Extrapulmonary factors of alveolar hypoventilation are associated with mechanical limitation of chest wall and diaphragmatic mobility, as well as impairments in the central respiratory regulatory structures. They lead to pronounced restriction of respiratory excursions and a decrease in basic spirometric parameters.
Key parameterFVC directly reflects the degree of pulmonary restriction
Thoracic cageOssification of costal cartilages and chest compression
Pleural cavityPresence of blood, exudate, transudate, or air
Centrogenic levelDamage to the respiratory center and cerebral cortex
Chest Wall and Pleural Pathology
Disorders of the musculoskeletal framework and serous membranes lead to restricted mobility of the chest wall and diaphragm.
Chest wall pathology: Includes mechanical compression, reduced joint mobility, and ossification of costal cartilages.
Pleural pathology: Inflammatory processes (pleuritis) and fibrous changes.
Pathological contents: Accumulation of air (pneumothorax), blood (hemothorax), as well as exudate or transudate (hydrothorax).
Extrapulmonary Restriction and Spirometry
Restrictive disorders cause a limitation in the magnitude of lung respiratory excursions. Such conditions include exudative pleuritis, pronounced ossification of costal cartilages, decreased mobility of chest joints in osteochondrosis, and mechanical compression (e.g., during structural collapses and motor vehicle accidents).
In this form of pathology, the following parameters predictably decrease:
Total Lung Capacity (TLC).
Residual Volume (RV).
Forced Vital Capacity (FVC) / Vital Capacity (VC) — a key parameter that directly reflects the severity of restriction (the lower it is, the more severe the condition).
Centrogenic Level of Hypoventilation
Central regulation disorders are considered a critical cause of alveolar hypoventilation. Based on the topographic criterion, the centrogenic level affects the respiratory center and the cerebral cortex.
Main damaging factors:
Trauma and neoplasms in the medulla oblongata region.
Brain compression due to edema, inflammation, or hemorrhage.
Acute hypoxia.
Exogenous and endogenous intoxications (ethanol, narcotic drugs, uremia).
Destructive processes of brain tissue (encephalitis, multiple sclerosis, syringomyelia, syphilis).
Clinically significant forms include apneustic and periodic breathing patterns.
Which neuromuscular diseases lead to extrapulmonary alveolar hypoventilation?
Extrapulmonary hypoventilation is caused by diseases affecting neuromuscular junctions, nerve trunks, and the respiratory muscles themselves.
Poliomyelitis, myasthenia gravis, and polyneuritis cause impaired impulse transmission at the neuromuscular junctions of the intercostal muscles and diaphragm.
Botulism leads to the blockade of acetylcholine release, causing respiratory muscle paresis and acute respiratory failure.
Myalgia and myodystrophies are associated with direct damage to the intercostal muscles and impaired function.
How does the Tiffeneau index change in restrictive hypoventilation?
In restrictive hypoventilation, the Tiffeneau index remains within normal limits, i.e., equal to or greater than 70%.
This is due to the fact that when lung expansion is limited, both key spirometric parameters decrease proportionally: Forced Expiratory Volume in 1 second (FEV₁) and Forced Vital Capacity (FVC). As a result, their percentage ratio (FEV₁/FVC), which represents the Tiffeneau index, does not decrease.
How does apneustic breathing differ from periodic breathing?
Apneustic breathing is characterized by a cycle described as a prolonged low-depth inspiration → short expiration → another prolonged inspiration. Its mechanism: prolonged inspiration is associated with reduced amplitude of impulses from all types of respiratory neurons except the post-inspiratory pool; post-inspiratory neuron activity is prolonged, and synchronization of inspiratory neurons in the respiratory rhythm generator is disrupted.
Periodic breathing forms include Biot's, Cheyne-Stokes, and Kussmaul breathing:
Cheyne-Stokes breathing: A period of apnea from several seconds to 1 minute → shallow breathing → gradual increase in depth to a noisy maximum around the 5th to 7th breath → gradual decrease in depth → a new period of apnea.
Biot's breathing: Alternation of uniform, rhythmic, and deep respiratory movements with periods of apnea.
Kussmaul breathing: Uniform cycles of slow, deep, and noisy inspiration followed by a forced expiration.
What spinal cord lesions cause respiratory disorders?
Respiratory disorders are caused by the following spinal cord and pathway lesions:
Lesions of pathways from the respiratory center to the diaphragm in spinal cord ischemia or trauma, multiple sclerosis, poliomyelitis. The pathogenesis is loss of respiratory automatism; breathing becomes irregular and ceases during sleep.
Corticospinal tract lesions in tumors, trauma, spinal cord ischemia, syringomyelia. The pathogenesis is loss of voluntary respiratory control; the patient cannot voluntarily alter the rhythm or depth of breathing.
Lesions of descending spinal pathways and motor neurons in spinal cord trauma or ischemia, poliomyelitis. Clinically, a decrease in the amplitude of respiratory movements and periodic apnea are described.
Cervical lesion in tick-borne viral encephalitis: Paralysis of the diaphragmatic musculature is associated with motor neurons of the anterior horns of C4; combined lesion of the neck muscles and diaphragm causes peripheral-type respiratory impairment.
Vertebrospinal trauma at the cervical and upper levels: Monitoring and prevention of hypoventilation are recommended for such patients.
Which spirometric parameters decrease in extrapulmonary restriction?
Total Lung Capacity (TLC), Residual Volume (RV), and Vital Capacity (VC) predictably decrease.
What does the Vital Capacity (VC) reflect in restriction?
VC directly reflects the degree of pulmonary restriction: the lower this indicator, the more pronounced the limitation of respiratory excursions.
What are the main causes of damage to the centrogenic level of respiratory regulation?
These include trauma and tumors of the medulla oblongata, brain compression from edema or hemorrhage, acute hypoxia, intoxications (exogenous and endogenous), and destructive changes in brain tissue.
Go deeper
Afferent and efferent levels of neural regulation of respiration
Clinical features of apneustic and periodic breathing
Pathogenesis of compressive atelectasis in pneumothorax and hemothorax
Crush syndrome of the chest wall
Differential diagnosis of obstructive and restrictive disorders