A 65-year-old diabetic man has orthostatic hypotension (BP drops from 130/80 supine to 90/60 standing) without a compensatory rise in heart rate. Which is the most likely site of autonomic dysfunction explaining the absent tachycardia?
- A Efferent sympathetic cardioaccelerator nerve fibres to the sinoatrial node are damaged; cardiac baroreflex arc is broken at its efferent limb, preventing noradrenaline-mediated HR increase ✓
- B Afferent baroreceptor fibres in the carotid sinus are damaged; hypotension is not detected, so no reflex is initiated
- C The nucleus tractus solitarius has been selectively damaged by hyperglycaemia, blocking central processing of baroreflex signals
- D Parasympathetic withdrawal normally mediates standing tachycardia; vagal efferent fibres are specifically damaged
Explanation
In diabetic autonomic neuropathy, orthostatic hypotension occurs when efferent sympathetic vasoconstrictor and cardioaccelerator fibres are damaged. Normally, standing activates arterial baroreceptors → NTS → increased sympathetic outflow → peripheral vasoconstriction (to prevent BP fall) and cardiac acceleration via noradrenaline on SA node β1 receptors. When sympathetic efferents are neuropathic, neither vasoconstriction nor tachycardia can occur—hence the combination of hypotension without reflex tachycardia. Although parasympathetic withdrawal also contributes to initial standing tachycardia (option D), this operates normally; the absent HR rise here is due to the missing sympathetic acceleration that normally sustains tachycardia beyond the first 15 beats.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.