Professional Guide to Signs and Symptoms
5th Edition

Chest expansion, asymmetrical
Asymmetrical chest expansion is the uneven extension of portions of the chest wall during inspiration. During normal respiration, the thorax uniformly expands upward and outward, then contracts downward and inward. When this process is disrupted, breathing becomes uncoordinated, resulting in asymmetrical chest expansion.
Asymmetrical chest expansion may develop suddenly or gradually and may affect one or both sides of the chest wall. It may occur as delayed expiration (chest lag), as abnormal movement during inspiration (for example, intercostal retractions, paradoxical movement, or chest-abdomen asynchrony), or as unilateral absence of movement. This sign usually results from pleural disorders, such as life-threatening hemothorax or tension pneumothorax. (See Recognizing life-threatening causes of asymmetrical chest expansion.) However, it can also result from a musculoskeletal or urologic disorder, airway obstruction, or trauma. Regardless of its underlying cause, asymmetrical chest expansion produces rapid and shallow or deep respirations that increase the work of breathing.
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HISTORY AND PHYSICAL EXAMINATION
If you don’t suspect flail chest and if the patient isn’t experiencing acute respiratory distress, obtain a brief history. Asymmetrical chest expansion commonly results from mechanical airflow obstruction, so
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find out if the patient is experiencing dyspnea or pain during breathing. If so, does he feel short of breath constantly or intermittently? Does the pain worsen his feeling of breathlessness? Does repositioning, coughing, or any other activity relieve or worsen the patient’s dyspnea or pain? Is the pain more noticeable during inspiration or expiration? Can he inhale deeply?
Ask if the patient has a history of pulmonary or systemic illness, such as frequent upper respiratory tract infections, asthma, tuberculosis, pneumonia, or cancer. Has he had thoracic surgery? (This typically produces asymmetrical chest expansion on the affected side.) Also, ask about blunt or penetrating chest trauma, which may have caused pulmonary injury. Obtain an occupational history to find out if the patient may have inhaled toxic fumes or aspirated a toxic substance.
Next, perform a physical examination. Begin by gently palpating the trachea for midline positioning. (Deviation of the trachea usually indicates an acute problem requiring immediate intervention.) Then examine the posterior chest wall for areas of tenderness or deformity. To evaluate the extent of asymmetrical chest expansion, place your hands—fingers together and thumbs abducted toward the spine—flat on both sections of the lower posterior chest wall. Position your thumbs at the 10th rib, and grasp the lateral rib cage with your hands. As the patient inhales, note the uneven separation of your thumbs, and gauge the distance between them. Then repeat this technique on the upper posterior chest wall. Next, use the ulnar surface of your hand to palpate for vocal or tactile fremitus on both sides of the chest. To check for vocal fremitus, ask the patient to repeat “99” as you proceed. Note any asymmetrical vibrations and areas of enhanced, diminished, or absent fremitus. Then percuss and auscultate to detect air and fluid in the lungs and pleural spaces. Finally, auscultate all lung fields for normal and adventitious breath sounds. Examine the patient’s anterior chest wall, using the same assessment techniques.
MEDICAL CAUSES
  • Bronchial obstruction. Life-threatening loss of airway patency may occur gradually or suddenly in bronchial obstruction. Typically, lack of chest movement indicates complete obstruction; chest lag signals partial obstruction. If air is trapped in the chest, you may detect intercostal bulging during expiration and hyperresonance on percussion. You may also note dyspnea, accessory muscle use, decreased or absent breath sounds, and suprasternal, substernal, or intercostal retractions.
  • Flail chest. In this life-threatening injury to the ribs or sternum, the unstable portion of the chest wall collapses inward during inspiration and balloons outward during expiration (paradoxical movement). The patient may have ecchymoses, severe localized pain, or other signs of traumatic injury to the chest wall. He may also exhibit rapid, shallow respirations, tachycardia, and cyanosis.
  • Hemothorax. Hemothorax is life-threatening bleeding into the pleural space that causes chest lag during inspiration. Other findings include signs of traumatic chest injury, stabbing pain at the injury site, anxiety, dullness on percussion, tachypnea, tachycardia, and hypoxemia. If hypovolemia occurs, you’ll note signs of shock, such as hypotension and rapid, weak pulse.
  • Kyphoscoliosis. Abnormal curvature of the thoracic spine in the anteroposterior direction (kyphosis) and the lateral direction (scoliosis) gradually compresses one lung and distends the other. This produces decreased chest wall movement on the compressed-lung side and expands the intercostal muscles during inspiration on the opposite side. It can also produce ineffective coughing, dyspnea, back pain, and fatigue.
  • Myasthenia gravis. Progressive loss of ventilatory muscle function produces asynchrony of the chest and abdomen during inspiration (“abdominal paradox”), which can lead to acute respiratory distress. Typically, the patient’s shallow respirations and increased muscle weakness
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    cause severe dyspnea, tachypnea and, possibly, apnea.
  • Phrenic nerve dysfunction. In this disorder, the paralyzed hemidiaphragm fails to contract downward, causing asynchrony of the thorax and upper abdomen on the affected side during inspiration (“abdominal paradox”). Its onset may be sudden, as in trauma, or gradual, as in infection or spinal cord disease. If the patient has underlying pulmonary dysfunction that contributes to hyperventilation, his inability to breathe deeply or to cough effectively may cause atelectasis of the affected lung.
  • Pleural effusion. Chest lag at end-inspiration occurs gradually in this life-threatening accumulation of fluid, blood, or pus in the pleural space. Usually, some combination of dyspnea, tachypnea, and tachycardia precedes chest lag; the patient may also have pleuritic pain that worsens with coughing or deep breathing. The area of the effusion is delineated by dullness on percussion and by egophony, bronchophony, whispered pectoriloquy, decreased or absent breath sounds, and decreased tactile fremitus. The patient may have a fever if infection caused the effusion.
  • Pneumonia. Depending on whether fluid consolidation in the lungs develops unilaterally or bilaterally, asymmetrical chest expansion occurs as inspiratory chest lag or as chest-abdomen asynchrony. The patient typically has fever, chills, tachycardia, tachypnea, and dyspnea along with crackles, rhonchi, and chest pain that worsens during deep breathing. He may also be fatigued and anorexic and have a productive cough with rust-colored sputum.
  • Pneumothorax. Entrapment of air in the pleural space can cause chest lag at end-inspiration. This life-threatening condition also causes sudden, stabbing chest pain that may radiate to the arms, face, back, or abdomen and dyspnea unrelated to the chest pain’s severity. Other findings include tachypnea, decreased tactile fremitus, tympany on percussion, decreased or absent breath sounds over the trapped air, tachycardia, restlessness, and anxiety.
    Tension pneumothorax produces the same signs and symptoms as pneumothorax, but they’re much more severe. A tension pneumothorax rapidly compresses the heart and great vessels, causing cyanosis, hypotension, tachycardia, restlessness, and anxiety. The patient may also develop subcutaneous crepitation of the upper trunk, neck, and face and mediastinal and tracheal deviation away from the affected side. Auscultation of a crunching sound over the precordium with each heartbeat indicates pneumomediastinum.
  • Poliomyelitis. In this rare disorder, paralysis of the chest wall muscles and diaphragm produces chest-abdomen asynchrony (“abdominal paradox”), fever, muscle pain, and weakness. Other findings include decreased reflex response in the affected muscles and impaired swallowing and speaking.
  • Pulmonary embolism. This acute, life-threatening disorder causes chest lag; sudden, stabbing chest pain; and tachycardia. The patient usually has severe dyspnea, blood-tinged sputum, pleural friction rub, and acute anxiety.
OTHER CAUSES
  • Treatments. Asymmetrical chest expansion can result from pneumonectomy and surgical removal of several ribs. Chest lag or the absence of chest movement may also result from intubation of a mainstem bronchus, a serious complication typically due to incorrect insertion of an endotracheal tube or movement of the tube while it’s in the trachea.
SPECIAL CONSIDERATIONS
If you’re caring for an intubated patient, regularly auscultate breath sounds in the lung peripheries to help detect a misplaced tube. If this occurs, prepare the patient for a chest X-ray to allow rapid repositioning of the tube. Because asymmetrical chest expansion increases the work of breathing, supplemental oxygen is usually given during acute events.
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PEDIATRIC POINTERS
Children are at greater risk than adults for inadvertent intubation of a mainstem bronchus (especially the left bronchus). Their breath sounds are usually referred from one lung to the other because of the small size of the thoracic cage, so use chest wall expansion as an indicator of correct tube position in children. Children also develop asymmetrical chest expansion, paradoxical breathing, and retractions with acute respiratory illnesses, such as bronchiolitis, asthma, and croup.
Congenital abnormalities, such as cerebral palsy and diaphragmatic hernia, can also cause asymmetrical chest expansion. In cerebral palsy, asymmetrical facial muscles usually accompany chest-abdomen asynchrony. In a life-threatening diaphragmatic hernia, asymmetrical expansion usually occurs on the left side of the chest.
GERIATRIC POINTERS
Asymmetrical chest expansion may be more difficult to determine in elderly patients because of the structural deformities associated with aging.