THE RESPIRATORY SYSTEM

Jayvee Eduardson Avisa, RN

The respiratory system functions primarily to maintain the exchange of oxygen and
carbon dioxide in the lungs and tissues and to regulate acid-base balance. Any change in this
system affects every other body system. Conversely, changes in other body systems may reduce
the lungs’ ability to provide oxygen and eliminate carbon dioxide

The respiratory system consists of the airways, lungs, bony thorax, and respiratory
muscles and functions in conjunction with the central nervous system (CNS). These structures
work together to deliver oxygen to the blood-stream and remove excess carbon dioxide from the
body.

Airways
The airways are divided into the upper and lower airways. The upper airways include the
nasopharynx (nose), oropharynx (mouth), laryngopharynx, and larynx. Their purpose is to warm,
filter, and humidify inhaled air. They also help make sound and send air to the lower airways.

The epiglottis is a flap of tissue that closes over the top of the larynx when the patient
swallows. It protects the patient from aspi-rating food or fluid into the lower airways.

The larynx is located at the top of the trachea and houses the vocal cords. It’s the
transition point between the upper and lower airways.

The lower airways begin with the trachea, which then divides into the right and left
mainstem bronchial tubes. The mainstem bron-chi divide into the lobar bronchi, which are lined
with mucus-producing ciliated epithelium, one of the lungs’ major defense systems.

The lobar bronchi then divide into secondary bronchi, tertiary bronchi, terminal
bronchioles, respiratory bronchioles, alveolar ducts and, finally, into the alveoli, the gas-
exchange units of the lungs. The lungs in a typical adult contain about 300 million alveoli.

Lungs
Each lung is wrapped in a lining called the visceral pleura. The larger of the two lungs,
the right lung has three lobes: upper, middle, and lower. The smaller left lung has only an upper
and a lower lobe. The lungs share space in the thoracic cavity with the heart, great vessels,
trachea, esopha-gus, and bronchi. All areas of the thoracic cavity that come in contact with the
lungs are lined with parietal pleura.A small amount of fluid fills the area between the two layers
of the pleura. This pleural fluid allows the layers of the pleura to slide smoothly over one another
as the chest expands and contracts. The parietal pleurae also contain nerve endings that transmit
pain signals when inflammation occurs.

Thorax
The bony thorax includes the clavicles, sternum, scapula, 12 sets of ribs, and 12 thoracic
vertebrae. Ribs are made of bone and cartilage and allow the chest to expand and contract during
each breath. All ribs attach to the ver-tebrae. The first seven ribs also attach directly to the
sternum. The 8th, 9th, and 10th ribs attach to the costal cartilage of the ribs above. The 11th and
12th ribs are called floating ribs because they don’t attach to anything in the front.

Pulmonary circulation
Oxygen-depleted blood enters the lungs from the pulmonary artery off the right ventricle,
then flows through the main pulmo-nary vessels into the pleural cavities and the main bronchi,
where it continues to flow through progressively smaller vessels until it reaches the single-celled
endothelial capillaries serving the alveoli. Here, oxygen and carbon dioxide diffusion takes
place.

DIAGNOSTIC TESTS

ABG analysis
A practitioner will typically order an ABG analysis as one of the first tests to assess
respiratory status because it helps evaluate gas exchange in the lungs. ABG analysis includes
several measures:
1. An indication of hydrogen ion concentration in the blood, pH shows the blood’s acidity
or alkalinity.
2. Known as the respiratory parameter, partial pressure of arterial carbon dioxide (Pa CO2),
reflects the adequacy of the lungs’ ventilation and carbon dioxide elimination.
3. Partial pressure of arterial oxygen (Pa O2) reflects the body’s ability to pick up oxygen
from the lungs.
4. Known as the metabolic parameter, the • bicarbonate (HCO3–) level reflects the
kidneys’ ability to retain and excrete bicar-bonate.

Sputum analysis
Analysis of a sputum specimen (the material expectorated from a patient’s lungs and
bronchi during deep coughing) helps diagnose respiratory disease, determine the cause of
respiratory infection (including viral and bacterial causes), identify abnormal lung cells,
and manage lung disease.

Endoscopic and imaging tests

Endoscopic and imaging tests include bronchoscopy, chest X-ray, magnetic resonance
imaging (MRI), pulmonary angiography, tho-racic computed tomography (CT) scan, and
ventilation-perfusion (V) scan.

Bronchoscopy
Bronchoscopy is direct inspection of the trachea and bronchi through a flexible fiber-
optic or rigid bronchoscope. It allows the doctor to determine the location and extent of
pathologic pro-cesses, assess resectability of a tumor, diagnose bleeding sites, collect tissue or
sputum specimens, and remove foreign bodies, mucus plugs, or excessive secretions.

Chest X-ray
Because normal pulmonary tissue is radiolucent, foreign bodies, infiltrates, fluids,
tumors, and other abnormalities appear as densities (white areas) on a chest X-ray. It’s most
useful when compared with the patient’s previous films, which allows the radiologist to detect
changes. By itself, a chest X-ray film may not provide information for a definitive diagnosis. For
example, it may not reveal mild to moderate obstructive pulmonary disease. Even so, it can show
the location and size of lesions and identify structural abnormalities that influence ventilation
and diffusion. Examples of abnormali-ties visible on X-ray include pneumothorax, fibrosis,
atelectasis, and infiltrates.

MRI
MRI is a noninvasive test that employs a powerful magnet, radio waves, and a computer
to help diagnose respiratory disorders. It provides high-resolution, cross-sectional images of lung
structures and traces blood flow. MRI’s greatest advantage is its ability to “see through’’ bone
and to delineate fluid-filled soft tissue in great detail, without using ionizing radiation or contrast
media.

Pulmonary angiography
Also called pulmonary arteriography, pulmonary angiography allows radiographic
examination of the pulmonary circulation.

Thoracic CT scan
A thoracic CT scan provides cross-sectional views of the chest by passing an X-ray
beam from a computerized scanner through the body at different angles and depths. The CT scan
provides a three-dimensional image of the lung, allowing the doctor to assess abnormalities in
the configuration of the trachea or major bronchi and evaluate masses or lesions, such as tumors
and abscesses, and abnormal lung shadows.

V scan
Although less reliable than pulmonary angiography, a V scan carries fewer risks. This
test indicates lung perfusion and venti-lation. It’s used to evaluate V mismatch, to detect
pulmonary emboli, and to evaluate pulmonary function, particularly in preop-erative patients
with marginal lung reserves.

Pulse oximetry
Pulse oximetry is a continuous noninvasive study of arterial blood oxygen saturation
using a clip or probe attached to a sensor site (usually an earlobe or a fingertip). The percentage
expressed is the ratio of oxygen to Hb

Thoracentesis
Also known as pleural fluid aspiration, thoracentesis is used to obtain a sample of pleural
fluid for analysis, relieve lung compres-sion and, occasionally, obtain a lung tissue biopsy
specimen.

PFTs
PFTs can measure either volume or capacity. These tests aid diagnosis in patients with
suspected respiratory dysfunction. The practitioner orders these tests to:
1. evaluate ventilatory function through spirometric measurements
2. determine the cause of dyspnea
3. assess the effectiveness of medications, such as bronchodilators and steroids
 4. determine whether a respiratory abnormality stems from an obstructive or restrictive
disease process
5. evaluate the extent of dysfunction.

Drug therapy
Drugs are used for airway management in such disorders as bron-chial asthma and
chronic bronchitis and may include: xanthines (theophylline and derivatives) and adrenergics to
dilate bronchial passages and reduce airway resistance, making it easier for the patient to breathe
and allowing sufficient ventilationcorticosteroids to reduce inflammation and make the airways
more responsive to bronchodilatorsantihistamines, antitussives, and expectorants to help
suppress coughing and mobilize secretionsantimicrobials to reduce or eliminate infective
organisms leukotrine receptor modifiers to help block the bronchoconstrictive effect of
leukotrinesantihistamines to block or reverse inflammation caused by sensitivity to allergens.

SURGERY

Tracheotomy
A tracheotomy provides an airway for an intubated patient who needs prolonged
mechanical ventilation and helps remove lower tracheobronchial secretions in a patient who
can’t clear them. It’s also performed in emergencies when endotracheal (ET) intubation isn’t
possible, to prevent an unconscious or paralyzed patient from aspirating food or secretions, and
to bypass upper airway obstruction due to trauma, burns, epiglottiditis, or a tumor.

Chest tube insertion

A chest tube may be required to help treat pneumothorax, hemothorax, empyema, pleural
effusion, or chylothorax. Inserted into the pleural space, the tube allows blood, fluid, pus, or air
to drain and allows the lungs to reinflate.

Thoracotomy
A thoracotomy is the surgical removal of all or part of a lung; it aims to spare healthy
lung tissue from disease. Lung excision may involve a pneumonectomy, lobectomy, segmental
resection, or wedge resection.

Inhalation therapy
Inhalation therapy uses carefully controlled ventilation techniques to help the patient
maintain optimal ventilation in the event of respiratory failure. Techniques include mechanical
ventilation, continuous positive airway pressure (CPAP), and oxygen therapy.

Mechanical ventilation
Mechanical ventilation corrects profoundly impaired ven-tilation, evidenced by
hypercapnia, hypoxia, and signs of respiratory distress (such as nostril flaring, intercostal
retractions, decreased blood pressure, and diaphoresis). Typically requiring an ET or
tracheostomy tube, it delivers up to 100% room air under positive pressure or oxygen- enriched
air in concentrations up to 100%.
CPAP
As its name suggests, CPAP ventilation maintains positive pres-sure in the airways
throughout the patient’s respiratory cycle. Originally delivered only with a ventilator, CPAP may
now be delivered to intubated or nonintubated patients through an artifi-cial airway, a mask, or
nasal prongs by means of a ventilator or a separate high-flow generating system.

Oxygen therapy
In oxygen therapy, oxygen is delivered by mask, nasal prongs, nasal catheter, or
transtracheal catheter to prevent or reverse hypoxemia and reduce the work of breathing.
Possible causes of hypoxemia include emphysema, pneumonia, Guillain-Barré syndrome, heart
failure, and myocardial infarction (MI).

Chest physiotherapy
Chest physiotherapy is usually performed with other treatments, such as suctioning,
incentive spirometry, and administration of such medications as small-volume nebulizer aerosol
treatments and expectorants. Recent studies indicate that percussional vibration isn’t an effective
treatment for most diseases; exceptions include cystic fibrosis and bronchiectasis. Improved
breath sounds, increased Pa O2, sputum production, and improved airflow suggest successful
treatment.

COMMON RESPIRATORY DISORDERS

Acute respiratory distress syndrome

A form of pulmonary edema that leads to ARF, acute respiratory distress syndrome
(ARDS) results from increased permeability of the alveolocapillary membrane. Although severe
ARDS may be fatal, recovering patients may have little or no permanent lung damage.

ARDS may result from:

1. aspiration of gastric contents , sepsis (primarily gram-negative), trauma (such as lung
contusion, head injury, and long-bone fracture with fat emboli)
2. oxygen toxicity, viral, bacterial, or fungal pneumonia, microemboli (fat or air emboli or
disseminated intra-vascular coagulation)
3. drug overdose (such as barbiturates and opioids)
4. blood transfusion •

Pathophysiology
In ARDS, fluid accumulates in the lung interstitium, alveolar s paces, and small
airways, causing the lung to stiffen. This impairs ventilation and reduces oxygenation of
pulmonary capillary blood.

Assess your patient for the following signs and symptoms:

1. rapid, shallow breathing; dyspnea; and hypoxemia
2. tachycardia
3. intercostal and suprasternal retractions, crackles, and rhonchi
4. restlessness, apprehension, mental sluggishness, and motor dysfunction.
Acute respiratory failure
When the lungs no longer meet the body’s metabolic needs, ARF results. In patients with
essentially normal lung tissue, ARF usually means PaCO2above 50 mm Hg and Pa O2 below 50
mm Hg. These limits, however, don’t apply to patients with COPD, who commonly have a
consistently high Pa CO2and low PaO2. In patients with COPD, only acute deterioration in ABG
values, with corresponding clinical deterioration, indicates ARF.

ARF may develop from any condition that increases the work of breathing and decreases
the respiratory drive. Respiratory tract infections, such as bronchitis and pneu-monia, are the
most common precipitating factors but bronchospasm or accumulated secretions due to cough
suppression can also lead to ARF. Other causes of ARF include:
1. CNS depression — head trauma or injudicious use of sedatives, narcotics, tranquilizers,
or oxygen
2. cardiovascular disorders — MI, heart failure, or pulmonary emboli
3. airway irritants — smoke or fumes

Pathophysiology
Respiratory failure results from impaired gas exchange, when the lungs don’t oxygenate
the blood adequately and fail to prevent car-bon dioxide retention. Any condition associated with
hypoventila-tion (a reduction in the volume of air moving into and out of the lung), V mismatch
(too little ventilation with normal blood flow or too little blood flow with normal ventilation), or
intrapulmo-nary shunting (right-to-left shunting in which blood passes from the heart’s right side
to its left without being oxygenated) can cause ARF if left untreated.

Patients with ARF experience hypoxemia and acidemia affecting all body organs,
especially the central nervous, respiratory, and cardiovascular systems. Although specific
symptoms vary with the underlying cause, you should always assess for:
1. altered respirations (increased, decreased, or normal rate; shallow, deep, or alternating
shallow and deep respirations; possible cyanosis; crackles, rhonchi, wheezes, or
diminished breath sounds on chest auscultation)
2. altered mentation (restlessness, confusion, loss of concentration, irritability,
tremulousness, diminished tendon reflexes, or papilledema)
3. cardiac arrhythmias (from myocardial hypoxia) tachycardia (occurs early in response to
low PaO2)
4. pulmonary hypertension (increased pressures on the right side of the heart, elevated
jugular veins, enlarged liver, and peripheral edema).

ARF is an emergency requiring immediate action to correct the underlying cause and restore
adequate pulmonary gas exchange. If significant respiratory acidosis persists, the patient may
require mechanical ventilation through an ET or a tracheostomy tube. If he doesn’t respond to
conventional mechanical ventilation, the practitioner may try HFV; prone positioning may also
help. Treatment routinely includes antibiotics for infection, bronchodilators and possibly
steroids.
Atelectasis
Atelectasis (collapsed or airless condition of all or part of the lung) may be chronic or
acute and commonly occurs to some degree in patients undergoing abdominal or thoracic
surgery. The prognosis depends on prompt removal of airway obstruction,
relief of hypoxia, and reexpansion of the collapsed lobules or lung.

Atelectasis may result from:

1. bronchial occlusion by mucus plugs (a common problem in heavy smokers or people
with COPD, bronchiectasis, or cystic fibrosis)
2. occlusion by foreign bodies
3. bronchogenic carcinoma
4. inflammatory lung disease
5. oxygen toxicity
6. pulmonary edema
7. any condition that inhibits full lung expansion or makes deep • breathing painful, such as
abdominal surgical incisions, rib frac-tures, tight dressings, obesity, and neuromuscular
disorders
8. prolonged immobility
9. mechanical ventilation using constant small tidal volumes without intermittent deep
breaths
10. CNS depression (as in drug overdose), which eliminates periodic sighing.

Pathophysiology
In atelectasis, incomplete expansion of lobules (clusters of alveoli) or lung segments
leads to partial or complete lung col-lapse. Because parts of the lung are unavailable for gas
exchange,

How it’s treated

Atelectasis is treated with incentive spirometry, chest percussion, postural drainage, and
frequent coughing and deep-breathing exercises. If these measures fail, bronchoscopy may help
remove secretions. Humidity and bronchodilators can improve mucocili-ary clearance and dilate
airways and are sometimes used with a nebulizer. Atelectasis secondary to an obstructing
neoplasm may require surgery or radiation therapy.

Bronchiectasis
An irreversible condition marked by chronic abnormal dilation of bronchi and destruction
of bronchial walls, bronchiectasis can occur throughout the tracheobronchial tree or can be
confined to one segment or lobe. However, it’s usually bilateral, involving the basilar segments
of the lower lobes. It affects people of both sexes and all ages.

Bronchiectasis may be caused by such conditions as:

1. cystic fibrosis
2. immunologic disorders
3. recurrent, inadequately treated bacterial respiratory tract infections such as TB, measles,
pneumonia, pertussis, or influenza
4. obstruction by a foreign body, tumor, or stenosis associated with recurrent infection
 5. inhalation of corrosive gas or repeated aspiration of gastric content into the lungs.

Pathophysiology
Bronchiectasis results from repeated damage of bronchial walls and abnormal
mucociliary clearance that causes breakdown of supportive tissue adjacent to the airways. This
disease has three forms: cylindrical (fusiform), varicose, and saccular (cystic).

Initially, bronchiectasis may not produce symptoms. Assess your patient for a chronic
cough that produces copious, foul-smelling, mucopurulent secretions, possibly totaling several
cupfuls daily (classic symptom). Other characteristic findings include:coarse crackles during
inspiration over involved lobes or segments, occasional wheezes, dyspnea, weight loss, malaise,
clubbing, recurrent fever, chills, and other signs of infection. •

Treatment for bronchiectasis includes:

1. antibiotics given by mouth or I.V. for 7 to 10 days or until sputum production decreases
bronchodilators, with postural drainage and chest percussion, to help remove secretions if
the patient has bronchospasm and thick, tenacious sputumbronchoscopy used
occasionally to aid removal of secretions oxygen therapy for hypoxemia lobectomy or
segmental resection for severe hemoptysis.

Chronic obstructive pulmonary disease

COPD is an umbrella term that could refer to emphysema and chronic bronchitis and,
more commonly, a combination of these conditions. Asthma was once classified as a type of
COPD and shares some of the same characteristics but it’s now considered a distinct chronic
inflammatory disorder. The most common chronic lung disease, COPD affects an estimated 30
million Ameri-cans, and its incidence is rising. It now ranks fourth among the major causes of
death in the United States.

COPD may result from:

1. cigarette smoking
2. recurrent or chronic respiratory tract infection
3. allergies
4. familial and hereditary factors such as alpha 1-antitrypsin defi-ciency.

Pathophysiology
Smoking, one of the major causes of COPD, impairs ciliary action and macrophage
function and causes inflammation in the airways, increased mucus production, destruction of
alveolar septa, and peribronchiolar fibrosis. Early inflammatory changes may reverse if the
patient stops smoking before lung disease becomes exten-sive.The mucus plugs and narrowed
airways trap air, as occurs in chronic bronchitis and emphysema, and the alveoli hyperinflate on
expiration. On inspiration, airways enlarge, allowing air to pass beyond the obstruction, but they
narrow on expiration, preventing gas flow. Air trapping (also called ball valving) occurs
commonly in asthma and chronic bronchitis.
What to look for
The typical COPD patient is asymptomatic until middle age, when the following signs
and symptoms may occur:
1. reduced ability to exercise or do strenuous work
2. productive cough
3. dyspnea with minimal exertion. •

Treatment for COPD aims to relieve symptoms and prevent

complications. Most patients receive beta-agonist bronchodila-tors (albuterol [Proventil HFA] or
salmeterol), anticholinergic bronchodilators (ipratropium [Atrovent]), and corticosteroids
(beclomethasone [Beconase AQ]). These drugs are usually given by metered dose inhaler.

Pleural effusion
Pleural effusion is an excess of fluid in the pleural space. Nor-mally this space contains a
small amount of extracellular fluid that lubricates the pleural surfaces. Increased production or
inadequate removal of this fluid results in transudative or exuda-tive pleural effusion. Empyema
is the accumulation of pus and necrotic tissue in the pleural space.

Transudative pleural effusion can stem from:

1. heart failure
2. hepatic disease with ascites
3. peritoneal dialysis
4. hypoalbuminemia
5. disorders resulting in overexpanded intravascular volume.
6. Exudative pleural effusion can stem from: TB, subphrenic abscess, esophageal rupture ,
pancreatitis, bacterial or fungal pneumonitis or empyema.

Pathophysiology
In transudative pleural effusion, excessive hydrostatic pressure or decreased osmotic
pressure allows excessive fluid to pass across intact capillaries, resulting in an ultrafiltrate of
plasma containing low concentrations of protein. In exudative pleural effusion, capil-laries
exhibit increased permeability, with or without changes in hydrostatic and colloid osmotic
pressures, allowing protein-rich fluid to leak into the pleural space. Empyema is usually
associated with infection in the pleural space.

Assess your patient for the following signs and symptoms:

1. dyspnea, dry cough
2. pleural friction rub
3. possible pleuritic pain that worsens with coughing or deep breathing
4. dullness on percussion
5. tachycardia, tachypnea
6. decreased chest motion and breath sounds. •
Pneumonia
Pneumonia is an acute infection of the lung parenchyma that com-monly impairs gas
exchange. The prognosis is usually good for people who have normal lungs and adequate host
defenses before the onset of pneumonia; however, bacterial pneumonia is the fifth leading cause
of death in debilitated patients. The disorder occurs in primary and secondary forms.

Pneumonia is caused by an infecting pathogen (bacterial or viral) or by a chemical or other

irritant (such as aspirated material). Certain predisposing factors increase the risk of pneumonia.
For bacterial and viral pneumonia, these include:
1. chronic illness and debilitation
2. cancer (particularly lung cancer)
3. abdominal and thoracic surgery
4. atelectasis, aspiration
5. colds or other viral respiratory infections
6. chronic respiratory disease, such as COPD, asthma, bronchiectasis, and cystic fibrosis
7. smoking, alcoholism
8. malnutrition
9. sickle cell disease
10. tracheostomy

Pathophysiology
In general, the lower respiratory tract can be exposed to patho gens by inhalation,
aspiration, vascular dissemination, or direct contact with contaminated equipment such as
suction catheters. After pathogens are inside, they begin to colonize and infection develops

The five cardinal signs and symptoms of early bacterial pneumo-nia are:
1. coughing
2. sputum production
3. pleuritic chest pain
4. shaking chills
5. fever.

Other signs vary widely, ranging from diffuse, fine crackles to signs of localized or extensive
consolidation and pleural effusion.

Antimicrobial therapy varies with the infecting agent. Therapy should be reevaluated early in
the course of treatment. Supportive measures include:
1. humidified oxygen therapy for hypoxemia
2. mechanical ventilation for respiratory failure
3. a high-calorie diet and adequate fluid intake
4. bed rest
5. an analgesic to relieve pleuritic chest pain.
Pneumothorax
In pneumothorax, air or gas accumulates between the parietal and visceral pleurae,
causing the lungs to collapse. The amount of air or gas trapped determines the degree of lung
collapse. In some cases, venous return to the heart is impeded, causing a life-threatening
condition called tension pneumothorax.

Spontaneous pneumothorax can result from:

1. ruptured congenital blebs
2. ruptured emphysematous bullae
3. tubercular or malignant lesions that erode into the pleural space
4. interstitial lung disease such as eosinophilic granuloma.

Traumatic pneumothorax can result from:

1. insertion of a central venous access device
2. thoracic surgery
3. thoracentesis or closed access device
4. penetrating chest injury
5. transbronchial biopsy. Tension pneumothorax can develop from either spontane-ous or
traumatic pneumothorax.

Spontaneous pneumothorax may not produce symptoms in mild cases, but profound
respiratory distress occurs in moderate to severe cases. Weak and rapid pulse, pallor, jugular vein
distention, and anxiety indicate tension pneumothorax. In most cases, look for these symptoms:
1. sudden, sharp, pleuritic pain
2. asymmetrical chest wall movement
3. shortness of breath
4. cyanosis
5. decreased or absent breath sounds over the collapsed lung
6. hyperresonance on the affected side
7. crackling beneath the skin on palpation (subcutaneous emphysema).

Treatment is conservative for spontaneous pneu-mothorax in cases where no signs of

increased pleural pressure appear, lung collapse is less than 30%, and the patient shows no
signsof dys-pnea or other indications of physiologic compro-mise. Such treatment consists of:
1. bed rest or activity as tolerated by the patient
2. careful monitoring of blood pressure, pulse rate, and respiration
3. oxygen administration
4. in some cases, needle aspiration of air with a large-bore needle attached to a syringe.
5. Conservative treatment for spon-taneous pneumotho-rax includes bed rest.

Pulmonary embolism and infarction

Pulmonary embolism is an obstruction of the pulmonary arterial bed by a dislodged
thrombus or foreign substance. Pulmonary infarction, or lung tissue death from a pulmonary
embolus, is sometimes mild and may not produce symptoms. However, when a massive
embolism occurs involving more than 50% obstruction of pulmonary arterial circulation, it can
be rapidly fatal.
Pulmonary embolism usually results from dislodged thrombi that originate in the leg veins. Other
less common sources of thrombi are the pelvic, renal, hepatic, and arm veins and the right side of
the heart.

Pathophysiology
Trauma, clot dissolution, sudden muscle spasm, intravascular pressure changes, or a
change in peripheral blood flow can cause the thrombus to loosen or fragmentize. Then the
thrombus — now called an embolus — floats to the heart’s right side and enters the lung through
the pulmonary artery. There, the embolus may dis-solve, continue to fragmentize, or grow.

Total occlusion of the main pulmonary artery is rapidly fatal; smaller or fragmented emboli
produce symptoms that vary with the size, number, and location of the emboli. Dyspnea is
usually the first symptom of pulmonary embolism and may be accompa-nied by anginal or sharp
pleuritic chest pain that worsens with inspiration. Other clinical features include tachycardia,
productive cough (sputum may be blood-tinged), and low-grade fever. Less common signs
include massive hemoptysis, splinting of the chest, and leg edema. A large embolus may produce
right-sided heart failure with cyanosis, syncope, and distended jugular veins. Signs of shock
(such as weak, rapid pulse and hypotension) and hypoxia (such as restlessness) may also occur.
Cardiac aus-cultation occasionally reveals a right ventricular third heart sound audible at the
lower sternum and increased intensity of a pulmo-nary component of the second heart sound.
Crackles and a pleural friction rub may be heard at the infarction site.

Treatment aims to maintain adequate car-diovascular and pulmo nary function as the
obstruction resolves and to prevent recurrence. Because most emboli resolve within 10 days,
treatment consists of oxygen therapy as needed and anticoagulation with heparin to inhibit new
thrombus for-mation.

Tuberculosis
TB is an acute or chronic infection characterized by pulmonary infiltrates and formation
of granulomas with caseation, fibrosis, and cavitation. The American Lung Association estimates
that active TB afflicts nearly 5 out of every 100,000 people. The prog-nosis is excellent with
correct treatment.

Mycobacterium tuberculosis is the major cause of TB. Other strains of mycobacteria may
also be involved. Several factors increase the risk of infection, including:
1. Gastrectomy
2. uncontrolled diabetes mellitus
3. Hodgkin’s disease
4. Leukemia
5. treatment with corticosteroid therapy or immunosuppressant therapy
6. silicosis
7. human immunodeficiency virus infection.
 In primary infection, the disease usually doesn’t produce symp-toms. However, it may
produce nonspecific signs and symptoms such as:
1. fatigue
2. cough
3. anorexia
4. weight loss
5. night sweats
6. low-grade fever.

In reinfection, the patient may experience cough, productive mucopurulent sputum, and chest
pain.

Antitubercular therapy with daily oral doses of isoniazid, rifampin (Rifadin), and
pyrazinamide (and sometimes with ethambutol [Myambutol] or streptomycin) for at least 6
months usually cures TB. After 2 to 4 weeks, the disease is typically no longer infectious, and
the patient can resume his normal lifestyle while continuing to take medication. The patient with
atypical myco-bacterial disease or drug-resistant TB may require second-line
drugs, such as capreomycin (Capastat), streptomycin, cycloserine (Seromycin), amikacin, and
quinolones.