RESPIRATORY DISTURBANCES

Gas Exchange Disorders

Asthma

A chronic inflammatory disease of the airways which causes airway HYPERRESPONSIVENESS, MUCOSAL EDEMA,
and MUCUS PRODUCTION
Unlike any other obstructive lung diseases, asthma is largely reversible, either spontaneously or with treatment.
Patients with asthma may experience symptom-free periods alternating with acute exacerbations that last from
minutes to hours or days.
Strongest predisposing factor for asthma: Allergy
Common allergens: Seasonal (grass, tree, and weed pollens), perennial (mold, dust, roaches, animal dander)
Common triggers: Airway irritants (air pollutants, cold, heat, weather changes, strong odors or perfumes, smoke,
occupational exposure), foods (shellfish, nuts), exercise, stress, hormonal factors, medications, vital respiratory tract
infections, and gastroesophageal reflux
Complications: status asthmaticus, respiratory failure, pneumonia, atelectasis
STATUS ASTHMATICUS: severe asthma attack that doesn't improve with traditional treatments, such as inhaled
bronchodilator and may last for a few minutes or even hours; considered as life-threatening

Clinical Manifestations/Symptoms:
Cough
Chest tightness
WHEEZING
Dyspnea
Expiration requires effort and becomes prolonged
As the exacerbation progresses, DIAPHORESIS (excessive sweating), tachycardia, and widened pulse pressure
may occur along with hypoxemia (secondary to ventilation-perfusion mismatch and readily responds to
supplemental oxygenation) and central cyanosis (late sign of poor oxygenation).

Interventions:
 Key to quality asthma care: KNOWLEDGE
 Fluid administration: people with asthma are frequently dehydrated from diaphoresis and insensible fluid loss
with hyperventilation
 Pharmacologic therapy: quick-relief medications
SHORT-ACTING BETA 2 ADRENERGIC AGONIST (SABA) - used to relax smooth muscle of the lungs; used
up to three treatments at 20-minute intervals as needed
 Examples: albuterol/salbutamol, levalbuterol, pirbuterol
ANTICHOLINERGIC AGENTS inhibit muscarinic cholinergic receptors and reduce intrinsic vagal tone of
the airway
 Example: ipratropium
 Pharmacologic therapy: long-acting medications
LONG-ACTING BETA 2 AGONIST (LABA) - used with anti-inflammatory medications to control asthma
symptoms; reduces swelling in the airways
Corticosteroids (anti-inflammatory agents)
 Inhaled corticosteroids: beclomethasone, budesonide, ciclesonide, flunisolide, fluticasone,
mometasone, triamcinolone acetonide, salmeterol
 Systemic corticosteroids: methylprednisolone, prednisolone
 Anti-inflammatory medications are primarily used since the underlying pathology of asthma is
inflammation
 Examples:
 MAST CELLSSTABILIZERS (cromolyn sodium, nedocromil) - inhibit the release of
mediators of inflammation
 LEUKOTRINE RECEPTOR ANTAGONIST (montelukast, zarfilukast) - block the action of
leukotrienes, one cause of the inflammation and nasal congestion associated with
allergies to keep bronchial tubes and lung airways from constricting
XANTHINE BRONCHODILATOR
Example: XANTHINE BRONCHODILATOR - a mild to moderate bronchodilator that is usually used in
addition to inhaled corticosteroids
MONOCLONIAL ANTIBODY/ IMMUNOMODULATORS
 Example: omalizumab - inhibits the binding of IgE to the high-affinity IgE receptor in the surface
of mast cells and basophils, thereby reducing the release of mediators of the allergic response.
Therefore, it prevents an allergic response by acting on the body's immune system.
 Oxygen supplementation
 PEAK FLOW MONITORING- measures the highest airflow during a forced expiration, measures the ability to
push air out of the lungs
Nursing Management:
 Assess respiratory status (monitoring severity of symptoms, breath sounds, peak flow, pulse oximetry, and
vital signs)
 Obtain history or allergic reactions to medications, food, environmental, or other triggers (exercise, weather
changes, stress)
 Administer the prescribed medications and monitor the patient's responses
 Administer fluids if patient is dehydrated
 Acute respiratory failure needing intubation, the nurse assists in the intubation procedure, continues close
monitoring of the patient, and keeps the patient and family informed about the procedures
 Patient education:
 Nature of asthma as a chronic inflammatory disease
 Definitions of inflammation and bronchoconstriction
 Purpose and action of each medication
 Triggers to avoid and how to avoid them
 Proper inhalation technique
 How to perform peak flow monitoring
 How to implement an asthma action plan

CYSTIC FIBROSIS (CF)

Most common fatal autosomal recessive disease among Caucasians, but less frequently found among Hispanic,
Asian, and African Americans
CF was once a fatal childhood disease; however, the median expected survival age is now in the late 30s
Major manifestation of CF when diagnosed later in life: respiratory symptomps
CF is caused by mutations/dysfunctions in the protein
CYSTIC FIBRTOSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) gene
A person must inherit a defective copy of the CF gene (one from each parent) to have CF
CF manifestations are characterized by thick, viscous secretions in the lungs, pancreas, liver, intestine, and
reproductive tract as well as increased salt content and sweat gland secretions
Hallmark pathology of CF:
 o BRONCHIAL MUCUS PLUGGING
o inflammation
o BRONCHIECTASIS (which commonly starts in the upper lobes and progresses to involve all lobes)

Clinical Manifestations/Symptoms:
Productive and chronic cough with sputum production
Persistent infection consistent with typical CF pathogens (S. aureus, H. influenzae, P. aeruginosa)
Wheezing
Upper respiratory symptoms: sinusitis, nasal polyps
Gastrointestinal tract and nutritional abnormalities:
o PRANCEATIC INSUFFICIENCY
o recurrent pancreatitis
o biliary cirrhosis
o portal hypertension
o CF-related diabetes
o recurrent abdominal pain
o vitamin deficiencies
o recurrent pancreatitis
o weight loss
Genito-urinary problems: male and female infertility
Chest x-ray: hyperinflation of the lung fields; evidence of bronchiectasis and chronic sinusitis, often with nasal
polyps
Pulmonary function test: results are consistent with the obstructive disease of the airways
SWEAT CHLORIDE TEST: measures the amount of chloride (a component of salt) in the sweat; gold
standard for diagnosing CF

Medical management:
 Chronic bacterial infection: control of the infection through IV and nebulized antibiotics
 Acute airway exacerbations: airway clearance (the DORNASE ALFA), antibiotics (based on sputum culture
results)

Nursing/Collaborative Management:
 CHEST PHYSIOTHERAPY (postural drainage, chest percussion, chest vibration)
 Deep breathing exercises
 Remind the patient to reduce the risk factors associated with respiratory infections (e.g., exposure to crowds
or to people with known infections)
 Instruct the patient about the early signs and symptoms of respiratory infection and disease progression that
may warrant to notify his/her doctor
 Emphasize adequate fluid (to promote removal of secretions) and dietary intake (to ensure adequate
nutritional status)
 Since CF is a lifelong disorder, patients often have to learn to modify their daily activities to accommodate
their symptoms and treatment modalities.
 HIGH FREQUENCY CHEST WALL OSCILLATION- an inflatable vest that is attached to a machine is worn, and
the machine mechanically performs chest physical therapy by vibrating at high frequency - in order to loosen
and thin the mucus, after five minutes, the person stops the machine and coughs or huffs
 AUTOGENIC DRAINAGE (also means "self-drainage") - use large breaths out (exhalation) to loosen mucus in
the lungs
  POSITIVE EXPIRATORY PRESSURE (PEP) mask - application of positive expiratory pressure via
mask/mouthpiece as an airway clearance technique aimed at increasing lung volumes by mobilizing,
transporting, and evacuating secretions in spontaneously breathing patients
 FLUTTER DEVICE
 provide an oscillatory expiratory pressure pattern with PEP and assist with expectoration of secretions
 vibrates the airways (which loosens mucus from the airway walls)
 intermittently increase endobronchial pressure (which helps maintain patency of the airways during
exhalation so that mucus does not become trapped as it moves up the airways
 accelerate expiratory airflow (which facilitates the upward movement of mucus through the airways so
that it can be more easily cleaned
 Anti-inflammatory agents to treat the inflammatory response in the airways
 Inhaled bronchodilators [salmeterol, tiotropium bromide (Spiriva)] may be used for those who have significant
bronchoconstrictive component
 Oral pancreatic enzyme supplementation during meal time as 90% of the patients have pancreatic exocrine
insufficiency
 Mainstay of CF treatment:
 MUCOLYTIC AGENTS
 antibiotics
 inhaled beta agonists
 anti-inflammatory agents
 CFTR modulator: IVACAFOTR (Kalydeco) LUMACAFTOR (Orkambi)
 Supplemental oxygen if pulmonary deterioration advances
 Lung transplantation (for small selected population of patients with CF)

ATELECTASIS
The closure or collapse of alveoli
One of the most commonly encountered abnormalities seen on chest x-ray
Types of atelectasis:
 NONOBSTRUCTIVE atelectasis
1. COMPRESSIVE atelectasis
Excessive pressure on the lung tissue which restricts normal lung expansion on inspiration
Caused by fluid accumulating in the pleural space (pleural effusion), air in the pleural
space (pneumothorax), or blood in pleural space (hemothorax)
2. Adhesive atelectasis
Alveoli collapse because of the absence of a pulmonary surfactant (this keeps the
alveoli stable)
Example: Respiratory distress syndrome, bruised lung (pulmonary contusion)
3. Cicatricial atelectasis
Lung tissue has scars which keeps them from being able to hold as much air as they should
Example: Sarcoidosis
4. Rounded atelectasis
Aka folded lung
Linked to pleural diseases; pleural thickening
Round, triangular, or oval-shaped mass adjacent to the pleura
Example: Asbestosis (asbestos settles and damages the pleural space)
5. Acceleration atelectasis
When pilots flu straight up really fast, the acceleration can close the airways in their lungs

 OBSTRUCTIVE atelectasis
 Any blockage that obstructs passage of air to and from the alveoli
Most common type
Trapped alveoli air is absorbed back into the bloodstream. As a result, the affected portion
of the lung becomes airless and the alveoli collapse
Causes:
o Foreign body
o Tumor/abnormal growth in the airway
o Altered breathing patterns
o Retained secretions
o Pain
o Smoking
o Alterations in small airway function
o Prolonged supine positioning / long-term bedrest
o Increased abdominal pressure
o Old age
o Obesity
o Reduced lung volumes due to musculoskeletal or neurologic disorders/condition that damages the
nerves/muscles such as spinal cord injury or muscular dystrophy
o Restrictive defect
o Specific surgical procedures (e.g., upper abdominal, thoracic, or open heart surgery)
o Post-operation (due to a monotonous, low tidal breathing pattern which may cause small airway closure and
alveolar collapse; results from the effects of anesthesia/analgesic agents, supine positioning, splinting of
chest wall due to pain, abdominal distention, secretion retention, airway obstruction, impaired cough reflex,
patient's reluctance to cough because of the pain)
Signs and symptoms
Dyspnea
Cough
Sputum production
Tachycardia
Tachypnea
Pleural pain
CENTRAL CYANOSIS (a bluish skin hue that is a late sign of hypoxemia)
Assessment and diagnostic findings:
o Decreased breath sounds and/or crackles heard over the affected area upon auscultation
o Chest x-ray: patchy infiltrates or consolidated areas
o Low oxygen saturation
Nursing/Collaborative Management:
 Frequent turning
 Early mobilization/ambulation
 Voluntary deep breathing exercises
 Use of incentive spirometry
 Secretion management techniques: directed cough, suctioning, aerosol nebulizer treatments, chest
physiotherapy (postural drainage and chest percussion)
 Pressurized metered-dose inhaler to dispense a bronchodilator rather than an aerosol nebulizer
 Large pleural effusion: THORACENTESIS (removal of the fluid by needle aspiration) or insertion of a chest
tube
 Encourage the patient to quit smoking and assist in smoking cessation programs
 Bronchoscopy to clear the blockages
 ACUTE TRACHEOBRONCHITIS
Inflammation of the mucous membranes of the trachea and bronchial tree, often follows after an URTI
Caused by:
o Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Aspergillus; done
via sputum culture
o Inhalation of physical and chemical irritants, gases, or other air contaminants
Clinical Manifestations/Symptoms:
Dry, irritating cough
Scanty amount of mucoid sputum
Sternal soreness (from coughing)
Fever, chills, night sweats
Headache
General malaise
Shortness of breath
Inspiratory stridor and expiratory wheeze
Purulent (pus-filled) sputum if the infection progresses
Severe tracheobronchitis: blood-streaked secretions as a result of the irritation of the mucosa of the
airways
Nursing/Collaborative Management:
 Antibiotic treatment
 Antihistamines are not prescribed as they can cause excessive drying and make the secretions more
difficult to expectorate
 Increase fluid intake to thin viscous and tenacious secretions
 Suctioning and bronchoscopy to remove secretions
 Endotracheal intubation (in rare cases) in patients who are severely debilitated or who have
coexisting diseases that also impair the respiratory system
 Treatment of tracheobronchitis is largely symptomatic: increasing moisture content (such as steam
inhalations) in the airway reduces airway irritation, moist heat in the chest may help relieve soreness
and pain, mild analgesics may be prescribed
 Bronchial hygiene: increased fluid intake, directed coughing
 Instruct patient to complete the full course of antibiotics as prescribed

PNEUMONIA
Inflammation of the LUNG PARENCHYMA caused by various microorganisms (bacteria,
mycobacteria, fungi, viruses)
PNEUMONITIS - a general term that describes an inflammatory process in the lung tissue that may predispose
or place the patient at risk for microbial invasion
Types of pneumonia:
1. COMMUNITY-ACQUIRED PNEUMONIA
o Occurs in the community setting or within the first 48 hours after hospitalization
o Caused by S. pneumoniae (most common cause of CAP), H. influenzae, M. pneumoniae, and
other viruses (cytomegalovirus - most common viral pathogen)
2. HEALTHCARE ASSOCIATED PNEUMONIA
o Occurs in a non-hospitalized patient with extensive health care contact with one or more of
the following:
Hospitalization for more or equal to 2 days in an acute care facility within 90 days
of infection
Residence in a nursing home or long-term care facility
 Antibiotic therapy, chemotherapy, or wound care within 30 days of current infection
Hemodialysis treatment at a hospital or clinic
Home infusion therapy or home wound care
Family member with infection due to multidrug resistant bacteria
o Important distinction: causative pathogens are often multi-drug resistant (MDR); initial antibiotic
treatment for HCAP is often different from that for CAP due to possibility of MDR bacteria
3. HOSPITAL-ACQUIRED PNEUMONIA
o Occurs more or equal to 48 hours after hospital admission that did not appear to be incubating at
the time of admission
o HAP is associated with a high mortality rate because of:
Virulence of the organisms
Resistance to antibiotics
Patient's underlying disorder
4. VENTILATOR ASSOCIATED PNEUMONIA
o A subtype of HAP that develops more or equal to 48 hours after endotracheal tube intubation
5. ASPIRATION PNEUMONIA
o Entry of endogenous or exogenous substances into the lower airway which results in pulmonary
consequences
o Most common form: bacterial infection from aspiration of bacteria that normally reside in the
upper airways
o May occur in community/hospital setting
Pneumonia in the Immunocompromised Host (use of corticosteroids/other immunosuppressants, chemotherapy,
nutritional depletion, use of broad-spectrum antimicrobial agents, AIDS, genetic immune disorders, long-term
advanced life support technology (mechanical ventilation):
 PNEUMOCYSTIS PNEUMONIA (PCP)
o Causative agents: Pneumocystis jiroveci, fungal pneumonias, and Mycobacterium tuberculosis.
Risk Factors:
Travel/exposure to certain environments
Residence in a long-term care facility
Immunocompromised patients
Heart failure
Diabetes
Alcoholism
COPD
AIDS
Cystic fibrosis
Complications:
Shock and respiratory failure
Pleural effusion
Clinical Manifestations/Symptoms:
Sudden onset of chills
Fever
Pleuritic chest pain aggravated by deep breathing and coughing
Tachypnea
Shortness of breath
Use of accessory muscles in respiration
URTI: NASAL CONGESTION, SORE THROAT/PHARYNGITIS
Headache
Myalgia
 Rash
Mucoid/mucopurulent sputum
Flushed cheeks and lips
CENTRAL CYANOSIS (late sign of poor oxygenation - hypoxemia)
Orthopnea
Poor appetite
Diaphoresis
Easy fatigability
Physical findings that indicate lung tissue consolidation: increased tactile fremitus (vocal vibration detected
on palpation), percussion dullness, bronchial breath sounds, egophony (when auscultated, the spoken "E"
becomes a loud, nasal-sounding "A"), whispered pectoriloquy (whispered sounds are easily auscultated
through the chest wall)
o These changes occur because sound is transmitted better through solid/dense tissue (consolidation)
than through normal air-filled tissue
Clinical Diagnosis:
o History (particularly of a recent respiratory tract infection)
o Physical examination
o Chest x-ray
o Blood culture (bacteremia occurs frequently)
o Sputum examination
Nursing/Collaborative Management:
 Antibiotics (determined by culture and sensitivity results)
 Viral pneumonia - supportive treatment (hydration, antipyretics, antitussives, warm & moist inhalations,
antihistamines, nasal decongestants, bed rest until infection shows signs of clearing, oxygen for hypoxemia)
 ARTERIAL BLOOD GAS : to obtain a baseline measure of the patient's oxygenation and acid-base status
 Pulse oximetry: continuously monitor the patient's oxygen saturation and response to therapy
 Assessment
 Fever
 Chills
 Night sweats
 Pleuritic-type pain
 Fatigue
 Tachypnea/Tachycardia
 Use of accessory muscles for breathing
 Coughing (note for frequency and severity)
 Purulent sputum
 Auscultation of the lung
 Mental, hydration status
 Baseline diagnostic findings: chest x-ray
 Diagnosis
 Ineffective Airway Clearance related to copious tracheobronchial secretions
 Fatigue and activity intolerance related to impaired respiratory function
 Risk for deficient fluid volume related to fever and a rapid respiratory rate
 Imbalanced nutrition: less than body requirements
 Deficient knowledge about the treatment regimen and preventive measures

 Planning
 Improved airway patency
 Increased activity
  Maintenance of proper fluid volume
 Maintenance of adequate nutrition
 Understanding of the treatment protocol and preventive measures
 Absence of complications
 Interventions:
 Remove secretions (proper coughing, oral/endotracheal/nasotracheal/tracheal suctioning)
 Encourage to increase oral fluid intake
 Humidification to loosen and liquefy secretions and improve ventilation
 Administer oxygen as prescribed
 Lung expansion maneuvers (deep breathing exercises, use of incentive spirometer)
 Chest Physiotherapy (percussion and postural drainage)
 Promote rest and avoid overexertion
 Small, frequent meals and maintaining adequate nutrition
 Avoid smoking and alcohol intake
 Promote patient's knowledge
 Monitor and manage potential complications
 Evaluates patient's adherence to the therapeutic regimen
 Evaluation:
Demonstrates improved airway patency, as evidenced by adequate oxygenation by pulse oximetry or
arterial blood gas analysis, normal
temperature, normal breath sounds, and effective coughing
 Rests and conserves energy by limiting activities and remaining in bed while symptomatic and then
slowly increasing activities
 Maintains adequate hydration, as evidenced by an adequate fluid intake and urine output and normal
skin turgor
 Consumes adequate dietary intake, as evidenced by maintenance or increase in body weight without
excess fluid gain
 Verbalizes increased knowledge about management strategies
 Complies with management strategies
 Exhibits no complications
 Exhibits acceptable vital signs, pulse oximetry, and arterial blood gas measurements
 Reports productive cough that diminishes over time
 Has absence of signs or symptoms of sepsis, septic shock, respiratory failure, or pleural effusion
 Remains oriented and aware of surroundings
 Maintains or increases weight
 Adheres to treatment protocol and prevention strategies

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) / CHRONIC AIRFLOW LIMITATION (CAL)

A preventable and treatable slowly progressive respiratory disease of airflow obstruction involving airways,
pulmonary parenchyma (any form if lung tissue, including bronchioles, bronchi, blood vessels, interstitium, and
alveoli), or both
Airflow limitation/obstructions is fully reversible
COPD patients present with overlapping signs and symptoms of
emphysema and chronic bronchitis (both are two distinct disease
processes).
o CHRONIC BRONCHITIS
Presence of cough and sputum production for at least 3 months in each of 2 consecutive years
These cause airway irritation resulting in increased inflammation and hypersecretion of mucus:
smoke and other environmental pollutants
 Constant irritation -> goblet cells and submucosal glands increase in number -> increased mucus
production -> mucus plugging of the airway -> reduced ciliary function -> bronchial walls become
thickened and narrows the bronchial lumen -> alveoli adjacent to the bronchioles may become
damaged and fibrosed -> altered function of the alveolar macrophages -> patient becomes more
susceptible to respiratory infection
o EMPHYSEMA
Abnormal distention of the airspaces beyond the terminal bronchioles and destruction of the walls
of the alveoli, resulting in impaired oxygen and carbon dioxide exchange
Recurrent/chronic infections -> decrease alveolar surface area in direct contact with pulmonary
capillaries -> increase in dead space (lung area where no gas exchange can occur) -> impaired
oxygen diffusion -> hypoxemia
In the later stages, carbon dioxide elimination is impaired -> increased carbon dioxide tension in
arterial blood (hypercapnia) -> respiratory acidosis
As the alveolar walls continue to break down-> reduced size of the pulmonary capillary bed ->
resistance to pulmonary blood flow is increased -> right ventricle is forced to maintain a higher
blood pressure in the pulmonary artery -> pulmonary hypertension -> cor pulmonale (one
complication for emphysema) - right-sided heart failure brought on by long-term high blood
pressure in the pulmonary arteries
Types of emphysema:
a. PANLOBULAR (PANCINAR)
o destruction of the respiratory bronchiole, alveolar duct, and alveoli; airspaces within the
lobule are enlarged
o S/S: hyperinflated chest, marked dyspnea on exertion, weight loss - since expiration
during breathing becomes an active act and requires muscular effort (To move air into
and out of the lungs, negative pressure is required during inspiration, and an adequate
level of positive pressure must be attained and maintained during expiration)
b. CENTRILOBULAR (CENTROCINAR)
o pathologic changes occur in the lobule and the peripheral portions of the acinus/alveoli
are preserved
o There is a disorder in the ventilation-perfusion ratios
o S/S: chronic hypoxemia, hypercapnia, polycythemia, episodes of right-sided heart
failure, peripheral edema, central cyanosis, respiratory failure
Risk Factors:
CIGARETTE SMOKING (first-hand, second-hand, third-hand) - smoking depresses the activity of
scavenger cells and affects the respiratory tract's ciliary cleansing mechanism, which keeps the
breathing passages free of inhaled irritants, bacteria, and other foreign matter; smoking also irritates
the goblet cells and mucous glands
Occupational exposure: dust, chemicals
Indoor and outdoor air pollution
Genetic abnormalities: deficiency of ALPHA 1 ANTITRYPSIN, an enzyme inhibitor that normally
counteracts the destruction of lung tissue by certain other enzymes; also protects the lung
parenchyma from injury
Increased age
Clinical Manifestations/Symptoms:
Three primary symptoms: CHRONIC COUGH, MUCUS PRODUCTION, DYSPNEA
Weight loss - since dyspnea interferes with eating and the work of breathing is energy depleting (i.e.,
use of accessory muscles)
BARREL CHEST - since the lungs are chronically overinflated with air, so the rib cage stays partially
expanded all the time
 Leaning forward and uses the accessory muscles to breathe (upper shoulder girdle moving upward)
causing the supraclavicular fossae to retract on inspiration
Advanced emphysema: abdominal muscles may contract
Musculoskeletal wasting
Metabolic syndrome
Depression
Assessment and Diagnostic Findings:
o Pulmonary function tests -determines the severity and progression of the disease
o Spirometry - to evaluate airflow obstructions
o Arterial blood gas - to assess baseline oxygenation and gas exchange
o Chest x-ray
o High-resolution CT scan
o Screening for alpha1-antitrypsin deficiency (for patients younger than 45 years old, family history
of COPD)
COPD classification (measured by pulmonary function tests)

Complications:
o Respiratory insufficiency and failure
o Pneumonia
o Chronic atelectasis
o Pneumothorax
o Pulmonary arterial hypertension (COR PULMONALE)
Medical/Surgical management:
o Smoking cessation
o Bronchodilators
 Inhaled therapy (pressurized metered-dose inhaler, dry powder inhaler, nebulization)
 May also be given orally (pills/tablets/liquid form)
o Corticosteroids (inhaled or systemic)
o Anticholingerics
o Supplemental oxygen therapy
  HYPOXIC DRIVE - it is a very small part of the overall stimulus driving the respiratory system
 Given for patients who desaturate
o BULLECTOMY
 BULLAE - enlarged airspaces that do not contribute to ventilation but occupy a space in the
thorax which compresses the affected area of the lung and may impair gas exchange
o LUNG VOLUME REDUCTION SURGERY
 For patients with advanced or end-stage COPD (Grade IV) and is a palliative surgical option
 Removal of a portion of the diseased lung parenchyma
 This surgery does not cure the disease but may improve life expectancy, decrease dyspnea,
improve lung function, exercise tolerance, and quality of life
o Lung Transplantation
 For severe COPD in selected patients
o PULMONARY REHABILITATION
 a program of education and exercise that helps you manage your breathing
problem, increase your stamina (energy) and decrease your breathlessness
 Goals: reduce symptoms, improve quality of life, increase physical and emotional
participation in everyday activities
 For patients with Grade II through IV COPD
 Services are multidisciplinary and include assessment, education, smoking cessation,
physical reconditioning, nutritional counseling, skills training, and psychological support
 Patient education
 Breathing exercises
 Activity pacing
 Self-care activities
 Physical conditioning
 Oxygen therapy
 Nutritional therapy
 Coping measures
 Palliative care

Nursing Management
o Assessing the patient
o Achieving airway clearance
o Improving breathing patterns
o Improving activity tolerance
o Monitoring and managing potential complications

BRONCHIECTASIS
A chronic, irreversible dilation of the bronchi and bronchioles that results from destruction of muscles and
elastic connective tissue
Pulmonary infection -> inflammatory process -> damage to the bronchial wall -> loss of the supporting structure and
thick sputum that obstructs the bronchi -> walls become permanently distended and distorted, impairing
mucociliary clearance -> obstruction towards the alveoli -> atelectasis -> inflammatory scarring or fibrosis replaces
the functioning lung tissue - respiratory insufficiency
Is usually localized, affecting a segment/lobe of the lung, most frequently in the lower lobes
Clinical manifestations:
Chronic cough
 Purulent sputum
Hemoptysis
Clubbing of fingers
Have repeated episodes of pulmonary infection
Assessment and diagnostic findings:
 Symptoms can be mistaken as chronic bronchitis. However, a definite sign is a prolonged history
of productive chronic cough with sputum consistently negative for tubercle bacilli
 CT scan: bronchial dilation
Management:
 Promote bronchial drainage
 Clear excessive secretions from the affected portions
 Postural drainage
 Removal of mucopurulent sputum through bronchoscopy
 Chest physiotherapy (percussion and postural drainage)
 Smoking cessation
 Antibiotics
 Vaccination against influenza and pneumococcal pneumonia
 Bronchodilators
 Nebulized mucolytics
 Ensure adequate hydration
 Surgical removal - to conserve normal pulmonary tissue and to avoid infectious complications
 SEGMENTAL WEDGE RESECTION- removes a part of a lung but smaller than a lobe
 LOBECTOMY- removal of a lung lobe
 PNEUMONECTOMY- removal of the entire lung

PULMONARY TUBERCULOSIS
 An infectious disease that primarily affects the lung parenchyma
 May be transmitted to other parts of the body (meninges, kidneys, bones, lymph nodes)
 Primary infectious agent: M. TUBERCULOSIS
 Mode of transmission: AIRBORNE
 Person inhales mycobacteria -> bacteria goes through the airways and to the alveoli -> bacteria multiplies ->
bacteria travels to other body parts through the lymph system and bloodstream -> inflammatory reaction of the
body -> accumulation of exudates on the alveoli -> bronchopneumonia
Risk factors:
Close contact
Immunocompromised status (e.g., HIV/AIDS, cancer, prolonged high-dose corticosteroid therapy)
Person without adequate healthcare (homeless, impoverished)
Pre-existing medical conditions (e.g., diabetes, chronic kidney injury, malnourishment, transplanted
organ)
Immigration from or recent travel to countries with high prevalence of TB (SE Asia, Africa, Latin
America, Carribean)
Institutionalization (e.g., long-term care facilities, psychiatric institutions, prisons)
Living in overcrowded, substandard housing
Being a health care worker performing high-risk activities
Clinical Manifestations/Symptoms:
Low-grade fever
Cough (non-productive, mucopurulent)
Hemoptysis
Night sweats
 Fatigue
Weight loss
Anorexia
Sputum production
Auscultating breath sounds: diminished bronchial sounds, crackles
Diagnostic findings:
 Sputum culture for ACID FAST BACILLI
 Tuberculin Skin Test
 result is read 48-72 hours after injection
 0-4 mm = NOT SIGNIFICANT
 More than 5 mm = significant for people who are high risk (HIV/AIDS patients, close contact
with another person who has an active TB)
 More than 10 mm = significant in people who have normal immunity
 Chest x-ray: usually reveals lesions at UPPER lobes
 Drug susceptibility testing
Medical Management:
 Anti-TB agents for 6-12 months
 People are considered noninfectious after 2-3 WEEKS of continuous medication therapy
 TB drug resistance types:
 Primary drug resistance: resistance to one of the first-line anti-TB agents in people who
have not had previous treatment
 Secondary/acquired drug resistance: resistance to one or more anti-TB agents in
patients undergoing therapy
 Multidrug resistance (MDR): resistance to two agents, isoniazid (INH) and rifampin;
populations at highest risk for MDR are those who are HIV positive, institutionalized, or
homeless
Nursing Management:
 Promote airway clearance
 Promote adherence to treatment regimen
 Promote activity and adequate nutrition
 Prevent transmission of TB infection

PULMONARY HYPERTENSION
 Blood pressure in the arteries of the lungs become ABNORMALLY ELEVATED
 Increased workload affects right ventricular functions
 Myocardium cannot meet the increasing demands imposed on it, leading to right ventricular hypertrophy
(enlargement and dilation) and heart failure
Clinical Manifestations/Symptoms:
Dyspnea on exertion and at rest
Substernal chest pain
Weakness
Fatigue
Syncope
Occasional hemoptysis
SIGNS OF RIGHT-SIDED HEART FAILURE : peripheral edema, ascites, distended neck veins,
liver engorgement, crackles, heart murmur
Anorexia
RUQ abdominal pain
Diagnostic findings:
 o Chest x-ray
o Pulmonary function studies
o ELECTROCARDIOGRAM (ECG)
 records the electrical signals of the heart
o ECHOCARDIOGRAPHY
 uses high frequency sound waves (ultrasound) to make pictures of the heart
o RIGHT HEART CATHETERIZATION
 to confirm the diagnosis of pulmonary hypertension; confirmed if mean pulmonary artery pressure
is greater than 25 mmHg
Medical management:
o Diuretics
o Oxygen
o Anticoagulants - may be considered for patients at risk for intrapulmonary thrombosis
o DIGOXIN- to improve right ventricular ejection fraction and control heart rate
o Exercise training
Surgical management:
o Lung transplant - if medical therapy is ineffective
o ATRIAL SEPTOSTOMY - shunting of blood from the right side of the heart to the left,
decreasing the strain of the right side of the heart and maintaining left ventricular output
Nursing management:
o Identify those at risk for pulmonary hypertension: COPD, PE, congenital heart disease, mitral valve
disease
o Administer oxygen therapy and medications appropriately
o Proper positioning, chest physiotherapy when the need arises
o Relieving anxiety

PULMONARY EMBOLISM (PE)

 Obstruction of the pulmonary artery or one of its branches by a THROMBUS that originates somewhere in the
venous system [such as deep vein thrombosis (DVT), presence of peripherally inserted central catheters]
 Commonly, PE is due to a BLOOD CLOT/THROMBUS. However, there are other types of emboli: air, fat, amniotic
fluid, and septic (from bacterial invasion of the thrombus)
 This thrombus completely/partially obstructs the pulmonary artery or its branches. Although there is ventilation in
the alveolar sacs of the lungs, there is no blood flow. Therefore, gas exchange is impaired or absent in this area.
 Death from acute PE commonly occurs within 1 hour after onset of symptoms
 PE is often a MEDICAL EMERGENCY
 Most effective approach: PREVENTION (active leg exercises to avoid venous stasis, early ambulation, use of
anti-embolism stockings)
Clinical Manifestations/Symptoms:
Symptoms of PE depend on the size of the thrombus and the area of the pulmonary artery occluded by
the thrombus
SUDDEN CHEST PAIN (may mimic angina pectoris or myocardial infarction)
Anxiety
Fever
Rapid and weak pulse
Apprehension
Cough
Diaphoresis
Hemoptysis
Syncope
 Dyspnea
Tachypnea
Diagnostic findings:
o Chest x-ray - may show infiltrates, atelectasis, elevation of the diaphragm on the affected side, or pleural
effusion
o ECG - sinus tachycardia and non-specific ST-T wave abnormalities (most common)
o Pulse oximetry
o ABG analysis - may show hypoxemia and hypocapnia (from tachypnea)
o Ventilation-perfusion (VQ) scan - examines airflow and blood flow in the lungs; aims to look for any
blood clot in the lungs
o PULMONARY ANGIOGRAPHY - for direct visualization under fluoroscopy of the arterial obstruction
and accurate assessment of the perfusion deficit
Medical management:
o General measures to improve respiratory and vascular status:
 Nasal oxygen
 For severe hypoxemia, endotracheal intubation and mechanical ventilatory support
 Establish IV lines with VASOPRESSOR agents (dobutamine, dopamine, norepinephrine)
 Insertion of an indwelling urinary catheter to monitor urinary output
 Small doses of IV morphine or sedatives to relieve patient's anxiety, improve tolerance of the
endotracheal tube, and ease adaptation to mechanical ventilator
o Anticoagulation therapy
 Low molecular weight heparin: ENAXAPARIN (Clexane)
 NEW ORAL ANTICOAGULANT (NOACs): dabigatran (Pradaxa), fondaparinux (Arixtra),
rivaroxaban (Xarelto), apixaban (Eliquis)
 Long-term treatment: warfarin and NOACs
 Thrombolytic (fibrinolytic) therapy
 Urokinase, TISSUE PLASMINOGEN ACTIVATOR
 This therapy resolves the thrombi or emboli quickly and restores normal hemodynamic
functioning of the pulmonary circulation, thereby reducing pulmonary hypertension and
improving perfusion, oxygenation, and cardiac output
 RISK FOR BLEEDING is significant

Surgical management:
o EMBOLECTOMY
 A surgery to remove a blood clot (embolus) from one of the blood vessels; an emergency procedure
o INFERIOR VENA CAVA filter
 A small device implanted inside the IVC that can stop blood clots from going up into the lungs
Nursing management:
o Minimize the risk of PE
o Preventing THROMBUS formation
 Encourage ambulation
 Active and passive leg exercises to prevent venous stasis in patients prescribed with bed rest
 Encourage patient not to sit/lie for prolonged periods, not to cross the legs, and not to wear any
constrictive clothing
 INTERMITTENT PNEUMATIC COMPRESSION DEVICES - may be used to prevent venous
thrombosis by enhancing blood flow in the deep veins of the legs
 IV catheters should not be left in place for prolonged periods
o Assessing potential for PE
o Monitoring thrombolytic therapy
 o Managing pain
 Place in semi-Fowler's position - more comfortable for breathing
 Frequent turning and repositioning
 Administer opioid analgesic agents as prescribed for SEVERE PAIN
o Managing oxygen therapy
 Careful use on proper use of oxygen
 Encourage patient to understand the need for continuous oxygen therapy
 Assess for signs of hypoxemia and monitor pulse oximetry values
 Encourage deep breathing exercises and use of incentive spirometry
 Nebulizer therapy as prescribed
 CHEST PHYSIOTHERAPY (percussion, postural drainage)
o Relieving anxiety
 Encourage to talk any fears/concerns
o Monitoring for complications
o Providing postoperative nursing care
 Post-op surgical embolectomy = measure the pulmonary arterial pressure (if applicable) and urinary
output; assess insertion site of the arterial catheter for hematoma formation and infection
 Instructs patient to discourage sitting for long periods as hip flexion compresses the large veins of
the legs
o Promoting home, community-based, and transitional care

PULMONARY EDEMA
 Abnormal accumulation of FLUID in the lung tissue, alveolar space, or both
 Classification:
o CARDIOGENIC- due to increased capillary hydrostatic pressure secondary to elevated pulmonary
venous pressure
o NONCARDIOGENIC- due to damage of the pulmonary capillary lining
 Direct (chest trauma, aspiration, smoke inhalation)
 hematogenous injury to the lung (sepsis, pancreatitis, multiple transfusions, cardiopulmonary
bypass)
 When the left ventricle begins to fail (left-sided congestive heart failure), blood backs up into the
pulmonary circulation, causing pulmonary interstitial edema
Clinical manifestations/symptoms:
Restless and anxious - due to decreased cerebral oxygenation
Sudden onset of breathlessness and sense of suffocation
Tachypnea
Noisy breathing
Low oxygen saturation rates
FROTHY PINK SPUTUM (BLOOD TINGED)- classic sign of pulmonary edema
Pale and cyanotic skin and mucous membranes
Jugular vein distention
Diagnostic findings
o Arterial blood gas
o Electrolytes
o BUN
o Creatinine
o Chest x-ray: to confirm the extent of pulmonary edema in the lung fields
Medical management:
o Oxygen therapy
 o Diuretics: FUROSEMIDE
o Vasodilators: Nitroglycerin, nitroprusside
Nursing management:
o Positioning the patient to promote circulation
 Position patient upright with legs dangling over the side of the bed to reduce the venous return to
the heart
o Providing psychological support
o Monitoring medications
 Diuretics: provide bedside commode, monitor urine output, measure vital signs (especially blood
pressure)

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

 Severe inflammatory process causing diffuse alveolar damage that results in sudden and progressive pulmonary
edema, increasing bilateral infiltrates on chest x-ray, hypoxemia UNRESPONSIVE to oxygen supplementation
regardless of the amount of PEEP, and absence of an elevated left atrial pressure
 Inflammation -> release of cellular and chemical mediators -> injury to the alveolar capillary membrane ->
structural damage to the lungs -> alveoli collapse; interstitial fluid and bronchial obstruction -> narrowed small
airways -> decreased lung capacity -> severe hypoxemia
Risk factors:
Aspiration (gastric secretions, drowning, hydrocarbons)
Drug ingestion and overdose
Hematologic disorders (disseminated intravascular coagulopathy, massive transfusions, cardiopulmonary
bypass)
Prolonged inhalation of high concentrations of oxygen, smoke, or corrosive substances
Localized infection (bacterial, fungal, viral pneumonia)
Metabolic disorders (pancreatitis, uremia)
Shock (any cause)
Trauma (pulmonary contusion, multiple fractures, head injury)
Major surgery
Fat or air embolism
Sepsis

Clinical manifestations/symptoms:
Rapid onset of dyspnea
Hypoxemia that does not respond to supplemental oxygen
Chest x-ray: findings are similar to those seen with cardiogenic pulmonary edema and are visible as
bilateral infiltrates that quickly worsen
INTERCOSTAL RETRACTIONS
Crackles upon auscultation of the lung field
Diagnostic tests:
o BRAIN NATRIURETIC PEPTIDE TEST - to distinguish between ARDS from cardiogenic pulmonary edema;
heart produces more BNP hormones if it works harder than usual over a long period of time such as heart
failure
o Echocardiography
o Pulmonary artery catheterization
o Arterial blood gas
o Pulmonary function test

Medical management:
 o Endotracheal intubation and mechanical ventilation
o Circulatory support
o Adequate fluid volume
o Nutritional support
o Supplemental oxygen
o Pulse oximetry
o No specific pharmacologic treatment for ARDS except SUPPORTIVE CARE (to improve patient-
ventilator synchronization and help decrease hypoxemia):
 NEUROMUSCULAR BLOCKING AGENTS
 Sedatives
 Analgesics
Nursing management:
o Oxygen administration
o Nebulizer therapy
o Chest physiotherapy
o Endotracheal tube/tracheostomy care
o SUCTIONING
o Frequent assessment of patient's status
o Decrease patient's anxiety