5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

Lung Volume and Capacity Findings

Arterial Blood Gases

Mild to Moderate Flail Chest

Acute Alveolar Hyperventilation With Hypoxemia1 (Acute Respiratory Alkalosis)

1See Fig. 5.2 and Table 5.4 and related discussion for the acute pH, PaCO2, and changes associated with acute alveolar hyperventilation.

Severe Flail Chest

Acute Ventilatory Failure With Hypoxemia2 (Acute Respiratory Acidosis)

2See Fig. 5.2 and Table 5.5 and related discussion for the acute pH, PaCO2, and changes associated with acute ventilatory failure.

3When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular PaCO2 level.

Oxygenation Indices4

5The 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.

4, Arterial-venous oxygen difference; DO2, total oxygen delivery; O2ER, oxygen extraction ratio; QS/QT, pulmonary shunt fraction; , mixed venous oxygen saturation; VO2, oxygen consumption.

Hemodynamic Indices6

Severe Flail Chest Disorder

6CO, Cardiac output; CI, cardiac index; 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 opacity (in atelectatic areas or areas with post-flail pneumonia).

•Rib fractures may need a special radiologic technique (rib series) to demonstrate.

•Because of the lung compression and atelectasis associated with flail chest, the density of the lung on the affected side increases. The increase in lung density is revealed on the chest radiograph as increased opacity (i.e., whiter in appearance). The chest radiograph may also

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show the rib fractures (Fig. 22.4).

FIGURE 22.4 (A) Chest x-ray of a 20-year-old woman with a severe right-sided flail chest. (B) Close-up of the same x-ray film, demonstrating rib fractures (arrows).

General Management of Flail Chest

In mild cases, analgesia and routine airway clearance therapies may be the only actions needed. In more severe cases, however, stabilization of the chest is usually required to allow bone healing and prevent atelectasis. Today, continuous mechanical ventilation, accompanied by positive end-expiratory pressure (PEEP), is commonly used to stabilize a flail chest. The use of pharmacologic paralytics may be required in severe flail chest for ventilatory control. Generally, mechanical ventilation for 5 to 10 days is adequate for sufficient bone healing to occur.1

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxia, decrease the work of breathing, and decrease myocardial work. It should be noted, however, that the hypoxemia that develops in flail chest 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 10.1).

Lung Expansion Therapy Protocol

Lung expansion techniques are commonly administered to offset and prevent the alveolar consolidation and atelectasis associated with flail chest (see Lung Expansion Therapy Protocol, Protocol 10.3). Mild analgesia may be helpful if the pulmonary expansion technique used causes excessive pain.

Mechanical Ventilation Protocol

Because acute ventilatory failure is associated with flail chest, continuous mechanical ventilation, often with PEEP, is often required to maintain an adequate ventilatory status (see Ventilator Initiation and Management Protocol, Protocol 11.1, and Ventilator Weaning Protocol, Protocol 11.2).

Case Study Flail Chest

Admitting History and Physical Examination

A 40-year-old obese male truck driver was involved in a major four-vehicle accident and was taken to the emergency department of a nearby medical center, where he was found to be markedly agitated and uncooperative. He was conscious and in obvious respiratory distress. His vital signs were blood pressure 80/62 mm Hg, pulse 90 beats/min, respiration rate 42 breaths/min and shallow. Paradoxical movement of the right chest wall was evident.

He had a laceration of the right eyelid and deep lacerations of the right thigh with rupture of the patellar tendon. Pain and tenderness were present on palpation of the right anterolateral chest wall. The ribs moved paradoxically inward with inspiration. The anteroposterior (AP) diameter of the chest was increased. Breath sounds were decreased bilaterally, and expiration was prolonged.

Chest radiographs revealed double fractures of ribs 2 through 10 on the patient's right anterolateral chest. He had 4+ hematuria, but his other laboratory findings were within normal limits.

The patient was intubated in the emergency department and placed on a mechanical ventilator with 5 cm H2O PEEP, a VT

of 8 mL/kg, and ventilatory rate of 12. An arterial line was placed, and the patient was taken to the operating room, where surgical repair of the eyelid and thigh was performed. In the operating room, with an FIO2 of 1.0, the patient's blood gas

values were pH 7.48, PaCO2 30 mm Hg, 23 mEq/L, PaO2 360 mm Hg, and SaO2 98%. His blood pressure was

110/70 mm Hg, and his heart rate was 100 beats/min. The patient was transferred to the surgical intensive care unit, where the respiratory therapist on duty made the following assessment.

Respiratory Assessment and Plan

S N/A—patient is intubated on a mechanical ventilator, sedated, and pharmacologically paralyzed (vecuronium bromide).

O No spontaneous respirations. No paradoxical movement of chest wall on ventilator. BP

110/70, HR 100 regular, RR 12 on vent. On FIO2 1.0, pH 7.48, PaCO2 30, 23, PaO2 360, SaO2 98%. Double fractures of ribs 2 through 10 on the patient's right anterolateral chest: No

pneumothorax, no hemothorax. A

•Flail chest (history, paradoxical chest movement, CXR)

•Acute alveolar hyperventilation with overoxygenation (arterial blood gas, ABG)

P Mechanical Ventilation Protocol: Decrease VT to correct acute alveolar hyperventilation and

maintain patient on controlled ventilation and PEEP per protocol until chest wall is stable. Wean oxygen per Ventilator Protocol (decreased to FIO2 0.40). Routine ABG monitoring.

Careful chest assessment and auscultation to monitor for secondary pneumothorax and pneumonia.

Over the next 72 hours, the patient was kept intubated and ventilated with an FIO2 of 0.40 and a mechanical ventilation

rate of 12/min. However, his hospital course was stormy. Aggressive fluid volume resuscitation with intravenous fluids at the rate of 100 mL/h was given. His sputum rapidly became thick and yellow. Lung Expansion Therapy Protocol was increased to a PEEP of 8 cm H2O. On the second day, a right pneumothorax was demonstrated and a chest tube was

inserted. A persistent air leak was present.

The next day, his pulse increased to 160 beats/min. His blood pressure was 142/82 mm Hg. His rectal temperature was 99.2°F. His ventilator rate was 12 breaths/min, with a PEEP of 10 cm H2O. Auscultation revealed bilateral crackles. On an

FIO2 of 0.70, his ABG values were pH 7.37, PaCO2 38 mm Hg, 23 mEq/L, PaO2 58 mm Hg, and SaO2 90%. Rapid

diuresis was initiated, and his cardiac function improved dramatically. Over the next few days, the chest radiograph showed dense infiltrates in both lungs, and it was difficult to maintain adequate oxygenation, even with high inspired oxygen concentrations. His sputum was yellow and thick. At this time, the respiratory assessment was as follows:

Respiratory Assessment and Plan

S N/A—intubated, sedated, and paralyzed.

O Afebrile. HR 160 regular, BP 142/82, RR 12 (on vent). Right chest tube shows air leak. Crackles bilaterally. CXR: Fractures appear in line; bilateral dense infiltrates. ABG on an FIO2

of 0.70 are pH 7.37, PaCO2 38, 23, PaO2 58, and SaO2 90%. Sputum thick, yellow. A

•Persistent right-sided flail chest (if allowed to breathe on his own) (CXR)

•Bilateral dense infiltrates suggest atelectasis versus pulmonary edema versus acute respiratory distress syndrome (ARDS) versus pneumonia (CXR)

•Adequate alveolar ventilation with moderate hypoxemia on present ventilator settings; oxygenation continues to worsen (ABG)

•Thick, yellow bronchial secretions (sputum)

•Pneumonia possible (despite normal temperature)

•Bronchopleural fistula on right side (chest tube bubbles)

P Mechanical Ventilation Protocol and Lung Expansion Therapy Protocol. Increase PEEP to 12 cm H2O. Oxygen therapy per protocol (maintain FIO2 of 0.70). Start Airway Clearance

Therapy Protocol (suction PRN; obtain sputum for Gram stain and culture). Continue SaO2 monitoring.

During the patient's first week of hospitalization, his blood urea nitrogen (BUN) increased to 60 mg/dL and his creatinine to 1.9 mg/dL, thought to be related to trauma. Liver function values remained within normal limits. The abnormal BUN and creatinine gradually returned to normal during the second week. The patient was slowly but successfully weaned off the ventilator over the next 2 weeks.

Discussion

This complicated case demonstrates the care of the traumatized patient with multiorgan failure. In this case, the second organ system affected was the cardiovascular system, probably secondary to fluid overload. Initial therapy included chest wall rest and internal stabilization with mechanical ventilation and PEEP. By the time of the second assessment, the more classic clinical manifestations of pulmonary parenchymal change secondary to flail chest had developed. The clinical scenarios of atelectasis (see Fig. 10.7) and/or alveolar consolidation (see Fig. 10.8) were well established, with oxygenrefractory pulmonary capillary shunting clearly in evidence.

Later, when what appeared to be acute respiratory distress syndrome (ARDS) supervened, additional PEEP was added, both for its effect on the ARDS and to stabilize the chest wall. Although these problems were dramatic enough, the therapist alertly noted the thick yellow bronchial secretions and suctioned as needed. The ordering of a sputum Gram stain and culture was appropriate. As the patient was being slowly weaned off the ventilator, pain control for the nonintubated patient was considered.

Clearly, a patient this ill should be assessed at least once—possibly more—per shift. Because this patient was hospitalized for 40 days, more than 120 such assessments were found in his chart. As we reviewed his case, this certainly did not seem to be excessive.

It is strongly suggested that notation of the ventilator settings in flail chest be a part of the “objective” recordings in the patient's SOAP notes—just as the FIO2 must accompany the patient's ABG values.

Self-Assessment Questions

1.In flail chest, which of the following occur?

1.Tidal volume (VT) increases

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C H A P T E R 2 3

Pneumothorax

CHAPTER OUTLINE

Anatomic Alterations of the Lungs

Etiology, Epidemiology, and Symptoms

Traumatic Pneumothorax

Spontaneous Pneumothorax

Iatrogenic Pneumothorax

Symptoms

Overview of the Cardiopulmonary Clinical Manifestations Associated With Pneumothorax

General Management of Pneumothorax

Respiratory Care Treatment Protocols

Pleurodesis

Case Study: Spontaneous Pneumothorax

Self-Assessment Questions

CHAPTER OBJECTIVES

After reading this chapter, you will be able to:

•List the anatomic alterations of the lungs associated with a pneumothorax.

•Describe the causes of a pneumothorax.

•List the cardiopulmonary clinical manifestations associated with a pneumothorax.

•Describe the general management of a pneumothorax.

•Describe the clinical strategies and rationales of the SOAPs presented in the case study.

•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

KEY TERMS

Bleomycin Sulfate

Closed Pneumothorax

Iatrogenic Pneumothorax

Open Pneumothorax

Pendelluft

Pleurisy

Pleurodesis

Sclerosant Agents

Spontaneous Pneumothorax

Sucking Chest Wound

Talc Pleurodesis

Tension Pneumothorax

Tetracycline Pleurodesis

Thoracic Free Air

Thoracostomy Chest Tube

Tracheal Shift

Traumatic Pneumothorax

Anatomic Alterations of the Lungs

A pneumothorax exists when gas (sometimes called thoracic free air) accumulates in the pleural space (Fig. 23.1). When gas enters the pleural space, the visceral and parietal pleura separate. This enhances the natural tendency of the lung to recoil, or collapse, and the natural tendency of the chest wall to move outward, or expand. As the lung collapses, the

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FIGURE 23.2 Sucking chest wound with accompanying pendelluft in an open right pneumothorax. The large arrow illustrates the chest wall injury.

A piercing chest wound also may result in a closed (valvular), or tension, pneumothorax through a one-way valve-like 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 (Fig. 23.3). This form of pneumothorax is the most serious of all because gas continues to accumulate in the intrapleural space and progressively increases the compressing pressures on the lungs and mediastinal structures of the affected area.

FIGURE 23.3 Closed (tension) pneumothorax produced by a right chest wall wound. The large arrow illustrates the chest wall injury and the parietal pleural “valve.”

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 people 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 (Fig. 23.4).

FIGURE 23.4 Right pneumothorax produced by a rupture in the visceral pleura that functions as a check valve. Progressive enlargement of the pneumothorax occurs, producing atelectasis on the affected side.

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 Fig. 23.4). 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

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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, as may a transthoracic needle biopsy of the lung itself. Thoracentesis, intercostal nerve block, cannulation of a subclavian vein, and tracheostomy are other possible causes of an iatrogenic pneumothorax. Rarely, bronchoscopy (particularly with lung biopsy) may produce an iatrogenic pneumothorax as well.

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).

Symptoms

The classic presentation of a pneumothorax is that of sudden crisis onset (see Fig. 3.9), with severe dyspneic pleuritic chest pain, cough, and cardiovascular collapse. Hemoptysis may occur, but it is usually not life-threatening. Occasionally, a pneumothorax may develop more slowly, but this is unusual.

Overview of the Cardiopulmonary Clinical Manifestations Associated With Pneumothorax

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by atelectasis (see Fig. 10.7)—the major anatomic alteration of the lungs associated with pneumothorax (see Fig. 23.1).

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 paradoxical movement of gas within the lungs is known as pendelluft. As a result of the pendelluft, the patient hypoventilates (see Fig. 23.2).

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 ventilation-perfusion ratio decreases. This leads to intrapulmonary shunting and venous admixture (Fig. 23.5). 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.

FIGURE 23.5 Venous admixture in pneumothorax.

Other Possible Mechanisms

•Relationship of decreased lung compliance to increased ventilatory rate

•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 (away from the affected side in a tension pneumothorax)

•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 and in the air spaces within the lung (Fig. 23.6). When this area is auscultated, however, the breath sounds are diminished (Fig. 23.7). 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.

FIGURE 23.6 Because the ratio of extrapulmonary gas to solid tissue increases in a pneumothorax, hyperresonant percussion notes are produced over the affected area.

FIGURE 23.7 Breath sounds diminish as gas accumulates in the intrapleural space.

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 (Fig. 23.8).

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FIGURE 23.8 As gas accumulates in the intrapleural space, the chest diameter increases on the affected side in a tension pneumothorax.

Clinical Data Obtained From Laboratory Tests and Special Procedures

Pulmonary Function Test Findings (Restrictive Lung Pathology)

Lung Volume and Capacity Findings

Arterial Blood Gases

Small Pneumothorax

Acute Alveolar Hyperventilation With Hypoxemia1 (Acute Respiratory Alkalosis)

Large Pneumothorax

Acute Ventilatory Failure With Hypoxemia2 (Acute Respiratory Acidosis)

3When tissue hypoxia is severe enough to produce lactic acid, the pH and HCO3– values will be lower than expected for a particular PaCO2 level.

1See Fig. 5.2 and Table 5.4 and related discussion for the acute pH, PaCO2, and HCO3– changes associated with acute alveolar hyperventilation.

2See Fig. 5.2 and Table 5.5 and related discussion for the acute pH, PaCO2, and HCO3– changes associated with acute ventilatory failure.

Oxygenation Indices4

oxygen saturation; V̇O2, oxygen consumption.

5The 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 Indices6

(Large Pneumothorax)