Understanding the respiratory system
The respiratory system consists of two lungs, conducting airways, and associated blood vessels.
The major function of the respiratory system is gas exchange. During ventilation, air is taken into
the body on inhalation (inspiration) and travels through respiratory passages to the lungs. Oxygen
(O2) in the lungs replaces carbon dioxide (CO2) in the blood (at the alveoli) during perfusion, and
then CO2 is expelled from the body on exhalation (expiration).
Disease or trauma may interfere with the respiratory system’s vital work, affecting any of the
following structures and functions:
• conducting airways
• lungs
• breathing mechanics
• neurochemical control of ventilation.
Conducting airways
The conducting airways allow air into and out of structures within the
lung that perform gas exchange. The conducting airways include the
upper airway and the lower airway
Upper airway
The upper airway consists of the:
• nose • mouth
• pharynx
• larynx.
Going up
The upper airway allows air flow into and out of the lungs. It warms,
humidifies and filters inspired air and protects the lower airway from
foreign matter.
Blocked!
Upper airway obstruction occurs when the nose, mouth, pharynx, or larynx becomes partially or
totally blocked, cutting off the O2 supply. Several conditions can cause upper airway obstruction,
including trauma, tumors, and foreign objects.
If not treated promptly, upper airway obstruction can lead to hypoxemia (insufficient O2 in the
blood) and then progress quickly to severe hypoxia (lack of O2 available to body tissues), loss of
consciousness, and death.
Lower airway
The lower airway consists of:
• trachea
• right and left main stem bronchi
• five secondary bronchi
• bronchioles.
The lower airways facilitate gas exchange. Each bronchiole descends from a lobule and contains
terminal bronchioles, alveolar ducts, and alveoli. Terminal bronchioles are “anatomic dead
spaces” because they don’t participate in gas exchange. The alveoli are the chief units of gas
exchange.
On the defense
In addition to warming, humidifying, and filtering inspired air, the lower airway provides the
lungs with defense mechanisms, including:
• irritant reflex
• muco-ciliary system
• secretory immunity.
The irritant reflex is triggered when inhaled particles, cold air, or toxins stimulate irritant
receptors. Reflex bronchospasm then occurs to limit the exposure, followed by coughing, which
expels irritant.
The muco-ciliary system produces mucus, which traps foreign particles. Foreign matter is then
swept to the upper airway for expectoration.
Secretory immunity protects the lungs by releasing an antibody in the respiratory mucosal
secretions that initiates an immune response against antigens contacting the mucosa.
Blocked again!
Like the upper airway, the lower airway can become partially or totally blocked as a result of
inflammation, tumors, foreign bodies, bronchospasm, or trauma. This can lead to respiratory
distress and failure.
Lungs are air-filled, sponge-like organs. They’re divided into lobes (three lobes on the right, two
lobes on the left). The lungs contain about 300 million pulmonary alveoli, which are grapelike
clusters of air-filled sacs at the ends of the respiratory passages, where gas exchange takes place
by diffusion.
All about alveoli
Alveoli consist of type I and type II epithelial cells:
Type I cells form the alveolar walls, through which gas exchange occurs.
Type II cells produce surfactant, a lipid-type substance that coats the alveoli. During inspiration,
the alveolar surfactant allows the alveoli to expand uniformly. During expiration, the surfactant
prevents alveolar collapse.
Trading places: O2 and CO2
How much O2 and CO2 trade places in the alveoli? That depends largely on the amount of air in
the alveoli (ventilation) and the amount of blood in the pulmonary capillaries (perfusion). The
ratio of ventilation to perfusion is called the V /Q ratio. The V/ ratio expresses the effectiveness of
gas exchange.
For effective gas exchange, ventilation and perfusion must match as closely as possible. In normal
lung function, the alveoli receive air at a rate of about 4 L/minute while the capillaries supply
blood to the alveoli at a rate of about 5 L/minute, creating aV /Q ratio of 4:5 or 0.8.
Asthma
Asthma is a chronic reactive airway disorder that can present as an acute attack. It causes episodic
airway obstruction resulting from bronchospasms, increased mucus secretion, and mucosa edema.
Asthma is one type of COPD, a long-term pulmonary disease characterized by airflow resistance.
Chronic bronchitis and emphysema are other types of COPD.
It usually strikes early
Cases of asthma continue to rise. Children account for a high number of asthma sufferer. Twice as
many boys than girls are affected.
It’s a family affair
About one-third of patients develop asthma between ages 10 and 30. In this group, incidence is the
same in both sexes. About one third of all patients share the disease with at least one immediate family
member.
How it happens
In asthma, bronchial linings overreact to various triggers, causing episodic smooth-muscle spasms that
severely constrict the airways. Mucosal edema and thickened secretions further block the airways. (See
Understanding asthma.)
What causes the overreaction can be attributed to: genetics and environment.
It’s all in the genes
Genetically induced asthma is a sensitivity to specific external allergens, which include pollen,
animal dander, house dust or mold, kapok or feather pillows, food additives containing sulfites,
cockroach allergen (major allergen for inner-city children), and any other sensitizing substance.
Genetically induced asthma begins in childhood and is commonly accompanied by other
hereditary allergies, such as eczema and allergic rhinitis.
Environmentally speaking
Environmentally induced asthma is a reaction to internal, non-allergenic factors. Most episodes
occur after a severe respiratory tract infection, especially in adults. Other predisposing conditions
include irritants, emotional stress, fatigue, endocrine changes, temperature and humidity
variations, and exposure to noxious fumes, such as nitrogen dioxide, which is produced by tobacco
smoking among family members and inadequately vented stoves and heating appliances. Many
asthmatics, especially children, have both genetically induced and environmentally induced
asthma.
What to look for
Signs and symptoms vary depending on the severity of a patient’s asthma.
From mild…
Patients with mild asthma have adequate air exchange and are asymptomatic between attacks.
Mild asthma is classified as either mild intermittent asthma or mild persistent asthma. With mild
intermittent asthma, the patient experiences symptoms of cough, wheezing, chest tightness, or
difficulty breathing less than twice per week. Flare-ups are brief but may vary in intensity.
Nighttime symptoms occur less than twice per month.
In mild persistent asthma, symptoms of cough, wheezing, chest tightness, or difficulty breathing
occur three to six times per week. Flare-ups may affect the patient’s activity level. Nighttime
symptoms occur three or four times per month.
…to not so bad…
Patients with moderate persistent asthma have normal or below normal air exchange as well as
signs and symptoms that include cough, wheezing, chest tightness, or difficulty breathing daily.
Flare-ups may affect the patient’s level of activity. Nighttime symptoms occur five or more times
per month.
…to worse
Patients with severe persistent asthma have below-normal air exchange and experience continual
symptoms of cough, wheezing, chest tightness, and difficulty breathing. Their activity level is
greatly affected. Nighttime symptoms occur frequently.
Patients with any type of asthma may develop status asthmaticus, a severe acute attack that
doesn’t respond to conventional treatment. The patient will have signs and symptoms that include:
• marked respiratory distress
• marked wheezing or absent breath sounds
• pulsus paradoxus greater than 10 mm Hg
• chest wall contractions. (See Treating asthma, page 88.)
What tests tell you
• Pulmonary function tests reveal signs of obstructive airway disease, low-normal or decreased
vital capacity, and increased total lung and residual capacities. Pulmonary function may be normal
between attacks
• Serum immunoglobulin (Ig) E levels may increase from an allergic reaction.
• Complete blood count (CBC) with differential reveals increased eosinophil count.
• Chest X-rays can diagnose or monitor asthma’s progress and may show hyperinflation with areas
of atelectasis.
• ABG analysis detects hypoxemia and guides treatment.
• Skin testing may identify specific allergens.
• Bronchial challenge testing evaluates the clinical significance of allergens identified by skin
testing.
• Pulse oximetry may show a reduced SaO2 level.
Chronic bronchitis
Chronic bronchitis, a form of COPD, is inflammation of the bronchi caused by irritants or
infection. In chronic bronchitis, hypersecretion of mucus and chronic productive cough last for 3
months of the year and occur for at least 2 consecutive years. The distinguishing characteristic of
bronchitis is obstruction of airflow caused by mucus.
How it happens
Chronic bronchitis occurs when irritants are inhaled for a prolonged period. The result is
resistance in the small airways and severe V/Q imbalance that decreases arterial oxygenation.
Patients have a diminished respiratory drive, so they usually hypoventilate. Chronic hypoxia
causes the kidneys to produce erythropoietin. This stimulates excessive RBC production, leading
to polycythemia. Hemoglobin levels are high, but the amount of reduced hemoglobin that comes
in contact with O2 is low; therefore, cyanosis is evident.
What to look for
Signs and symptoms of advanced chronic bronchitis include:
• productive cough
• dyspnea
• cyanosis
• use of accessory muscles for breathing
• pulmonary hypertension.
The pressure is on
As pulmonary hypertension continues, right ventricular end
diastolic pressure increases. This leads to cor pulmonale (right
ventricular hypertrophy with right-sided heart failure). Heart
failure results in increased venous pressure, liver engorgement,
epigastric distress, and dependent edema.
What tests tell you
• Chest X-rays may show hyperinflation and increased bronchovascular markings.
• Pulmonary function tests indicate increased residual volume,
decreased vital capacity and forced expiratory flow.
• ABG analysis displays decreased PaO2 and normal or
increased PaCO2.
• Sputum culture may reveal many microorganisms and
neutrophils.
• ECG may show atrial arrhythmias; and, occasionally, right
ventricular hypertrophy.
• Pulse oximetry shows a decreased SaO2 level.
Pneumonia
Pneumonia is an acute infection of the lung parenchyma that commonly impairs gas exchange. It
occurs in both sexes and at all ages. It’s the leading cause of
death from infectious disease. The prognosis is good for
patients with normal lungs and adequate immune systems.
However, bacterial pneumonia is the leading cause of death
in debilitated patients.
How it happens
Pneumonia is classified three ways:
Origin—Pneumonia may be viral, bacterial, fungal, or
protozoal in origin.
Location—Bronchopneumonia involves distal
airways and alveoli; lobar pneumonia involves part of
a lobe or an entire lobe.
Type—Primary pneumonia results from inhalation or
aspiration of a pathogen, such as bacteria or a virus, and
includes pneumococcal and viral pneumonia; secondary
pneumonia may follow lung damage from a noxious
chemical or other insult or may result from hematogenous
spread of bacteria; aspiration pneumonia results from
inhalation of foreign matter, such as vomitus or food
particles, into the bronchi.
Colonial expansion
In general, the lower respiratory tract can be exposed to pathogens by inhalation, aspiration,
vascular dissemination, or direct contact with contaminated equipment such as suction catheters.
After pathogens get inside, they begin to colonize and infection develops.
Stasis report
In bacterial pneumonia, which can occur in any part of the lungs, an infection initially triggers
alveolar inflammation and edema. This produces an area of low ventilation with normal perfusion.
Capillaries become engorged with blood, causing stasis. As the alveolocapillary membrane breaks
down, alveoli fill with blood and exudate, resulting in atelectasis (lung collapse). In severe
bacterial infections, the lungs look heavy and liverlike— reminiscent of ARDS.
Virus attack!
In viral pneumonia, the virus first attacks bronchiolar epithelial cells. This causes interstitial
inflammation and desquamation. The virus also invades
bronchial mucous glands and goblet cells. It then spreads to the alveoli, which fill with blood and
fluid. In advanced infection, a hyaline membrane may form. Like bacterial infections, viral
pneumonia clinically resembles ARDS.
Subtracting surfactant
In aspiration pneumonia, inhalation of gastric juices or hydrocarbons triggers inflammatory
changes and also inactivates surfactant over a large area. Decreased surfactant leads to alveolar
collapse. Acidic gastric juices may damage the airways and alveoli. Particles containing aspirated
gastric juices may obstruct the airways
and reduce airflow, leading to secondary bacterial pneumonia.
Risky business
Certain predisposing factors increase the risk of pneumonia. For
bacterial and viral pneumonia, these include:
• chronic illness and debilitation
• cancer (particularly lung cancer)
• abdominal and thoracic surgery
• atelectasis
• colds or other viral respiratory infections
• chronic respiratory disease, such as COPD, bronchiectasis, or
cystic fibrosis
• influenza
• smoking
• malnutrition
• alcoholism
• exposure to noxious gases
• aspiration
• immunosuppressive therapy
• premature birth.
Aspiration pneumonia is more likely to occur in elderly or debilitated patients, those receiving
nasogastric tube feedings, and those with an impaired gag reflex, poor oral hygiene, or a decreased
level of consciousness.
What tests tell you
• Chest X-rays confirm the diagnosis by disclosing infiltrates.
• Sputum specimen, Gram stain, and culture and sensitivity tests help differentiate the typemof
infection and the drugs that are effective in treatment.
• WBC count indicates leukocytosis in bacterial pneumonia and a normal or low count in viral or
mycoplasmal pneumonia.
• Blood cultures reflect bacteremia and are used to determine the causative organism.
• ABG levels vary, depending on the severity of pneumonia and the underlying lung state.
• Bronchoscopy or transtracheal aspiration allows the collection of material for culture.
• Pulse oximetry may show a reduced SaO2 level.
Pneumothorax
Pneumothorax is an accumulation of air in the pleural cavity that leads to partial or complete lung
collapse. When the amount of air between the visceral and parietal pleurae increases, increasing
tension in the pleural cavity can cause the lung to progressively collapse. In some cases, venous
return to the heart is impeded, causing a life-threatening condition called tension pneumothorax.
Spontaneous or traumatic?
Pneumothorax is classified as either traumatic or spontaneous.
Traumatic pneumothorax may be further classified as open (sucking chest wound) or closed (blunt
or penetrating trauma). Note that an open (penetrating) wound may cause closed pneumothorax if
communication between the atmosphere and the
pleural space seals itself off. Spontaneous pneumothorax, which is also considered closed, can be
further classified as primary (idiopathic) or secondary (related to a specific disease).
How it happens
The causes of pneumothorax vary according to classification.
Traumatic pneumothorax
A penetrating injury, such as a stab wound, a gunshot wound, or an impaled object, may cause
traumatic open pneumothorax, traumatic closed pneumothorax, or hemothorax (accumulation of
blood in the pleural cavity).
Blunt trauma from a car accident, a fall, or a crushing chest injury may also cause traumatic closed
pneumothorax or hemothorax.
Traumatic pneumothorax may also result from:
• insertion of a central line
• thoracic surgery
• thoracentesis
• pleural or transbronchial biopsy
• tracheotomy.
Tension pneumothorax can develop from either spontaneous or traumatic pneumothorax.
A change in atmosphere
Open pneumothorax results when atmospheric air (positive pressure) flows directly into the
pleural cavity (negative pressure). As the air pressure in the pleural cavity becomes positive, the
lung collapses on the affected side. Lung collapse leads to decreased total lung capacity. The
patient then develops V/Q imbalance leading to hypoxia.
A leak within the lung
Closed pneumothorax occurs when air enters the pleural space from within the lung. This causes
increased pleural pressure and prevents lung expansion during inspiration. It may be called
traumatic pneumothorax when blunt chest trauma causes lung tissue to rupture, resulting in air
leakage.
Rupture!
Spontaneous pneumothorax is a type of closed pneumothorax. It’s more common in men and in
older patients with chronic pulmonary disease. However, it also occurs in healthy young adults.
The usual cause is rupture of a subpleural bleb (a small cystic space) at the surface of the lung.
This causes air leakage into the pleural spaces; then the lung collapses, causing decreased total
lung capacity, vital capacity, and lung compliance—leading, in turn, to hypoxia. The total amount
of lung collapse can range from 5% to 95%.
What to look for
Although the causes of traumatic and spontaneous pneumothorax vary greatly, the effects are
similar. The cardinal signs and symptoms of pneumothorax include:
• sudden, sharp, pleuritic pain exacerbated by chest movement, breathing, and coughing
• asymmetric chest wall movement
• shortness of breath
• cyanosis
• hyperresonance or tympany heard with percussion
• respiratory distress.
The signs and symptoms of open pneumothorax also include:
• absent breath sounds on the affected side
• chest rigidity on the affected side
• tachycardia
• subcutaneous emphysema (air in the tissues) causing crackling beneath the skin upon palpation.
Tension pneumothorax produces the most severe respiratory symptoms, including:
• decreased cardiac output
• hypotension
• compensatory tachycardia
• tachypnea
• lung collapse due to air or blood in the intrapleural space
• mediastinal shift and tracheal deviation to the opposite side
• cardiac arrest. (See Treating pneumothorax.)
What tests tell you
• Chest X-rays confirm the diagnosis by revealing air in the pleural space and, possibly, a
mediastinal shift.
• ABG studies may show hypoxemia, possibly with respiratory acidosis and hypercapnia. SaO2
levels may decrease at first but typically return to normal within 24 hours.
• Pulse oximetry reveals hypoxemia.
Pulmonary edema
Pulmonary edema is a common complication of cardiac disorders. It’s marked by accumulated
fluid in the extravascular spaces of the lung. It may occur as a chronic condition or develop
quickly and rapidly become fatal.
How it happens
Pulmonary edema may result from left-sided heart failure caused by arteriosclerotic,
cardiomyopathic, hypertensive, or valvular heart disease.
Off balance
Normally, pulmonary capillary hydrostatic pressure, capillary permeability, and lymphatic
drainage are in balance. This prevents fluid infiltration to the lungs. When this balance changes, or
the lymphatic drainage system is obstructed, pulmonary edema results. If colloid osmotic pressure
decreases, the hydrostatic force
that regulates intravascular fluids is lost because nothing opposes it. Fluid flows freely into the
interstitium and alveoli, impairing gas exchange and leading to pulmonary edema.
What to look for
Signs and symptoms vary with the stage of pulmonary edema. Generally they include:
• dyspnea on exertion
• paroxysmal nocturnal dyspnea
orthopnea
• tachypnea
• increased then de4creased blood pressure
• dependent crackles
jugular vein distention
• diastolic S3 gallop
• cough producing frothy, bloody sputum
• arrhythmias
• cold, clammy skin
• diaphoresis
• cyanosis
• thready pulse. (See Treating pulmonary edema.)
What tests tell you
• ABG analysis usually shows hypoxia with variable PaCO2
• Chest X-rays show diffuse haziness of the lung fields and, usually, cardiomegaly and pleural
effusion.
• Pulse oximetry may reveal decreasing SaO2 levels.
• Pulmonary artery catheterization identifies left-sided heart failure and helps rule out ARDS.
• ECG may show previous or current myocardial infarction (MI).
Treatment for pulmonary edema has three aims:
1. reducing extravascular fluid
2. improving gas exchange and myocardial function
3. correcting the underlying disease, if possible.
Treatments include:
• high concentrations of oxygen (O2) administered by nasal cannula (the patient usually can’t
tolerate a mask)
• diuretics, such as furosemide to increase urination, which helps mobilize extravascular fluid
• positive inotropic agents, such as digoxin, milrinone, and inamrinone,
to enhance contractility in myocardial dysfunction
• pressor agents to enhance contractility and promote vasoconstriction
in peripheral vessels
• antiarrhythmics for arrhythmias related to decreased cardiac output
• arterial vasodilators, such as nitroprusside, to decrease peripheral vascular resistance, preload,
and afterload
• morphine to reduce anxiety and dyspnea and dilate the systemic venous bed, promoting blood
flow from pulmonary circulation to the periphery