Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute)
o Change in compliance reflexively stimulates the
RESPIRATORY FAILURE
Respiratory failure is an alteration in the function of the respiratory
system that causes the partial pressure of arterial oxygen (Pao 2) to
fall below 50 mm Hg (hypoxemia) and/or the partial pressure of
arterial carbon dioxide (Paco2) to rise above 50 mm Hg
(hypercapnia), as determined by arterial blood gas (ABG) analysis.
Respiratory failure is classified as acute, chronic, or combined acute
and chronic.
Classification
Acute Respiratory Failure
 Characterized by hypoxemia (Pao2 less than 50 mm Hg)
and/or hypercapnia (Paco2 greater than 50 mm Hg) and
acidemia (pH less than 7.35).
 Occurs rapidly, usually in minutes to hours or days.
Chronic Respiratory Failure
 Characterized by hypoxemia (decreased Pao 2) and/or
hypercapnia (increased Paco2) with a normal pH (7.35 to
7.45).
 Occurs over a period of months to years allows for
activation of compensatory mechanisms.
Acute and Chronic Respiratory Failure
 Characterized by an abrupt increase in the degree of
hypoxemia or hypercapnia in patients with preexisting
chronic respiratory failure.
 May occur after an acute upper respiratory infection or
pneumonia, or without obvious cause.
 Extent of deterioration is best assessed by comparing the
patient's present ABG levels with previous ABG levels
(patient normals).
Pathophysiology and Etiology
Oxygenation Failure
Characterized by a decrease in Pao2 and normal or decreased Paco2.
 Primary problem is inability to adequately oxygenate the
blood, resulting in hypoxemia.
 Hypoxemia occurs because damage to the alveolar-
capillary membrane causes leakage of fluid into the
interstitial space or into the alveoli and slows or prevents
movement of oxygen from the alveoli to the pulmonary
capillary blood.
o Typically, this damage is widespread, resulting in
many areas of the lung being poorly ventilated or
nonventilated.
o Consequences are severe ventilation-perfusion
imbalance and shunt.
 Hypocapnia results from hypoxemia and decreased
pulmonary compliance. Fluid within the lungs makes the
lung less compliant or stiffer.
mikEL rlh mantong
increased ventilation.
o Ventilation is also increased as a response to
hypoxemia.
o Ultimately, if treatment is unsuccessful, the Paco 2
will increase, and the patient will experience both
an increase in Paco2 and a decrease in Pao2.
 Etiology includes:
o Cardiogenic pulmonary edema (left ventricular
failure; mitral stenosis).
o Acute respiratory distress syndrome (ARDS).
Underlying causes of ARDS include shock of any
etiology; infectious causes, such as gram-negative
sepsis, viral pneumonia, bacterial pneumonia;
trauma, such as fat emboli, head injury, lung
contusion; aspiration of gastric fluid, near
drowning; inhaled toxins, such as oxygen in high
concentrations, smoke, corrosive chemicals;
hematologic conditions, such as massive
transfusions, post-cardiopulmonary bypass; and
metabolic disorders, such as pancreatitis, uremia.
Ventilatory Failure with Normal Lungs
Characterized by a decrease in Pao2, increase in Paco2, and a
decrease in pH.
 Primary problem is insufficient respiratory center
stimulation or insufficient chest wall movement, resulting
in alveolar hypoventilation.
 Hypercapnia occurs because impaired neuromuscular
function or chest wall expansion limits the amount of
carbon dioxide removed from the lungs.
o Primary problem is not the lungs. The patient's
minute ventilation (tidal volume times the number
of breaths per minute) is insufficient to allow
normal alveolar gas exchange.
 The carbon dioxide (CO 2) not excreted by the lungs
combines with water (H2O) to form carbonic acid (H2CO3).
This predisposes to acidemia and a fall in pH.
 Hypoxemia occurs as a consequence of hypercapnia. When
the Paco2 rises, the Pao2 must fall unless increased amounts
of oxygen are added to the inspired air.
 Etiology includes:
o Insufficient respiratory center activity (drug
intoxication, such as opioid overdose, general
anesthesia; vascular disorders, such as cerebral
vascular insufficiency, brain tumor; trauma, such
as head injury, increased intracranial pressure).
o Insufficient chest wall function (neuromuscular
disease, such as Guillain-Barré, myasthenia
gravis, poliomyelitis; trauma to the chest wall
resulting in multiple fractures; spinal cord trauma;
kyphoscoliosis).
Ventilatory Failure with Intrinsic Lung Disease
Characterized by a decrease in Pao2 and decreased pH.
 Primary problem is acute exacerbation or chronic
progression of previously existing lung disease, resulting in
CO2 retention.
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute)
 Hypercapnia occurs because damage to the lung
parenchyma and/or airway obstruction limits the amount
of CO2 removed by the lungs.
o Primary problem is preexisting lung disease usually
chronic bronchitis, emphysema, or severe asthma.
This limits CO2 removal from the lungs.
 The CO2 not excreted by the lungs combines with H 2O to
form H2CO3. This predisposes to acidemia and a fall in pH.
 Hypoxemia occurs as a consequence of hypercapnia. In
addition, damage to the lung parenchyma and/or airway
obstruction limits the amount of oxygen that enters the
pulmonary capillary blood.
 Etiology includes:
o Chronic obstructive pulmonary disease (COPD)
(chronic bronchitis, emphysema).
o Severe asthma.
o Cystic fibrosis.
Clinical Manifestations
 Hypoxemia restlessness, agitation, dyspnea, disorientation,
confusion, delirium, loss of consciousness.
 Hypercapnia headache, somnolence, dizziness, confusion.
 Tachypnea initially; then when no longer able to
compensate, bradypnea
 Accessory muscle use
 Asynchronous respirations
Diagnostic Evaluation
 ABG analysis show changes in Pao2, Paco2, and pH from
patient's normal; or Pao2 less than 50 mm Hg, Paco 2 greater
than 50 mm Hg, pH less than 7.35.
 Pulse oximetry decreasing Sao2.
 End tidal CO2 monitoring elevated.
 Complete blood count, serum electrolytes, chest X-ray,
urinalysis, electrocardiogram (ECG), blood and sputum
cultures to determine underlying cause and patient's
condition.
Management
 Oxygen therapy to correct the hypoxemia.
 Chest physical therapy and hydration to mobilize
secretions.
 Bronchodilators and possibly corticosteroids to reduce
bronchospasm and inflammation.
 Diuretics for pulmonary congestion.
 Mechanical ventilation as indicated. Noninvasive positive-
pressure ventilation using a face mask may be a successful
option for short-term support of ventilation.
Complications
 Oxygen toxicity if prolonged high Fio2 required.
 Barotrauma from mechanical ventilation intervention
mikEL rlh mantong
Nursing Assessment
 Note changes suggesting increased work of breathing
(tachypnea, diaphoresis, intercostal muscle retraction,
fatigue) or pulmonary edema (fine, coarse crackles or rales,
frothy pink sputum).
 Assess breath sounds.
o Diminished or absent sounds indicate inability to
ventilate the lungs sufficiently to prevent
atelectasis.
o Crackles indicate ineffective airway clearance, fluid
in the lungs.
o Wheezing indicates narrowed airways and
bronchospasm.
o Rhonchi and crackles indicate ineffective secretion
clearance.
 Assess level of consciousness (LOC) and ability to tolerate
increased work of breathing.
o Confusion, rapid shallow breathing, abdominal
paradox (inward movement of abdominal wall
during inspiration), and intercostal retractions
suggest inability to maintain adequate minute
ventilation.
 Assess for signs of hypoxemia and hypercapnia.
 Determine vital capacity (VC), respiratory rate, and
negative inspiratory force (NIF) and compare with values
indicating need for mechanical ventilation:
o VC < 10 to 15 mL/kg.
o Respiratory rate > 35 breaths/minute.
o NIF < 15 to 25 cm H2O.
 Analyze ABG and compare with previous values.
o If the patient cannot maintain a minute ventilation
sufficient to prevent CO2 retention, pH will fall.
o Mechanical ventilation or noninvasive ventilation
may be needed if pH falls to 7.30 or below.
 Determine hemodynamic status (blood pressure,
pulmonary wedge pressure, cardiac output, Svo 2) and
compare with previous values. If patient is on mechanical
ventilation and positive end-expiratory pressure (PEEP),
venous return may be limited, resulting in decreased
cardiac output.
Nursing Diagnoses
 Impaired Gas Exchange related to inadequate respiratory
center activity or chest wall movement, airway obstruction,
and/or fluid in lungs
 Ineffective Airway Clearance related to increased or
tenacious secretions
Nursing Interventions
Improving Gas Exchange
 Administer antibiotics, cardiac medications, and diuretics as
ordered for underlying disorder.
 Administer oxygen to maintain Pao2 of 60 mm Hg or Sao2 >
90% using devices that provide increased oxygen
concentrations (aerosol mask, partial rebreathing mask,
nonrebreathing mask).
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute)
 Monitor fluid balance by intake and output measurement,
urine specific gravity, daily weight, and direct measurement
of pulmonary capillary wedge pressure to detect presence
of hypovolemia or hypervolemia.
 Provide measures to prevent atelectasis and promote chest
expansion and secretion clearance, as ordered (incentive
spirometer, nebulization, head of bed elevated 30 degrees,
turn frequently, out of bed).
 Monitor adequacy of alveolar ventilation by frequent
measurement of respiratory rate, VC, inspiratory force, and
ABG levels.
 Compare monitored values with criteria indicating need for
mechanical ventilation (see section titled Nursing
Assessment). Report and prepare to assist with noninvasive
ventilation or intubation and initiation of mechanical
ventilation, if indicated.
STANDARDS OF CARE GUIDELINES
Respiratory Compromise
When caring for patients at risk for respiratory compromise,
consider the following assessments and interventions:
 Be aware of the status of the patient when assuming care
so comparison can be made with subsequent assessments.
 Perform thorough systematic assessment, including mental
status, vital signs, respiratory status, and cardiovascular
status.
 Document patient's condition to provide a record for
continuity of care.
 Evaluate for signs of hypoxia when anxiety, restlessness,
confusion, or aggression of new onset are noted. Do not
administer sedatives unless hypoxia has been ruled out by
performing respiratory assessment.
 Notify appropriate health care provider of significant
findings of hypoxia cyanosis, circumoral pallor, rapid and
shallow respirations, abnormal breath sounds, change in
behavior or level of consciousness. Request assessment
and intervention by health care provider as indicated.
 Use extreme caution in administering sedatives and opioids
to patients at risk for respiratory compromise.
Maintaining Airway Clearance
 Administer medications to increase alveolar ventilation
bronchodilators to reduce bronchospasm, corticosteroids
to reduce airway inflammation.
 Perform chest physiotherapy to remove mucus. Teach
slow, pursed-lip breathing to reduce airway obstruction.
 Administer I.V. fluids and mucolytics to reduce sputum
viscosity.
 Suction patient as needed to assist with removal of
secretions.
 If the patient becomes increasingly lethargic, cannot cough
or expectorate secretions, cannot cooperate with therapy,
or if pH falls below 7.30, despite use of the above therapy,
report and prepare to assist with intubation and initiation
of mechanical ventilation.
Patient Education and Health Maintenance
 Instruct patient with preexisting pulmonary disease to seek
early intervention for infections to prevent acute
respiratory failure.
mikEL rlh mantong
 Teach patient about medication regimen.
o Proper technique for inhaler use
o Dosage and timing of medications
o Monitoring for adverse effects of corticosteroids:
weight gain due to fluid retention, polyuria and
polydipsia due to hyperglycemia, mood changes;
report to health care provider
Community and Home Care Considerations
 Encourage patients at risk, especially the elderly and those
with preexisting lung disease, to get yearly influenza
immunizations and pneumococcal pneumonia
immunization.
o Pneumococcal vaccine is 60% to 70% effective in
preventing bacteremic pneumococcal infections in
adults and children at least age 2 years.
o If a person received their first pneumococcal
vaccination before age 65, they should be
revaccinated at age 65, if more than 5 years have
elapsed since the previous dose.
 Vaccinate people over age 2 and with the following
conditions for pneumococcal pneumonia, as recommended
by the Centers for Disease Control and Prevention (CDC):
o Chronic cardiovascular disease (including heart
failure).
o Chronic pulmonary disease (eg, emphysema).
o Diabetes.
o Alcoholism.
o Chronic liver disease (including cirrhosis).
o Cerebrospinal fluid leaks.
o Asplenia (including functional asplenia such as
sickle cell disease).
o Immunocompromised people (including human
immunodeficiency virus [HIV]).
o People living in environments at higher risk for
pneumococcal disease (Alaskan natives, certain
American Indian populations, and residents of
nursing homes and long-term care facilities).
 Immunize annually for influenza in the following groups,
according to the CDC:
o People age 50 and older
o Immunocompromised patients
o Residents of nursing homes or chronic care
facilities
o People with cardiovascular disease
o People with diabetes mellitus
o Patients receiving long-term aspirin therapy
o Pregnant women who will be in the second or
third trimester of pregnancy during flu season
o Health care workers
o Household contacts of people at risk
Evaluation: Expected Outcomes
 ABG values within patient's normal limits
 Decreased secretions; lungs clear
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute)
ACUTE RESPIRATORY DISTRESS
SYNDROME
ARDS is a clinical syndrome also called noncardiogenic pulmonary
edema in which there is severe hypoxemia and decreased
compliance of the lungs, which leads to both oxygenation and
ventilatory failure. Mortality is 50% to 60% but is improved with
early intervention.
Pathophysiology and Etiology
 Pulmonary and/or nonpulmonary insult to the alveolar-
capillary membrane causing fluid leakage into interstitial
spaces.
 Ventilation-perfusion ([V with dot above]/[Q with dot
above]) mismatch caused by shunting of blood (see Figure
11-1).
 Etiologies are numerous and can be pulmonary or
nonpulmonary. These include (but are not limited to):
o Pneumonia, sepsis, aspiration.
o Shock (any cause), trauma.
o Metabolic, hematologic, and immunologic
disorders.
o Inhaled agents smoke, high concentration of
oxygen, corrosive substances.
o Major surgery, fat or air embolism.
mikEL rlh mantong
Clinical Manifestations
 Severe dyspnea, use of accessory muscles.
 Increasing requirements of oxygen therapy. Hypoxemia
refractory to supplemental oxygen therapy.
 Severe crackles and rhonchi heard on auscultation.
Diagnostic Evaluation
 The hallmark sign for ARDS is a shunt; hypoxemia remains
despite increasing oxygen therapy.
 Decreased lung compliance; increasing pressure required
to ventilate patient on mechanical ventilation.
 Chest X-ray exhibits bilateral infiltrates.
 Pulmonary artery catheter readings: pulmonary artery
wedge pressure >18 mm Hg.
Management
 The underlying cause for ARDS must be determined so
appropriate treatment can be initiated.
 Ventilatory support with PEEP will be instituted. PEEP keeps
the alveoli open, thereby improving gas exchange.
Therefore, a lower oxygen concentration (Fio 2) can be used
to maintain satisfactory oxygenation.
 Fluid management must be maintained. The patient may
be hypovolemic due to the movement of fluid into the
interstitium of the lung. Pulmonary artery catheter
monitoring and inotropic medication can be helpful.
 Medications are aimed at treating the underlying cause.
Corticosteroids are used infrequently due to the
controversy regarding benefits of usage.
 Adequate nutrition should be initiated early and
maintained.
Complications
 Infections, such as pneumonia, sepsis.
 Respiratory complications, such as pulmonary emboli,
barotrauma, oxygen toxicity, subcutaneous emphysema, or
pulmonary fibrosis.
 GI complications, such as stress ulcer, ileus.
 Cardiac complications, such as decreased cardiac output
and dysrhythmias.
 Renal failure, disseminated intravascular coagulation.
Nursing Interventions
 Care is similar to patient with respiratory failure (page 281)
and pulmonary edema (page 416). Also see Mechanical
Ventilation, page 261.
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute)
ACUTE BRONCHITIS
Acute bronchitis is an infection of the lower respiratory tract that is
generally an acute sequela to an upper respiratory tract infection.
Pathophysiology and Etiology
 Primarily viral etiology, but may also arise from bacterial
agents.
 Airways become inflamed and irritated with increased
mucous production.
Clinical Manifestations
 Dyspnea, fever, tachypnea.
 Productive cough, clear to purulent sputum.
 Pleuritic chest pain, occasionally.
 Diffuse rhonchi and crackles heard on auscultation.
Management
 Antibiotic therapy for 7 to 10 days may be indicated for
patients with underlying respiratory problems or chronic
illness.
 Hydration and humidification.
 Secretion clearance interventions (controlled cough,
positive expiratory pressure valve therapy, chest physical
therapy).
 Bronchodilators for bronchospastic cough and bronchial
irritation.
 Symptom management for fever, cough.
Nursing Assessment
 Obtain history of upper airway infection, course and length
of symptoms.
 Assess severity of cough and characteristics of sputum
production.
 Auscultate chest for diffuse rhonchi and crackles as
opposed to localized crackles usually heard with
pneumonia.
Nursing Diagnosis
 Ineffective Airway Clearance related to sputum production
Nursing Interventions
Establishing Effective Airway Clearance
 Administer or teach self-administration of antibiotics as
ordered.
 Encourage mobilization of secretions, through hydration,
chest physical therapy, and coughing. Educate patient that
beverages with caffeine or alcohol do not promote
hydration because of their diuretic effect.
 If ordered, administer or teach self-administration of
inhaled bronchodilators to reduce bronchospasm and
enhance secretion clearance.
 Caution patients on the use of over-the-counter cough
suppressants, antihistamines, and decongestants that may
cause drying and retention of secretions. Cough
preparations containing the mucolytic guaifenesin may be
appropriate.
mikEL rlh mantong
Patient Education and Health Maintenance
 Instruct patient about medication regimen, including the
completion of the full course of antibiotics prescribed and
the effects of food on the absorption of the medications. If
patient is not being treated with antibiotics, assure patient
that the majority of cases of people recover from bronchitis
without antibiotic treatment.
 Encourage patient to seek medical attention for shortness
of breath and worsening condition.
 Advise patient that a dry cough may persist after bronchitis
due to irritation of the airways. A bedside humidifier and
avoidance of dry environments may help.
 Encourage patient to discuss alternative therapies with
health care provider. Some people use garlic as an
antimicrobial because it is believed to have antibacterial
and antiviral activity due to the antiseptic oil, which is
excreted through the lungs. It may also be helpful as part of
a broader approach to bronchitic asthma. Other herbs
believed to have antimicrobial activity for bronchitis are
echinacea, eucalyptus, and thyme. The antiseptic volatile
oils contained in eucalyptus and thyme can also be used in
the form of inhalations or baths.
Evaluation: Expected Outcomes
 Coughs up clear secretions effectively
PNEUMONIA
Pneumonia is an inflammatory process, involving the terminal
airways and alveoli of the lung, caused by infectious agents (see
Table 11-1, pages 288 to 291). It is classified according to its
causative agent.
Pathophysiology and Etiology
 The organism gains access to the lungs through aspiration
of oropharyngeal contents, by inhalation of respiratory
secretions from infected individuals, by way of the
bloodstream, or from direct spread to the lungs as a result
of surgery or trauma.
 Patients with bacterial pneumonia may have an underlying
disease that impairs host defense; pneumonia arises from
endogenous flora of the person whose resistance has been
altered, or from aspiration of oropharyngeal secretions.
o Immunocompromised patients include those
receiving corticosteroids or immunosuppressants,
those with cancer, those being treated with
chemotherapy or radiotherapy, those undergoing
organ transplantation, alcoholics, I.V. drug
abusers, and those with HIV disease and acquired
immunodeficiency syndrome.
o These people have an increased risk of developing
overwhelming infection. Infectious agents include
aerobic and anaerobic gram-negative bacilli;
Staphylococcus; Nocardia; fungi; Candida; viruses,
such as cytomegalovirus; Pneumocystis carinii
(also known as P. jiroveci); reactivation of
tuberculosis (TB); and others.
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute) mikEL rlh mantong
 When bacterial pneumonia occurs in a healthy person, procedures, seriously ill or debilitated patients,
there is usually a history of preceding viral illness. abnormalities of gag and swallowing reflexes
 Other predisposing factors include conditions interfering o NG tube feedings
with normal drainage of the lung, such as tumor, general o Obstetric patients from general anesthesia,
anesthesia, and postoperative immobility; depression of lithotomy position, delayed emptying of stomach
the central nervous system (CNS) from drugs, neurologic from enlarged uterus, labor contractions
disorders, or other conditions, such as alcoholism, and o GI conditions hiatal hernia, intestinal obstruction,
intubation or respiratory instrumentation. abdominal distention
 Pneumonia may be divided into three groups:  Effects of aspiration depend on volume and character of
o Community acquired, due to a number of aspirated material
organisms, including Streptococcus pneumoniae o Particulate matter mechanical blockage of airways
o Hospital or nursing home acquired (nosocomial), and secondary infection
due primarily to gram-negative bacilli and o Anaerobic bacterial aspiration from oropharyngeal
staphylococci secretions
o Pneumonia in the immunocompromised person o Gastric juice destructive to alveoli and capillaries;
 People over age 65 have a high mortality, even with results in outpouring of protein-rich fluids into the
appropriate antimicrobial therapy. interstitial and intra-alveolar spaces (Impairs
exchange of oxygen and CO2, producing
Clinical Manifestations hypoxemia, respiratory insufficiency, and
For most common forms of bacterial pneumonia: respiratory failure.)
 Sudden onset; shaking chill; rapidly rising fever of 101° F to Clinical Manifestations
105° F (38.3° C to 40.5° C).
 Cough productive of purulent sputum.  Tachycardia, fever.
 Pleuritic chest pain aggravated by respiration/coughing  Dyspnea, cough, tachypnea.
 Dyspnea, tachypnea accompanied by respiratory grunting,  Cyanosis
nasal flaring, use of accessory muscles of respiration,  Crackles, rhonchi, wheezing
fatigue  Pink, frothy sputum (may simulate acute pulmonary
 Rapid, bounding pulse edema)

Management Diagnostic Evaluation

 Antimicrobial therapy depends on laboratory identification
of causative organism and sensitivity to specific
antimicrobials, or presumptive therapy with broad
spectrum agent in milder cases.
 Oxygen therapy if patient has inadequate gas exchange
Complications
 Pleural effusion.
 Sustained hypotension and shock, especially in gram-
negative bacterial disease, particularly in elderly patients.
 Superinfection: pericarditis, bacteremia, and meningitis.
 Delirium this is considered a medical emergency.
 Atelectasis due to mucous plugs.
 Delayed resolution.
ASPIRATION PNEUMONIA
Aspiration is the inhalation of oropharyngeal secretions and/or
stomach contents into the lungs. It may produce an acute form of
pneumonia.
Pathophysiology and Etiology
 Chest X-ray may be normal initially; with time, shows
consolidation and other abnormalities.
Management
Depends on the material aspirated.
 Clearing the obstructed airway.
o If foreign body is visible, it may be removed
manually.
o Place the patient in tilted head-down position on
right side (right side more commonly affected if
patient has aspirated solid particles).
o Suction trachea/ET tube to remove particulate
matter.
 Laryngoscopy/bronchoscopy if patient has been
asphyxiated by solid material.
 Fluid volume replacement for correction of hypotension.
 Antimicrobial therapy if there is evidence of superimposed
bacterial infection.
 Correction of acidosis; respiratory acidosis and metabolic
acidosis indicate a severe reaction due to aspiration of
gastric contents.
 Oxygen therapy and assisted ventilation if adequate ABG
values cannot be maintained.

 Patients at risk and factors associated with risk: Complications

o Loss of protective airway reflexes (swallowing,  Lung abscess; empyema.
cough) caused by altered state of consciousness,  Necrotizing pneumonia
alcohol or drug overdose, during resuscitation
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute)
PULMONARY EMBOLISM
Pulmonary embolism refers to the obstruction of one or more
pulmonary arteries by a thrombus (or thrombi) originating usually in
the deep veins of the legs, the right side of the heart or, rarely, an
upper extremity, which becomes dislodged and is carried to the
pulmonary vasculature.
Pulmonary infarction refers to necrosis of lung tissue that can result
from interference with blood supply.
Pathophysiology and Etiology
 Obstruction, either partial or full, of pulmonary arteries,
which causes decrease or absent blood flow; therefore,
there is ventilation but no perfusion ([V with dot above]/[Q
with dot above] mismatch).
 Hemodynamic consequences:
o Increased pulmonary vascular resistance
o Increased pulmonary artery pressure (PAP)
o Increased right ventricular workload to maintain
pulmonary blood flow
o Right ventricular failure
o Decreased cardiac output
o Decreased blood pressure
o Shock
 Pulmonary emboli can vary in size and seriousness of
consequences.
 Predisposing factors include:
o Stasis, prolonged immobilization.
o Concurrent phlebitis.
o Previous heart (heart failure, myocardial infarction
[MI]) or lung disease.
o Injury to vessel wall.
o Coagulation disorders.
o Metabolic, endocrine, vascular, or collagen
disorders.
o Malignancy.
o Advancing age, estrogen therapy.
Clinical Manifestations
 Dyspnea, pleuritic pain, tachypnea, apprehension.
 Chest pain with apprehension and a sense of impending
doom occurs when most of the pulmonary artery is
obstructed.
 Cyanosis, tachyarrhythmias, syncope, circulatory collapse
and, possibly, death encountered in patients with massive
pulmonary embolism
 Subtle deterioration in patient's condition with no
explainable cause
 Pleural friction rub
mikEL rlh mantong
TUBERCULOSIS
TB is an infectious disease caused by bacteria (Mycobacterium
tuberculosis) that are usually spread from person to person through
the air. It usually infects the lung but can occur at virtually any site in
the body. HIV-infected patients are especially at risk. Drug-resistant
TB is of particular concern in certain parts of the United States.
Pathophysiology and Etiology
Transmission
 The term Mycobacterium is descriptive of the organism,
which is a bacterium that resembles a fungus. The
organisms multiply at varying rates and are characterized
as acid-fast aerobic organisms that can be killed by heat,
sunshine, drying, and ultraviolet light.
 TB is an airborne disease transmitted by droplet nuclei,
usually from within the respiratory tract of an infected
person who exhales them during coughing, talking,
sneezing, or singing.
 When an uninfected susceptible person inhales the
droplet-containing air, the organism is carried into the lung
to the pulmonary alveoli.
 Most people who become infected do not develop clinical
illness, because the body's immune system brings the
infection under control.
Pathology
 The bacilli of TB infect the lung, forming a tubercle (lesion).
 The tubercle:
o May heal, leaving scar tissue.
o May continue as a granuloma, then heal, or be
reactivated.
o May eventually proceed to necrosis, liquefaction,
sloughing, and cavitation.
 The initial lesion may disseminate tubercle bacilli by
extension to adjacent tissues, by way of the bloodstream,
by way of the lymphatic system, or through the bronchi.
 Extrapulmonary TB occurs more commonly in children and
immunocompromised individuals and can involve lymph
nodes, bones, joints, pleural space, pericardium, CNS, GU
tissue, and the peritoneum.
Clinical Manifestations
Patient may be asymptomatic or may have insidious symptoms that
may be ignored.
 Constitutional symptoms
o Fatigue, anorexia, weight loss, low-grade fever,
night sweats, indigestion.
o Some patients have acute febrile illness, chills, and
flu-like symptoms.
 Pulmonary signs and symptoms
o Cough (insidious onset) progressing in frequency
and producing mucoid or mucopurulent sputum.
o Hemoptysis; chest pain; dyspnea (indicates
extensive involvement).
 Extrapulmonary TB: pain, inflammation, and dysfunction in
any of the tissues infected.
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute)
PLEURISY
Pleurisy is a clinical term to describe pleuritis (inflammation of the
pleura, both parietal and visceral).
Pathophysiology and Etiology
 Inflammation of the pleura stimulates nerve endings,
causing pain.
 May occur in the course of many pulmonary diseases:
o Pneumonia (bacterial, viral).
o TB.
o Pulmonary infarction, embolism.
o Pulmonary abscess.
o Upper respiratory tract infection.
o Pulmonary neoplasm.
PLEURAL EFFUSION
Pleural effusion refers to a collection of fluid in the pleural space. It
is almost always secondary to other diseases.
Pathophysiology and Etiology
 May be either transudative or exudative.
 Transudative effusions occur primarily in noninflammatory
conditions; is an accumulation of low-protein, low cell
count fluid.
 Exudative effusions occur in an area of inflammation; is an
accumulation of high-protein fluid.
 Occurs as a complication of:
o Disseminated cancer (particularly lung and breast),
lymphoma.
o Pleuropulmonary infections (pneumonia).
o Heart failure, cirrhosis, nephrosis.
o Other conditions sarcoidosis, systemic lupus
erythematosus (SLE), peritoneal dialysis.
Clinical Manifestations
 Dyspnea, pleuritic chest pain, cough.
 Dullness or flatness to percussion (over areas of fluid) with
decreased or absent breath sounds
LUNG ABSCESS
A lung abscess is a localized, pus-containing, necrotic lesion in the
lung characterized by cavity formation.
Pathophysiology and Etiology
 Most commonly occurs due to aspiration of vomitus or
infected material from upper respiratory tract.
 Secondary causes include:
o Aspiration of foreign body into lung.
o Pulmonary embolus.
o Trauma.
o TB, necrotizing pneumonia.
mikEL rlh mantong
o Bronchial obstruction (usually a tumor) causes
obstruction to bronchus, leading to infection distal
to the growth.
 The right lung is involved more frequently than the left
because of dependent position of the right bronchus, the
less acute angle that the right main bronchus forms within
the trachea, and its larger size.
 In the initial stages, the cavity in the lung may
communicate with the bronchus.
 Eventually, the cavity becomes surrounded or encapsulated
by a wall of fibrous tissue, except at one or two points
where the necrotic process extends until it reaches the
lumen of some bronchus or pleural space and establishes a
communication with the respiratory tract, the pleural cavity
(bronchopleural fistula), or both.
 The organisms typically seen are Klebsiella pneumoniae
and Staphylococcus aureus.
Clinical Manifestations
 Cough, fever, and malaise from segmental pneumonitis and
atelectasis.
 Headache, anemia, weight loss, dyspnea, weakness.
 Pleuritic chest pain from extension of suppurative
pneumonitis to pleural surface.
 Production of mucopurulent sputum, usually foul-smelling;
blood streaking common; may become profuse after
abscess ruptures into bronchial tree.
 Chest may be dull to percussion, decreased or absent
breath sounds, intermittent pleural friction rub.
CANCER OF THE LUNG
(BRONCHOGENIC CANCER)
Bronchogenic cancer refers to a malignant tumor of the lung arising
within the wall or epithelial lining of the bronchus. The lung is also a
common site of metastasis by way of venous circulation or
lymphatic spread. Bronchogenic cancer is classified according to cell
type:
 Epidermoid (squamous cell) most common
 Adenocarcinoma
 Small cell (oat cell) carcinoma
 Large cell (undifferentiated) carcinoma
Pathophysiology and Etiology
Predisposing Factors
 Cigarette smoking amount, frequency, and duration of
smoking have positive relationship to cancer of the lung.
 Occupational exposure to asbestos, arsenic, chromium,
nickel, iron, radioactive substances, isopropyl oil, coal tar
products, petroleum oil mists alone or in combination with
tobacco smoke.
Staging
 Refers to anatomic extent of tumor, lymph node
involvement, and metastatic spread.
 Staging done by:
o Tissue diagnosis
Lippincott Manual of Nursing Practice, 8 th Ed Respiratory Disorders (Acute) mikEL rlh mantong
o Lymph node biopsy
o Mediastinoscopy

Clinical Manifestations
Usually occur late and are related to size and location of tumor,
extent of spread, and involvement of other structures
 Cough, especially a new type or changing cough, results
from bronchial irritation.
 Dyspnea, wheezing (suggests partial bronchial obstruction).
 Chest pain (poorly localized and aching)
 Excessive sputum production, repeated upper respiratory
infections
 Hemoptysis
 Malaise, fever, weight loss, fatigue, anorexia
 Paraneoplastic syndrome metabolic or neurologic
disturbances related to the secretion of substances by the
neoplasm
 Symptoms of metastasis bone pain; abdominal discomfort,
nausea and vomiting from liver involvement; pancytopenia
from bone marrow involvement; headache from CNS
metastasis
 Usual sites of metastasis lymph nodes, bones, liver