ringer for ECF deficit, and 5% glucose for total-body-water deficit.
▶Why should perfusion parameters (not BP alone) be monitored in shock?
BP is maintained by compensation and falls later than CO, so it underestimates the severity of inadequate tissue perfusion.
▶Which baroreceptors detect the fall in venous return during hemorrhage?
High-pressure baroreceptors (aortic arch, carotid) and low-pressure baroreceptors (atria, large veins).
▶What is reverse stress relaxation in hemorrhagic shock?
A rapid compensatory mechanism where reduced volume causes the vessel wall (especially veins) to tense and push blood out, helping maintain filling.
▶How do the kidneys conserve fluid during hemorrhagic shock?
RAAS and ADH (V2) drive Na⁺/water retention, ADH (V1) causes vasoconstriction, and ANP is decreased.
▶Why does venous constriction help in compensated hemorrhagic shock?
Veins hold most of the blood volume; constricting them mobilizes stored blood and increases venous return to the heart.