Objective. Students will identify primary and accessory muscles of inspiration and expiration, explain the role of intrapleural pressure in lung expansion, and describe how pneumothorax disrupts normal mechanics.
This lesson, its worked examples and its practice questions has not yet been verified by a licensed clinician in the field or by a certification or approval body. It is a study draft and may contain errors. Do not use it to make decisions about any patient or medication. Always follow your instructor, your supervising professional, and current official references and regulations.
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Breathing looks effortless, but it depends on precise coordination of muscles, bones, and pressure gradients. The lungs have no skeletal muscle of their own; they expand and recoil passively in response to volume changes created by the thoracic cage. Understanding this mechanism is essential for every respiratory therapist because disruption—from disease, trauma, or poor technique—directly threatens patient safety.
The thoracic cage is a bony and cartilaginous structure formed by the sternum, twelve pairs of ribs, costal cartilages, and the thoracic vertebrae. When its volume increases, pressure inside the lungs falls below atmospheric pressure and air flows in. When volume decreases, pressure rises and air flows out. This is a direct application of Boyle's Law: at constant temperature, pressure and volume are inversely related.
Diaphragm. The diaphragm is the dominant muscle of quiet inspiration. It is a dome-shaped musculotendinous sheet separating the thoracic and abdominal cavities. When it contracts, the dome descends, increasing the vertical dimension of the thoracic cavity. At rest, diaphragmatic contraction accounts for the majority of tidal volume in a healthy adult.
External intercostals. Eleven pairs of external intercostal muscles run obliquely downward and forward between adjacent ribs. When they contract, they elevate the rib cage in what is described as a bucket-handle motion (lateral expansion) and a pump-handle motion (anterior elevation of the sternum). Both movements increase thoracic volume.
During forced or labored inspiration, additional muscles are recruited:
Clinical note: visible use of accessory muscles at rest—neck muscles straining, shoulders rising—signals increased work of breathing and is a key assessment finding that must be reported and addressed promptly.
Quiet expiration is passive: the diaphragm and external intercostals simply relax, elastic recoil of the lung and chest wall returns the thorax to resting volume, and air flows out. No muscular work is required in a healthy person at rest.
Forced expiration (coughing, exercise, playing wind instruments) recruits:
Patients with neuromuscular disease or abdominal surgery often lose expiratory muscle strength; this impairs cough and increases pneumonia risk—a direct patient-safety concern.
The pleural space is a potential space between the visceral pleura (covering the lung) and the parietal pleura (lining the chest wall). It contains only a thin film of fluid. Because the lung's elastic recoil pulls inward while the chest wall's recoil pulls outward, the pleural space is normally under negative pressure relative to the atmosphere (approximately –3 to –5 cm H₂O at end-expiration in a healthy adult at rest).
When the diaphragm descends and the rib cage expands, the pleural space enlarges. Intrapleural pressure becomes even more negative (approximately –8 to –9 cm H₂O at peak inspiration). This negative pressure is transmitted across the visceral pleura and draws the lung outward, expanding alveoli and lowering alveolar pressure below atmospheric. Air then flows down its pressure gradient from the mouth into the alveoli.
The pleural fluid also acts as a coupling agent: it holds the visceral and parietal pleurae together by surface tension while still allowing them to slide, so the lung follows every movement of the chest wall.
A pneumothorax occurs when air enters the pleural space—through a chest wall wound, a ruptured alveolus, or an iatrogenic injury such as line placement. Once air is present, the negative intrapleural pressure is lost. The affected lung collapses toward the hilum because its elastic recoil is no longer opposed. The chest wall may spring outward.
A tension pneumothorax is a life-threatening emergency. Air enters the pleural space through a one-way valve mechanism and cannot escape; pressure builds with each breath. Rising positive pressure in the affected hemithorax compresses the lung on that side, then pushes the mediastinum toward the opposite side (mediastinal shift). This kinks the great vessels, reduces venous return to the heart, drops cardiac output, and can be rapidly fatal. Signs include absent breath sounds on the affected side, tracheal deviation away from the affected side, hypotension, and severe respiratory distress. Immediate needle decompression followed by chest tube placement is required. Respiratory therapists must recognize these signs and communicate them urgently to the medical team within scope of practice.
Answer each question, then check it. Nothing is recorded; this is your own practice.
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