Why is a patient with a spinal cord injury above T6 in bradycardia?

Bradycardia in Spinal Cord Injury Above T6

Bradycardia occurs in patients with spinal cord injury above T6 due to acute loss of supraspinal control over sympathetic neurons, resulting in unopposed parasympathetic (vagal) stimulation of the heart. 1

Pathophysiologic Mechanism

Loss of Sympathetic Control

• Spinal cord injuries at or above T6 disrupt descending pathways from central autonomic control centers to spinal sympathetic neurons located in the intermediolateral nuclei of T1-L2 spinal cord segments. 1, 2, 3
• This disruption causes loss of supraspinal control over the sympathetic nervous system, resulting in reduced overall sympathetic activity below the injury level. 2, 4, 3
• The sympathetic innervation to the heart originates primarily from T1-T4 spinal segments, so injuries above T6 effectively denervate cardiac sympathetic control. 4, 3

Unopposed Parasympathetic Dominance

• With sympathetic tone diminished or absent, the vagus nerve exerts unopposed parasympathetic influence on the heart, leading to severe sinus bradycardia. 1, 2
• The vagus nerve remains intact because it originates from the brainstem (cranial nerve X), not the spinal cord, allowing continued parasympathetic cardiac control without sympathetic counterbalance. 2, 3

Spinal Shock Phenomenon

• During the acute phase after injury, spinal shock occurs—a temporary loss or depression of all spinal reflex activity below the injury level, including autonomic reflexes. 2, 3
• This neurogenic shock component consists of severe bradycardia combined with profound hypotension due to loss of cardiovascular sympathetic innervation. 2, 4, 3

Clinical Severity and Risk

Incidence and Timing

• Severe sinus bradycardia is common in the acute recovery phase after spinal cord injury, with both incidence and severity directly related to the level and severity of injury. 1
• Cardiac arrest, most often from sinus arrest and asystole, occurs in 16% of patients with severe cervical spinal injury during the first 2-4 weeks after trauma. 1, 2

Common Triggers

• Bradycardia episodes are frequently triggered by tracheal suctioning, turning the patient, and other positional changes that further stimulate vagal reflexes. 1, 5, 2
• These episodes can be persistent and refractory to atropine and other adrenergic drugs because the underlying problem is absence of sympathetic tone rather than excessive parasympathetic activity. 1, 2, 6

Key Clinical Pitfall

A critical mistake is assuming atropine will be effective. While atropine blocks parasympathetic receptors, it cannot restore the absent sympathetic tone that is the primary problem. 1, 2, 6 This explains why aminophylline or theophylline may be more effective than traditional atropine therapy in this specific population, as methylxanthines work by inhibiting adenosine's suppressive effects on the sinoatrial node rather than relying on sympathetic-parasympathetic balance. 1, 6

Duration and Resolution

• Bradycardia typically resolves after either a few weeks or removal of noxious stimuli, as conservative therapy is generally successful for managing the acute phase. 1
• Treatment with agents like theophylline can usually be withdrawn after 4-6 weeks as autonomic function gradually improves. 1, 6
• Permanent pacemaker placement should not be rushed as bradycardia is typically self-limited and resolves as spinal shock recedes. 5