RESPONSES TO ALTERED RESPIRATORY FUNCTION

REVIEW OF THE ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY SYSTEM

A. The Upper Respiratory System

1. Nose – external opening of the respiratory system.

 Nostrils – external nares, are 2 cavities within the nose separated by the nasal septum.
- The cavities contains hair follicles, sweat glands and sebaceous glands.
- Nasal hairs filter the air as it enter the nares
- Rest of the cavity is lined with mucous membranes that contain olfactory
neurons and goblet cells that secrete thick mucus.

2. Sinuses – located in the frontal, ethmoid, sphenoid, and maxillary bones.

- Lighten the skull, assist in speech and produce mucus that drains into the nasal
cavities to help trap debris.

3. Pharynx – a funnel-shaped passageway about 5 inches (13cm) long.

- Serves as a passageway for both air and food.

4. Larynx – about 2 inches (5 cm) long.

- Provides an airway and routes air and food into the proper passageway.
- Contains the vocal cords, necessary for voice production.

5. Trachea – about 4-5 inches (12-15 cm) long and 1 inch in diameter.
- It contains 16-20 C-shaped rings of cartilage joint by connective tissue.
- The mucosa lining the trachea consists of pseudostratified ciliated columnar
epithelium containing seromucous glands that produce thick mucus.

B. The Lower Respiratory System

1. Lungs – are elastic connective tissue called stroma, and are soft and spongy.
- The two lungs differ in size and shape. Left lung is smaller and has 2 lobes,
whereas the right lung has 3 lobes.
- The vascular system of the lungs consists of the pulmonary arteries, which
deliver blood to the lungs for oxygenation and the pulmonary veins which
deliver oxygenated blood to the heart.

2. Pleura – is a double-layered membrane that covers the lungs and the inside of the thoracic
cavities.
- Produces pleural fluid, a lubricating, serous fluid that allows the lungs to move
easily over the thoracic wall during breathing.

3. Bronchi
– right and left pulmonary bronchi – secondary (lobar) bronchi – tertiary (segmental)
bronchi – bronchioles – collectively called bronchial or respiratory trees
- Right primary bronchus – shorter, wider and situated more vertically

1
 - During inspiration, air enters the lungs through the primary bronchus and then
moves through the increasingly smaller passageway to the alveoli.

4. Alveoli – cluster around the alveolar sacs.

- Adult lung has approximately 300 million alveoli.
- This is where oxygen and carbon dioxide exchange occurs.

FACTORS AFFECTING VENTILATION AND RESPIRATION

1. CHANGES IN RESPIRATORY VOLUME AND CAPACITY
- Affected by gender, age, weight and health status.

Tidal Volume (TV) – amount of air moved in and out of the lungs with each normal, quiet
breath.
Inspiratory Reserve Volume (IRV) – amount of air that can be inhaled forcibly over the tidal
volume.
Expiratory Reserve Volume (ERV) – is the approximately 100 mL of air that can be forced
out over the tidal volume.
Residual Volume (RV) – volume of air that remains in the lungs after a forced expiration.
Vital Capacity (VC) – total amount of air that can be exhaled after a maximal inspiration.
- Calculated by adding together the IRV, TV, and the ERV

2. OXYGEN, CARBON DIOXIDE AND HYDROGEN ION CONCENTRATIONS

- The respiratory centers and the chemoreceptors respond to changes in the concentration of
O2, CO2 and hydrogen ions.

3. AIRWAY RESISTANCE, LUNG COMPLIANCE AND ELASTICITY

- Respiratory passageway resistance is created by the friction encountered as gases move along
the respiratory passageways, by constriction of the passageways, by accumulation of mucus
or infectious material, and by tumors.
- Lung compliance is the distensibility of the lungs. It depends on the elasticity of the lung
tissue and the flexibility of the rib cage.
- Lung Elasticity – is essential for lung distention during inspiration and lung recoil during
expiration.

4. ALVEOLAR SURFACE TENSION

- At any gas-liquid boundary, the molecules of liquid are more strongly attracted to each other
that to gas molecules, this produces a state of tension called the surface tension.
- Surfactant, interferes with this adhesiveness of the water molecules, reducing surface tension
and helping expand the lungs.

CARE OF CLIENT WITH RESPIRATORY DISORDERS

A. REACTIVE AIRWAY DISORDERS

1. Chronic Obstructive Pulmonary Disease (COPD)

- Is a progressive, nonreversible process of airway narrowing and loss of supporting tissue.

2
a. CHRONIC BRONCHITIS
- A disorder of excessive bronchial mucus secretion, characterized by a productive
cough lasting 3 or more months in 2 consecutive years.

CAUSES: Cigarette Smoking, Inhaled Irritants

MANIFESTATIONS
 Cough – persistent, productive of copious mucopurulent sputum
 Evidence od right sided heart failure – distended neck veins, edema, liver
engorgement, enlarged heart
 Adventitious lung sounds, including loud rhonchi and possible wheezes on
auscultation
 Hypercapnia and hypoxemia
 Respiratory acidosis

b. EMPHYSEMA
- Characterized by destruction of the walls of the alveoli, with resulting enlargement of
abnormal air spaces.

CAUSES: Cigarette Smoking, Deficiency of a1-antitrypsin

MANIFESTATIONS:
 Dyspnea – initial symptom; initially occurring only with exertion but may progress
to become severe even at rest.
 Cough – absent or mil with scant clear sputum, if any
 Barrel chest
 Appears thin and cachectic
 Tachypneic and uses accessory muscles of respiration and often assumes a tripod
position

CLASSIFICATION OF COPD BY SEVERITY

Stage 0 - At risk – lung function normal, but with chronic cough and sputum production
are present
Stage 1 – Mild COPD – mild airflow limitation, usually with chronic cough and sputum
production
Stage 2 – Moderate COPD – worsening airflow limitation, usually with progressing
manifestations including dyspnea on exertion
Stage 3 – Severe COPD – further worsening of airflow limitation, increased SOB, and
repeated exacerbations impacting quality of life.
Stage 4 – Very Severe COPD – severe airflow limitation with significantly impaired
quality of life and potentially life-threatening exacerbations

LABORATORY/DIAGNOSTIC TESTS (for both chronic bronchitis & emphysema)

 Pulmonary Function Testing – performed to establish the diagnosis and evaluate the
extent and progress of COPD.

3
 - A noseclip is applied and the unsedated client breathes into an incentive
spirometer
- The client is instructed to inhale as deeply as possible and then exhale to the
maximal extent possible.
- Using measured lung volumes, respiratory capacities are calculated to assess
pulmonary status
RESULT: in COPD, the total lung capacity and residual volume are increased.
The forced expiratory volume (FEV1) and forced vital capacity (FVC) are
decreased.

How to use the

incentive
spirometer?
1) Sit on the edge of the bed if possible, or sit up.
2) Hold the incentive spirometer in an upright
position.
3) Place the mouthpiece in the mouth and seal the lips
tightly around it.
4) Breathe in slowly and as deeply as possible.
Notice the piston rising toward the top of the
column, it should reach the blue outlined area.
5) Hold breath as long as possible. Then exhale
slowly and allow the piston to fall to the bottom of
the column.

4
 Serum 1-antitrypsin (1AT) levels – used to screen for deficiency, particularly in clients
with a family history of obstructive airway disease, those with an early onset, women, and
nonsmokers.
- Normal adult range: 80-260 mg/dl
- Fasting is not required prior to this test
 Arterial Blood Gas Analysis – are drawn to evaluate, particularly during acute exacerbations
of COPD.
- Collected in a heparinized needle and syringe
- Sample is placed on an icebag and taken immediately to the lab
- Apply pressure to puncture site for 2-5 minutes or longer if needed
 Pulse oximetry – used to monitor oxygen saturation of the blood
- May be continuously monitored to assess the need for supplemental oxygen.
Nsg. Care: Assess factors that may alter findings.
 CBC – shows increased RBCs and hematocrit
 Chest X-ray – may show flattening of the diaphragm due to hyperinflation and evidence of
pulmonary infection.

MANAGEMENT (for both chronic bronchitis & emphysema)

 Lifestyle modification
- Smoking cessation – can not only prevent COPD from developing but also can
improve lung function once the disease has been diagnosed.
 Exposure to other airway irritants and allergents shoud be avoided.
 Pulmonary hygiene measures.
 Hydration
 Effective coughing
 Percussion
 Postural drainage
 A program of regular aerobic exercise designed to gradually increase exercise tolerance is
recommended.
 Breathing exercises are used to slow respiratory rate and relieve accessory muscle fatigue.
 Long-term oxygen therapy is used for severe and progressive hypoxemia.
 Medications:
 Broad spectrum antibiotics are prescribed
 Bronchodilators
 Corticosteroid therapy
 a1-antitrypsin replacement therapy
 immunization – pneumococcal vaccine and yearly flu vaccine

Nursing Management
 Assess respiratory status every 1 to 2 hours or as indicated.
 Monitor ABG results.
 Monitor I & O and assess mucous membranes and skin turgor.
 Encourage a fluid intake of at least 2000-2500 ml per day unless contraindicated.
 Place in Fowler’s, high fowler’s or orthopneic position.
 Assist with coughing and deep breathing at least every 2 hours while awake.
 Provide tissues and a paper bag to dispose expectorated sputum.

5
  Provide supplemental O2 as ordered.
Nursing Diagnosis
 Ineffective Airway Clearance
 Impaired Gas Exchange
 Imbalanced Nutrition: less than body requirements
 Compromised Family Coping
 Activity Intolerance
 Decisional conflict: smoking

2. BRONCHIAL ASTHMA
- Chronic inflammatory disorder of the airways characterized by recurrent episodes of wheezing,
breathlessness, chest tightness and coughing.

RISK FACTORS
a. Extrinsic Factors
a.1 pollens
a.2 animal dander
a.3 household dust
a.4 tobacco use & exposure to secondhand smoke
a.5 irritant gases

b. Intrinsic Factors
b.1 respiratory infections
b.2 nasal polyp
b.3 emotional stress

MANIFESTATIONS
 Chest tightness
 Cough
 Dyspnea
 Wheezing
 Tachypnea and
tachycardia
 Anxiety and
apprehension

 Status Asthmaticus
– severe, prolonged
asthma that does not
respond to routine
treatment.

LABORATORY/DIAGNOSTIC TESTS
 Pulmonary Function Test/s (PFTs) – used to evaluate the degree of airway obstruction.
- Done before and after use of aerosol inhaler – helps determine the reversibility of airway
obstruction.

6
 Challenge or Bronchial Provocation Testing – uses an inhaled substance such as histamine with PFTs
to confirm the diagnosis of asthma.
 ABGs – drawn during an acute attack to evaluate oxygenation,carbon dioxide elimination and acid-
base status.
 Skin Testing – may be done to identify specific allergens if an allergic trigger is suspected for asthma
attacks.

MANAGEMENT
 PREVENTIVE MEASURES
 Modifying the home environment by controlling dust, removing carpets, covering matresses and
pillows to reduce dust mite populations.
 Installing sir filtering systems may be useful.
 Pets may need to be removed from the household.
 Eliminating all tobacco smoke in the home is vital.
 Wearing a mask that retains humidity and warm air while exercising in cold weather.
 Early treatment of respiratory infections.
 Emotional stress

 MEDICATIONS
 BRONCHODILATORS
 Adrenergic Stimulants (B2-agonists) – affect receptors on smooth muscle cells of the
respiratory tract, causing smooth muscle relaxation and bronchodilation.
o Inhaled short-acting beta-adrenergic agonists – administered by metered-dose inhaler
or dry powder inhaler-treatment of choice for quick relief.
o Long-acting adrenergic stimulants in conjunction with anti-inflammatory drugs are
used to control symptoms.
 Anticholinergic agents – prevent bronchoconstriction by blocking parasympathetic input to
bronchial smooth muscle.
 Methylxantines – used as adjunctive treatment for asthma.
- Relax bronchial smooth muscle and may also inhibit the release of chemical
mediators of the inflammatory process.
- Theophylline, Aminophylline

 ANTI-INFLAMMATORY AGENTS
- Suppress airway inflammation and reduce asthma symptoms.
 Corticosteroids – block the late response to inhaled allergens and reduce bronchial
hyperresponsiveness.
 Cromolyn Sodium and Nedocromil – are used to prevent acute episodes of asthma.

 LEUKOTRIEN MODIFIERS
- Reduce the inflammatory response in asthma.
- Improve lung function, diminish symptoms, and reduce the need for short-acting
bronchodilators.
- Montelukast (Singulair), Zafirlukast (Accolate), Zilueton (Zyflo)

 NURSING MANAGEMENT
 Monitor skin color and temperature and LOC.

7
  Monitor vital signs and laboratory results.
 Assess ABG results and pulse oximetry readings.
 Place in fowler’s. high fowler’s or orthopneic (with head and arms supported on the overbed
table) position to facilitate breathing and lung expansion.
 Administer oxygen as ordered. If a mask is used, monitor closely for feelings of claustrophobia or
suffocation.
 Initiate or assist with chest physiotherapy, including percussion and postural drainage.
 Increase fluid intake.
 Administer nebulizer treatments.
 Assist with ADLs as needed.
 Provide rest periods between scheduled activities and treatments.
 Teach and assist to use techniques to control breathing pattern: pursed-lip breathing, Abdominal
breathing, relaxation techniques.

NURSING DIAGNOSES
 Ineffective airway clearance
 Ineffective breathing pattern
 Anxiety

3. CYSTIC FIBROSIS
- Autosomal recessive disorder that affects epithelial cells of the respiratory, gastrointestinal and
reproductive tracts and leads to abnormal exocrine gland secretions.
- It can affect many organ systems, but is particularly damaging the lungs, leading to COPD in
childhood and early childhood.

MANIFESTATIONS
 Recurrent pneumonia
 Exercise intolerance
 Chronic cough
 Clubbing of the fingers and toes
 Barrel chest
 Crackles on auscultation
 Hyoerresonant percussion tone
 Manifestations of right sided heart failure
 Abdominal pain
 Steatorrhea

LABORATORY/DIAGNOSTIC TESTS
 Analysis of chloride concentration in sweat – used to
confirm the diagnosis
- In CF, the CI concentration is >70 mEq/L
- Pilocarpine and a small electric current are
used to increase sweat production on the
forearm.
- Absorbent paper or gauze is used to collect
the sweat for analysis.
 ABGs – show hypoxemia

8
  Pulmonary Function Test – reveals reduced airflow, reduced forced vital capacity and reduced
total lung capacity.
MANAGEMENT
 MEDICATIONS
 Influenza vaccine – yearly
 Measles and pertussis boosters as needed
 Bronchodilator inhalers – used to control airway constriction.
 Antibiotic therapy – for acute pulmonary infections
 Dornase alfa – recombinant human DNase, breaks down the excess DNA in the sputum
of clients with CF.

 TREATMENTS
 Chest physiotherapy – percussion and postural drainage
 Use of the “huff” cough technique with specified breathing cycles or patterns.

 Oxygen therapy – for hypoxemia

 NURSING MANAGEMENT
 Assess respiratory status, including v/s breath sounds, SaO2, and skin color.
 Assess cough and sputum (amount, color consistency and possible odor).
 Monitor ABG results.
 Place in fowler’s or high fowler’s position. Encourage position changes and ambulation
as allowed.
 Assist to cough, deep breath and use assistive devices.
 Provide fluid intake of at least 2500 to 3000 ml per day.
 Encourage client and family to express their feelings, fears and concerns.

NURSING DIAGNOSES
 Ineffective Airway Clearance
 Anticipatory Grieving

4. BRONCHIECTASIS
- Characterized by permanent abnormal dilation of one or more large bronchi and destruction of the
bronchial walls.

CAUSES
 Cystic fibrosis
 Bacterial infection
 Exposure to toxic gases
 Abnormal lung or immunologic defenses
 Localized airway obstruction

9
 MANIFESTATIONS
 Chronic cough with mucopurulent sputum
 Hemoptysis
 Recurrent pneumonia
 Wheezing
 Shortness of breath
 Right sided heart failure
 Cor pulmonale

LABORATORY/DIAGNOSTIC TESTS
 Chest x-ray
 CT scan
 Bronchoscopy – direct visualization
of the larynx, trachea and bronchi
through a bronchoscope.
- May be used to clear retained
secretions/obstruction or to
evaluate hemoptysis.

COLLABORATIVE MANAGEMENT
 Antibiotics – prophylactic use
 Bronchodilators
 Chest physiotherapy
 Supplemental oxygen may be prescribed.

5. ATELECTASIS
- Is not a disease but a condition associated with many respiratory disorders.
- It is a state of partial or total lung collapse or airlessness.
- It may be acute or chronic.

CAUSES
 Obstruction of bronchus ventilating a segment of lung tissue
 Compression of the lung by pneumothorax
 Pleural effusion
 Tumor
 Loss of pulmonary surfactant

MANIFESTATIONS
 Diminished breath sounds – if small atelectasis
 Large lung area is affected – tachycardia, tachypnea, dyspnea, cyanosis, signs of hypoxemia,
reduced chest expansion and breath sounds, fever

10
MANAGEMENT
 Prevention for high risk clients (COPD, smokers undergoing surgery, prolonged bed rest or on
mechanical ventilation)
 Vigorous chest physiotherapy
 Frequent assessment of respiratory status
 For Clients with Atelectasis
 Vigorous coughing and chest physiotherapy

TECHNIQUES IN CHEST PHYSIOTHERAPY

a. Postural Drainage

b.

 Bronchoscopy may be necessary

 Antibiotic therapy
 Nursing Care
 Position client to the unaffected side.
 Encourage frequent changes, ambulation, coughing and deep breathing.
 Unless contraindicated, encourage fluids.
 Teach client at high risk for developing atelectasis about pulmonary care measures, fluid
intake and preventing pulmonary infections.

11
B. PULMONARY VASCULAR DISORDERS
1. PULMONARY EMBOLISM
- Obstruction of blood flow in part of the
pulmonary vascular system by an embolus.
- It is a medical emergency – 50% of deaths
occur within the first 2 hours following
embolization.

CAUSES
a. Blood clots that developed in the venous system
or right side of the heart
b. Tumors that have invaded venous circulation
c. Fat or bone marrow
d. Amniotic fluid released into the circulation
during childbirth
e. Intravenous injection of air or foreign substances

MANIFESTATIONS
a. Dyspnea
b. Pleuritic chest pain
c. Anxiety and apprehension
d. Cough
e. Tachycardia
f. Crackles (rales)
g. Low-grade fever
h. Diaphoresis
i. Hemoptysis
j. Syncope
k. Cyanosis
l. S3 and/or S4 gallop

LABORATORY/DIAGNOSTIC TESTS
a. Plasma D-dimer levels – highly specific to the presence of a thrombus.
- Elevated blood levels indicate thrombus formation and lysis.
b. Chest CT with contrast – principal test used to diagnose pulmonary embolism.
c. Lung scans – including perfusion and ventilation scans
 Perfusion lung scan – radiotagged albumin is injected intravenously and distributed in the
lungs by the pulmonary blood flow. The lungs are then scanned for distribution of the
isotope.
 Ventilation scan – a radiotagged gas is inhaled and the lungs are scanned for gas
distribution.
d. Pulmonary Angiography – definitive test for pulmonary embolism when other, less invasive test
are inconclusive.
- A contrast medium is injected into the pulmonary arteries illustrates the pulmonary
vascular system on x-ray.
e. Chest x-ray – shows pulmonary infiltration and occasionally pleural effusion.
f. ABGs – usually show hypoxemia and respiratory alkalosis.
g. Coagulation Studies – ordered to monitor the response to therapy.

12
  Activated partial thromboplastin time (aPTT or PTT)is used to assess the intrinsic
pathway and the response to heparin therapy.

MANAGEMENT
a. Pharmacological Management
a.1 Anticoagulant therapy – standard treatment to prevent pulmonary embolism.
 Heparin therapy – initiated with an IV bolus of 5000 to 10000 units, followed by
continuous infusion rate of 1000 to 1500 units/hour.
 Warfarin Sodium (Coumadin) – oral anticoagulant is initiated at the same time.
- Alters the synthesis of vitamin K dependent factors and requires 5 to 7 days to be fully
effective.

Nsg. Considerations of Anti-coagulant therapy

 Assess signs of bleeding.
 Report coagulation study results outside the desired range.
 Keep protamine sulfate available for heparin therapy and vitamin K available
for warfarin therapy.
a.2 Fibrinolytic therapy – used to treat massive pulmonary embolus and hypotension
- Reduce the incidence of pulmonary hypertension which develops 3 to 5 years after an
embolism.
Nsg. Considerations of Fibrinolytic therapy
 Avoid invasive procedures, injections and venous punctures when possible.
 Maintain firm pressure on injection and venipuncture sites.
 Maintain adequate fluid intake. Administer stool softeners as ordered.

b. Surgery
 Insertion of an umbrella like filter – inserted into the inferior vena cava to trap large
emboli while allowing continued blood flow.
- The filter is inserted percutaneously via either the femoral or jugular vein.

c. Nursing
Management
 Frequently assess respiratory status, including rate, depth, effort, lung sounds and oxygen
saturation.
 Monitor ABG results, reporting abnormal findings as indicated.
 Monitor cardiac rhythm, assess skin color and temperature.

13
  Maintain bed rest.
 Place in fowler’s or high fowler’s position with the lower extremities dependent.
 Monitor pulmonary artery pressures, neck vein distention and peripheral edema. Report
findings as indicated.

2. PULMONARY HYPERTENSION
- Abnormal elevated of the pulmonary arterial pressure

a. Primary Pulmonary Hypertension

- Is an uncommon disorder without identified cause.
- In the familial form, a gene transmitted in an autosomal dominant pattern affects a protein
receptor in the walls of pulmonary arteries leading to abnormal vessel growth.

b. Secondary Pulmonary Hypertension

- More common than primary

CAUSES
 Chronic lung disease – emphysema
 Sleep apnea
 Hypoventilation due to obesity or neuromuscular disease
 Left ventricular failure
 Mitral Stenosis

MANIFESTATIONS
a. Progressive dyspnea
b. Fatigue
c. Angina
d. Syncope with exertion

Complication:
COR PULMONALE – condition of the right ventricular hypertrophy and failure resulting from long-
standing pulmonary hypertension.
- COPD is the most common cause

Manifestations
 Chronic productive cough
 Progressive dyspnea
 Wheezing
 Peripheral edema
 Distended neck veins
 Skin – warm, moist, ruddy and cyanotic

LABORATORY/DIAGNOSTIC TESTS
a. CBC – shows polycythemia
b. ABGs and Oxygen Saturation
c. Chest X-ray – reveals right heart enlargement and dilation of central pulmonary arteries.
d. ECG – right ventricular hypertrophy
e. Doppler ultrasonography – noninvasive means of estimating pulmonary artery pressure.

14
 f. Cardiac catheterization – definitive diagnostic test
MANAGEMENT

a. Pharmacological Management
 Calcium Channel Blockers
 Short-acting direct vasodilators
 Oral anticoagulant
 Diuretic therapy

b. Supportive Management
 Oxygen administration
 If polycythemia is present, phlebotomy is performed.

c. Nursing Management
 Monitor breath sounds, RR, skin color and use of accessory muscles.
 Salt and water restriction – if with cor pulmonale
 Positioning for optimal lung expansion
 Coughing, deep breathing and chest physiotherapy

Nursing Diagnoses
a. Impaired Gas Exchange
b. Activity Intolerance
c. Decreased Cardiac Output
d. Excess Fluid Volume
e. Ineffective Individual Coping
f. Anticipatory Grieving
g. Hopelessness

C. RESPIRATORY FAILURE
- The lungs are unable to oxygenate the blood and remove carbon dioxide adequately to meet the
body’s needs, even at rest.

1. ACUTE RESPIRATORY FAILURE

- Not a disease but a consequence of severe respiratory dysfunction.
- It is often defined by ABG values.

CAUSES
a. COPD
b. Chest injury
c. Inhalation trauma
d. Neuromuscular disorders
e. Cardiac diseases

MANIFESTATIONS
a. Hypoxemia – dyspnea, restlessness, apprehension, impaired judgment, motor impairment,
tachycardia and hypertension, cyanosis
- As hypoxia progresses – dysrhythmias, hypotension, decreased CO

15
b. Hypercapnia – headache, peripheral and conjunctival vasodilation, papilledema, neuromuscular
irritability and decreased LOC, respiratory acidosis
LABORATORY/DIAGNOSTIC TESTS
a. ETCO2 – used to evaluate alveolar ventilation.
b. ABGs – used to evaluate alveolar ventilation and gas exchange.

COLLABORATIVE MANAGEMENT
a. Pharmacological
 Beta-adrenergic or anticholinergic – by inhalation to promote bronchodilation.
 Methylxantines – Theophylline – may be given intravenously
 Corticosteroids – reduce airway edema
 Antibiotics – to treat any underlying infection
 Anti-anxiety/anxiolytics – used for sedation and to inhibit respiratory drive.
 IV morphine or fentanyl – provides analgesia and also inhibits respiratory drive.
 Neuromuscular blocking agent – may be necessary to induce paralysis and suppress the
ability to breathe.

b. Oxygen Therapy
 Administered to reverse hypoxemia.
 The goal is to achieve an oxygen
saturation of 90% or greater without
oxygen toxicity.
 CPAP (continuous positive airway
pressure) is used when respiratory failure
is caused by hypoventilation or usual
oxygen delivery systems do not correct
hypoxemia.
- It increases lung volume, opening
previously closed alveoli,
improving ventilation of
underventilated alveoli and
improving ventilation-perfusion
relationships.

c. Airway Management
 Endotracheal tube insertion
 Done if upper airway is obstructed or
positive pressure mechanical ventilation
is necessary to correct hypoxemia and
hypercapnia.
 To maintain positive pressure
ventilation, the tube is cuffed with an air
filled or foam sac just above the end of
tube.

16
  Tracheostomy – for long term ventilator
support.
Disadv: Require surgical incision
Increase risk of lower respiratory infection

d. Mechanical Ventilation
- Indicated when alveolar ventilation is inadequate to
maintain blood oxygen and carbon dioxide levels.

e. Nursing Management
 Assess and document v/s and oxygen saturation.
 Promptly report worsening ABGs and oxygen saturation levels.
 Administer O2 as ordered.
 Place in Fowler’s or high-Fowler’s position.
 Minimize activities and energy expenditures.
 Prepare for endotracheal intubation and mechanical ventilation:
 Obtain an intubation tray with a selection of sterile endotracheal tubes and laryngoscope with
a variety of adult baldes.
 Check laryngoscope lamp, replace battery pack or bulb as needed.
 Set up endotracheal suction, bringing suction machine, sterile catheter, sterile gloves and
sterile NSS to the bedside.
 Notify respiratory therapist to set up the ventilator.
 Notify radiology that a portable chest x-ray will be needed on completion of intubation to
verify correct placement of the endotracheal tube.
 Explain the procedure and its purpose to the family.
 Suction as needed to maintain a patent airway.
 Perform chest physiotherapy as ordered.
 Firmly secure endotracheal or tracheostomy tube.

2. ACUTE RESPIRATORY DISTRESS SYNDROME

- Characterized by noncardiac pulmonary edema and progressive refractory hypoxemia.

CONDITIONS ASSOCIATED WITH ARDS

a. Shock
b. Inhalation injuries
c. Infections
d. Drug overdose
e. Trauma

MANIFESTATIONS
a. Dyspnea
b. Tachypnea
c. Anxiety
d. Intercostal retractions
e. Use of accessory muscles
f. Cyanosis
g. Crackles and rhonchi

17
h. Agitation
i. Confusion
j. Lethargy
LABORATORY/DIAGNOSTIC TESTS
a. ABGs
b. Chest x-ray – diffuse infiltrates, progressing to
a “white out” pattern.
c. Chest CT Scan – provides a better illustration
of the pattern of alveolar consolidation and
atelectasis.
d. Pulmonary function testing – shows decreased
lung compliance with reduced vital capacity,
minute volume and functional vital capacity.
e. Pulmonary artery pressure monitoring – shows
normal pressure in ARDS, helping distinguish
ARDS from cardiogenic pulmonary edema.

MANAGEMENT
a. Pharmacological
 Inhaled nitric oxide – improves oxygenation by dilating blood vessels in better ventilated areas of
the lungs.
 Surfactant therapy – reduces surface tension, helps maintain open alveoli, decreasing the work of
breathing, improving compliance and gas exchange and preventing atelectasis.
 NSAIDs and Corticosteroids – to block inflammatory response.
 Antibiotic therapy – to treat any infection
 Anticoagulant therapy

b. Mechanical ventilation
 Mainstay management for ARDS is endotracheal intubation and mechanical ventilation.

c. Nursing Management
 Monitor and record vital signs including apical pulse.
 Assess LOC and lung sounds frequently.
 Frequently provide good skin care, keeping skin clean and dry and protecting pressure points.
 Maintain IVF as ordered.
 Enteral or parenteral feeding is necessary to maintain nutritional status.
 Place in Fowler’s or high-Fowler’s position.
 Assist in the weaning process:
 Remain with the client during initial periods following changes of ventilator settings.
 Limit procedures and activities during weaning periods.
 Provide diversion such as television or radio.
 Begin weaning procedures in the morning when the client is well rested and alert.
 Avoid administering drugs that may depress respirations during the process.
 Keep oxygen at the bedside following weaning and extubation.
 Provide pulmonary hygiene with percussion and postural drainage.

18
19