A 34-year-old man with a T6 spinal cord injury from a motorcycle accident develops a distended bladder. He suddenly develops pounding headache, profuse sweating above the level of injury, nasal congestion, and a blood pressure of 210/130 mmHg with a heart rate of 48 bpm. The primary pathophysiological mechanism responsible for the severe hypertension is:
- A Loss of supraspinal inhibitory control over spinal sympathetic reflexes below the lesion, with intact parasympathetic compensatory mechanisms above it ✓
- B Loss of supraspinal sympathetic inhibition below the lesion causing massive catecholamine release
- C Unopposed vagal stimulation below the lesion causing reflex systemic vasoconstriction
- D Disruption of the renin-angiotensin-aldosterone system leading to unregulated angiotensin II production
Correct answer: A. Loss of supraspinal inhibitory control over spinal sympathetic reflexes below the lesion, with intact parasympathetic compensatory mechanisms above it
Explanation
This is autonomic dysreflexia. The noxious stimulus (distended bladder) below the spinal lesion activates intact spinal sympathetic reflexes that are disconnected from brainstem inhibitory control, causing massive vasoconstriction and hypertension below the lesion. The intact baroreceptor reflex above the lesion triggers compensatory bradycardia (via vagal stimulation to the SA node) and vasoconstriction fails below the lesion. Option C incorrectly invokes vagal activity below the lesion. Option B describes neurogenic shock physiology, not autonomic dysreflexia.
Reference: Ganong's Review of Medical Physiology, 26th ed.
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