A pneumothorax exists when gas (sometimes called free air) accumulates in the pleural space (see Figure 22-1). When gas enters the pleural space, the visceral and parietal pleura separate. This enhances the natural tendency of the lungs to recoil, or collapse, and the natural tendency of the chest wall to move outward, or expand. As the lung collapses, the alveoli are compressed and atelectasis ensues. In severe cases, the great veins may be compressed and cause the venous return to the heart to diminish.

A pneumothorax is a restrictive lung disorder. The major pathologic or structural changes associated with a pneumothorax are as follows:

• Lung collapse

• Atelectasis

• Chest wall expansion (in tension pneumothorax)

• Compression of the great veins and decreased cardiac venous return

Etiology and Epidemiology

Gas can gain entrance to the pleural space in the following three ways:

1. From the lungs through a perforation of the visceral pleura

2. From the surrounding atmosphere through a perforation of the chest wall and parietal pleura or, rarely, through an esophageal fistula or a perforated abdominal viscus

3. From gas-forming microorganisms in an empyema in the pleural space (rare)

A pneumothorax may be classified as either closed or open according to the way gas gains entrance to the pleural space. In a closed pneumothorax, gas in the pleural space is not in direct contact with the atmosphere. An open pneumothorax, on the other hand, is a condition in which the pleural space is in direct contact with the atmosphere such that gas can move freely in and out. A pneumothorax in which the intrapleural pressure exceeds the intraalveolar (or atmospheric) pressure is known as a tension pneumothorax. Some forms of pneumothorax are identified on the basis of origin, as follows:

• Traumatic pneumothorax

• Spontaneous pneumothorax

• Iatrogenic pneumothorax

OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Pneumothorax

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8)—the major anatomic alteration of the lungs associated with pneumothorax (see Figure 22-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate.

Stimulation of Peripheral Chemoreceptors (Hypoxemia)

As gas moves into the pleural space, the visceral and parietal pleura separate and the lung on the affected side begins to collapse. As the lung collapses, atelectasis develops, and alveolar ventilation decreases.

If the patient has a pneumothorax as a result of a sucking chest wound, an additional mechanism also may promote hypoventilation. In other words, when a patient with this type of pneumothorax inhales, the intrapleural pressure on the unaffected side decreases. As a result the mediastinum often moves to the unaffected side, where the pressure is lower, and compresses the normal lung. The intrapleural pressure on the affected side also may decrease, and some air may enter through the chest wound and further shift the mediastinum toward the normal lung. During expiration the intrapleural pressure on the affected side rises above atmospheric pressure, and gas escapes from the pleural space through the chest wound. As gas leaves the pleural space, the mediastinum moves back toward the affected side. Because of this back-and-forth movement of the mediastinum, some gas from the normal lung may enter the collapsed lung during expiration and cause it to expand slightly. During inspiration, however, some of this “rebreathed dead space gas” may move back into the normal lung. This paradoxic movement of gas within the lungs is known as pendelluft. As a result of the pendelluft, the patient hypoventilates (see Figure 22-2).

Therefore when a patient has a pneumothorax, alveolar ventilation is reduced because of lung collapse and atelectasis. If the pneumothorax is accompanied by a sucking chest wound, alveolar ventilation may be further decreased by pendelluft.

As a result of the reduced alveolar ventilation, the patient’s ratio decreases. This leads to intrapulmonary shunting and venous admixture (Figure 22-5). Because of the venous admixture, the Pao₂ and Cao₂ decrease. As this condition intensifies, the patient’s arterial oxygen level may decline to a point low enough to stimulate the peripheral chemoreceptors. Stimulation of the peripheral chemoreceptors in turn initiates an increased ventilatory rate.