Traumatic Pneumothorax

Penetrating wounds to the chest wall from a knife, a bullet, or an impaling object in an automobile or industrial accident are common causes of traumatic pneumothorax. When this type of trauma occurs, the pleural space is in direct contact with the atmosphere, and gas can move into and out of the pleural cavity. This condition is known as a sucking chest wound and is classified as an open pneumothorax (Figure 22-2).

A piercing chest wound also may result in a closed (valvular) or tension pneumothorax through a one-way valvelike action of the ruptured parietal pleura. In this form of pneumothorax, gas enters the pleural space during inspiration but cannot leave during expiration because the parietal pleura (or, more infrequently, the chest wall itself) acts as a check valve. This condition may cause the intrapleural pressure to exceed the atmospheric pressure in the affected area. Technically this form of pneumothorax is classified as a tension pneumothorax (Figure 22-3). This form of pneumothorax is the most serious of all.

When a crushing chest injury occurs, the pleural space may not be in direct contact with the atmosphere, but the sharp end of a fractured rib may pierce or tear the visceral pleura. This may permit gas to leak into the pleural space from the lungs. Technically, this form of pneumothorax is classified as a closed pneumothorax.

Spontaneous Pneumothorax

When a pneumothorax occurs suddenly and without any obvious underlying cause, it is referred to as a spontaneous pneumothorax. A spontaneous pneumothorax is secondary to certain underlying pathologic processes such as pneumonia, tuberculosis, and chronic obstructive pulmonary disease (COPD). A spontaneous pneumothorax is sometimes caused by the rupture of a small bleb or bulla on the surface of the lung. This type of pneumothorax often occurs in tall, thin persons aged 15 to 35 years. It may result from the high negative intrathoracic pressure and mechanical stresses that take place in the upper zone of the upright lung (Figure 22-4).

A spontaneous pneumothorax also may behave as a tension pneumothorax. Air from the lung parenchyma may enter the pleural space via a tear in the visceral pleura during inspiration but is unable to leave during expiration because the visceral tear functions as a check valve (see Figure 22-4). This condition may cause the intrapleural pressure to exceed the intraalveolar pressure. This form of pneumothorax is classified as both a closed pneumothorax and a tension pneumothorax.

Iatrogenic Pneumothorax

An iatrogenic pneumothorax sometimes occurs during specific diagnostic or therapeutic procedures. For example, a pleural or liver biopsy may cause a pneumothorax. Thoracentesis, intercostal nerve block, cannulation of a subclavian vein, and tracheostomy are other possible causes of an iatrogenic pneumothorax.

An iatrogenic pneumothorax is always a hazard during positive-pressure mechanical ventilation—particularly when high tidal volumes or high system pressures are used. This is particularly common in COPD and in human immunodeficiency virus (HIV)–related acute respiratory distress syndrome (ARDS). Indeed, when very high mean airway pressures are required to ventilate such patients, prophylactic bilateral tube thoracostomies are often mandatory.

 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.

Other Possible Mechanisms

• Decreased lung compliance–increased ventilatory rate relationship

• Activation of the deflation receptors

• Activation of the irritant receptors

• Stimulation of the J receptors

• Pain, anxiety

Increased Heart Rate (Pulse) and Blood Pressure (Small Pneumothorax)

Cyanosis

Chest Assessment Findings

• Hyperresonant percussion note over the pneumothorax

• Diminished breath sounds over the pneumothorax

• Tracheal shift

• Displaced heart sounds

• Increased thoracic volume on the affected side (particularly in tension pneumothorax)

As gas accumulates in the pleural space, the ratio of air to solid tissue increases. Percussion notes resonate more freely throughout the gas in the pleural space as well as in the air spaces within the lung (Figure 22-6). When this area is auscultated, however, the breath sounds are diminished (Figure 22-7). When intrapleural gas accumulates, and intrathoracic pressure is excessively high, the mediastinum may be forced to the unaffected side. If this is the case, there will be a tracheal shift and the heart sounds will be displaced during auscultation.

Finally, the gas that accumulates in the pleural space enhances not only the natural tendency of the lungs to collapse but also the natural tendency of the chest wall to expand. Therefore in a large pneumothorax the chest often appears larger on the affected side. This is especially true in patients with a severe tension pneumothorax (Figure 22-8).

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings

(Restrictive Lung Pathology)

LUNG VOLUME AND CAPACITY FINDINGS

VT	IRV	ERV	RV
N or ↓	↓	↓	↓
VC	IC	FRC	TLC	RV/TLC ratio
↓	↓	↓	↓	N

Arterial Blood Gases

SMALL PNEUMOTHORAX

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco2		Pao2
↑	↓	↓ (slightly)	↓

LARGE PNEUMOTHORAX

Acute Ventilatory Failure with Hypoxemia (Acute Respiratory Acidosis)

pH*	Paco2	*	Pao2
↓	↑	↑ (slightly)	↓

^*When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular Paco₂ level.

Oxygenation Indices*

	Do2†			O2ER
↑	↓	N	↑ (severe)	↑	↓

---

^*, Arterial-venous oxygen difference; DO₂, total oxygen delivery; O₂ER, oxygen extraction ratio; , pulmonary shunt fraction; , mixed venous oxygen saturation; , oxygen consumption.

^†The Do₂ may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the Do₂ is normal, the O₂ER is usually normal.

Hemodynamic Indices‡

(Large Pneumothorax)

CVP	RAP		PCWP	CO	SV
↑	↑	↑	↓	↓	↓
SVI	CI	RVSWI	LVSWI	PVR	SVR
↓	↓	↑	↓	↑	↓

---

^‡CO, Cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; , mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.

RADIOLOGIC FINDINGS

Chest Radiograph

• Increased translucency (darker lung fields) on the side of pneumothorax

• Mediastinal shift to unaffected side in tension pneumothorax

• Depressed diaphragm

• Lung collapse

• Atelectasis

Ordinarily, the presence of a pneumothorax is easily identified on the chest radiograph in the upright posteroanterior view. A small collection of air is often visible if the exposure is made at the end of maximal expiration because the translucency of the pneumothorax is more obvious when contrasted with the density of a partially deflated lung. The pneumothorax is usually seen in the upper part of the pleural cavity when the film is exposed while the patient is in the upright position. Severe adhesions, however, may limit the collection of gas to a specific portion of the pleural space. Figure 22-9, A shows the development of a tension pneumothorax in the lower part of the right lung. Figure 22-9, B shows progression of the same pneumothorax 30 minutes later. Figure 22-10 shows the classic body shape of a 19-year-old male, who is 6 feet 5 inches tall, who experienced a spontaneous left-sided pneumothorax while playing a round of golf.

Oxygenation Indices*

	Do2†			O2ER
↑	↓	N	↑ (severe)	↑	↓

---

^†The Do₂ may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the Do₂ is normal, the O₂ER is usually normal.

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. It should be noted, however, that the hypoxemia that develops in a pneumothorax is most commonly caused by the alveolar atelectasis and capillary shunting associated with the disorder. Hypoxemia caused by capillary shunting is often refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

Pleurodesis

On occasion, a thoracentesis may be performed before a procedure called pleurodesis. During this procedure a chemical or medication (talc, tetracycline, or bleomycin sulfate) is injected into the chest cavity. The chemical substance or medication causes an intense inflammatory reaction over the outer surface of the lung and inside of the chest cavity. This procedure is performed to cause the surface of the lung to adhere to the chest cavity, thus preventing or reducing recurrent fluid accumulation or pneumothorax. An intense pleuritis is produced, which may be quite painful (pleurisy).

Respiratory Assessment and Plan

The patient stated that he was more comfortable on the oxygen mask, but that some left-sided chest pain was still present. His physical findings were unchanged from his initial evaluation. The chest radiograph confirmed the diagnosis of a 50% left-sided pneumothorax, lung collapse, and mediastinal shift to the right. The arterial blood gas values on a partial rebreathing mask were pH 7.53, Paco₂ 29, 21, and Pao₂ 56. The physician was still busy with the patient in the next room. With this new information, the respiratory therapist charted the following.

Respiratory Assessment and Plan

Approximately 15 minutes later, the attending physician entered the room and quickly reviewed the clinical data and assessments. Moments later, he inserted a thoracostomy tube and began underwater drainage. The respiratory therapist placed a CPAP mask on the patient’s face at 5 cm H₂O. The Fio₂ on the mask was adjusted to 0.8. Over the next 30 minutes, the lung expanded well and the patient’s ventilatory and oxygenation status quickly improved. The chest tube was removed after 48 hours. Follow-up examination after 2 weeks revealed full expansion of the left lung. There was no evidence of blebs or bullae. A tuberculin skin test result was negative, and the cause of the pneumothorax was never found.

Discussion

Few respiratory conditions persist with a “crisis” onset, and this is one of them. Other instances include foreign body aspiration, pulmonary embolism, anaphylactic shock, and some cases of asthma.

This case nicely demonstrates the signs and symptoms of Atelectasis and intrapulmonary shunting (see Figure 9-8). The physician and respiratory therapist could not hear crackles, however, presumably because the atelectatic segments were separated (distant) from the chest wall and the examiner’s stethoscope.

Although the respiratory care administered in this case (oxygen therapy) was fairly pedestrian, the therapist’s assistance in the assessment of this patient and his presence at bedside made a great difference in the speed and ease with which the patient was treated. The value of an assessing and treating therapist in this situation cannot be overestimated.