A 30-year-old man with complete spinal cord transection at the T5 level develops pounding headache, profuse sweating above the level of the lesion, flushing of the face, and BP of 210/115 mmHg shortly after bladder catheterisation. His pulse is 40/min. The combination of severe hypertension with bradycardia is best explained by:

• A Stimulation of the Bezold-Jarisch reflex by distension of the urinary bladder wall
• B Excess circulating catecholamines from the adrenal medulla acting on intact cardiac receptors
• C Loss of descending vasomotor control causing simultaneous vagal and sympathetic activation throughout
• D Unopposed sympathetic discharge below the lesion with intact baroreceptor-mediated vagal slowing above it ✓

Explanation

In lesions above T6, a noxious stimulus below the injury triggers a massive sympathetic discharge that cannot be modulated by supraspinal centres, causing intense vasoconstriction and hypertension. Carotid and aortic baroreceptors above the lesion remain intact and connected to the medulla, so they mount a brisk vagal reflex producing bradycardia, while the vagus still reaches the heart because cardiac innervation exits above the lesion. Adrenal catecholamines are not the main driver.

Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.