Congestive heart failure is the most common cause of pleural effusion. Both right- and left-sided heart failure can result in pleural effusion. In general, left-sided heart failure is more likely to produce pleural effusion than right-sided heart failure. In right-sided heart failure (cor pulmonale), an increase in the hydrostatic pressure in the systemic circulation can (1) increase the rate of pleural fluid formation and (2) decrease lymphatic drainage from the pleural space because of the elevated systemic venous pressure. In left-sided heart failure, an increase in hydrostatic pressure in the pulmonary circulation can (1) decrease the rate of pleural fluid absorption through the visceral pleura and (2) cause fluid movement through the visceral pleura into the pleural space.

About two thirds of malignant pleural effusions occur in women. Malignant pleural effusions are highly associated with breast and gynecologic malignancies.

Other Pathologic Fluids That Separate the Parietal from the Visceral Pleura

In addition to transudate and exudate, other pathologic fluids can separate the parietal pleura from the visceral pleura.

Hemothorax

The presence of blood in the pleural space is known as a hemothorax. Most of these are caused by penetrating or blunt chest trauma. An iatrogenic hemothorax may develop from trauma caused by the insertion of a central venous or pulmonary artery catheter.

Blood can gain entrance into the pleural space from trauma to the chest wall, diaphragm, lung, or mediastinum. A hematocrit of the pleural fluid should always be obtained if the pleural fluid looks like blood. A hemothorax is said to be present only when the hematocrit of the pleural fluid is at least 50%.

 OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Pleural Effusion and Empyema

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-7)—the major anatomic alteration of the lungs associated with pleural effusion (see Figure 24-1).

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)

• Decreased lung compliance–increased ventilatory rate relationship

• Activation of the deflation receptors

• Activation of the irritant receptors

• Stimulation of J receptors

• Pain, anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Chest Pain, Decreased Chest Expansion

Cyanosis

Cough (Dry, Nonproductive)

Chest Assessment Findings

• Tracheal shift

• Decreased tactile and vocal fremitus

• Dull percussion note

• Diminished breath sounds

• Displaced heart sounds

• Pleural friction rub (occasionally)

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 PLEURAL EFFUSION

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco2		Pao2
↑	↓	↓ (slightly)	↓

LARGE PLEURAL EFFUSION

Acute Ventilatory Failure with Hypoxemia (Acute Respiratory Acidosis)

pH*	Paco2	*	Pao2
↓	↑	↑ (slightly)	↓

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^*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* (Large Pleural Effusion)

	Do2†		C(a-)o2	O2ER
↑	↓	N	↑ (severe)	↑	↓

---

^*C(a-)O₂, 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 Pleural Effusion)

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

• Blunting of the costophrenic angle

• Fluid level on the affected side (see Figure 23-2)

• Depressed diaphragm

• Mediastinal shift (possibly) to unaffected side

• Atelectasis

• “Meniscus sign”

The diagnosis of a pleural effusion is generally based on the chest x-ray film. A pleural effusion of less than 300 mL usually cannot be seen on an upright chest x-ray film. In moderate pleural effusion (>1000 mL) in the upright position, an increased density usually appears at the costophrenic angle. The fluid first accumulates posteriorly in the most dependent part of the thoracic cavity between the inferior surface of the lower lobe and the diaphragm. As the fluid volume increases, it extends upward around the anterior, lateral, and posterior thoracic walls in the so-called “meniscus sign” (see Figure 23-3). Interlobar fissures are sometimes highlighted as a result of fluid filling.

As nicely illustrated in the chest radiograph of a pleural effusion shown in Figure 23-2, the lateral costophrenic angle is usually obliterated, and the outline of the diaphragm on the affected side is lost. In severe cases the weight of the fluid may cause the diaphragm to become inverted (concave). Clinically this inversion is seen only in left-sided pleural effusions; the gastric air bubble is pushed downward, and the superior border of the left diaphragmatic leaf is concave. In addition, the mediastinum may be shifted to the unaffected side, and the intercostal spaces may appear widened.

Pleural effusion, atelectasis, and parenchymal infiltrates can obliterate one or both diaphragms. Therefore when a posteroanterior or lateral chest radiograph suggests pleural effusion, additional radiographic studies are generally necessary to document the presence of pleural fluid or other pathology. The lateral decubitus radiograph is recommended because free fluid gravitates to the most dependent part of the pleural space and layers out there (Figure 23-3).

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in pleural effusion is mostly caused by the atelectasis and pulmonary shunting associated with the disorder. Hypoxemia caused by capillary shunting is often refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

Physical Examination

The woman appeared malnourished, exhibited poor personal hygiene, and had yellow tobacco stains around her fingers. She appeared to be in moderate to severe respiratory distress. Her nails and mucous membranes were cyanotic, and her shirt was wet from perspiration. She demonstrated an occasional hacking, nonproductive cough. She stated that she could not take a deep breath and that maybe the problem stemmed from “that spot” on her lung.

Her vital signs were as follows: blood pressure 130/60, heart rate 112 bpm, and respiratory rate 36/min with shallow respirations. She was slightly febrile, with an oral temperature of 37.7° C (99.8° F). Palpation showed that the trachea was shifted slightly to the left. Dull percussion notes were found over the right middle and right lower lobes. Auscultation revealed normal vesicular breath sounds over the left lung fields and upper right lobe. No breath sounds could be heard over the right middle and right lower lobes.

The patient’s chest x-ray film showed a large, right-sided pleural effusion. The right costophrenic angle demonstrated blunting, the right hemidiaphragm was depressed, and the right middle and lower lung lobes were partially collapsed and showed changes consistent with pneumonia. The arterial blood gas values (ABGs) on a 3 L/min oxygen nasal cannula were as follows: pH 7.48, Paco₂ 24, 17, and Pao₂ 37. The oxygen saturation measured by pulse oximetry (Spo₂) was 72%. The doctor, assisted by the respiratory therapist, performed a thoracentesis on the patient at the bedside. Slightly more than 2 L of yellow fluid was withdrawn. The patient then was started on intravenous antibiotics. A portable chest x-ray examination was ordered, and a respiratory care consultation was requested. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

3 Hours after Admission

At this time the patient was sitting up in bed. She stated that although she was feeling better, she did not feel great. She still had an occasional dry-sounding, nonproductive cough. Her skin appeared pale. She was still cyanotic. She was no longer perspiring, as she was when she was first admitted. Her vital signs were as follows: blood pressure 135/85, heart rate 100 bpm, respiratory rate 24/min, and temperature normal. Her respiratory efforts, however, no longer appeared shallow. Palpation of the chest was not remarkable. Dull percussion notes were found over the right middle and right lower lobes. Normal vesicular breath sounds were heard over the left lung and upper right lung. Loud bronchial breath sounds were audible over the right middle and right lower lobes.

The patient’s chest x-ray showed a small, right-sided pleural effusion. Increased opacity was still present in the right middle and lower lung, consistent with pneumonia. The patient’s trachea and mediastinum were in their normal positions. On an Fio₂ of 0.50, her ABGs were as follows: pH 7.52, Paco₂ 29, 22, and Pao₂ 57. Her Spo₂ was 92%. At this time, the following SOAP was charted.

Respiratory Assessment and Plan

5 Hours after Admission

The patient was sitting in a semi-Fowler’s position. She appeared relaxed and alert. She stated that she had finally caught her breath. Although she still appeared pale, she did not look cyanotic. No spontaneous cough was observed at this time.

Her vital signs were as follows: blood pressure 128/79, heart rate 88 bpm, respiratory rate 16/min, and temperature normal. Palpation of the chest was unremarkable. Dull percussion notes were found over the right middle and right lower lobes. Normal vesicular breath sounds were heard over the left lung and right upper lobe. Bronchial breath sounds were audible over the right middle and right lower lobes. No current chest x-ray was available. The patient’s ABG values on an Fio₂ of 0.60 were as follows: pH 7.45, Paco₂ 36, 24, and Pao₂ 77. Her Spo₂ was 95%. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

Discussion

This case illustrates a patient with postpneumonic pleural effusion, one of the pleural diseases that generally can be improved with appropriate therapy (in this case a 2-L thoracentesis).

During the first assessment, the respiratory care practitioner recognizes that the patient has significant respiratory morbidity. Indeed, the patient has an extensive right-sided pneumonia and pleural effusion and partially collapsed right middle and lower lobes. Clearly the patient is in respiratory distress. The patient’s acute alveolar hyperventilation and severe hypoxemia are a direct result of the partial collapse of the lung lobes. Because of the extremely low Pao₂ noted on the initial arterial blood gas, the presence of lactic acid is very likely. In fact, this was confirmed by the respiratory practitioner with the Pco₂//pH nomogram. Understanding that Atelectasis is the main pathophysiologic mechanism operating in this case (see Figure 9-8), the practitioner correctly assesses the situation as one that requires careful monitoring and begins the Lung Expansion Therapy Protocol (Protocol 9-3) (with incentive spirometry) and the Oxygen Therapy Protocol (Protocol 9-1) (with a high concentration of oxygen).

A trial of bronchopulmonary hygiene therapy would not be unwarranted in this case, given the patient’s cigarette smoking history alone or the degree of severity of the condition. Admittedly, the physical findings in this patient (no sputum production) did not indicate such therapy. Given the patient’s history, the respiratory care practitioner also would be interested in the results of the cytologic studies for malignancy in both the sputum and thoracentesis fluid. Frequently, blood gases do not improve immediately after a thoracentesis, despite the fluid removal, because the atelectasis under the pleural effusion takes some time (hours or days) to dissipate. For this reason, the Lung Expansion Therapy Protocol, after thoracentesis, is appropriate.

At the time of the second assessment, the patient was beginning to improve, although she still had signs of right middle and lower lobe Consolidation (Figure 9-9). Good breath sounds were heard over the left lung and upper right lung, although bronchial breath sounds reflecting consolidation were still noted on the right. The respiratory care practitioner was appropriately concerned that atelectasis was still present, and in such a case he or she should increase the Lung Expansion Therapy Protocol (Protocol 9-3). In this case, the practitioner selected a continuous positive airway pressure (CPAP) mask at 10 cm H₂O every 2 hours for 15 minutes. The practitioner could have also intensified use of incentive spirometry, carefully used intermittent positive-pressure breathing (IPPB) or extended the amount of time the patient was using the CPAP mask.

In the last assessment the patient continued to do fairly well, although she was far from returning to baseline values. The pneumonitis, atelectasis, and mild hypoxemia, which persisted despite supplemental oxygen therapy, suggested the need for continued significant (though unchanged) therapy. This case demonstrates that in-place therapy often does not need to be changed at each assessment. Indeed, this guide may apply to as many as 50% to 60% of accurately performed seriatim assessments. For pedagogic reasons, this option has not been exercised often in this text. However, this third assessment (in a patient with pleural effusion and underlying atelectasis and pneumonia) is a good case in point.