Pathophysiology
II-24. Organ manifestations of circulatory shock (MODS)
循環性ショックの臓器症状（MODS）
Organ Manifestations of Circulatory Shock (MOF/MODS)
- The irreversible stage = multiple organ failure / multiple organ dysfunction syndrome, driven by sustained hypoperfusion
Heart — Cardiac Pump Failure
- CO keeps falling even when the cause is stable: ↓coronary flow → ↓pump function → ↓CO → ↓arterial pressure → further ↓coronary flow (vicious cycle) → subendocardial necrosis
- Aggravated by ATP depletion, acidosis, toxins (e.g. endotoxin)
CNS
- Failure of cardiorespiratory and other vegetative regulatory functions → autonomic nervous system loses its function
Lungs — “Shock Lung” (ARDS)
- Hyaline membrane disorder; activated alveolar macrophages + cytokines → ↑endothelial permeability → plasma exudate → ↑O₂ diffusion distance
- Epithelial damage → ↓surfactant → alveolar collapse; exudate fills alveoli → ↓gas-exchange surface → respiratory failure
Kidneys — “Shock Kidney” (ATN, acute kidney failure)
- ↓pressure + renal vasoconstriction (↑SYM, ↑ANGII, endothelial dysfunction) → ischemia
- Tubular hypoxia → ↓ATP → depolarization, Ca²⁺ influx, cytoskeletal rearrangement; Na⁺/K⁺ ATPase mislocalization → ↓Na⁺ reabsorption → ↑Na⁺ at macula densa → tubuloglomerular feedback → ↓GFR; brush-border loss, cell death/detachment → tubular obstruction
Liver
- Hypoxia around the central vein (O₂ gradient) → centrilobular necrosis → liver failure (impaired metabolic & detoxifying functions)
GI Tract
- Strong GI vasoconstriction (blood redistribution) → very slow flow → RBC sludging → microthrombi/blockage → loss of intestinal barrier function → septicemia (sepsis)
Blood Viscosity
- Plasma/fluid loss (burns, diarrhea, diuresis, sweating) → hemoconcentration → ↑viscosity → ↓tissue perfusion → more RBC sludging
一問一答
▶What is MODS in the context of circulatory shock?
Multiple organ dysfunction syndrome — the irreversible stage characterized by failure of multiple organs driven by sustained hypoperfusion.
▶Describe the cardiac vicious cycle in shock-induced pump failure.
↓Coronary flow → ↓pump function → ↓CO → ↓arterial pressure → further ↓coronary flow, leading to subendocardial necrosis.
▶What aggravates cardiac pump failure in shock?
ATP depletion, acidosis, and toxins (e.g., endotoxin).
▶How does shock affect the CNS at the organ level?
Failure of cardiorespiratory and other vegetative regulatory functions — the autonomic nervous system loses its function.
▶What is 'shock lung' (ARDS) and how does it develop?
A hyaline membrane disorder: activated alveolar macrophages + cytokines → ↑endothelial permeability → plasma exudate → ↑O₂ diffusion distance.
▶What causes renal ischemia in 'shock kidney'?
Decreased pressure plus renal vasoconstriction (↑SYM, ↑ANGII, endothelial dysfunction) leading to acute tubular necrosis.
▶How does tubuloglomerular feedback reduce GFR in shock kidney?
Tubular hypoxia → Na⁺/K⁺ ATPase mislocalization → ↓Na⁺ reabsorption → ↑Na⁺ at the macula densa → tubuloglomerular feedback → ↓GFR.
▶Why does surfactant loss worsen shock lung?
Epithelial damage → ↓surfactant → alveolar collapse; exudate fills alveoli → ↓gas-exchange surface → respiratory failure.
▶How does tubular cell injury cause obstruction in shock kidney?
Brush-border loss and cell death/detachment block the tubular lumen, causing tubular obstruction.
▶Why does the liver develop centrilobular necrosis in shock?
Hypoxia is worst around the central vein (oxygen gradient), causing centrilobular necrosis and liver failure.
▶How does GI involvement in shock lead to sepsis?
Strong GI vasoconstriction → very slow flow → RBC sludging → microthrombi → loss of intestinal barrier → septicemia.
▶How does blood viscosity change in shock and why does it matter?
Plasma/fluid loss (burns, diarrhea, diuresis, sweating) → hemoconcentration → ↑viscosity → ↓tissue perfusion and more RBC sludging.
▶What is subendocardial necrosis and why is the subendocardium vulnerable?
Necrosis of the inner myocardium; the subendocardium is most vulnerable to ischemia because it is perfused last and compressed most during systole.
▶Why does increased O₂ diffusion distance impair gas exchange in shock lung?
Plasma exudate and edema thicken the alveolar-capillary barrier, so oxygen must diffuse further, reducing oxygenation.
▶What renal lesion underlies 'shock kidney'?
Acute tubular necrosis (ATN) causing acute kidney failure.
▶Why is loss of the intestinal barrier dangerous in shock?
Gut bacteria/toxins translocate into the circulation, triggering septicemia that worsens the systemic state.
▶Why does cardiac output keep falling even when the original cause is stable?
Because the self-reinforcing coronary perfusion vicious cycle continues independently of the initial trigger.
▶What cellular events follow tubular ATP depletion in shock kidney?
Depolarization, Ca²⁺ influx, cytoskeletal rearrangement, and Na⁺/K⁺ ATPase mislocalization.
▶Which mediators drive endothelial permeability in shock lung?
Activated alveolar macrophages and the cytokines they release.
▶How does hemoconcentration create a further vicious cycle in shock?
↑Viscosity → ↓tissue perfusion → more RBC sludging → further ↓perfusion.