What is the etiology of orthostatic hypotension in patients with central nervous system (CNS) injuries and paralysis?

Etiology of Orthostatic Hypotension in CNS Injuries and Paralysis

Impaired sympathetic nervous system function is the primary etiology of orthostatic hypotension in patients with central nervous system injuries and paralysis, causing inadequate vasoconstriction and venous pooling in the legs. 1

Pathophysiological Mechanisms

Primary Mechanism: Sympathetic Nervous System Dysfunction

• In patients with CNS injuries and paralysis, functional and structural impairments of the autonomic nervous system lead to inadequate increase in peripheral resistance and heart rate upon standing 1
• Cardiovascular sympathetic fibers are unable to increase total peripheral vascular resistance in the upright posture 1
• This results in:
  • Venous pooling of blood below the diaphragm
  • Decreased venous return
  • Reduced cardiac output
  • Low blood pressure 1

Specific Autonomic Deficits

1. Inadequate vasoconstriction:

   • Failure of peripheral vasoconstriction is the key mechanism 1
   • Normally, standing triggers arterial baroreceptors to signal the vasomotor center in the medulla, which then increases sympathetic outflow to blood vessels
   • CNS injuries disrupt this pathway, preventing appropriate vasoconstriction

2. Chronotropic incompetence:

   • Blunted heart rate response to standing (usually <10 beats per minute) 1, 2
   • While not the primary contributor to orthostatic hypotension, it compounds the problem

3. Loss of skeletal muscle pump:

   • Paralysis eliminates the normal muscle contractions that assist with venous return
   • This exacerbates venous pooling in the lower extremities 1

Distinguishing Features from Other Forms of Orthostatic Hypotension

• In neurogenic OH due to CNS injuries, the heart rate increase is blunted (usually <10 bpm) 1, 2
• This contrasts with non-neurogenic OH (e.g., hypovolemia), where heart rate increase is preserved or enhanced 1
• The onset typically occurs within 3 minutes of standing (classical OH) 1

Clinical Manifestations

Symptoms result from cerebral hypoperfusion and include:

• Dizziness and lightheadedness
• Weakness and fatigue
• Visual disturbances
• Hearing disturbances
• Neck and back pain
• Syncope in severe cases 1

Common Pitfalls in Understanding OH in CNS Injuries

• Misconception: Increased skeletal muscle pump is NOT an etiology of orthostatic hypotension; rather, the LOSS of this mechanism contributes to the problem
• Misconception: Parasympathetic nervous system impairment is NOT a primary cause of orthostatic hypotension in CNS injuries
• Misconception: Impaired absorption of antihypertensive medications is NOT a significant mechanism in this population

Summary

The orthostatic hypotension observed in patients with CNS injuries and paralysis is primarily due to impaired sympathetic nervous system function, resulting in inadequate vasoconstriction, venous pooling, and reduced venous return. This is compounded by chronotropic incompetence and loss of the skeletal muscle pump that would normally assist with venous return.