Pathophysiology
II-20. Definition and classification of circulatory shock
循環性ショックの定義と分類
Circulatory Shock — Definition
- Complex acute systemic circulatory failure → inadequate tissue blood supply → cell and organ damage → ultimately multiple organ failure and death without intervention
Classification
- Hypovolemic (↓blood/plasma volume): hemorrhagic, or plasma loss (vomiting, diarrhea, burns)
- Cardiogenic (cardiac-origin ↓CO): ischemic, myopathic, arrhythmic
- Obstructive (large-vessel occlusion → ↓CO): pulmonary embolism, cardiac tamponade, tension pneumothorax
- Distributive (increased vascular capacity): septic, anaphylactic, neurogenic
Hemodynamic Types
- Hypodynamic / vasoconstrictive (hypovolemic, cardiogenic, obstructive): primary ↓CO → compensatory general vasoconstriction (↑TPR) to maintain BP
- Hyperdynamic / vasodilative (distributive): initial ↓TPR (vasodilation) → ↓afterload, transiently ↑CO → then ↓venous return → ↓CO (resembles hypodynamic shock)
- Septic shock is most frequent (>50% of cases)
Causes of ↓CO by Type
- Hypovolemic & distributive: ↓preload → ↓CO
- Cardiogenic: loss of myocardial pump function
- Obstructive: ↑afterload → ↓CO
Forces Returning Blood to the Heart
- Vis a fronte — diastolic suction (depends on lusitropic capacity)
- Vis a tergo — forward push (large-vessel stretch and developed pressure)
- Hypovolemic shock: ↓blood volume → ↓filling pressure → ↓preload → ↓CO
- Distributive shock: the unstressed/stressed volume boundary shifts right → normal volume no longer generates adequate filling pressure → ↓preload → ↓CO
一問一答
▶What causes obstructive shock?
Large-vessel occlusion reducing CO — pulmonary embolism, cardiac tamponade, and tension pneumothorax.
▶What is the definition of circulatory shock?
A complex acute systemic circulatory failure causing inadequate tissue blood supply → cell and organ damage → ultimately multiple organ failure and death without intervention.
▶What causes hypovolemic shock?
Decreased blood/plasma volume — hemorrhagic, or plasma loss from vomiting, diarrhea, and burns.
▶What are the four etiological classes of circulatory shock?
Hypovolemic, cardiogenic, obstructive, and distributive.
▶What are the subtypes of cardiogenic shock?
Ischemic, myopathic, and arrhythmic (a cardiac-origin decrease in CO).
▶What are the types of distributive shock?
Septic, anaphylactic, and neurogenic (increased vascular capacity).
▶What characterizes hypodynamic (vasoconstrictive) shock?
Hypovolemic, cardiogenic, and obstructive shock: primary ↓CO → compensatory general vasoconstriction (↑TPR) to maintain BP.
▶What characterizes hyperdynamic (vasodilative) shock?
Distributive shock: initial ↓TPR (vasodilation) → ↓afterload, transiently ↑CO → then ↓venous return → ↓CO (resembling hypodynamic shock).
▶Which type of shock is most frequent?
Septic shock (>50% of cases).
▶How does CO fall in each shock type by mechanism?
Hypovolemic & distributive: ↓preload → ↓CO; cardiogenic: loss of myocardial pump function; obstructive: ↑afterload → ↓CO.
▶What are vis a fronte and vis a tergo?
Vis a fronte = diastolic suction (depends on lusitropic capacity); vis a tergo = forward push from large-vessel stretch and developed pressure — the forces returning blood to the heart.
▶How does hypovolemic shock reduce cardiac output via the Frank-Starling mechanism?
↓Blood volume → ↓filling pressure → ↓preload → ↓CO.
▶How does distributive shock reduce preload despite a normal blood volume?
The unstressed/stressed volume boundary shifts right, so a normal volume no longer generates adequate filling pressure → ↓preload → ↓CO.
▶Why does distributive shock eventually resemble hypodynamic shock?
After an initial transient ↑CO from vasodilation, venous return falls → CO drops, mimicking the low-output hypodynamic state.
▶What is the final common consequence of untreated shock?
Multiple organ failure (MOF/MODS) and death.
▶Why is cardiac output a better early indicator than blood pressure in shock?
Compensatory vasoconstriction maintains BP initially, so CO falls before BP — making BP a misleading late marker.
▶How does the hemodynamic profile of obstructive shock compare to hypovolemic shock?
Both are hypodynamic/vasoconstrictive with low CO and compensatory ↑TPR, but obstructive shock results from ↑afterload (large-vessel occlusion) rather than volume loss.
▶Why does diastolic suction (vis a fronte) depend on lusitropic capacity?
Active myocardial relaxation (lusitropy) generates the diastolic suction that helps draw blood back into the heart.
▶Which shock types are unified by a fall in preload?
Hypovolemic and distributive shock both reduce CO via decreased preload.
▶Why does compensatory vasoconstriction in hypodynamic shock harm tissues despite maintaining BP?
Raising TPR supports blood pressure but reduces perfusion to peripheral tissues, contributing to later cell/organ damage.