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ФИЗИОЛОГИЯ И ПАТОФИЗИОЛОГИЯ ДИАФРАГМЫ
The diaphragm is the primary muscle responsible for inspiration during relaxed tidal volume breathing. When a person takes a breath, signals from the medulla travel down descending pathways to activate the anterior horn cells of the spinal cord. Nerve roots at C3-C5 form the phrenic nerves, which innervate the diaphragm.
The diaphragm is an elliptical muscle with a central tendon and muscular domes that attach to the inner aspect of the lower ribs, the sternum, and the lumbar vertebrae.2 It is innervated by the phrenic nerve, which arises from motor neurons at C3-C5. This muscle contracts during inspiration, moving in a caudal direction, which produces negative pleural and intrathoracic pressure. This negative intrathoracic pressure is transmitted to the alveoli, and as alveolar pressure drops below atmospheric pressure, air is driven from the atmosphere into the lung. If the caudal contraction of the diaphragm were its only action, the negative intrathoracic pressure created would result in inward displacement of the rib cage, which, in turn, would lead to expiration of air from the chest. However, the diaphragm’s zone of apposition —the part of the muscle that lies directly against the inner aspect of the lower rib cage — is exposed to positive abdominal pressure, so diaphragmatic contraction leads to expansion of the rib cage. Contraction of the zone of apposition results in outward displacement of the lower rib cage, resulting in chest expansion and negative intrathoracic pressure. Interestingly, in obstructive lung disease, the lungs are hyperinflated, which decreases the size of the zone of apposition. This results in a mechanical disadvantage for inspiration.2
Accessory muscles of inspiration include the intercostal muscles, scalenes, sternocleidomastoids, and trapezii. During tidal volume breathing, the activity of the intercostal muscles serves to stabilize the rib cage. However, all these muscles become active during times of increased ventilation, or to achieve inspiration of tidal volume during diaphragmatic paralysis.
Expiration to functional residual capacity (FRC) normally occurs passively as a result of the inherent recoil of the lung. With ventilatory stress, expiratory muscles actively contribute to expiration. In diaphragmatic paralysis, the expiratory muscles are recruited during expiration, pushing the diaphragm upward into the thorax at end-expiration. Then, during inspiration, there is passive descent of the diaphragm to FRC. In this way, recruitment of expiratory muscles optimizes positioning of the paralyzed diaphragm, preventing paradoxical ascent and net expiratory activity of the diaphragm during inspiration.3
Because the accessory muscles of inspiration and the muscles of expiration largely compensate for the paralyzed diaphragm, isolated diaphragmatic paralysis rarely leads to alveolar hypoventilation and respiratory failure. However, this outcome is much more likely when the underlying disease process also results in generalized neuromuscular weakness.4
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