5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

FIGURE 19.7 Cavitary reactivation tuberculosis showing a left upper lobe cavity and localized pleural thickening (arrows). (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)

FIGURE 19.8 Miliary tuberculosis showing widespread uniformly distributed fine nodulation of the lung. (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)

General Management of Tuberculosis

Because the tubercle bacillus can exist in open cavitary lesions, in closed lesions, and within the cytoplasm of macrophages, a drug that may be effective in one of these environments may be ineffective in another. In addition, some of the TB bacilli are drug-resistant. Because of this problem, several drugs usually are prescribed concurrently for individuals with TB. Because toxicity is associated with some of the antituberculosis drugs, frequent examinations are performed to identify toxicity manifested in the kidneys, liver, eyes, and ears.

Pharmacologic Agents Used to Treat Tuberculosis

The standard pharmacologic agents used to treat M. tuberculosis consist of two to four drugs for 6 to 9 months. Examples of these protocols are as follows:

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•Six-month treatment protocol: For the first 2 months (called the induction phase) the patient takes a daily dose of isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), and either ethambutol (EMB, E) or streptomycin (SM). For the next 4 months the patient takes isoniazid and rifampin daily or twice weekly.

•Nine-month treatment protocol: For the first 1 to 2 months the patient takes a daily dose of isoniazid and rifampin, followed by twice-weekly isoniazid and rifampin until the full 9-month period has been completed.

Isoniazid and rifampin (Rifadin) are first-line agents prescribed for the entire 9 months. Isoniazid is considered the most effective first-line antituberculosis agent. Rifampin is bactericidal and is most commonly used in combination with isoniazid. Although patients with TB usually are not contagious after a few weeks of treatment, a full course of treatment is necessary to kill all the bacteria. The prophylactic use of isoniazid is often prescribed as a daily dose for 1 year in individuals who have been exposed to the TB bacillus or who demonstrate a positive tuberculin reaction (even when the acid-fast sputum stain is negative).

When the TB bacterium is resistant to one or more of these agents, at least three or more antibiotics must be added to the treatment regimen and the duration should be extended. A major problem with TB therapy is noncompliance on the part of the patient to take the TB medication as prescribed. Even under the best circumstances, it is very difficult to maintain a regimen of multiple TB antibiotics on a daily basis for months. Unfortunately, most TB patients are not living under the best of circumstances. In addition, failure to adhere to an antibiotic regimen often leads to antibiotic resistance in the slow-growing microorganism. In fact, many M. tuberculosis isolates are now found to be multiple drug–resistant TB (MDR-TB).

In response to the problem of noncompliance, it is recommended that all such patients with TB be treated by directly observed therapy (DOT)—that is, the ingestion of medication is directly observed by a responsible individual. In communities where DOT has been used, the rate of drug-resistant TB and the rate of TB relapse have been shown to decrease.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. Because of the hypoxemia associated with TB, supplemental oxygen may be required. The hypoxemia that develops in patients with lung abscess is usually caused by pulmonary capillary shunting. Hypoxemia caused by capillary shunting is often refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 10.1).

Airway Clearance Therapy Protocol

Because of the excessive mucus production and accumulation sometimes associated with severe TB, a number of airway clearance therapies may be used to enhance the mobilization of bronchial secretions. Infection control measures must be followed (see Airway Clearance Therapy Protocol, Protocol 10.2).

Mechanical Ventilation

Because acute ventilatory failure is occasionally associated with TB, mechanical ventilation may be required to maintain an adequate ventilatory status. Continuous mechanical ventilation is justified when the acute ventilatory failure is thought to be reversible—for example, when pneumonia complicates the condition (see Ventilator Initiation and Management Protocol, Protocol 11.1, and Ventilator Weaning Protocol, Protocol 11.2).

Infection Control Measures

Patients hospitalized with active tuberculosis are kept in respiratory isolation until three sputum AFB smears are negative, taken over 3 consecutive days.

Case Study Tuberculosis

Admitting History and Physical Examination

This 60-year-old male patient had been in good health until about 4 months before admission, when he first noted the onset of night sweats, occasionally accompanied by chills. About 3 months ago he noted that his appetite was decreasing, and he lost about 25 lb after that time.

Approximately 3 weeks before his admission, he noted that his long-standing “smoker's cough” had become more productive. For the 2 weeks before admission, his daily sputum production had increased to about a cup of thick yellow sputum with an occasional fleck or two of blood. There was a concomitant increase in dyspnea. About 10 days before admission, he had a gradual onset of moderately sharp left-sided chest pain. It was aggravated by deep breathing but did not radiate.

The history gave little useful information. About 35 years previously, he was told during a routine medical examination that he had a positive TB skin test but that he had no pulmonary problems. Subsequently he had several chest x-ray examinations in mobile chest x-ray units, once for an insurance application. The last x-ray examination was performed 5 years ago.

For the previous 35 years, he had been employed in a foundry as a “cone maker” and “shaker.” He volunteered the information that he worked in a “dusty” environment and that he had worn a protective mask only for the previous few months. His family history was noncontributory. He and his wife lived in the same house with his married daughter and two young granddaughters.

Physical examination revealed a thin man who appeared to be both chronically and acutely ill. His vital signs were blood pressure 132/90, heart rate 116 beats/min, respiratory rate 32 breaths/min, and oral temperature 102.4°F. His room air SpO2 was 90%. He was coughing up large amounts of yellow, blood-streaked sputum. There was marked dullness to

percussion in both apical areas, and diffuse inspiratory and expiratory coarse crackles were present in the right upper and middle lobes. A chest x-ray film demonstrated extensive bilateral apical calcification, cavity formation in the right upper lobe, and diffuse infiltrate and consolidation in the right middle lobe. He was admitted to the hospital and placed in respiratory isolation.

The following initial respiratory assessment was entered into the patient's chart.

Respiratory Assessment and Plan

S Productive cough, slight hemoptysis; appears short of breath (moderate). History of leftsided chest pain for 10 days.

O Febrile to 102.4°F. RR 32, HR 116, BP 132/90. Room air SpO2 90%. Productive cough: Large

amounts yellow, blood-streaked sputum. Inspiratory and expiratory coarse crackles in right upper and middle lobes. CXR: Apical calcification; RUL cavity; RML infiltrate/consolidation. A

•Probable tuberculosis (patient possibly infectious)

•Excessive airway secretions (yellow sputum, cough)

•Mild hypoxemia (SpO2 90%)

P Flag chart: Continue respiratory isolation pending AFB smear results. Obtain sputum for routine, anaerobic, and acid-fast cultures and cytology—induce if necessary. Obtain baseline ABG on room air. Airway Clearance Therapy Protocol: C&DB q2h. Based on ABG results, titrate oxygen therapy per Oxygen Therapy Protocol. Discuss need for bedside spirogram with physician.

Discussion

Two primary clinical scenarios were activated in this case. First, the alveolar consolidation (see Fig. 10.8) identified on the chest x-ray film reflected the patient's challenged immune response. This was further manifested by the objective data noted at the patient's bedside—fever, dull percussion notes, and increased heart rate, blood pressure, and respiratory rate. In addition, the alveolar consolidation undoubtedly contributed to the patient's pulmonary shunting and mild hypoxemia (see Fig. 10.8).

Second, clinical manifestations associated with excessive bronchial secretions (see Fig. 10.11) also were present in this patient: daily cough, yellow sputum production, and coarse crackles. His oxygen desaturation was mild (SpO2 90%), and a

room air ABG and subsequent oxygen titration (presumably with low-flow oxygen by nasal cannula) were appropriate.

As expected, the patient produced sputum containing acid-fast organisms. The attending physician prescribed isoniazid, rifampin, and streptomycin for 2 months, followed by an outpatient course of isoniazid and rifampin for 4 months. The patient also was instructed regarding several different airway clearance therapy protocols (see Protocol 10.2) to perform at home. He remained in the hospital for 14 days, until three consecutive sputum acid-fast bacillus smears were negative, and he was no longer febrile. The patient did well through 1 year of follow-up.

Self-Assessment Questions

1.Which of the following are known as the first stage of tuberculosis?

1.Reinfection tuberculosis

2.Primary tuberculosis

3.Secondary tuberculosis

4.Primary infection stage

a.2 only

b.3 only

c.1 and 3 only

d.2 and 4 only

2.What is the name of the protective wall that surrounds and encases lung tissue infected with tuberculosis? 1. Miliary tuberculosis

2. Reinfection tuberculosis

3.Granuloma

4.Tubercle

a.1 only

b.3 only

c.4 only

d.3 and 4 only

3.The tubercle bacillus is: 1. Highly aerobic

2.Acid-fast

3.Capable of surviving for months outside of the body

4.Rod-shaped

a.2 only

b.4 only

c.2 and 3 only

d.1, 2, 3, and 4

4.At which size wheal is a tuberculin skin test considered to be positive?

a.Greater than 4 mm

b.Greater than 6 mm

c.Greater than 8 mm

d.Greater than 10 mm

5.Which of the following is often prescribed as a prophylactic daily dose for 1 year in individuals who have been exposed to tuberculosis bacilli?

a.Streptomycin

b.Ethambutol

c.Isoniazid

d.Rifampin

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C H A P T E R 2 0

Pulmonary Edema

CHAPTER OUTLINE

Anatomic Alterations of the Lungs

Etiology and Epidemiology

Cardiogenic Pulmonary Edema

Noncardiogenic Pulmonary Edema

Overview of the Cardiopulmonary Clinical Manifestations Associated With Pulmonary Edema

General Management of Pulmonary Edema

Noncardiogenic Pulmonary Edema

Cardiogenic Pulmonary Edema

Respiratory Care Treatment Protocols

Case Study: Pulmonary Edema

Self-Assessment Questions

CHAPTER OBJECTIVES

After reading this chapter, you will be able to:

•List the anatomic alterations of the lungs associated with pulmonary edema.

•Describe the causes of pulmonary edema.

•List the cardiopulmonary clinical manifestations associated with cardiogenic and noncardiogenic pulmonary edema.

•Describe the general management of pulmonary edema.

•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

Afterload Reduction

Albumin

Angiotensin-Converting Enzyme (ACE) Inhibitors

Antidysrhythmic Agents

Brain Natriuretic Peptide (BNP)

Captopril

Cardiogenic Pulmonary Edema

Cardiomegaly

Cephalogenic Pulmonary Edema

Cheyne-Stokes Respiration

Congestive Heart Failure (CHF)

Decompression Pulmonary Edema

Digitalis

Dobutamine

Dopamine

Echocardiogram

Enalapril

Furosemide (lasix)

High-Altitude Pulmonary Edema

Increased Capillary Permeability

Kerley A and B Lines

Left Ventricular Ejection Fraction (LVEF)

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age at the first heart attack is 65.6 years for males and 72.0 years for females. Approximately every 40 seconds, an American will have a heart attack. From 2005 to 2015, the annual death rate attributable to coronary heart disease declined 34.4 percent and the actual number of deaths declined 17.7% – but the burden and risk factors remain alarmingly high. The estimated direct and indirect cost of heart disease in 2013 to 2014 (average annual) was $204.8 billion. Heart attacks ($12.1 billion) and Coronary Heart Disease ($9.0 billion) were 2 of the 10 most expensive conditions treated in US hospitals in 2013. Between 2013 and 2030, medical costs of Coronary Heart Disease are projected to increase by about 100 percent.

Cardiac pulmonary edema occurs when the left ventricle is unable to pump out a sufficient amount of blood during each ventricular contraction. The ability of the left ventricle to pump blood can be determined by means of the left ventricular ejection fraction (LVEF) with a noninvasive cardiac imaging procedure echocardiogram that reflects the patient's left ventricular systolic cardiac contractility. Poor ventricular function also may be caused by an increased ventricular stiffness or impaired myocardial relaxation. This condition is called diastolic dysfunction and is associated with a relatively normal LVEF. Normal values for the LVEF range between 55% and 70%. An LVEF less than 40% may confirm heart failure; an LVEF less than 35% is life-threatening, and cardiac arrhythmias are likely.

When the patient's LVEF is low, the blood pressure inside the pulmonary veins and capillaries increases as a result. This action literally causes fluid to be pushed through the capillary walls and into the alveoli in the form of a transudate. The basic pathophysiologic mechanism for this action is described in the following sections.

Ordinarily, hydrostatic pressure of about 10 to 15 mm Hg tends to move fluid out of the pulmonary capillaries into the interstitial space. This force is normally offset by colloid osmotic forces of about 25 to 30 mm Hg that tend to keep fluid in the pulmonary capillaries. The colloid osmotic pressure is referred to as oncotic pressure and is produced by the albumin and globulin in the blood. The stability of fluid within the pulmonary capillaries is determined by the balance between hydrostatic and oncotic pressures. This relationship also maintains fluid stability in the interstitial compartments of the lung.

Movement of fluid in and out of the capillaries is expressed by the Starling equation:

where J is the net fluid movement out of the capillary, K is the capillary permeability factor, Pc and Pi are the hydrostatic pressures in the capillary and interstitial space, and πc and πi are the oncotic pressures in the capillary and interstitial space.

Although conceptually valuable, this equation has limited practical use. Of the four pressures, only the oncotic and hydrostatic pressures of blood in the pulmonary capillaries can be measured with any certainty. The oncotic and hydrostatic pressures within the interstitial compartments cannot be readily determined.

When the hydrostatic pressure within the pulmonary capillaries rises to more than 25 to 30 mm Hg, the oncotic pressure loses its holding force over the fluid within the vessels. Consequently, fluid starts to spill into the interstitial spaces and alveoli of the lungs (see Fig. 20.1).

Clinically, the patient with left ventricular failure often has activity intolerance, weight gain, anxiety, delirium, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue, cardiac arrhythmias (particularly atrial fibrillation), and adventitious breath sounds. Because of poor peripheral circulation, such patients often have cool skin, diaphoresis, cyanosis of the digits, and peripheral pallor. Major organ failure of the brain and kidney may be the result of hypoperfusion. Increased pulmonary capillary hydrostatic pressure is the most common cause of pulmonary edema. Box 20.1 provides common causes of cardiogenic pulmonary edema. Box 20.2 provides common risk factors for coronary heart disease (CHD).

Box 20.1

Common Causes of Cardiogenic Pulmonary Edema

•Arrhythmias (e.g., premature ventricular contractions or bradycardia producing low cardiac output)

•Systemic hypertension

•Congenital heart defects

•Coronary heart disease (see Box 20.2)

•Excessive fluid administration

•Left ventricular failure

•Mitral or aortic valve disease

•Myocardial infarction

•Cardiac tamponade

•Pulmonary embolus

•Renal failure

•Rheumatic heart disease (myocarditis)

•Cardiomyopathies (e.g., viral)

Box 20.2

Risk Factors for Coronary Heart Disease (CHD)

•Age

•Males older than 45 years

•Females older than 55 years

•Family history of CHD

•Male relative with CHD: Younger than 55 years

•Female relative with CHD: Younger than 65 years

•Cigarette smoker

•Obesity

•Hypertension: Blood pressure >140/90 mm Hg or on antihypertensive agents

•High level of low-density-lipoprotein cholesterol (LDL-C): >130 mg/dL (“bad cholesterol”)

•Low level of high-density-lipoprotein cholesterol (HDL-C): <35 mg/dL (“good cholesterol”)

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Overview of the Cardiopulmonary Clinical Manifestations Associated With Pulmonary Edema

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by atelectasis (see Fig. 10.7), increased alveolar-capillary membrane thickness (see Fig. 10.9), and, in severe cases, excessive bronchial secretions (see Fig. 10.11)—the major anatomic alterations of the lungs associated with pulmonary edema (see Fig. 20.1).

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 and baroreceptors

•Anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Cheyne-Stokes Respiration

Cheyne-Stokes respiration may be seen in patients with severe left-sided heart failure and pulmonary edema. Some authorities have suggested that the cause of Cheyne-Stokes respiration in these patients may be related to the prolonged circulation time between the lungs and the central chemoreceptors. Cheyne-Stokes respiration is a classic clinical manifestation in central sleep apnea (see Chapter 32, Sleep Apnea).

Paroxysmal Nocturnal Dyspnea and Orthopnea

Patients with pulmonary edema often awaken with severe dyspnea after several hours of sleep. This condition is called paroxysmal nocturnal dyspnea (PND). This condition is particularly prevalent in patients with cardiogenic pulmonary edema. While the patient is awake, more time is spent in the erect position and, as a result, excess fluids tend to accumulate in the dependent portions of the body. When the patient lies down, however, the excess fluids from the dependent parts of the body move into the bloodstream and cause an increase in venous return to the lungs. This action raises the pulmonary hydrostatic pressure and promotes pulmonary edema. The pulmonary edema in turn produces pulmonary shunting, venous admixture, and hypoxemia. When the hypoxemia becomes severe, the peripheral chemoreceptors are stimulated and initiate an increased ventilatory rate (see Figs. 3.5 and 3.6). The decreased lung compliance, J receptor stimulation, and anxiety may also contribute to the paroxysmal nocturnal dyspnea commonly seen in this disorder at night. A patient is said to have orthopnea when dyspnea increases while the patient is lying in a recumbent position.

Cyanosis

Cough and Sputum (Frothy and Pink in Appearance)

Chest Assessment Findings

•Increased tactile and vocal fremitus

•Crackles and wheezing

Clinical Data Obtained From Laboratory Tests and Special Procedures

Pulmonary Function Test Findings

Moderate to Severe Pulmonary Edema (Restrictive Lung Pathology)

Forced Expiratory Volume and Flow Rate Findings1

Lung Volume and Capacity Findings

1The decreased forced expiratory volumes and flow rate findings are primarily caused by the low vital capacity associated with the restrictive pulmonary disorder.

Arterial Blood Gases

Mild to Moderate Pulmonary Edema

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Acute Alveolar Hyperventilation With Hypoxemia2 (Acute Respiratory Alkalosis)

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

Severe Pulmonary Edema

Acute Ventilatory Failure With Hypoxemia3 (Acute Respiratory Acidosis)

3See Fig. 5.2 and Table 5.5 and related discussion for the acute pH, PaCO2, and changes associated with acute and chronic ventilatory failure.

4When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular PaCO2 level (metabolic acidosis). This is particularly common when systemic hypotension is present.

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

5, 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 Indices7 Cardiogenic Pulmonary Edema

(Moderate to Severe)

Other Important Hemodynamic Indices:

Left Ventricular Ejection Fraction (LVEF)

8Decreased LVEF when cardiogenic pulmonary edema is present. May be normal in noncardiogenic pulmonary edema.

7CO, 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; LVEF, left ventricular ejection fraction.

Abnormal Laboratory Test and Procedure Results

•Serum potassium: Low

•Serum sodium: Low

•Serum chloride: Low

•Brain natriuretic peptide (BNP): Elevated

Hypokalemia, hyponatremia, and hypochloremia are often seen in patients with left-sided heart failure and may result from diuretic therapy or excessive fluid retention. The brain natriuretic peptide (BNP), also known as B-type natriuretic peptide or ventricular natriuretic peptide (still BNP) is an important biomarker used to help establish the diagnosis of congestive heart failure (CHF). The BNP hormone is produced by the heart and reflects how well the heart is functioning. Normally, only a low amount of BNP (<100 pg/mL) is found in blood. However, when the heart is working harder than normal over a long period, the heart releases more of the substance, increasing the blood level of BNP. The following provides various BNP levels and the cardiac status associated with these levels:

•BNP levels below 100 pg/mL indicate no heart failure.

•BNP levels of 100 to 300 pg/mL suggest heart failure may be present.

•BNP levels above 300 pg/mL indicate mild heart failure.