5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

Although the man was able to enjoy a couple of relatively good years of retirement with his wife, his health declined rapidly. His cough and dyspnea quickly became a daily problem. Despite his deteriorating health, the man continued to smoke. When he was 72 years old, he was hospitalized for 8 days for treatment of pneumonia and severe respiratory distress. When he was discharged at that time, his PFTs still showed a moderate to severe restrictive disorder. He started using oxygen at home regularly.

Approximately 10 months before the current admission, the man was hospitalized because of congestive heart failure. He was treated aggressively and sent home within 5 days. At the time of discharge, his PFTs showed that he had a worsening restrictive respiratory disorder. His arterial blood gas (ABG) values on 2 L/min oxygen by nasal cannula were pH 7.38,

PaCO2 86 mm Hg, 49 mEq/L, PaO2 63 mm Hg, and SaO2 91%.

Approximately 3 hours before the current admission, the man awoke from an afternoon nap extremely short of breath. His wife stated that he coughed almost continuously and had difficulty speaking. She measured his oral temperature, which read 38°C (100°F). Concerned, she drove her husband to the hospital emergency department (ED).

Physical Examination

As the man was wheeled into the ED, he appeared nervous, weak, and in obvious respiratory distress. He was on 1.5 L/min oxygen by nasal cannula, which was connected to an E-tank attached to the wheelchair. His skin felt damp and clammy. He appeared pale and cyanotic. His neck veins were distended, and his fingers and toes were clubbed. He demonstrated a frequent but weak cough productive of a moderate amount of thick, whitish-yellow secretions. He had 3+ peripheral edema of the ankles and feet. He said this was the worst his breathing had ever been.

The patient's vital signs were blood pressure 180/96 mm Hg, heart rate 108 beats/min, respiratory rate 32 breaths/min, and oral temperature 38.3°C (100.8°F). Palpation of the chest was negative. Percussion produced bilateral dull notes in the lung bases. Coarse crackles were auscultated throughout both lungs. A pleural friction rub could be heard over the right middle lobe between the sixth and seventh ribs, between the anterior axillary line and midaxillary line.

The patient's lower lobes had a diffuse, ground-glass appearance on the chest radiograph. Irregularly shaped opacities in the right and left lower pleural spaces were identified by the radiologist as calcified pleural plaques. A possible infiltrate consistent with pneumonia was also visible in the right middle lobe. In addition, the chest x-ray suggested that the right side of the heart was moderately enlarged. His ABGs on a 1.5 L/min oxygen nasal cannula were pH 7.56, PaCO2 51 mm Hg,

43 mEq/L, PaO2 47 mm Hg, and SaO2 86%.

The physician started the patient on intravenous furosemide (Lasix) to treat the man's cor pulmonale and began administering an antibiotic to treat suspected pneumonia. A respiratory therapist was called to obtain a sputum culture, perform a respiratory care evaluation, and outline further respiratory therapy. The physician said that she did not want to commit the patient to a ventilator unless absolutely necessary. On the basis of this information, the following SOAP was recorded.

Respiratory Assessment and Plan

S “This is the worst my breathing has ever been.”

O Vital signs: BP 180/96, HR 108, RR 32, T 38.3°C (100.8°F); weak appearance; skin: cyanotic, damp, and clammy; distended neck veins and digital clubbing; cough: frequent, weak, moderate amount of thick, whitish-yellow secretions; peripheral edema 3+ of ankles and feet. Bilateral dull percussion notes in lung bases. Over both lungs: coarse crackles; pleural friction rub over right middle lobe between sixth and seventh ribs, between anterior axillary line and midaxillary line; CXR: ground-glass appearance in lower lobes; calcified pleural plaques in right and left lower pleural spaces; consolidation in right middle lung lobe; right heart

enlargement; ABGs (1.5 L/min O2 by nasal cannula) pH 7.56, PaCO2 51, 43, PaO2 47, SaO2 86%.

A

•Respiratory distress (general appearance, vital signs, ABGs, history of congestive heart failure)

•Pulmonary fibrosis (history, diagnosis of asbestosis, CXR)

•Alveolar consolidation in right middle lobe (CXR)

•Pleurisy (asbestosis or pneumonitis) in area of right middle lobe (pleural friction rub)

•Excessive bronchial secretions (coarse crackles, sputum production)

•Chest infection likely (yellow sputum, fever)

•Acute alveolar hyperventilation superimposed on chronic ventilatory failure with moderate to severe hypoxemia (history, ABGs)

•Impending ventilatory failure (ABGs)

P Up-regulate Oxygen Therapy Protocol (air entrainment mask at FIO2 0.35). Airway Clearance

Therapy Protocol (DB&C q4h; obtain sputum for Gram stain and culture). Initiate Lung Expansion Therapy Protocol (incentive spirometry followed by C&DB). Monitor with pulse oximeter, set SpO2 alarm at 85%.

The Next Morning

Throughout the night the patient's condition remained unstable. He continued to cough frequently but could not expectorate secretions adequately on his own. When the therapist assisted the patient during coughing episodes, a moderate amount of thick, white and yellow sputum was produced. Even though he was conscious, alert, and able to follow simple directions, he did not answer any of the respiratory therapist's specific questions about his breathing.

His skin was cold and damp to the touch, and he appeared short of breath. His color was improved, but he still appeared pale and cyanotic. His neck veins were still distended, although not so severely as they had been on admission, and edema of his ankles and feet could still be seen. The patient's vital signs were blood pressure 192/108 mm Hg, heart rate 113 beats/min, respiratory rate 34 breaths/min, and oral temperature 38°C (100.4°F). Palpation of the chest was negative.

Dull percussion notes were elicited over the lung bases. Coarse crackles continued to be auscultated throughout both lungs. A pleural friction rub could still be heard over the right middle lung between the sixth and seventh ribs, between the anterior axillary line and midaxillary line. No recent chest radiograph was available. His ABGs (FIO2 0.35) were pH 7.57,

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corrected hypoxemia (ABGs)

•Alveolar hyperventilation and overoxygenation caused by mechanical ventilator and FIO2 setting

P Down-regulate Oxygen Therapy Protocol (reduce FIO2 to 0.50). Down-regulate Mechanical Ventilation Protocol (e.g., decrease the tidal volume to increase the PaCO2 to patient's baseline

—e.g., 80 to 90 mm Hg). Continue Airway Clearance Therapy Protocol and Aerosolized Medication Protocol. Continue Lung Expansion Therapy Protocol (10 cm H2O PEEP, but monitor

mean airway pressure). Continue to closely monitor and reevaluate.

Discussion

The admitting history revealed that the patient had been diagnosed with moderate pneumoconiosis (probable asbestosis). Not surprisingly, pulmonary function tests in the past had shown mild to moderate restrictive pulmonary disorders.

Significant new findings were the recent history suggesting congestive heart failure and the ABG values on his discharge from the hospital 10 months before the admission under discussion, which demonstrated chronic ventilatory failure. The patient's recent fever and cough and purulent sputum production both before and in his ED admission suggested an infectious cause for his symptoms. His cyanosis, neck-vein distention, and digital clubbing suggested chronic hypoxemia. The sputum purulence confirmed that infection may indeed have been present and that the assessing therapist's desire to obtain a sputum culture was appropriate. This was not followed up in subsequent SOAP notes. The pleural rub demonstrated by this patient could have been related to his asbestosis or to a pneumonic infiltrate extending to the pleural surface.

In the initial assessment the patient's severe hypertension and his fever were noted. Both deserved vigorous therapy if his pulmonary function were to improve at all. The patient's severe hypoxemia reflected common clinical indicators caused by alveolar-capillary membrane thickening (see Fig. 10.9) and excessive bronchial secretions (see Fig. 10.11). Although there is no therapy available to reverse the increased alveolar membrane thickening, which reflects the alveolitis from his almost certain asbestosis, the excessive bronchial secretions can be effectively treated in most cases.

The patient was hyperventilating with respect to his earlier outpatient blood gases. During such an assessment the patient's underlying pulmonary conditions (chronic pulmonary fibrosis, bronchitis, and congestive heart failure) should be recorded, but the assessment should really zero in on the treatable issues, specifically in this case the pulmonary infection, as suggested by the patient's fever, sputum purulence, and chest radiograph.

At the time of the second evaluation, the patient's hypoxemia had worsened despite oxygen therapy. If not already being used, Venturi oxygen mask therapy was indicated there, and aggressive endotracheal suctioning also could be indicated. A trial of Lung Expansion Therapy Protocol (Protocol 10.3) was appropriate to attempt to offset the pathologic effects of the alveolar consolidation and, possibly, atelectasis. The physician may have ordered a trial of diuretic therapy to reduce the fluid retention and also a course of antibiotic therapy. It was not clear whether appropriate (culture-based) antibiotic therapy was selected in this case.

The last assessment revealed ventricular arrhythmias. The change in the patient's sputum from thick and white to greenish-yellow suggests superinfection with another organism, and reculture of the sputum was appropriate. The respiratory therapist responded quickly and appropriately to readjust the mechanical ventilator. The FIO2 was decreased to

0.50 to correct the patient's overoxygenation (PaO2 246), and the tidal volume was reduced to increase the PaCO2 to the

baseline—80 to 90 mm Hg, according to the ABG history. Ventilator parameters should be adjusted to provide good pulmonary expansion while avoiding high mean airway pressures. A cautious trial of PEEP would have been in order.

Despite all that was done for this patient, he died 4 days later as a result of left-sided congestive heart failure and pneumonia complicating his pulmonary asbestosis.

Self-Assessment Questions

1.Which of the following is another name for hypersensitivity pneumonitis?

a.Sarcoidosis

b.Extrinsic allergic alveolitis

c.Alveolar proteinosis

d.Idiopathic pulmonary hemosiderosis

2.Which of the following is(are) considered pulmonary vasculitides?

1.Rheumatoid arthritis

2.Wegener granulomatosis

3.Lymphomatoid granulomatosis

4.Churg-Strauss syndrome

a.1 only

b.3 only

c.2, 3, and 4 only

d.1, 2, and 3 only

3.Which of the following disorders is associated with desquamative interstitial pneumonia and usual interstitial pneumonia?

a.Idiopathic pulmonary fibrosis

b.Eosinophilic granuloma

c.Rheumatoid arthritis

d.Sarcoidosis

4.Which of the following is(are) systemic connective tissue diseases?

1.Pulmonary Langerhans cell histiocytosis

2.Rheumatoid arthritis

3.Sjögren syndrome

4.Alveolar proteinosis

a.3 only

b.2 and 4 only

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PA R T X

Diffuse Alveolar Disease

OUTLINE

Chapter 28 Acute Respiratory Distress Syndrome

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FIGURE 28.1 Cross-sectional view of alveoli in acute respiratory distress syndrome. AC, Alveolar consolidation; AT, atelectasis; HM, hyaline membrane; M, macrophage.

The major pathologic or structural changes associated with ARDS are as follows:

•Interstitial and intraalveolar edema and hemorrhage

•Alveolar consolidation

•Intraalveolar hyaline membrane formation

•Pulmonary surfactant deficiency or qualitative abnormality

•Atelectasis

Historically, ARDS was first referred to as the “shock lung syndrome” when the disease was first identified in combat casualties during World War II. Since that time the disease has appeared in the medical literature under many different names, all based on the conditions believed to be responsible for the disease. In 1967 the disease was first described as a specific entity, and the term acute respiratory distress syndrome was suggested. This term is predominantly used today. Box 28.1 provides some of the other names that have appeared in the medical journals to identify ARDS.

Box 28.1

Previous Names for Acute Respiratory Distress Syndrome

•Adult hyaline membrane disease

•Adult respiratory distress syndrome

•Capillary leak syndrome

•Congestion atelectasis

•Da Nang lung (because of the high incidence of ARDS in the Vietnam War)

•Hemorrhagic pulmonary edema

•Noncardiac pulmonary edema

•Oxygen pneumonitis

•Oxygen toxicity

•Postnontraumatic pulmonary insufficiency

•Postperfusion lung

•Postpump lung

•Posttraumatic pulmonary insufficiency

•Shock lung syndrome

•Stiff lung syndrome

•Wet lung

•White lung syndrome

Etiology and Epidemiology

ARDS accounts for 10% to 15% of all intensive care unit admissions and about 25% of patients on mechanical ventilation. A multitude of causative factors may produce ARDS. Although more than 60 possible pulmonary insults have been identified to cause ARDS, only a few common causes account for most cases of ARDS. Box 28.2 provides some of the better-known causes. The clinical manifestations associated with ARDS usually appear within 6 to 72 hours of an inciting event and worsen rapidly. The patient typically presents with dyspnea, cyanosis, bilateral crackles, tachypnea, tachycardia, diaphoresis, and use of accessory muscles of inspiration. Systemic hypotension is frequently an early event, and the dyspnea is often out of proportion to the extent of the radiologic abnormality. A cough and chest pain also may be present. The general clinical course is characterized by several days of hypoxemia that requires moderate to high concentrations of inspired oxygen. The bilateral alveolar infiltrates and diffuse crackles worsen during this period, and the patient's overall health status is often fragile as a result of severe hypoxemia. Between 12% and 35% of patients die within the first 72 hours. Most patients who survive this initial clinical course begin to show oxygenation improvements and decreasing alveolar infiltrates over the next several days.

Box 28.2

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Causes of Acute Respiratory Distress Syndrome

Most Common

•Sepsis: The most common cause of ARDS. It should be the first cause considered whenever ARDS develops in an adult patient.

•The risk factors are especially high in patients with sepsis who also have a history of alcoholism.

•Aspiration (e.g., of gastric contents). ARDS occurs in about one-third of patients who have a recognized episode of aspiration of gastric contents.

•Pneumonia: Community-acquired pneumonia is one of the most common causes of ARDS that develops outside of the hospital. Common pathogens include Streptococcus pneumoniae, Legionella pneumophila, Pneumocystis jiroveci (formerly called Pneumocystis carinii), Staphylococcus aureus, enteric gram-negative organisms, and a variety of respiratory viruses.

•Severe trauma: ARDS is a common complication of severe trauma. Such trauma often includes the following:

•Bilateral lung contusion caused by blunt trauma (e.g., steering wheel smashed into the chest during a car accident).

•Fat embolism from a long-bone fracture (e.g., ARDS symptoms typically appear 12 to 48 hours after the trauma).

•Sepsis: Perhaps the most common cause of ARDS that develops several days after severe trauma.

•Massive traumatic tissue injury: Predisposes the patient to ARDS.

•Massive blood transfusion (in stored blood the quantity of aggregated white blood cells, red blood cells, platelets, and fibrin increases; these blood components may in turn occlude or damage small blood vessels).

•Lung and hematopoietic stem cell transplantation: Patients are at risk for ARDS resulting from a variety of infectious and noninfectious causes.

•Drug abuse (e.g., heroin, barbiturates, morphine, methadone).

Other Causes

•Central nervous system (CNS) disease (particularly when complicated by increased intracranial pressure)

•Cardiopulmonary bypass (especially when the bypass is prolonged).

•Disseminated intravascular coagulation (seen in patients with shock; it is a condition of paradoxical simultaneous clotting and bleeding that produces microthrombi in the lungs).

•Inhalation of toxins and irritants (e.g., chlorine gas, nitrogen dioxide, smoke, ozone; oxygen may also be included in this category of irritants).

•Immunologic reactions (e.g., allergic alveolar reaction to inhaled material or Goodpasture syndrome).

•Oxygen toxicity (e.g., prolonged exposure to FIO2 >0.60).

Diagnostic Criteria for Acute Respiratory Distress Syndrome

As shown in Box 28.3, the Berlin Definition of ARDS is used as the diagnostic criteria for ARDS. Note that the Berlin Definition of ARDS requires that all the elements listed in Box 28.3 must be present to diagnose ARDS. For the most part, ARDS is a diagnosis of exclusion—that is, excluding other possible causes of acute hypoxemic respiratory failure with bilateral alveolar infiltrates. Cardiogenic pulmonary edema is the primary alternative that needs to be ruled out. Other possible alternative causes of acute hypoxemic respiratory failure with bilateral alveolar infiltrates include diffuse alveolar hemorrhage, idiopathic acute exacerbation of preexisting interstitial lung disease, acute eosinophilic pneumonia, cryptogenic organizing pneumonia, acute interstitial pneumonia, and rapidly disseminating (metastatic) malignancy.

Box 28.3

Berlin Definition of Acute Respiratory Disease Syndrome: Diagnostic

Criteria

•Respiratory symptoms associated with ARDS have manifested within 1 week of a known clinical event or new or worsening symptoms over the past 7 days.

•Bilateral opacities similar to pulmonary edema appear on the chest radiograph or computed tomography scan. The opacities cannot be fully explained by pleural effusion, lobar or lung collapse, or pulmonary nodules.

•The patient's respiratory failure cannot be fully explained by heart failure or fluid overload. An objective assessment to rule out hydrostatic pulmonary edema is required if risk factors for ARDS are not present.

•A moderate to severe impairment of oxygenation must be present, as defined by the ratio of arterial oxygen

tension to fraction of inspired oxygen ratio (PaO2/FIO2 ratio). The severity of the hypoxemia defines the severity of the ARDS*:

•Mild ARDS: The PaO2/FIO2 is >200, but ≤300, on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H2O.

•Moderate ARDS: The PaO2/FIO2 is >100, but ≤200, on ventilator settings that include PEEP ≥5 cm H2O.

•Severe ARDS: The PaO2/FIO2 is ≤100 on ventilator settings that include PEEP ≥5 cm H2O.

*To determine the PaO2/FIO2 ratio, the PaO2 is measured in mm Hg and the FIO2 is expressed as a decimal fraction between 0.21 and 1. For example, if a patient has a PaO2 of 60 mm Hg while receiving 85% oxygen, then the PaO2/FIO2 is 60/0.85 = 70. The normal PaO2/FIO2 ratio is between 350 and 450.

Modified from ARDS Definition Task Force. (2012). Acute respiratory distress syndrome: The Berlin Definition. Journal of the American Medical Association 307(23), 2526-2533.

Overview of the Cardiopulmonary Clinical Manifestations Associated With Acute Respiratory Distress Syndrome

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by atelectasis (see Fig. 10.7), alveolar consolidation (see Fig. 10.8), and increased alveolar-capillary membrane thickness (see Fig. 10.9)—the major anatomic alterations of the lungs associated with ARDS (see Fig. 28.1).

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)

•Relationship of decreased lung compliance to increased ventilatory rate

•Stimulation of J receptors

•Anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Substernal or Intercostal Retractions

Cyanosis

Chest Assessment Findings

•Dull percussion note

•Bronchial breath sounds

•Crackles

Clinical Data Obtained From Laboratory Tests and Special Procedures

Pulmonary Function Test Findings

(Restrictive Lung Pathophysiology)

Forced Expiratory Volume and Flow Rate Findings

Lung Volume and Capacity Findings

DECREASED DIFFUSION CAPACITY (DLCO)

Arterial Blood Gases1

Mild to Moderate Acute Respiratory Distress Syndrome

Acute Alveolar Hyperventilation With Hypoxemia2

(Acute Respiratory Alkalosis)

Severe Acute Respiratory Distress Syndrome

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1NOTE: The use of the SpO2/FIO2 ratio (which does not require ABG analysis) has simplified the monitoring, diagnosis, and treatment of ARDS compared with the PaO2/FIO2 difference, which does require an arterial blood gas stick (see Chapter 6, Assessment of Oxygenation).

2See Fig. 5.2 and Table 5.4 and related discussion for the acute pH, PaCO2, and changes associated with acute alveolar hyperventilation.

Oxygenation Indices5

6The 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 (rare), or (3) a combination of both. When the DO2 is normal, the O2ER is usually normal.

oxygen saturation; V̇O2, oxygen consumption.

Hemodynamic Indices7 Severe ARDS

8A normal PCWP (<18 mm Hg) is the hallmark of ARDS, distinguishing it from cardiogenic pulmonary edema, in which the PCWP is elevated.

9If sepsis with systemic hypotension is present.

7CO, 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, diffusely throughout lungs

Because of the bilateral alveolar infiltrates that develop in ARDS, an increased radiodensity is seen on the chest radiograph. The increased lung density resists x-ray penetration and is revealed on the radiograph as increased opacity. Therefore the more severe the ARDS, the denser the lungs become and the “whiter” the radiograph (Fig. 28.2). Ultimately, the lungs may have a ground-glass appearance. This is in contrast to cardiogenic pulmonary edema, where the infiltrates appear more central.

FIGURE 28.2 Chest radiograph of a patient with moderately severe acute respiratory distress syndrome.

Other Clinical Manifestations Associated With Acute Respiratory Distress Syndrome