In a patient with severe haemorrhagic shock (class III, >30% blood volume loss), which compensatory response maintains mean arterial pressure for the longest duration?
- A Stress relaxation of arterial walls, which increases arterial compliance and reduces systolic pressure load within the first minute
- B Sympathetic-mediated arteriolar vasoconstriction (increased TPR) and venoconstriction (increased venous return) — these are activated within seconds by arterial baroreceptors and maintained for hours, providing sustained MAP support ✓
- C ADH (vasopressin) acting on vascular V1 receptors — this is the first and most rapid response, occurring within seconds via baroreceptor-mediated release
- D Renin-angiotensin-aldosterone activation providing long-term volume restoration within 15–30 minutes of haemorrhage through immediate renal Na⁺ reabsorption
Explanation
In haemorrhagic shock, arterial baroreceptors immediately (within seconds) detect reduced MAP and withdraw parasympathetic and increase sympathetic outflow. Sympathetic stimulation causes: (1) arteriolar vasoconstriction (increasing TPR, sustaining MAP); (2) venoconstriction (reducing venous capacitance, increasing venous return and cardiac output); (3) increased heart rate and contractility. These responses are sustained for hours. Baroreceptor-mediated ADH release is important (within seconds to minutes) but V1-mediated vasoconstriction is a secondary mechanism. RAAS-mediated aldosterone acts over 1–2 hours for renal Na⁺ retention but does not provide immediate volume. Stress relaxation would reduce vascular resistance, which is counterproductive in shock.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.