Guillain-Barré Syndrome (GBS) is a rare neurological disorder in which the body’s immune system attacks the peripheral nervous system. This causes rapid-onset muscle weakness, typically beginning in the feet and legs and progressing upward, affecting both sides of the body symmetrically. The involvement of the muscles controlling breathing is the most serious complication of GBS. Up to 30% of affected individuals experience respiratory compromise requiring mechanical ventilation. The resulting nerve damage leads to a specific type of ventilatory failure, necessitating close medical monitoring.
The Neurological Basis of Guillain-Barré Syndrome
The pathology of GBS is rooted in an aberrant immune response, often triggered by a preceding infection, such as a respiratory illness or gastroenteritis. The immune system mistakenly targets components of the peripheral nerves, a process thought to involve molecular mimicry. In the most common form, immune cells attack the myelin sheath, the fatty layer that insulates nerve fibers outside the brain and spinal cord.
Myelin enables the rapid transmission of nerve impulses to the muscles. When this sheath is damaged (demyelination), the nerve signal slows down or is interrupted, preventing effective communication from the central nervous system to the skeletal muscles. In other variants of GBS, the immune attack targets the axon itself, the central core of the nerve fiber.
Regardless of the target, the result is a functional block in nerve conduction. This disruption prevents muscles from receiving signals to contract, leading to progressive weakness and paralysis. This generalized nerve damage eventually reaches the motor neurons that control the physical mechanism of breathing.
Respiratory Muscle Failure in GBS
The generalized nerve damage in GBS extends to the nerves controlling the primary muscles of inspiration, causing neuromuscular respiratory failure. The diaphragm is the most important muscle for breathing, responsible for approximately 70% of air volume exchanged during quiet respiration. It is innervated by the phrenic nerve, and weakness impairs its ability to contract downward and expand the chest cavity.
The intercostal muscles, located between the ribs, also help expand the rib cage during a breath. When GBS attacks the nerves supplying these muscles, the ability to fully expand the chest wall is compromised. The combined weakening of the diaphragm and intercostals leads to a failure of the ventilatory pump.
This mechanical failure results in shallow, rapid breathing, reducing the volume of air exchanged. As paralysis progresses, the patient cannot generate the force needed to maintain adequate ventilation. This inability to move sufficient air causes respiratory distress, even though the lungs themselves are structurally sound.
Classification as Type II Respiratory Failure
The respiratory compromise caused by Guillain-Barré Syndrome is classified as Type II Respiratory Failure, also known as hypercapnic or ventilatory failure. Respiratory failure is categorized into two main types based on blood gas imbalance. Type I, or hypoxemic failure, involves low oxygen but near-normal carbon dioxide levels, typically resulting from impaired gas exchange within the lung tissue.
Type II failure involves low oxygen levels alongside elevated carbon dioxide levels (hypercapnia). This condition arises not from a defect in the lungs’ ability to exchange oxygen, but from a failure of the mechanical apparatus—the muscles and nerves—responsible for moving air. GBS causes paralysis of the breathing muscles, making it a clear example of neuromuscular weakness leading to Type II classification.
The core issue is the inadequate expulsion of carbon dioxide (CO2), a waste product of cellular metabolism. When breathing muscles are too weak to expel CO2 efficiently, the gas builds up in the bloodstream, causing hypercapnia. This accumulation shifts the body’s acid-base balance toward acidity, resulting in respiratory acidosis.
Hypercapnia can cause confusion, drowsiness, and headache. If the acid-base disturbance is not corrected, it can lead to coma and organ dysfunction. The rise in carbon dioxide levels is a defining marker that necessitates immediate intervention to support the patient’s breathing mechanics.
Immediate Clinical Intervention
Continuous monitoring of respiratory function is necessary for all GBS patients, usually in an intensive care setting. Clinicians rely on measurements of the Forced Vital Capacity (FVC), which quantifies the maximum volume of air a patient can exhale after a maximal inhalation. A progressively declining FVC indicates worsening respiratory muscle weakness.
When the FVC drops below a specific threshold, typically 20 milliliters per kilogram of body weight, the patient is at high risk for ventilatory failure. The standard intervention for impending Type II respiratory failure is intubation and mechanical ventilation. This involves placing a tube into the trachea and connecting the patient to a ventilator that takes over the work of the paralyzed breathing muscles.
Mechanical ventilation ensures adequate oxygenation and the clearance of accumulated carbon dioxide. This supportive measure is temporary, allowing time for the peripheral nerves to heal and muscle strength to return. The decision to intubate is based on FVC trends, signs of an ineffective cough, and the overall work of breathing.