A patient with complete T4 spinal cord transection (acute phase) is given IV atropine for symptomatic bradycardia. Why are patients with high cervical/thoracic spinal cord injury particularly prone to bradycardia and hypotension?

• A Spinal shock elevates spinal parasympathetic outflow from sacral segments
• B Loss of afferent baroreceptor signals from the aortic arch to the medulla
• C Spinal cord oedema compresses the phrenic nerve, reducing cardiac sympathetic drive
• D Loss of descending sympathetic pathways from the rostral ventrolateral medulla leaves vagal tone unopposed to the heart and disrupts splanchnic vasoconstriction ✓

Explanation

Cardiac sympathetic innervation originates from T1–T5 spinal segments and descends from the rostral ventrolateral medulla (RVLM). A high thoracic or cervical transection interrupts these descending sympathetic pathways, leaving cardiac vagal (parasympathetic) tone unopposed and causing bradycardia. Simultaneously, loss of descending sympathetic drive to splanchnic and peripheral vasculature causes vasodilation and neurogenic hypotension — the 'sympathectomized' state of neurogenic shock. This distinguishes it from hypovolaemic shock where tachycardia is expected.

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

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