RESPIRATORY SYSTEM

Five Parts to Respiration

1. Pulmonary ventilation = breathing;
2. External respiration = air into lungs; gas exchange (O2 load/ CO2 unload); air out;
3. Transport of respiratory gases = gases in blood transported from lungs to body cells and back to lungs;
4. Internal respiration = exchange of gases at body capillaries (O2 unload/CO2 load).
5. Cellular respiration = use of oxygen by cells to produce energy (production of CO2).

ORGANS OF THE RESPIRATORY SYSTEM

UPPER RESPIRATORY ORGANS

The upper respiratory organs are lined with mucous membranes:
• The mucus functions to trap debris.
• The cilia beats the debris to the pharynx to be swallowed and destroyed by digestive enzymes.
• This tissue also serves to warm and moisten incoming air.

Nose (external nares or nostrils)

Nasal cavity (separated by nasal septum)
• bone & cartilage lined with mucous membranes;
• turbinates warm and moisten incoming air;
• olfactory reception;
• resonating chambers for speech;
• olfactory (smell) nerve endings are located in roof of nasal cavity.

Nasal conchae (within nasal cavity)

• lined by mucous membranes;
• increase turbulence of incoming air to better warm, moisten and filter.

Paranasal sinuses
• within 4 skull bones (frontal, ethmoid, sphenoid, maxillary);
• drain into nasal cavity;
• lined with mucous membranes;
• reduce weight of skull;
• resonating chambers for speech.

Pharynx (or throat)

• wall of skeletal muscle lines with mucous membranes;
• passageway for air and food;
• resonant chamber for speech sounds;
• three parts:
o nasopharynx (uppermost), contains lymph tissue called adenoids;
o oropharynx (middle), contains lymph tissues called tonsils;
o laryngopharynx (lowest).

Larynx (or voice box)

Thyroid cartilage (Adam's apple);

Epiglottis closes off the airway during swallowing;

Trachea (windpipe)
• Location = mediastinum; anterior to esophagus; extends from larynx to T5;
• Structure:
o Function = support against collapse; continue to warm, moisten & filter air;
o Lined by mucous membranes;
o Carina = point where trachea divides into right & left bronchus…highly sensitive and touching it causes coughing.
LOWER RESPIRATORY ORGANS

Bronchial tree within lungs

• a main-stem bronchus leads into each lung (right one is shorter, wider and straighter, so aspiration is more likely in the
right lung than the left). The main-stem bronchus then branches into…
• lobar bronchi which branch to each lobe and then branch into …
• segmental bronchi that divide into…
• sub-segmental bronchi which branch into tubes called…
• terminal (respiratory) bronchioles. Bronchoconstriction/dilation occurs here.
• With this extensive branching:
• Epithelium changes from ciliated pseudostratified columnar epithelium to non-ciliated simple columnar epithelium in
terminal bronchioles;
• Cartilage decreases;
• Smooth muscle increases (innervated by ANS and hormones:
o Parasympathetic and histamine constrict bronchioles (i.e. bronchoconstriction);
o Sympathetic and epinephrine dilate bronchioles (i.e. bronchodilation).
• Further branching is microscopic into…
• respiratory bronchioles…
• alveolar ducts…
• alveolar sacs…
• alveoli.

CHEST WALL AND LUNGS

• Location = thoracic cavity;
• Chest wall is shaped, supported and protected by 24 ribs (12 per side).
o covered by pleural (serous) membranes:
 visceral pleura;
 parietal pleura;
 intrapleural space between the pleura is filled with a thin film of fluid (20-25 mL)
• pleural fluid has a very high surface tension that allows the two membranes to act as one (vs.
lubrication function of other serous fluids).
• Pleural fluid is drained by the lymphatic circulation. Some pathologic conditions may cause the
accumulation of greater amounts of fluid, called pleural effusion.
• Purulent pleural fluid with bacterial infection is called empyema.
• Lung Anatomy:
o Each lung is divided into lobes by fissures:
 Right lung has 3 lobes;
 Left lung has 2 lobes.
 Each lobe:
• receives a secondary bronchus;
• is divided into lobules.
• Each lobule:
 is wrapped in elastic connective tissue;
 contains a lymphatic vessel, an arteriole, a venule, and a branch from a terminal
bronchiole.
 Microscopic anatomy:
 Each terminal bronchiole subdivides into microscopic branches called…
 respiratory bronchioles (lined by simple squamous epithelium), which subdivide into several …
 alveolar ducts, which terminate into numerous…
 alveoli and alveolar sacs (2-3 alveoli that share a common opening).

ALVEOLI (microscopic air sacs)

 Are interconnected by pores of Kohn, which allow movement of air (and bacteria) from
 alveolus to alveolus.
 Wall consist of two types of epithelial cells and macrophages;
o Type I Alveolar cells form a continuous simple squamous lining of the alveolar
wall;
o Type II Alveolar cells interrupt above lining and secrete surfactant:
 complex mixture = detergent;
 lowers surface tension and prevents alveolar collapse.
 Stretching of alveoli during a sigh stimulates secretion of surfactant.
o Alveolar Macrophages remove dust particles and other debris from alveolar
spaces.
 Alveolar-Capillary (Respiratory) Membrane
o Structure = thin (0.5 um in thickness).
o Function = allows for rapid diffusion of gases (from [high] to [low]).

The lungs contain more than 300 million alveoli = Surface area the size of a tennis court
for gas exchange at one time!

VENTILATION AND RESPIRATION

BLOOD SUPPLY TO LUNGS (two fold):

 Pulmonary circuit (deoxygenated blood);
 Oxygenated blood is delivered through bronchial arteries (off thoracic aorta).

Recall that the function of the respiratory system is to supply cells with oxygen and remove carbon dioxide. The three basic processes
are pulmonary ventilation, external respiration and internal respiration.

PULMONARY VENTILATION (Breathing):

 BREATHING involves two actions, inspiration & expiration.

o Inspiration (inhalation) = breathing air in.
 The thoracic cavity has a given size and volume.
 When the diaphragm is at rest (curved upward), the air pressure outside the lungs is equal to the air
pressure inside the lungs (1 atm or 760 mm Hg)
 During inspiration:
• The diaphragm muscle pushes downward;
• The size of thoracic cavity increases;
• The pressure in the thoracic cavity decreases (758 mm Hg);
• The air pressure inside the thoracic cavity (lungs) is less than the atmospheric pressure and
therefore air rushes into lungs to equalize the pressure gradient.
 Pleural Membranes aid in inspiration:
o Serous fluid between membranes primarily contains water;
o The water in the serous fluid has great surface tension and therefore…
 Membranes move together:
• thoracic cage expands;
• parietal pleura expands;
• visceral pleura expands;
• lungs expand.
 Contraction of the external intercostal muscles also aid inspiration.

o Expiration (exhalation) = breathing out depends on two factors:

 The elastic recoil of tissues that were stretched during inspiration (i.e. tissues bouncing back to shape).
 The inward pull of surface tension due to the alveolar fluid.

 Atelectasis (Collapsed Lung)

• At the end of an expiration, the alveoli tend to recoil inward and collapse on themselves;
 • Surfactant (mixture of phospholipid & proteins) produced by Type II Alveolar cells decreases the
surface tension in the lungs;
• As the alveoli become smaller during expiration, the surfactant overcomes the pressure differential
and allows the alveoli to remain inflated.
o Respiratory Distress Syndrome (RDS) in newborns (collapsed lungs) occurs due to the
lack of surfactant in the alveoli.
Modified Respiratory Movements
 Usually the result of reflexes:
o Cough = sends blast of air through and clears upper respiratory tract;
o Sneeze = forcefully expels air through nose & mouth;
o Laugh = a deep breath released in a series of short convulsive expirations;
o Hiccup = spasmodic contraction of diaphragm;
o Yawn = deep inspiration through open mouth; (ventilates alveoli?).
Factors that influence breathing:
 Stretch of Tissues;
 Low blood oxygen;
 High Blood carbon dioxide;
 Low pH;
 Others: temperature, pain, irritation of airways.
RESPIRATORY AIR VOLUMES
Respiratory air volumes are measured by spirometry and include:

 Anatomical Dead Space (VD) = volume of air that fills the space between the nose and the bronchioles; approximately
150 ml;

 Tidal Volume (VT) = volume of air that enters the lungs during normal inspiration and leaves the lungs during normal
expiration; approximately 500 ml (of which 150 ml is VD);

 Inspiratory Reserve Volume (IRV) = the amount of air the can be forcibly inhaled after a normal tidal expiration;
approximately 3000 ml;

 Expiratory Reserve Volume (ERV) = the amount of air that can be forcibly exhaled after a normal tidal expiration;
approximately 1100 ml;

 Vital Capacity (VC) = the maximum amount of air that can be exhaled after a maximum inhalation;

 VC = TV + IRV + ERV = 4600 ml.

 Residual Volume = amount of air that always remains in lungs =1200 ml;

 Total Lung Capacity = VC + RV = approximately 6 L.

EXTERNAL RESPIRATION:

 Definition = the exchange of oxygen and carbon dioxide between the alveoli and lung blood capillaries.
 The pressure of gas determines the rate at which it will diffuse from region to region (Dalton's Law).
o Air is a mixture of gases:
 78% Nitrogen
 21% Oxygen
 0.04% Carbon Dioxide
o In a mixture of gases, the amount of pressure that each gas creates = partial pressure.
 In air: O2 = 21%; PaO2 = 104 mm Hg
 In air: CO2 = .04%; PaCO2 = 40 mm Hg
 The partial pressure of a gas is directly related to the concentration of that gas in a mixture.
 Diffusion of gases through the respiratory membrane proceeds from where a gas is at high partial pressure
to low partial pressure.

ALVEOLUS CAPILLARY
 PaCO2 PaCO2
40 mmHg 45 mmHg
PaO2 PaO2
104 mmHg 40 mmHg

 Therefore, CO2 will flow from lung capillary ----> alveolus & O2 will flow from alveolus ----> lung capillary.

o The rate of diffusion of gases also depends on a number of factors, including the following:
 gas exchange surface area;
 diffusion distance;
 breathing rate and depth.
INTERNAL RESPIRATION

 Definition = the exchange of oxygen and carbon dioxide between tissue blood capillaries and tissue cells.
o In tissue cell: PaCO2 = 45; PaO2 = 40;

o In tissue capillary: PaCO2 = 40; PaO2 = 95.

CELL CAPILLARY
PaCO2 PaCO2
45 mmHg 40 mmHg
PaO2 PaO2
40 mmHg 95 mmHg

o Therefore, oxygen moves from the tissue capillary into the tissue cell and carbon dioxide moves from the tissue cell
into the tissue capillary.

TRANSPORT OF GASES (IN BLOOD)

 Oxygen
o Oxygen is carried in the blood in two forms: dissolved and bound to hemoglobin.
 Dissolved oxygen is called partial pressure or arterial tension (PaO2) expressed as mmHg
 Bound oxygen is called oxygen saturation (SaO2) expressed as a percentage
• Oxygen binds with hemoglobin (Hb) in red blood cells to form oxyhemoglobin;
• A weak bond is formed so oxygen can be delivered (released) to tissues when needed.
• The release of oxygen from hemoglobin depends on many factors:
o Increases with high blood PaCO2; decreases with low blood PaCO2;
o Increases when low blood pH (acidosis); decreases when high blood pH (alkalosis);
o Increases when high blood temperature; decreases when low blood temperature.
• Carbon monoxide (CO) binds to hemoglobin more efficiently than oxygen.
o If the hemoglobin (that is suppose to bind with oxygen) is bound to CO, much less Hb is
available to bind and transport oxygen to the tissues; Hypoxia results.
 Carbon Dioxide (CO2)
o CO2 is transported in 3 forms:
 dissolved CO2= 7% (PaCO2)
 carbaminohemoglobin=23%
 bicarbonate ions= 70% (HCO3-)
o In tissues, CO2 is produced by cellular respiration.
 This CO2 combines with H2O to form H2CO3 (carbonic acid) which then…
 dissociates under the influence of carbonic anhydrase to release…
 H+ and bicarbonate ion (HCO3-): CO2 + H2O <------> H2CO3 <-------> H+ + HCO3-
• Reaction is reversed in lungs & CO2 is expelled during expiration.
 Assessment Values (Normals)
o ABG = arterial blood gases
 pH = 7.35 – 7.45
 PaO2 = 80 – 100 mmHg
 SaO2 = >95%
 PaCO2 = 35 – 45 mmHg
 HCO3- = 22 – 26 mEq/L
o VBG = venous blood gases
 pH = 7.34 – 7.37
 VO2 = oxygen consumption
  PvO2 = mixed venous oxygen tension = 38 – 42 mmHg
 SvO2 = venous oxygen saturation = 60% – 80%
 PvCO2 = mixed venous carbon dioxide tension = 44 – 46 mmHg
 HCO3- = 24-30 mEq/L
o Oximetry = arterial oxygen saturation with pulse oximetry
 SpO2 = >95%
• Less accurate when SpO2 is less than 70% or when hemoglobin variants are present.
• Motion, low perfusion, anemia, bright lights, IV dyes, thick acrylic nails, dark skin color also make
pulse ox less accurate

RESPIRATORY DEFENSE MECHANISMS

 Filtration of air
o Nasal hairs
o Turbulence: change in airflow direction at nasopharynx and larynx
o Mucuous trapping
o Particle size greater than 5 um are usually removed before reaching alveoli
 Mucociliary clearance
o Mucous is continually secreted
 Rate approx. 100 ml per day by goblet cells and submucosal glands
 Secretory immunoglobulin A (IgA) in mucous protects against viruses and bacteria
o Cilia move particles to mouth to be swallowed and destroyed by digestive enzymes
 May be impaired by dehydration, smoking, high O2 concentrations, infection and drugs like atropine,
anesthetics, alcohol, cocaine, cystic fibrosis and chronic bronchitis.
 Cough reflex
o Only effective in removing secretions above the subsegmental level (large/main airways)
o Lower secretions must be moved upward by mucociliary elevator
 Reflex bronchoconstriction
o In response to inhalation of large amounts of irritating substances, bronchi constrict.
 Alveolar macrophages
o Alveoli do not have cilia, but have macrophages instead.
o Rapidly phagocytize inhaled foreign particles like bacteria.
o Debris moved to the level of bronchioles forremoval by cilia or lymph system.
o Impaired by cigarettes

LIFE SPAN CHANGES

 Exposure to pollutants, smoke, etc, increases the risk of developing respiratory illnesses.
 Loss of cilia, thickening of mucus, and impaired macrophages increases the risk of infection as one ages.
 Breathing becomes more difficult as one ages due to:
o calcified cartilage
o skeletal changes
o altered posture
o replacement of bronchiole smooth muscle by fibrous connective tissue.
 Vital Capacity decreases with age.

DIAGNOSTIC STUDIES

 Blood
o Hemoglobin (Hg) and hematocrit (Hct)
o ABGs
o Oximetry (SpO2 and SvO2)

 Sputum Studies
o Expectoration
o Tracheal suction
o Bronchoscopy
 o Observe for color, blood, volume, viscosity

 Skin Tests
o Allergy testing and TB
o Intradermal injection of an antigen
o Look for induration and measure diameter in mm.

 Radiologic Studies
o Chest X-Ray
o Computed tomography (CT) 3-D views
o Magnetic Resonance Imaging (MRI)
o Ventilation-Perfusion Scan
 For diagnosis of pulmonary embolus
o Pulmonary Angiography
 Confirmation of ambolus if lung scan is inconclusive
 Also diagnoses congenital and acquired lesions of the pulmonary vessels
o Positron Emission Tomography (PET)
 For benign vs. malignant solitary pulmonary nodules
 Graphs glucose metabolism (increased in malignancies)

 Endoscopic Exams
o Bronchoscopy
 Visualization of bronchi with a fiberoptic tube.
• For biopsies
• To remove mucous plugs or foreign bodies
• Bronchoalveolar lavage (BAL): 30 mL of sterile saline injected through the scope and withdrawn to
examine for cells.
o BAL diagnoses Pneumocystis carinii pneumonia
o Mediastinoscopy
 Inspects and biopsy of lymph nodes in mediastinal area
 Lung Biopsy
o Specimens obtained by transbronchial (through bronchoscope tube) or open lung.
 Thoracentesis
o Insertion of a needle through the chest wall into the pleural space to obtain specimens for diagnosis
 Pulmonary Function Tests (PFTs)
o Measure lung volumes and airflow.
o Diagnose pulmonary disease
o Performed with a spirometer
 Exercise Testing
o Walking on a treadmill while expired oxygen/carbon dioxide, respiratory rate, heart rate and rhythm are monitored.
o Timed walk measures exercise capacity.
UPPER RESPIRATORY PROBLEMS Chapter 26

STRUCTURAL AND TRAUMATIC DISORDERS OF THE NOSE

Deviated Septum
Definition: A deflection of the normally straight nasal septum to one side that alters the passage of air.
Cause: Trauma to the nose or congenital disproportion (septum is not proportional to the size of the nose).
Signs/Symptoms: Variable. May experience obstruction to nasal breathing, nasal edema, dryness of nasal mucosa with
bleeding. Severely deviated septum may block drainage of mucous resulting in sinus infection.
Treatment: Allergy control or surgery (“nasal septoplasty”).

Nasal Fracture
Cause: Trauma to the nose or middle part of the face.
Signs/Symptoms: Unilateral fracture: little or no displacement
Bilateral fracture: (most common) nose looks flattened
Complex: Caused by powerful frontal blows which may also shatter frontal bones.
Inability to breathe through each side of the nose, edema, bleeding, hematoma, ecchymosis (bruising)
under one or both eyes. Internally, look for septal deviation, hemorrhage or clear drainage which may
be CSF.
Treatment: Maintain a patent airway, reduce edema with ice, prevent complications, provide emotional support,
realign fractured parts with surgery (rhinoplasty or septoplasty).

Rhinoplasty
Definition: Surgical reconstruction of the nose for cosmetic purposes or to improve airway function R/T trauma or
deformities.
Role of the Nurse: Pre-op: Assess patient’s expectations of surgery (actual or perceived alteration in body image). Inform
patient not to take aspirin or NSAIDs for 2 weeks to reduce the risk of bleeding. Post-op: Assess
respiratory status, pain, surgical site for hemorrhage/edema.

Epistaxis
Definition: Nosebleed. Occurs especially in children (usually anterior bleeding) and in elderly adults (usually
posterior bleeding).
Cause: Trauma, foreign bodies, nasal spray abuse, street drug use, anatomic malformation, allergic rhinitis or
tumors. Hypertension does not cause nosebleed, but it can make a nosebleed more difficult to control.
First Aid: Keep the patient quiet; place patient in a sitting position, leaning forward; apply direct pressure by
pinching the entire soft lower portion of the nose for 10 to 15 minutes; apply ice compresses to thenose
and have the patient suck on ice; partially insert a small gauze pad into the bleeding nostril and apply
pressure if bleeding continues; get medical assistance if bleeding does not stop.
Treatment: Application of vasoconstrictive agent, cauterization, anterior packing, posterior packing.
Role of the Nurse: Posterior packing predisposes patient to bacterial infection, is painful and may alter respiratory status
(especially in elderly). Monitor respiratory rate, heart rate/rhythm, oxygen saturation (pulse ox), LOC
and observe for signs of aspiration. Patient should receive a mild narcotic analgesic for pain and an
antibiotic effective against Staph. Home teaching includes: sneezing with an open mouth and
avoidance of aspiring-containing products/NSAIDS, vigorous nose blowing, strenuous activity, lifting and
straining for 4 to 6 weeks after discharge.
INFLAMMATION AND INFECTION OF NOSE AND SINUSES
Allergic Rhinitis
Definition: The reaction of the nasal mucosa to a specific allergen.
Cause: Seasonal: caused by pollen, flowers, grasses and occur in spring/fall; last several weeks while allergens
are high. Perennial: caused by specific environmental triggers like pet dander, dust mites, molds,
cockroaches; is present intermittently or constantly and symptoms resemble the common cold.
Signs/Symptoms: Nasal congestion; sneezing; itchy, watery eyes and nose; altered sense of smell; thin, watery nasal
discharge; turbinates appear pale, boggy and swollen and may obstruct sinus drainage resulting in
sinusitis. Headache, congestion, pressure, post-nasal drip, nasal polyps, snoring may result in chorinic
allergies.
Treatment: Identify and avoid triggers (keep a diary to track activities that precipitate an allergic reaction). Drug
therapy includes nasal sprays, antihistamines, decongestants, intranasal corticosteroid sprays and
cromolyn sprays. Omalizumad (Xolair) is being investigated as a monoclonal antibody to
immunoglobulin E (IgE) that prevents the allergic cascade response. Immunotherapy (allergy shots)
attempt to control allergies through frequent, small exposures to triggers with the goal of decreasing
sensitivity to the allergens.
Role of the Nurse: Alert patients using antihistamines that sedation is a major side effect of the first-generation drugs
(benadryl). Patients using nasal inhalers need careful instructions about proper use of the equipment.
Teach patients that nasal decongestant sprays can cause a rebound effect from prolonged use.

Acute Viral Rhinitis

Definition: Common cold (“acute coryza”).
Cause: Virus that invades the upper respiratory tract. Is the most prevalent infectious disease in the world and
is spread by airborne droplets.
Signs/Symptoms: Tickling and irritation of throat, sneezing, dryness of the nose or nasopharynx, followed by copious
nasal secretions, some nasal obstruction, watery eyes, elevated temperature, headache, and general
malaise. Complications include laryngitis, sinusitis, otitis media, tonsillitis, and lung infection.
Treatment: Rest, fluids, proper diet, antipyretics, analgesics, and drugs to reduce annoying symptoms such as
antihistamines and decongestants. Antibiotics are not effective. Frequent hand washing and avoidance
of hand-to-face contact may prevent direct spread of infection.
Echinacea, an herbal therapy, stimulates immune system and has antibacterial and anti-inflammatory
properties. Considered safe when taken at recommended doses for 10 to 14 days. Do not take for
more than 8 weeks. Patients with immune disorders should not use Echinacea.
Role of the Nurse: Teach patient to recognize the symptoms of secondary bacterial infections: temperature above 100.4 F;
purulent nasal exudate; tender, swollen glands and a sore, red throat. In patients with pulmonary
disease, look for changes in consistency/color/volume of sputum. Antibiotics may be given sooner to
patients with respiratory disease.

Influenza
Definition: “Flu”
Cause: Three groups of viruses (A, B & C, though C has little pathogenic effects)
Signs/Symptoms: Abrupt onset of cough, fever, and myalgia often accompanied by headache and sore throat. Other cold-
like symptoms may also appear. Symptoms of uncomplicated flu usually subside within 7 days. Some
experience weakness and lassitude, hyperactive airways and chronic cough that may persist for weeks
(older adults, especially).
Persons over 50; adults with chronic illness, cardiac or respiratory problems; nursing home residents;
people hospitalized in the past year; immunocompromised adults; women in 2nd or 3rd trimester of
pregnancy; and people with known exposure to the virus are all at significantly higher risk.
PNEUMONIA is the most common complication of flu.
Treatment: Vaccine is 70 to 90% effective in preventing flu when given in the fall (mid-Oct) before exposure occurs.
All people over 50 and all healthcare workers are encouraged to get vaccinated. Soreness at the
injection site is the only side effect of the vaccine (but vaccine is contraindicated in people allergic to
eggs). FluMist (a nasal vaccine) is available to adults under 49 years of age.
 Primary treatment: Relieve symptoms and prevent secondary infections.
Rimantadine (Flumadine) or amantadine (Symmetrel) and antivirals used against influenza A. (Side
effects may include heartburn and hallucinations). Zanamivir (Relenza) and oseltamivir (Tamiflu) are
effective against influenza A and B. They prevent the virus from budding and spreading to other cells.
Start treatments within 2 days of symptoms to reduce duration and severity of flu infection.

Sinusitis
Definition: Infection of the sinuses occurring as a result of blockage to the ostia (sinus exit) by inflammation or
swelling of the mucosa.
Cause: Bacteria, viruses and fungi all may grow in the secretions trapped in the sinuses and cause infection.
Bacterial infection is most commonly Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella
catarrhalis. Viral infection follows upper respiratory infection when virus invades mucous membrane
and decreases ciliary action. Fungal sinusitis is uncommon and is usually only in debilitated and
immunocompromised patients. Forty percent of intubated patients contract nosocomial sinusitis.
Two forms: Acute and Chronic.
Acute: results from upper respiratory infection, allergies, swimming or dental manipulation.
Chronic: (a persistent infection) associated with allergies and nasal polyps.
Signs/Symptoms: Acute: Significant pain over affected sinus, purulent nasal drainage, nasal obstruction, congestion,
fever and malaise. Patient looks and feels sick. Mucosa appears hyperemic, swollen and tender.
Headaches may change in intensity with position change or when secretions drain.
Chronic: Difficult to diagnose because symptoms are non-specific. Patient rarely presents with fever.
Symptoms may mimic allergies. X-Ray/CT Scan may show sinuses filled with thick fluid. Nasal
endoscopy may be used to examine sinuses and obtain a drainage culture.
Asthma and sinusitis are closely linked for unknown reasons. Appropriate treatment of sinusitis may
reduce asthma symptoms.
Treatment: Most cases of sinusitis resolve on their own without treatment within 2 weeks.
Keep well-hydrated; irrigate the nose with salt water; take hot showers/use steam inhaler to loosen
secretions; monitor for temperature >100.4 F; use analgesics for pain, decongestants/expectorants for
symptoms and antibiotics for infection; administer nasal sprays correctly; do not smoke. Avoid first-
generation antihistamines (Benadryl) as they thicken secretions. Second-generation (non-drowsy)
antihistamines are effective in relieving symptoms.
Broad-spectrum antibiotics taken for 4 to 6 weeks may be required with chronic sinusitis R/T mixed
bacterial flora present in infection.
Antibiotics reduce by 50% incidence of clinical failure

• Amoxicillin or Amox w/ clavulanate

• TMP/SMZ
• Cephalexin
• Cefuroxime
• Cefalor
• Quinolones
• Macrolides
Antibiotics and other drugs may not resolve condition and infection may worsen or recur, or infection may be
drug resistant.
Complications include Osteomyelitis and Mucocele. In elderly – any respiratory infection may lead to
pneumonia.
Unresolved sinusitis may need referral to a specialist (ENT)
NASAL/SINUS OBSTRUCTIONS

Polyps
Definition: Benign mucous membrane masses which appear as bluish, glossy projections in the nare. Can exceed
the size of a grape!
Cause: Form slowly in response to repeated inflammation of the sinus or nasal mucosa.
Signs/Symptoms: Nasal obstruction, nasal discharge (usually clear), and speech distortion.
Treatment: Removal with endoscopic or laser surgery (but recurrence is common). Topical or systemic
cortiocosteroids may slow polyp growth.
Role of the Nurse: Monitor patient for anxiety R/T fear of malignancy.

Foreign Bodies
Signs/Symptoms: Inorganic items (buttons, beads, etc.) may have no symptoms, may lie undetected and be accidentally
discovered upon examination. Organic items (wood, cotton, beans, peas, raisins, paper) produce a
local inflammatory response with nasal discharge which may become purulent and foul smelling.
Treatment: Remove item from nose through the route of entry. Sneezing with the opposite nostril closed may be
effective in assisting the removal of foreign bodies. Do NOT irrigate or push the item further into the
nose as this can cause aspiration and airway obstruction. If removal is not possible…see a health care
provider!

PROBLEMS RELATED TO THE PHARYNX

Acute Pharyngitis
Definition: An acute inflammation of the pharyngeal walls (including tonsils, palate and uvula).
Cause: 70% are nonspecified viral infections. 15% to 20% are bacterial “Strep throat” infections caused by
beta-hemolytic Streptococcus invasion. Fungal pharyngitis, especially candidiasis can develop with
prolonged use of antibiotics or inhaled corticosteroids (especially in immunosuppressed patients –
HIV/AIDS)
Signs/Symptoms: Range from “scratchy throat” to pain so severe that swallowing is impaired. Both viral and bacterial
appear as red, edematous pharynx with or without yellow patchy exudate. Appearance is not
diagnostic! Cultures/rapid strep antigen tests must be done to determine cause and therefore treatment
course. Irregular white patches suggest fungal infection (Candida albicans). Gray-white
pseudomembrane covering the oro/naso/laryngo pharynx and trachea indicates diphtheria.
Treatment: Washing hands may prevent infections! Goals are infection control, symptom relief and prevention of
secondary infection. Bacterial infections may be treated with antibiotics. Candida infections are treated
with nystatin (swish medicine in mouth as long as possible before swallowing).
Increase fluid intake; cool/bland liquids and gelatin are non-irritating. Avoid citrus juices which irritate.

Peritonsillar Abscess
Definition: A complication of acute pharyngitis or acute tonsillitis when bacterial infection invades one or both
tonsils.
Signs/Symptoms: Tonsil enlarge sufficiently to threaten airway patency; high fever; leukocytosis; chills.
Treatment: IV antibiotics, needle aspiration/incision to drain abscess and possibly an emergency tonsillectomy.

Obstructive Sleep Apnea

Definition: Partial or complete upper airway obstruction during sleep causing apnea (cessation of spontaneous
respirations) and hypopnea (abnormally shallow and slow respirations).
Cause: Tongue and soft palate fall backward and partially or completely obstruct the pharynx. The obstruction
may last 15 to 90 seconds. Apnea results in hypoxemia (decreased O2) and hypercapnia (increased
CO2) which causes patient to partially awaken with a startle response, snort and gasp which brings the
 tongue and palate forward opening the airway. Patient may startle awake 200 to 400 times in 8 hours of
sleep.
Signs/Symptoms: Frequent awakening at night; insomnia; excessive daytime sleepiness; witnessed apneic episodes;
loud, uncontrolled snoring; morning headaches (from hypercapnia’s vasodilation of cerebral blood
vessels); personality changes; irritability; complications include systemic hypertension and cardiac
arrhythmias.
Diagnosis: Polysomnography in a sleep laboratory or home sleep study. Measures patient’s chest/abdominal
movement; oral airflow; nasal airflow; pulse ox; ocular movement and heart rate/rhythm. Multiple
episodes of apnea or hypopnea (airflow diminished 30 to 50%) confirm diagnosis.
Treatment: Avoid sedatives/alcohol within 3 to 4 hours of sleep; lose weight; use an oral appliance that prevents
tongue from obstructing pharynx; nasal continuous positive airway pressure (nCPAP) or bilevel positive
airway pressure (BiPAP) machines are effective in reducing sleep apnea, but compliance by patients is
low; surgical treatments are available and effective in about 60% of patients.

PROBLEMS RELATED TO THE TRACHEA AND LARYNX

Airway Obstruction
Definition: Any mechanical impediment to the delivery of air to the lungs or to the absorption of oxygen in the
lungs. May be partial or complete. Complete obstruction is a medical emergency.
Cause: Aspiration of food or a foreign body; laryngeal edema following extubation; laryngeal or tracheal
stenosis; CNS depression; allergic reactions (anaphylactic).
Signs/Symptoms: Stridor, use of accessory muscles, suprasternal and intercostal retractions, wheezing, restlessness,
tachycardia and cyanosis.
Treatment: Prompt assessment is required as partial obstruction can quickly progress to complete obstruction.
Reestablish a patent airway (Heimlich’s maneuver), cricothyroidtomy (an emergency incision into the
larynx performed to open the airway in a person who is choking); endotracheal intubation and
tracheostomy. Unexplained or recurring symptoms need additional tests (chest XRay, pulmonary
function tests and bronchoscopy).

Tracheostomy
Definition: A tracheotomy is a surgical incision into the trachea for the purpose of establishing an airway. A
tracheostomy is the stoma (opening) that results from the tracheotomy.
Purpose: Bypass an upper airway obstruction; facilitate the removal of secretions; permit long-term mechanical
ventilation; permit oral intake and speech in the patient with long-term mechanical ventilation.
Advantages: Compared to endotracheal tubes, tracheostomies have less risk of long-term damage to the airway; are
more comfortable for patient because no tube is in the mouth; allows the patient to eat and speak; and
is more secure so mobility for the patient is enhanced.
Role of the Nurse: Care of the patient with a tracheostomy involves suctioning the airway to remove secretions; cleaning
around the stoma; changing tracheostomy ties; inner cannula care; continuously assessing the risk of
aspiration and educating the patient about the care of his/her tracheostomy.

Laryngeal Polyps
Definition: Growths on the vocal cords.
Cause: Vocal abuse or irritation (intubation, cigarettes).
Signs/Symptoms: Hoarseness
Treatment: Surgical removal of large polyps that cause stridor and dyspnea may be required. Polyps are usually
benign, but may later become malignant.

Head/Neck Cancer
Definition: Malignant tumors, typically squamous cell in origin, that arise from mucosal surfaces of the paranasal
sinuses, oral cavity and naso/oropharynx and larynx.
Cause: Though this type of cancer is rare in the general population, 90% of cases occur in adults 50 years or
older after prolonged use of tobacco and alcohol. Twice as many males as females are affected.
Signs/Symptoms: Disability is great because of potential loss of voice, facial disfigurement and social consequences.
Early signs/symptoms vary with tumor location:
 Oral cavity cancer may start as a painless growth in the mouth or ulcer that does not heal. Pain is
a late symptom that may be aggravated by acidic food.
 -pharynx and supraglottic larynx cancers rarely produce early symptoms and are diagnosed in late
stages when patient complains of persistent unilateral sore throat or ear pain.
 Laryngeal cancer may have hoarseness as an early symptom.
 Lumps in the neck or hoarseness that lasts longer than 2 weeks requires a medical evaluation.
Late signs/symptoms are easily detected: pain, dysphagia, decreased mobility of tongue, airway
obstruction, cranial nerve neuropathy.
Diagnosis: Thorough examination of oral cavity is required, including under the tongue and dentures; The floor of
the mouth, tongue and lymph nodes in the neck should be palpated. Look for thickening of the normally
soft and pliable oral mucosa. Leukoplakia (white patches) or erythroplakia (red patches) may be seen
and should be biopsied.
Indirect laryngoscopy and/or flexible nasopharyngoscope may be used to visually inspect the larynx and
vocal cords for lesions and tissue mobility. CT scans or MRIs may be used to detect local/regional
spread of cancer. Typically, multiple biopsy specimens are required to determine the extent of the
disease.
TNM Staging is used to classify the disease process. (T) = tumor size; (N) = number/location of
involved nodes and (M) = extent of metastasis. TNM is classified in stages I to IV and stage guides the
treatment.
Treatment: Stage I or II may undergo radiation therapy or surgery with the goal of cure.
Laryngeal cancer:
Radiation
• Radiation effectively cures early vocal cord lesions without damaging the voice.
o Brachytherapy: Thin, hollow needles are inserted into the tumor area and radioactive
iridium seeds are placed in the needles. This delivers a concentrated, but localized,
dose of radiation to the tumor but does not affect surrounding tissues. May be used
alone or in conjunction with external radiation.
Surgical Interventions:

• Cordectomy (partial removal of one vocal cord). Voice is preserved.

• Hemilaryngectomy: removal of one vocal cord or part of a cord and requires a temporary
tracheostomy. Voice is preserved but quality is hoarse and breathy.

• Supraglottic laryngectomy: removal of structures above the true vocal cords (false cords and
epiglottis). Patient is left with high risk of aspiration and requires a temporary tracheostomy.
Voice is preserved, but quality is hoarse and breathy.

• Total laryngectomy: removal of entire larynx and pre-epiglottic region with permanent
tracheostomy.

• Neck dissection: often accompany total laryngectomies and involves excision of lymph nodes
and lymph channels (to reduce risk of spreading disase).
o Radical neck dissection: Wide excision of nodes and lymph channels, and includes
removal or transaction of sternocleidomastoid muscles (and other neck muscles),
internal jugular vein, mandible, submaxillary gland, part of the thyroid/parathyroid
glands and the spinal accessory nerve. Usually is only performed on one side of the
neck.
o Modified neck dissection: Spares as many structures as possible to limit
disfigurement and functional loss. Removes major cervical lymph vessels but spares
nerves, veins and muscles when possible. When cancer lesion is midline, bilateral
neck dissections are required, but a modified procedure will be performed on at least
one side.
 o Nutrition Therapy for Neck Dissections
 Parenteral fluids for 24-48 hours. Tube feedings via NG, nasointestinal or
gastrostomy tube may be required. (Watch for intolerance of feeding—
nausea/vomiting/diarrhea/distention).
 When patient can swallow, watch for choking and aspiration.
 Anticipate swallowing issues. Teach supraglottic swallow to minimize
aspiration risks.
 Avoid thin, watery fluids, instead use non-pourable pureed foods of foods
thickened with an agent (thicker foods allow more control in swallowing).
 Give antiemetics and analgesias before meals to reduce nausea and mouth
pain.
 Always feed with head of bed elevated.

Planning: Goals: a patent airway; no spread of cancer; no complications related to therapy; adequate nutritional
intake; minimal to no pain; ability to communicate; acceptable body image.
Interventions Immediately after surgery: maintain patent airway; place patient in semi-Fowler’s position (decrease
edema); monitor vital signs for hemorrhage and respiratory compromise; use would suction system as
needed.
Radiation therapy: Dry mouth may be treated with increased fluid intake, sugarless gum, sugarless
candy, nonalcoholic mouth wash, artificial saliva, oral hygiene. Stomatitis (dry lips at the corners of
mouth) may be treated with water/hydrogen peroxide (3:1 ratio) rinse, or baking soda and water (1t to 8
oz of water) to clean/soothe irritated tissue. Avoid commercial mouthwash and hot/spicy foods. Altered
skin integrity is common.
Teach patient about changes in speech and alternate ways to communicate (prostheses, esophageal
speech method). Teach about stoma care.
Monitor patient for signs of depression (loss of function, disfigurement, body image and sexuality
issues.)
Prognosis: Overall, the cure rate for head/neck cancer is low for advanced stages, despite surgical and radiation
interventions. Metastatic cancer is painful and leaves patients in a severely debilitated state.
LOWER RESPIRATORY PROBLEMS Chapter 27

Acute Bronchitis
Definition: Inflammation of the bronchi in the lower respiratory tract usually due to infection. One of the most
common conditions seen in primary care.
Cause: Usually occurs as a complication of an upper respiratory tract infection brought on by a virus
(rhinovirus, influenza, corona virus, respiratory synctial virus (RSV), adenovirus, influenza A and B,
parainfluenza).
Bacterial infections are also common
• Smokers usually infected with Strep pneumoniae and Haemophilus influenzae;

• Non-smokers usually infected with Mycoplasma pneumoniae, Chlamydia pneumoniae;

• Unusual bacteria: Bordetella pertussis, Bordetella parapertussis, Legionella species

Signs/Symptoms: Persistent cough following an acute upper airway infection (rhinitis/pharyngitis)
• Productive cough with clear to purulent sputum
• Rhinitis
• Pharyngitis
• Mild fever
• Headache
• Malaise
• Shortness of breath on exertion
• Elevated pulse and respiratory rate
• Normal breath sounds or rhonchi and expiratory wheezing
• Chest discomfort
Diagnosis: Clues to diagnosis:
• Hoarseness…
o Suggests Chlamydia pneumoniae

• Paroxysmal, barking cough, worse at night, interferes with completing a sentence…

o Suggests Bordetella species

• Impressive constitutional symptoms (shaking chills, high fever, fatigue, sweats, muscle
aches)…
o Suggest influenza
• Recurrent episodes of acute bronchitis…
o Concern for HIV infection
When symptoms are severe, chest x-rays can differentiate acute bronchitis from pneumonia (acute
bronchitis has no evidence of consolidation or infiltrates).
Treatment: Usually self-limiting; treatment is supportive…
• Fluids
• Rest
• Anti-inflammatory agents
• Antiviral medications
• Cough suppressant or bronchodilators for symptomatic treatment of nocturnal
cough/wheezing
• Other symptom relief to reduce complaints
Pharmacotherapy
• Antibiotics are not usually prescribed unless person has prolonged infection, is a smoker
 or has COPD.
• No proven value in using antibiotics in acute bronchitis
• Increases medical costs
• Fosters drug resistance
• Contributes to drug toxicity
• When prescribed, the drug of choice is a broad-spectrum antibiotic for multi-flora
infections.
o In acute exacerbation of chronic bronchitis, early intervention with antibiotics
can reduce hospitalizations and decrease risk of relapse. If untreated, acute
exacerbation of chronic bronchitis can lead to respiratory failure.
• For Flu: amantadine or rimantadine within 48 hours may help
• For wheezing: albuterol inhaler

Pneumonia
Definition: An acute inflammation of the lung parenchyma that commonly impairs gas exchange. Bacterial
pneumonia is the leading cause of death in debilitated patients.
Cause: Pneumonia may be viral, bacterial, fungal, protozoal (parasitic), or chemical in origin.
• Primary pneumonia results from inhalation or aspiration of a pathogen;

• Secondary pneumonia may follow lung damage from noxious chemicals or other insults,
or may result from hematogenous spread of bacteria (bacteria in the blood).
• Aspiration pneumonia results from inhalation of foreign matter (vomitus, food particles)
into the bronchi.
• Pneumonia can also be transmitted by direct contact with contaminated equipment
(suction catheters, bronchoscopes).
Bacterial pneumonia:
• Infection initially triggers alveolar inflammation and edema, which produces an area of low
ventilation with normal perfusion.
• Capillaries become engorged with blood, causing stasis.
• As alveolocapillary membrane breaks down, alveoli fill with blood and exudate, resulting in
atelectasis (lung collapse)
• Lungs look heavy and liver-like.
Viral pneumonia:
• The virus first attacks bronchiolar epithelial cells, which causes interstitial inflammation
and desquamation.
• The virus also invades bronchial mucous glands and goblet cells.
• It spreads to the alveoli, which fill with blood and fluid.
Aspiration pneumonia:
• Inhalation of gastric juices or hydrocarbons trigger inflammation and inactivates surfactant
over a large area.
• Decreased surfactant leads to alveolar collapse.
• Acidic gastric juices may damage the airways and alveoli. Particles containing aspirated
gastric juices may obstruct the airways and reduce airflow, leading to secondary bacterial
pneumonia.
Risk Factors: Factors predisposing to pneumonia:
• Aging
• Air pollution
• Altered consciousness (alcoholism, head injury, seizures, anesthesia, drug overdose,
stroke)
• Altered oropharyngeal flora
• Bed rest/prolonged immobility
 • Chronic disease (COPD, diabetes mellitus, heart disease, cancer, end-stage renal
disease)
• Debilitating illness
• HIV
• Immunosuppresive drugs (corticosteroids, cancer chemotherapy, organ transplant)
• Inhalation or aspiration of noxious substances
• Intestinal and gastric feedings
• Malnutrition
• Smoking
• Tracheal intubation
• Upper respiratory tract infection

Types & Classifications: Community-Acquired Pneumonia (CAP)

• “A lower respiratory tract infection of the lung parenchyma with onset in the community or
during the first 2 days of hospitalization.”
o Category 1: Outpatients with no history of cardiopulmonary disease and no
modifying factors
 Treated with latest-generation macrolide (Zithromax, Biaxin)
 or doxycycline
o Category 2: Outpatients with cardiopulmonary disease and/or modifying factors

 Treated with beta-lactam (Ceftin, Augmentin) plus macrolide/doxycycline

 or anti-Pseudomonal fluoroquinolone (Cipro, Levaquin)
o Category 3: Inpatients, not admitted to ICU
o Category 4: ICU patients
o Modifying factors = age >65, alcoholism, multiple medical co-morbidities and
immunosuppressive disease.
• Likely organisms of CAP:
o Streptococcus pneumoniae (most common)
o Mycoplasma pneumoniae
o Haemophilus influenzae
o Respiratory viruses
o Chlamydia pneumoniae
o Legionella pneumophila
o Oral anaerobes
o Moraxella catarrhalis
o Staphylococcus aureus
o Nocardia
o Enteric aerobic Gram (-) bacteria (Klebsiella)
o Fungi
o Mycobacterium tuberculosis
• Highest incidence in winter months
• Smoking is a high risk factor
Hospital-Acquired Pneumonia (HAP)
• “Pneumonia occurring 48 hours or longer after hospital admission and not incubating at
the time of hospitalization.”
• Likely organisms of HAP:
o Pseudomonas aeruginosa
 o Enterobacter
o Escherichia coli
o Proteus
o Klebsiella
o Staphylococcus aureus
o Streptococcus pneumoniae
o Oral anaerobes
• Categories of HAP
o Group 1: Patients without unusual risk factors who have mild to moderate HAP
with onset at any time during hospitalization or severe HAP of early onset (<5
days after admission)
 Enteric, gram-negative bacilli (Enterobacter, E. coli, Proteus, Klebsiella,
H. influenzae)
 MRSA
 Streptococcus pneumoniae
 Treatment…
• Cephalosporin (2nd generation)
• Beta-lactam/beta-lactamase inhibitor
• Fluoroquinolone if allergic to penicillin
o Group 2: Patients with specific risk factors who have mild to moderate HAP
occurring any time during hospitalization.
 Abdominal surgery; aspiration…
• Anaerobes…
o Clindamycin or beta-lactam
 Coma, head trauma, diabetes mellitus, renal failure…
• Staphylococcus aureus…
o Vancomycin until MRSA ruled out
 High-dose corticosteroids…
• Legionella…
o Erythromycin with/without rifampin

 Prolonged ICU stay, corticosteroids, antibiotics, lung disease…

• Pseudomonas aeruginosa…
o Treat as severe HAP!
o Group 3: Patients with severe HAP either of early onset with specific risk factors
or of late onset (>5 days after admission).
 Pseudomonas aeruginosa
 Acinetobacter species
 Treatment…
• Aminoglycoside or ciprofloxacin PLUS one of the following…
o Antipseudomonal penicillin
o Beta-lactam/beta-lactamase inhibitor
o Ceftazidime
o Cefoperazone
o Imipenem (Primaxin)
o Aztreonam (Azactam)
 MRSA
• Treatment…vancomycin
 • Risk for HAP in mechanically ventilated patients is 6 to 20 times higher than other
patients.
• Inpatient mortality rates much higher than mortality for CAP (1-5% vs. 12%)
Aspiration Pneumonia
• “The sequelae occurring from abnormal entry of secretions or substances into the lower
airway. Usually follows aspiration of material from the mouth or stomach into the trachea
and subsequently the lungs.”
• Usually patient has a history of loss of consciousness (seizure, anesthesia, head injury,
stroke, alcohol intake), with gag and cough reflex depression or is on tube feedings.
• Three forms of aspiration pneumonia:
o Inert substance (mechanical obstruction is first manifestation). Example: barium,
peanut, small bead.
o Chemical (non-infectious) pneumonitis (chemical injury to the lungs with infection
as a secondary event 48 to 72 hours later). Example: toxic fluids, gastric juices.
o Bacterial infection (usually normal oropharyngeal flora or multiple organisms
inhaled into lungs). Antibiotic therapy is based on severity of illness, HAP/CAP,
and type of organism.
Opportunistic Pneumonia
• Affects patients with compromised immune systems.
o Pneumocystis carinii = HIV/AIDS. Chest x-ray shows diffuse bilateral alveolar
pattern of infiltration. In widespread disease, lungs are massively consolidated.
Treat with Bactrim.
o Cytomegalovirus (type of herpes virus) = organ transplant patients. Gives rise to
latent infections and reactivation with virus shedding. May be mild or can be
fulminant and produce pulmonary insufficiency leading to death. In pneumonia,
may be combined with other bacteria and fungi. Treat with Cytovene.
Signs/Symptoms: Pneumococcal Pneumonia:
• CONGESTION Phase: outpouring of fluid into the alveoli; organisms multiply and spread.
• RED HEPATIZATION Phase: Massive dilation of the capillaries and alveoli are filled with
organisms, neutrophils, RBCs and fibrin. Lung appears red and granular like liver.
• GRAY HEPATIZATION Phase: Decreased blood flow and WBCs/fibrin consolidate in the
affected part of lung.
• RESOLUTION Phase: Complete resolution and healing occur if no complications arise.
CAP Symptoms:
• S. Pneumoniae:
o Sudden onset of fever, chills, cough productive of purulent sputum and pleuritic
chest pain.
o Elderly or debilitated patient may have confusion or stupor R/T hypoxia.
o Pulmonary consolidation (dullness to percussion, increased fremitus, bronchial
breath sounds and crackles)
• Mycoplasma, Legionella, Chlamydia pneumoniae:
o Gradual onset
o Dry cough
o Extrapulmonary manifestations…
 Headache
 Myalgias
 Fatigue
 Sore throat
 Nausea
 Vomiting
 Diarrhea
  Crackles on auscultation
• Septic Staphylococcus aureus:
o Patient is very sick
o Only pulmonary symptoms may be dyspnea and fever
o Necrotizing infection destroys lung tissue
• Viral pneumonia:
o Chills
o Fever
o Dry, non-productive cough
o Extrapulmonary symptoms
o Can be caused by flu
o May also be found with measles, varicella-zoster, and herpes simplex

Complications: Pneumonia in an otherwise healthy adult usually resolves without complications. However, in
compromised patients, complications include…
• Pleurisy – inflammation of the pleura
• Pleural effusion – usually effusion is sterile and reabsorbed in 1 to 2 weeks
• Atelectasis – collapsed, airless alveoli in part of one lobe. Usually clears with effective
coughing and deep breathing
• Delayed resolution – results from persistent infection with residual consolidation (elderly,
malnourished, alcoholic or COPD at highest risk)
• Lung abscess – usually S. aureus and Gram-negative pneumonias
• Empyema – accumulation of purulent exudate in the pleural cavity (needs antibiotics and
drainage via chest tube or surgery)
• Pericarditis – spread of infection from lungs to heart lining
• Arthritis – systemic spread of infection affects joints
• Meningitis – can be caused by S. pneumoniae. Look for disorientation, confusion,
somnolent symptoms.
• Endocarditis – spread of infection to valves of the heart.
Diagnosis: Chest x-ray…
• Lobar/segmental consolidation = bacterial cause, usually Strep pneumoniae or Klebsiella

• Diffuse pulmonary infiltrates = virus, Legionella or pathogenic fungi

• Cavitary shadows = necrotizing infection/destruction of tissue by S. aureus, Gram (-)

bacteria and Mycobacterium tuberculosis.
• Pleural effusion = 30% of patients with CAP
Sputum cultures…
• For drug-resistant pathogens
• Organisms not responsive to empiric treatment (broad-spectrum antibiotics)
• Should be done before administration of antibiotics
Blood tests…
• For seriously ill patients, collect two cultures before treatment
• ABGs usually reveal hypoxemia
• Leukocytosis found in bacterial pneumonia (>15,000/microliter)
Clues to diagnosis…
• Sudden onset; single, shaking chill; sustained temperature of 102 to 104 F; commonly
preceded by upper respiratory infection = Streptococcus
• Alcoholics, COPD, Diabetics; fever, recurrent chills; cough producing rusty, bloody,
 viscous sputum (currant jelly); cyanosis of lips and nail beds; shallow, grunting respirations
= Klebsiella
• Patients with viral illness (flu/measles) or cystic fibrosis; temperature of 102 to 104;
recurrent shaking chills; bloody sputum; dyspnea; tachypnea; hypoxemia =
Staphylococcus
• Insidious onset; generally affects young adults; sore throat; fever; cough; chills; malaise;
small amt of mucoid sputum; retrosternal chest pain; anorexia; rhinitis; adenopathy;
scattered crackles; rhonchi = Adenovirus
• Infants and children; listlessness; irritability; tachypnea with retraction of intercostal
muscles; slight sputum production; fever; severe malaise; possible cough or croup; fine,
moist crackles = Respiratory Syncytial Virus (RSV)
Treatment: Supportive measures:
• Oxygen therapy (hypoxemia)
• Analgesics for chest pain
• Antipyretics (aspirin/Tylenol) for fever
• Restrict activity and encourage rest
Viral pneumonia
• No definitive treatment is recommended
• Prevent or treat flu
o Flu vaccine
oEmpiric treatment of flu includes amantadine, rimantadine or a neuraminidase
inhibitor
Pneumococcal vaccine
• For people at risk…
o Chronic illness (lung/heart disease; diabetes)
o Recovering from severe illness
o 65 years or older
o Living in a long-term care facility
o Revaccinate every 5 years if immunocompromised
Antibiotics
• Main caution is drug resistant bacteria and allergic reactions to certain antibiotics
• Non-categorized patients usually given empiric, broad-spectrum antibiotic.
• CAP (Category 1)
o Antibiotic is macrolide (Zithromax) or clarithromycin (Biaxin)
o If allergic to macrolides, use doxycycline (though doxycycline is not as reliable
against pneumococcus organisms)
o Do not use erythromycin, Penn V K, Rifampin or Bactrim…they are not effective
against pneumococcal bacteria.
• HAP
o Empiric antibiotic treatment should be based on likely pathogen of various groups
o When using empiric therapy, it is important to recognize the nonresponsive
patient quickly. Patients with ventilator-associated pneumonia can deteriorate
rapidly. Aggressive assessment and treatment are required.
Nutritional therapy
• Fluid intake of at least 3 L per day to support treatment; may need to be administered by
IV
• Minimum of 1500 calories per day
• Eat small, frequent meals.
Role of Nurse: Goals
• Clear breath sounds
 • Normal breathing patterns
• No signs of hypoxia
• Normal chest x-ray
• No complications related to pneumonia

Tuberculosis
Definition: An infectious disease caused by Mycobacterium tuberculosis. Usually involves the lungs, but may
occur in the larynx, kidneys, bones, adrenal glands, lymph nodes and meninges and can be
disseminated throughout the body.
• TB kills more people worldwide than any other infectious disease.
• In the late 1940s, streptomycin and isoniazid (INH) brought about a dramatic decrease in
TB prevalence.
• Between 1985 and 1992, there was a significant increase in TB prevalence due to...
o HIV infection
o Multidrug-resistant (MDR) strains of M. tuberculosis
o Poor compliance with drug therapy
o Treatment failure
o Poor follow-up treatment
o Decreased vigilance in treating patients
• Prevalence has again decreased since 1993 due to improvements in TB control programs.
Cause: M. tuberculosis is a gram-positive, acid-fast bacillus that is spread from person to person via
airborne droplets, which are produced when the infected individual with pulmonary or laryngeal TB
coughs, sneezes, speaks or sings.
Risk factors:
• Poor, under-served minorities
• Homeless people
• Residents of inner-city neighborhoods
• Foreign-born people
• Older adults
• Institutionalized people
• IV/injection drug users
• Socioeconomically disadvantaged
• Medically underserved of all races
• Immunosuppressed people (HIV, cancer, organ transplant)
• Native American population (Arizona, New Mexico)
• Mexican border
• Health care workers
TB is not highly infectious and transmission usually requires close, frequent or prolonged exposure.
Pathophysiology:
o Bacilli are inhaled and implant in bronchioles or alveoli
o After implantation, bacilli multiply with no initial resistance from host
o Bacilli are engulfed by phagocytes
o Continue to multiply within the phagocytes
o Phagocytes/macrophages spread the bacilli through the lymphatic system into the blood
stream before a cellular immune response can be activated
o Kidneys, epiphyses of bones, cerebral cortex and adrenal glands are target sites
of TB
o Eventually cellular immunity limits further spread of infection.
 o A characteristic tissue reaction called epithelioid cell granuloma results from
cellular immune reaction
 Granuloma is result of fusion of the infiltrating macrophages
 Granuloma is surrounded by lymphocytes within 10 to 20 days
 Central part of granuloma lesion is called Ghon tubercle which
undergoes necrosis characterized by a cheesy appearance named
caseous necrosis.
 The lesion may also undergo liquefactive necrosis in which the liquefied
remains of the lesion drains into connecting bronchi and produces a
cavity.
 The tubercular material may enter the tracheobronchial system, allowing
airborne transmission of infectious particles.
o Healing of lesion involves resolution, fibrosis and calcification.

 The granulation tissue surrounding the lesion may become more fibrous
and form a collagenous scar around the tubercle. A Ghon complex is
formed, consisting of the Ghon tubercle and regional lymph nodes.
 Calcified Ghon complexes may be seen on chest x-ray.
o The disease enters a latent phase in which it may persist without clinical
symptoms.
o If the initial immune response is not adequate, control of the organisms is not
maintained and clinical illness results.
 People at risk for clinical illness are usually immunosuppressed…
• HIV infection
• Cancer with chemotherapy
• Long-term corticosteroid use
• Diabetes mellitus
Signs/Symptoms: Early Stage:
• Usually symptom-free; many cases are found incidentally with routine chest x-ray,
especially in older adults
• Systemic manifestations…
o Fatigue
o Malaise
o Anorexia
o Weight loss
o Low-grade fever
o Night sweats
• Pulmonary manifestations…
o Frequent cough that produces mucoid or mucopurulent sputum
o Dyspnea is unusual
o Chest pain characterized as dull or tight
o Hemoptysis is uncommon and is usually associated with advanced stages
Acute Onset:
• High fever
• Chills
• Generalized flu-like symptoms
• Pleuritic pain
• Productive cough
Complications: Complications of TB include…
• Miliary (Hematogenous) TB
 o A necrotic Ghon complex erodes through a blood vessel and large numbers of
organisms invade the blood stream and spread throughout the body.
• Patient may be acutely ill with fever, dyspnea and cyanosis or…
• Chronically ill with systemic manifestations of weight loss, fever and GI
disturbance.
• Hepatomegaly, splenomegaly and generalized lymphadenopathy may
be present.
• Pleural Effusion and Empyema
o Release of caseous material into the pleural space triggers an inflammatory
reaction and a pleural exudate of protein-rich fluid.
o Dry pleurisy may result from a superficial tuberculosis lesion involving the pleura.
o Empyema is less common but may occur from large numbers of organisms
spilling into the pleural space from a ruptured cavity.
• Tuberculosis Pneumonia
o Results when large amounts of bacilli spill from the liquefied necrotic lesion into
the lung or lymph nodes.
o Symptoms resemble bacterial pneumonia…
• Chills
• Fever
• Productive cough
• Pleuritic pain
• Leukocytosis
• Other Organ Involvement
o Meninges
o Bone and joint tissue
o Kidneys
o Adrenal glands
o Lymph nodes
o Female and male genital tracts

Diagnosis: Classification of TB
o Class 0: No TB exposure
o Class 1: TB exposure, no infection (negative skin test)
o Class 2: Latent TB infection, no disease (positive skin test; other tests negative)
o Class 3: TB clinically active (positive skin test; other tests positive; symptomatic of TB)
o Class 4: TB, not clinically active (positive skin test; documented history of disease; x-
ray shows evidence of past infection; bacteriology tests negative; no symptoms)
o Class 5: TB Suspect (diagnosis pending…no more than 3 months in this class)
Tuberculin Skin Testing
o Antigen/Antibody reaction test…uses purified protein derivative (PPD) of tuberculin to
detect TB antibodies from a previous immune response.
o Once acquired, sensitivity to TB persists throughout life.
o Reaction of >5 mm induration is positive for patients with…
o Recent close contact with person diagnosed with infectious TB
o Chest x-ray with fibrotic lesions likely to be healed TB
o Known or suspected HIV infection
o Organ transplants and other immunosuppressive conditions
o Reaction of >10 mm induration is positive for patients…
 o With other medical risk factors known to substantially increase risk of TB once
infection has occurred (diabetes, renal disease, cancer)
o Who recently immigrated from (in past 5 years) from areas of high prevalence
o Who are medically under-served or homeless
o Who reside in long-term care facilities and prisons
o Who use IV drugs
o Who are health care workers
o Who are low risk for TB
o Reaction of >15 mm induration is positive for all others at low risk.
Chest X-ray
o It is not possible to make a diagnosis of TB solely on the basis of a chest x-ray.
o Chest x-ray in TB patient most commonly shows multinodular lymph node involvement
with cavitation in the upper lobes of the lungs.
o Calcification of lesions occurs within several years of infection.
Bacteriologic Studies
o True diagnosis can only be made by demonstrating the presence of tubercle bacilli.
o Stained sputum smear for acid-fast bacilli is usually the first bacteriologic evidence of
infection.
o Three consecutive sputum specimens collected on different days are tested.
o Gastric washes, cerebrospinal fluid and pus from an abscess can all be stained and
tested.
o Nucleic acid amplification (NAA) is a new, rapid diagnostic test for TB. Results are
available in a few hours, but the NAA test does not replace routine sputum smears and
cultures.
Treatment: Outpatient Treatment
o Patient may continue to work and maintain lifestyle
o Hospitalization is only for diagnosis or for severe illness, adverse drug reactions or
treatment failures.
Drug Therapy
o Active Disease
o Multidrug-resistant TB occurs when resistance develops to two or more anti-TB
drugs
o Treatment usually consists of a combination of at least four drugs.
o Five primary drugs currently used are:
 Isoniazid (INH)
 Rifampin (Rifamate)
 Pyrazinamide
 Streptomycin
 Ethambutol (Myambutol)
o Fixed-dose combo drugs (INH/rifampin and INH/rifampin/pyrazinamide) are
available and may enhance compliance to treatment
o HIV patients on antiretroviral drugs cannot take rifampin because it impairs the
effectiveness of the antiretroviral drug.
o Newer drugs include the quinolones (ciprofloxacin/Cipro) and rifapentine (Priftin).
o Therapy must be continued for 6 to 9 months.
o Drug regimens should be adapted to the resistance pattern evident from sputum
culture.
o Monitor the effectiveness of drugs and the development of toxic side effects.
o Test sputum samples weekly and then monthly to assess effectiveness.
 Regimen is considered effective if the patient converts to a negative TB
sputum status.
o Follow-up care ensures adherence to the treatment regimen with Directly
 Observed Therapy (DOT) with patients known to be at risk for noncompliance.
o Teaching patients about the side effects of these drugs and when to seek prompt
medical attention is critical.
o The major side effect of INH, rifampin and pyrazinamide is HEPATITIS.
 Monitor liver function tests regularly.
Latent Infections
o Latent TB Infection (LTBI) occurs when an individual become infected but does
not become ill.
o Drug therapy can be used to prevent a TB infection from developing into a
clinical disease.
o INH administered orally once daily for 6 to 9 months can prevent illness.
 HIV patients and those with fibrotic lesions on chest X-ray take INH for
full 9 months.
Vaccine
o Immunization with bacilli Calmette-Guerin (BCG) vaccine prevents.
o Is currently in use in many parts of the world.
o The PPD skin test of vaccinated individuals results in an induration of less than
10 mm. Therefore a “positive” TB test for vaccinated indivduals is defined as “an
increase in induration by 10 mm from a previous PPD test.” (American Thoracic
Society)
Role of Nurse: Goals:
o Patient will comply with therapeutic regimen
o Patient will have no recurrence of disease
o Patient will have normal pulmonary function
o Patient will take appropriate measures to prevent the spread of disease.
Interventions:
o Assess symptomatic patient for exposure to persons with TB.
o Patients strongly suspected of having TB should…
o Be placed on respiratory isolation
o Receive four-drug therapy
o Receive an immediate medical work-up, including chest x-ray, sputum smear and
culture
o Use a negative pressure isolation room that offers six or more exchanges per
hour to isolate patient.
o Teach patient to cover the nose and mouth with paper tissue every time he or she coughs,
sneezes or produces sputum. The tissues should be burned, flushed down the toilet or
thrown into a paper bag and disposed of with the trash.
o Instruct the patient about certain factors that could reactivate TB such as
immunosuppressive therapy, malignancy and prolonged debilitation.

Atypical Mycobacteria
Definition and Cause:
Pulmonary Fungal Infections
Definition and Cause:
A pulmonary disease that closely resembles TB but caused by atypical acid-fast mycobacteria.
o Is indistinguishable from TB except by bacteriologic culture.
o These organisms are a common cause of opportunistic infections in HIV patients.
o Treatment depends on specific organsism, but many of the drugs used in TB are effective
in atypical mycobacteria.
Organisms include…
o Histoplasma capsulatum
o Coccidioides immitis
o Blastomyces dermatitidis
o Cryptococcus neoformans
 o Aspergillus niger or A. fumigatus
o Candida albicans
o Actinomyces Israeli
o Nocardia asteroides
Found most frequently in seriously ill patients being treated with corticosteroids, antineoplastics,
immunosuppressive drugs and multiple antibiotics and in patients with AIDS and cystic fibrosis.
• Fungi not transmitted person to person so patient does not have to be placed in isolation.
• Signs and symptoms are similar to those of bacterial pneumonia
• Identification in sputum specimen or other body fluid is best diagnostic indicator.
Treatment Amphotericin B is the drug most widely used in treating serious systemic fungal infections.
• Must be given intravenously to achieve adequate blood and tissue levels because it is
poorly absorbed from the GI tract.
• Is considered toxic with many possible side effects
o Hypersensitivity reactions
o Fever
o Chills
o Malaise
o Nausea/vomiting
o Thromobphlebitis at the injection site
o Abnormal renal function
o Avoid side effects by…
 Pre-medicating with an anti-inflammatory of diphenhydramine
(Benadryl) one hour before infusion
 Include small amount of hydrocortisone in the infusion to decrease
irritation of the veins
 Monitor renal function
 Ensure adequate hydration
• Is incompatible with most other drugs
• Administered every other day after an initial period of several weeks of daily therapy.
• Total treatment duration may range from 4 to 12 weeks.
Other oral drugs used to treat fungal infections include:
o Oral imidazole and triazole compounds with antifungal activity (ketoconazole,
fluconazole).
o May be used as alternative to amphotericin B.

Bronchiectasis
Definition: A permanent, abnormal dilation of one or more large bronchi resulting from destruction of the
elastic and muscular structures of the bronchial wall from bacterial infections.
o Two types:
o Saccular bronchiectasis occurs in large bronchi; characterized by cavity-like
dilations which end in large sacs.
o Cylindric bronchiectasis occurs in medium-sized bronchi that are mildly to
moderately dilated.
Cause: Almost all are associated with bacterial infections, including S. aureus, Klebsiella and anaerobes.
Viruses such as adenovirus and influenza can also cause bronchiectasis.
o Infections cause the bronchial walls to weaken, and pockets of infection begin to form.
When the walls of the bronchial system are injured, the mucociliary mechanism is
damaged allowing bacteria and mucus to accumulate within the pockets.
 o Mycobacteria avium-intracellulare presents a new threat because it can progress to
bronchiectasis.
Signs/Symptoms: Hallmark is persistent or recurrent cough with production of greater than 20 mL of purulent sputum
per day.
o Cough is paroxysmal and is stimulated with position change
o Copious (may be blood-streaked) sputum
o Exertional dyspnea
o Fatigue
o Weight loss
o Anorexia
o Fetid breath
o Crackles, rhonchi and wheezing may be heard
o Sinusitis frequently accompanies diffuse bronchiectasis
o Advanced, widespread bronchiectasis symptoms are generalized wheezing, digital
clubbing and cor pulmonale.
Diagnosis: Diagnostic studies…
• Chest x-rays show streaky infiltrates or may be normal;

• CT scan is excellent at detecting bronchiectasis;

• Bronchoscopy can identify source of secretions or sites of hemoptysis and can collect
sputum samples
• Sputum specimens may provide additional information regarding the severity of
impairment and the presence of active infections.
• Pulmonary function tests may be abnormal in advanced bronchiectasis showing a
decrease in vital capacity, expiratory flow and maximum voluntary ventilation.
• CBC may be normal or show leukocytosis
Treatment: Bronchiectasis is difficult to treat
• Treat acute flare-ups and prevent decline in lung function
• Antibiotics are mainstay of therapy and are given on basis of sputum culture
o Nebulized antibiotics are new therapy that appears effective in reducing
hospitalizations and flare-ups
o Antipseudomonal antibiotics (tobramycin/Nebcin) are commonly used
• Concurrent bronchodilator therapy is given to prevent bronchospasm.
• Mucolytic agents and expectorants are also used.
• Good hydration is required to liquify secretions
• Chest physical therapy and other airway clearance techniques are important to facilitate
expectoration of sputum
• Reduce exposure to excessive air pollutants and irritants
• Avoid cigarette smoking
• Obtain pneumococcal and influenza vaccinations
• Surgical resection of parts of the lungs is an option, but not used as often as in the past
o Surgery may be indicated in repeated bouts of pneumonia, hemoptysis and
disabling complications
o Surgery is not advised with diffuse or widespread involvement
• Lung transplantation is an option for bronchiectasis
Role of Nurse: Early detection and treatment of lower respiratory infections helps prevent complications like
bronchiectasis.
• Promptly remove any obstructive lesions or foreign bodies
• Promote drainage and removal of bronchial mucus
• Teach effective deep-breathing exercises and effective ways to cough
 • Some individuals require elevation of the foot of the bed by 4 to 6 inches to facilitate
drainage
• Flutter mucus clearance devices provide airway vibration during expiration (handheld
device); two to four 15-minutes sessions daily can provide satisfactory mucus clearance
• Positive expiratory pressure (PEP) therapy is a breathing maneuver against an expiratory
resistance often used in conjunction with nebulized medications
• Administration of prescribed antibiotics, bronchodilators or expectorants is important
• Rest is important to prevent overexertion
• Chilling and excess fatigue should be avoided
• Good nutrition is important and may be difficult to obtain
o Oral hygiene to cleanse the mouth and remove dried sputum crusts may improve
the patient’s appetite
o Offer appealing foods to increase desire to eat
• Drink at least 3 L of fluid daily
o Use low-sodium fluids to avoid systemic fluid retention
o Use a bland aerosol with normal saline solution to directly hydrate the respiratory
system (delivered via jet-type nebulizer)
• Avoid ultrasonic nebulizers because they often induce bronchospasm
• Steamy showers can prove effective at loosening mucus secretions
• Teach patient to recognize significant clinical symptoms…
o Increased sputum production
o Grossly bloody sputum
o Increasing dyspnea
o Fever
o Chills
o Chest pain

Lung Abscess
Definition: A pus-containing lesion of the lung parenchyma that gives rise to a cavity. The cavity is formed by
necrosis of the lung tissue.
Cause: Caused by aspiration of material from the oral cavity (gingival crevices) into the lungs.
Organisms include enteric gram-negative organisms (Klebsiella), S. aureus and anaerobic bacilli.
May also be caused by a lung infarct secondary to pulmonary embolism, malignant growth, TB and
various parasitic and fungal diseases of the lung.
Risk factors:
• Alcoholism
• Seizure disorders
• Neuromuscular diseases
• Drug overdose
• General anesthesia
• Stroke
Signs/Symptoms: Onset is usually insidious, especially with anaerobic organisms. Aerobic organisms cause a more
acute onset. Symptoms include…
• Cough-producing purulent sputum (often dark brown) this is foul smelling and foul tasting
• Hemoptysis is common, especially when abscess ruptures into bronchus
• Fever
• Chills
 • Prostration
• Pleuritic pain
• Dyspnea
• Cough
• Weight loss
• Dullness to percussion over affected areas
• Bronchial breath sounds to the periphery
• Crackles in later stages of condition
• Complications include…
o Chronic pulmonary abscess
o Bronchiectasis
o Brain abscess as a result of hematogenous spread of infection
o Broncopleural fistula
o Empyema from abscess perforation into the pleural cavity
Diagnosis: Chest x-ray reveals solitary cavitary lesion with fluid.
CT scanning confirms x-ray findings.
Lung abscesses do not require assisted drainage as long as there is drainage via the bronchus.
Routine sputum cultures are not reliable.
Pleural fluid and blood cultures may help identify bacteria.
Bronchoscopy may assist in draining abscess or in factors that suggest an underlying malignancy.
Treatment: Antibiotics given for a prolonged period (2 to 4 months) are usually the primary method of
treatment.
• Penicillin was once standard, but anaerobic bacteria produce beta-lactamase that resist
effects of penicillin.
• Clindamycin (Cleocin) is the new standard of treatment.
o Putrid lung abscesses show improvement with decreased fever within 3 to 4 days
of beginning clindamycin.
• Surgery is rarely indicated, but may be needed in reinfection of a large cavitary lesion.
o Usually lobectomy or pneumonectomy.
Role of Nurse: Interventions…
• Chest physiotherapy and postural drainage are sometimes used to drain abscesses
located in the lower or posterior portions of the lung.
• Teach patient to complete entire course of antibiotics.
• Teach patient to cough effectively.
• Frequent (every 2 to 3 hours) mouth care is needed to relieve the foul smelling odor and
taste from the sputum.
o Use diluted hydrogen peroxide and mouthwash
• Rest, good nutrition and adequate fluid intake are supportive interventions.

Environmental Lung Diseases

Definition: Lung disease resulting from inhaled dust or chemicals.
Cause: Inhaled particulates differ in exposures, but lung damage depends on these factors…
• Duration of exposure
• Amount of inhalant
• Susceptibility of the host
Signs/Symptoms: Conditions…
• Pneumoconiosis – “dust in the lungs” (silicosis, asbestosis, berylliosis)
o Diffuse parenchymal infiltration with phagocytic cells
o Leads to diffuse pulmonary fibrosis
 • Hantavirus – inhalation of aerosolized rodent excrement
• Chemical pneumonitis – exposures to toxic chemical fumes
o Diffuse lung injury characterized as pulmonary edema
o Normal chest x-ray or one that shows hyperinflation
• Hypersensitivity pneumonitis (extrinsic allergic alveolitis) – inhaled antigens to which the
individual is allergic (bird fancier’s lung; farmer’s lung)
• Lung cancer and mesothelioma – results from inhaled asbestos
o Minimum lapse of 15 to 19 years between exposure and development of cancer
o Greater exposure, greater risk of disease
Clinical Manifestations
• Pulmonary edema immediately following exposure to chemical fumes.
• Other diseases may have no symptoms for 10 to 15 years after the initial exposure
• Dyspnea and cough are often the earliest manifestations
• Chest pain and cough with sputum production usually occur later
• Reduced vital capacity
• Occupational Asthma
o Shortness of breath
o Wheezing
o Cough
o Chest tightness
o Results from exposure to fumes or dust that triggers allergic response
o Continued exposure may cause irreversible damage
o Best known cause: toluene diisocyanate (TDI) in production of rigid polyurethane
foam
• Complications include pneumonia, chronic bronchitis, emphysema and lung cancer; cor
pulmonale is a late complication (especially in diffuse pulmonary fibrosis)
Diagnosis: Chest x-ray shows lung involvement specific to primary problem. CT scans help in early detection
Treatment: Prevent or decrease environmental and occupational risks.
• Ventilation systems reduce exposure
• Wearing a mask reduces exposure
• Periodic inspection and workplace monitoring by OSHA/NIOSH help reduce exposures
• Avoid smoking cigarettes or being around smokers (second-hand smoke)
• Early detection is essential
o Periodic chest x-rays and pulmonary function studies help in detection
There is no specific treatment for most environmental lung diseases
• Provide symptomatic relief
• Treat coexisting problems (pneumonia, chronic bronchitis, emphysema, asthma)
Lung Cancer
Demographics: Most commonly occurs in individuals more than 50 year of age who have a long history of cigarette
smoking.
Cause: Cigarette smoking is the most important risk factor in the development of lung cancer.
• Causes 80-90% of all lung cancers
• Smoking causes a change in the bronchial epithelium which usually returns to normal
when smoking discontinues
• Smoking causes direct damage to DNA
• Risk of lung cancer is directly related to total exposure to cigarette smoke measured by
total number of cigarettes smoked in a lifetime, earlier age of smoking onset, depth of
inhalation, tar/nicotine content and use of unfiltered cigarettes.
• Childhood exposure to second-hand smoke is associated with asthma and likelihood of
 smoking in adulthood.
• Cigars and pipes are at increased risk (cigars more than pipes) over non-smokers
Other causes are exposure to asbestos, radon, nickel, iron and iron oxides, uranium, polycyclic
aromatic hydrocarbons, chromates, arsenic and air pollution.
• These exposures coupled with cigarette smoking significantly increases risk of lung
cancer
Pathophysiology: Pathogenesis of primary lung cancer is not well understood.
• Most originate from the epithelium of the bronchus.
• Grow slowly and it takes 8 to 10 years to reach 1 cm in size (detectable size on x-ray)
• Usually occur in segmental bronchi or beyond and have a preference for upper lobes of
lungs
• Changes in bronchial system show nonspecific inflammatory changes
o Hypersecretion of mucus
o Desquamation of cells
o Reactive hyperplasia of the basal cells
o Metaplasia of normal respiratory epithelium to stratified squamous cells
• Metastasizes usually by direct extension and via the blood and lymph system
o Common sites of metastasis are liver, brain, bones, scalene lymph nodes and
adrenal glands
• Two categories…
o Non-small cell lung cancer (NSCL) – which accounts of 75% of cases
o Small cell lung cancer (25% of cases)
 Some small cell cancers produce hormones, enzymes and antigens
which cause paraneoplastic syndrome, seen as hormonal,
dermatologic, neuromuscular, vascular, hematologic and connective
tissue syndromes.
Signs/Symptoms: Lung cancer is clinically silent for most individuals for a majority of its course.
• Symptoms are nonspecific and appear late in the disease process
• Depend on the type, location and metastatic spread of the cancer.
• Usually metastasis results in symptoms
• Persistent pneumonitis resulting from obstructed bronchi may be earliest symptom…
o Fever
o Chills
o Cough
• Persistent cough is most significant symptom, and one of the first to appear
• Blood-tinged sputum possible
o Hemoptysis is not a common early symptom
• Chest pain may be present and localized or unilateral (mild to severe)
• Dyspnea
• Auscultatory wheeze if bronchial obstruction
• Late symptoms…
o Anorexia
o Fatigue
o Weight loss
o Nausea/vomiting
o Hoarseness
o Unilateral paralysis of the diaphragm
o Dysphagia
o Superior vena cava obstruction (spread of malignancy)
 o Palpable lymph nodes in the neck or axilla
o Mediastinal involvement may lead to pericardial effusion, cardiac tamponade and
arrhythmias
Diagnosis Chest x-rays
• May show presence of the tumor or abnormalities related to obstructive features of the
tumor (atelectasis and pneumonitis)
• May show evidence of metastasis to the ribs or vertebrae
• May show pleural effusion
CT scan is the single most effective noninvasive technique for evaluating lung cancer
Identification of malignant cells is a definitive diagnosis.
• Sputum
o Early morning sputum specimen obtained by having patient cough deeply
provides best results
o Malignant cells may not be obtained even in the presence of lung cancer.
• Direct visualization
o Fiber optic bronchoscopy
 Allows biopsy specimens to be obtained
 Usually best, most reliable method
o Mediastinoscopy
 Insertion of a scope via a small anterior chest incision into the
mediastinum.
 Determines metastasis and staging of cancer
o Video-assisted thorascopy (VATS)
 Insertion of scope into a small thoracic incision to explore areas
inaccessible by mediastinoscopy
Pulmonary angiography and lung scans assess overall pulmonary status.
Fine needle aspiration (FNA) obtains a tissue sample to determine tumor histology.
• Most useful in cases involving a peripheral lesion near the chest wall
• Used in place of thoracotomy
• Thoracentesis to relieve a pleural effusion should have fluid analyzed for malignant cells.
STAGING
• Non-small cell lung cancers are staged with TNM system
o T = tumor size, location and degree of invasion
o N = lymph node involvement
o M = presence or absence of distant metastases
• Small cell lung cancer is classified as “limited” (confined to one hemothorax and to
regional lymph nodes) or “extensive” (any disease exceeding those boundaries).
Treatment Early screening has not proven effective, though high-resolution CT scan and/or sputum cytology
reduces morbidity and mortality rates in high risk patients.
Surgical resection is usually the only hope for cure in lung cancer.
• Depends on resectability of tumor…small cell cancers usually have widespread
metastasis at the time of diagnosis.
• Cardiopulmonary status must be evaluated before planning surgery
• Contraindications for surgery
o Hypercapnia
o Pulmonary hypertension
o Cor pulmonale
o Markedly reduced lung function
o Cardiac, renal, liver disease
• If operable, usually lobectomy (removal of one or more lobes of the lung) or
 pneumonectomy (removal of one entire lung) is performed.
Radiation
• Used as a curative approach in individual who has a respectable tumor but who is
considered a poor surgical risk.
• Adenocarcinomas are the least responsive to radiation.
• Radiation of small cell lung cancers does not usually improve mortality rate
• May be done as a palliative procedure to reduce symptoms such as cough, hemoptysis,
bronchial obstruction and superior vena cava syndrome
• May be used to treat pain caused by metastatic bone lesions or cerebral metastasis
Chemotherapy
• May be used in the treatment of non-resectable tumors or as adjuvant therapy to surgery
in non-small cell lung cancers.
• Chemo has improved survival in patients with advanced non-small cell lung cancers and is
now considered standard treatment.
Other therapies
• Prophylactic cranial radiation (toxicity of this therapy may include scalp erythema, fatigue
and alopecia)
• Bronchoscopic laser therapy (removes obstructing bronchial lesions to relieve symptoms)
• Phototherapy (injection of porfimer which is selectively concentrated in tumors is followed
by exposure of tumor to laser light…tumor is destroyed from toxic forms of oxygen and
debris is removed through bronchoscope)
• Airway stenting (redirects airway around obstruction…relieves dyspnea, cough or
respiratory insufficiency and supports airway wall against collapse or external
compression from tumor)
• Cryotherapy (destroying bronchogenic tumors by freezing them)
Role of the Nurse Goals
• Effective breathing pattern
• Adequate airway clearance
• Adequate oxygenation of tissues
• Minimal to no pain
• Realistic attitude toward treatment and prognosis
Interventions
• Help patients stop smoking
• Provide support and reassurance during the diagnostic evaluation
• Answer questions about condition honestly.
• Specific care depends on treatment plan.
• Major role is providing patient comfort, teaching methods to reduce pain and assessing
indications for hospitalization.
• Follow-up patients who have had surgical resection with intent to cure for manifestations
of metastasis.
o Contact physician if…
 Hemoptysis
 Dysphagia
 Chest pain
 Hoarseness
• Help patient with cancer manage pain.

Other Lung Tumors

• Primary lung tumors
 o Sarcomas
o Lymphomas
o Bronchial adenomas (considered malignant)
 Small, arise from lower trachea or major bronchi
 Locally invasive
 Frequently metastasize
 Symptoms:
 Hemoptysis, persistent cough, localized obstructive wheezing,
pneumonia
 Treated with surgical resection
• Lungs are a common site for secondary metastases from other malignancies
o Pulmonary capillaries are ideal sites for tumor emboli
o Also extensive lymphatic network
o Most commonly from:
 GI, GU, breast
 Symptoms: chest pain, nonproductive cough
• Benign tumors – called mesenchymal (rare)
o May become malignant

Chest Trauma/Thoracic Injuries

Trauma/Thoracic Injuries:
• Blunt trauma
o Occurs when the body is struck by a blunt object (like a steering wheel)
o Contrecoup trauma
 A type of blunt trauma caused by the impact of parts of the body against other objects (organs bouncing
around inside the body)
• Penetrating trauma
o Occurs when a foreign body impales or passes through the body tissues (like gunshot wounds, stabbings)

Pneumothorax
Definition: Air in pleural space, causes collapse of lung
• Closed Pneumothorax
o No external wound
o Often spontaneous caused by rupture of blebs (most commonly in underweight male
cigarette smokers 20 – 40 years of age)
o Other causes:
 Mechanical ventilation
 Insertion of subclavian catheter
 Perforation of esophagus
 Broken ribs
 Ruptured blebs or bullae in patient with COPD
• Open Pneumothorax
o Caused by an opening in the chest wall (penetrating injury)
o Should be covered with a vented dressing (secured on three sides with fourth side left
untapped)
o If object of penetration is present…do not remove it…secure it with bulky dressings.
 • Tension Pneumothorax (open or closed)
o Air accumulates rapidly in pleural space increasing intrapleural pressure with resultant
pressure on heart and great vessels.
o Occurs in mechanical ventilation and resuscitative efforts or when chest tubes are
clamped or obstructed
o Medical emergency leading to death from inadequate cardiac output
o May be relieved with large-bore needle insertion into chest wall to relieve trapped air
• Hemothorax (blood in pleural space)
o Caused by trauma, lung malignancy, complications of anticoagulant therapy, pulmonary
embolus and tearing of pleural adhesions.
• Chylothorax (lymph fluid in pleural space)
o Caused by a leak in the thoracic duct from trauma, surgical procedures, malignancy.
o Chest drainage, bowel rest, and total parenteral nutrition may be used for treatment
o Surgery and Pleurodesis (artificial production of adhesions between the parietal and
visceral pleura) are options for treatment
Signs/Symptoms: If small:
• mild tachycardia and dyspnea
If large:
• respiratory distress;
• shallow, rapid respirations, dyspnea, and air hunger;
• chest pain;
• cough with or without hemoptysis;
• No breath sounds over affected area
If tension pneumothorax:
• severe respiratory distress;
• tachycardia;
• hypotension;
• mediastinal displacement and trachea shifts to the unaffected side.

Fractured Ribs
Definition: Most common type of chest injury resulting from trauma.
• Ribs 5 through 10 are most commonly affected because they are least protected.
• Splintered or displaced ribs can damage the pleura and lungs.
Signs/Symptoms: Signs of fractured ribs include…
• Pain at site of injury (especially on inspiration)
• Bracing and splinting of affected area
• Shallow breathing
• Atelectasis
Treatment: Goals of treatment are decrease pain and promote good chest expansion.
• Intercostal nerve blocks with local anesthesia
o Lasts hours to days
o May need to be repeated
• Do NOT strap the chest or use a binder…it reduces lung expansion and may lead to
atelectasis

Flail Chest
Definition/Cause: Instability of chest wall caused by multiple rib fractures.
 Sign/Symptoms: The affected (flail) area will move paradoxically to the intact portion of the chest during respiration.
• During inspiration, flail area gets sucked inward
• During expiration, flail area bulges outward
• Prevents adequate ventilation and leads to hypoxemia
• Flail chest is apparent in an unconscious patient; but a conscious patient will brace/splint
the affected side preventing observation.
o Rapid, shallow respirations
o Tachycardia
o Poor air movement
o Asymmetric and uncoordinated movement of the thorax
Diagnosis: Palpation or respiratory movements; crepitus of the rib(s); chest x-ray and ABGs assist in
diagnosis.
Treatment: The definitive therapy is to reexpand the lung and ensure adequate oxygenation.
• Assist with ventilation
• Provide humidified oxygen
• Administer crystalloid IV solutions
• Short duration of intubation and mechanical ventilation
• Positive End-Expiratory Pressure (PEEP) used with mechanical ventilation

Restrictive Respiratory Disorders

Restrictive respiratory disorders are characterized by decreased compliance of the lungs or chest wall or both. Pulmonary function
tests are the best means to use in differentiating between restrictive and obstructive respiratory disorders.
Categories:
• Extrapulmonary: Disorders involving the central nervous system, neuromuscular system, and chest wall.

• Intrapulmonary: Disorders involving the pleura or lung tissue.

Pleural Effusion
Definition: Pleural effusion is a collection of fluid in the pleural space.
Types & Causes: Types:
• Transudate (hydrothorax)
o Occurs in noninflammatory conditions and is an accumulation of protein-poor,
cell-poor fluid.
o Caused by…
 Increased hydrostatic pressure (as in CHF)
 Decreased oncotic pressure (as in hypoalbuminemia from liver and
renal disease)
o Thoracentesis reveals clear, pale yellow fluid
• Exudative
o Occurs in inflammatory conditions and is an accumulation of fluid and cells.
o Is secondary to conditions such as pulmonary malignancies, pulmonary
infections, pulmonary embolization and GI disease (pancreatic disease,
esophageal perforation)
o Thoracentesis reveals high protein fluid that is dark yellow or amber
• Empyema
o A pleural effusion that contains pus.
o Caused by conditions such as pneumonia, TB, lung abscess, infection of surgical
wounds.
o Complication of empyema is fibrothorax in which fibrous fusion of the visceral
and parietal pleurae occurs.
 Signs/Symptoms: Common findings:
• Progressive dyspnea
• Decreased movement of the chest wall on affected side
• Pleuritic pain
• Dullness to percussion
• Absent or decreased breath sounds over affected area
• Chest X-ray indicates abnormality if effusion is >250 mL.
• Empyema symptoms…
o Fever
o Night sweats
o Cough
o Weight loss
Diagnosis: Thoracentesis obtains sample of fluid for analysis to determine type of effusion.
• Thoracentesis needle is inserted into the intercostal space and fluid is aspirated with a
syringe.
• 1000 to 1200 mL of pleural fluid is removed
• Complications include…
o Hypotension
o Hypoxemia
o Pulmonary edema
• Follow up with chest x-ray to rule out pneumothorax caused by thoracentesis.
• Monitor patient for respiratory distress during and after procedure.
Treatment: Main goal of treatment is to treat the underlying cause.
• Chemical pleurodesis may be used to sclerose the pleural space and prevent
reaccumulation of effusion fluid.
o Chest tubes are left in place after pleurodesis until fluid drainage is greater than
150 mL/day and no air leaks are noted
• Antibiotic therapy is needed in empyema to eradicate the causative organism.
o If a fibrothorax results from the empyema and causes severe pulmonary
restriction, a decortication surgical procedure is done to separate the
membranes.
Pleurisy
Definition & Cause: Pleurisy (pleuritis) in an inflammation of the pleura. Most common causes are pneumonia, TB,
chest trauma, pulmonary infarctions and neoplasms.
Two types…
• Fibrinous (dry) with fibrinous deposits on the pleural surface
• Serofibrinous (wet) with increased production of pleural fluid that may result in pleural
effusion
Signs/Symptoms: Pain of pleurisy is typically abrupt and sharp in onset and aggravated by inspiration.
• Breathing is shallow and rapid to avoid unnecessary movement of the pleura and chest
wall
• Friction rub is heard over areas where inflamed visceral/parietal pleurae rub against each
other
Treatment: Treatment is aimed at treating underlying cause
• Provide pain relief
o Analgesics
o Lie on or splint affected side
o Plint the rib cage when coughing
Atelectasis
Definition: Condition in which the alveoli are collapsed and airless. Commonly caused by airway obstruction
from retained exudates and secretions.
Treatment: Deep breathing prevents condition.
Chronic atelectasis may result in pulmonary fibrosis.

Idiopathic Pulmonary Fibrosis

Definition: Characterized by scar tissue in the connective tissue of the lungs as a sequela to inflammation or
irritation.
Risk Factors: Inhalation of organic and inorganic substances…
• Cigarette smoking
• History of chrinic aspiration
• Genetic risk factor?
Signs/Symptoms: Signs…
• Exertional dyspnea
• Nonproductive cough
• Inspirational crackles with or without clubbing
• Chest x-ray shows evidence consistent with restrictive lung disorder
Treatment: Treatment varies…
• 5 year survival rate of 30 to 50%
• Corticosteroid
• Cytotoxic agents
• Antifibrotic agents
• No good evidence that any of the treatments improves survival or quality of life
• Lung transplantation may be only hope.

Sarcoidosis
A chronic, multisystem granulomatous disease of unknown cause that primarily affects the lungs. It
may also affect the skin, eyes, liver, kidney, heart and lymph nodes.
• Acute, subacute and self-limiting
• May be chronic with remissions and exacerbations
• Marked pulmonary fibrosis in restrictive lung disease
• Complication includes cor pulmonale
• No specific treatment…is self-limiting and patient recovers without treatment
• Corticosteroids may relieve symptoms and suppress acute inflammation

Pulmonary Edema
An abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs.
• Usually presents as a complication of heart and lung diseases
• Is a medical emergency and may be life-threatening
• Results from increased hydrostatic pressure or decreased oncotic pressure in pulmonary
capillaries
• Fluid first enters the interstitial space (interstitial edema), and continues into the alveoli
(alveolar edema) if leak is not resolved
• Most common cause is left-sided CHF
• May be asymptomatic until pulmonary fibrosis occurs
• Early signs may be paroxysmal nocturnal dyspnea as a result of increased hydrostatic
 pressure in the lungs in the recumbent position
Pulmonary Embolism
A thromboembolism arising from venous circulation or right side of the heart (or from other sources
like amniotic fluid, air, fat, bone marrow or foreign intravenous material) that lodges in the
pulmonary vasculature.
• The result is a complete or partial occlusion of the pulmonary arterial blood flow to parts of
the lung.
• Lung tissue distal to the embolus is ventilated but not perfused.
May lead to pulmonary hypertension
Pulmonary Hypertension
Definition: Elevated pulmonary pressure resulting from an increase in pulmonary vascular resistance to blood
flow through small arteries and arterioles.
Cause: Primary Pulmonary Hypertension:
• Exact cause is unknown
• Characterized by mean pulmonary arterial pressure greater than 25 mmHg at rest or
greater than 30 mmHG with exercise
• Fen-Phen (diet drug) was linked to pulmonary hypertension
• Usually pulmonary circulation has low resistance and low pressure.
o A deficiency of vasodilator mediators from the epithelium may be a factor
Signs/Symptoms: Classic symptoms…
• Dyspnea on exertion and fatigue
• Exertional chest pain
• Dizziness
• Exertional syncope
• Cardiac output unable to increase in response to oxygen demands
• Right ventricular hypertrophy (cor pulmonale) occurs
• Leads to heart failure
Treatment: Relieve symptoms…
• Diuretics
• Calcium channel blockers
• Vasodilator therapy
• PROSTACYCLIN is standard of care. Promotes pulmonary vasodilation and reduces
pulmonary vascular resistance
o Must be administered by central line
o Very short half-life (6 mins)
o Complications result when medication is accidentally discontinued or when
infections develop at site of central line
Other: Secondary Pulmonary Hypertension
• Results from anatomic and vascular changes brought about by other disorders.
o Loss of capillaries as a result of alveolar wall damage (COPD);
o Stiffening of the pulmonary vasculature (pulmonary fibrosis); and
o Obstruction of blood flow (chronic emboli)
o Combination of conditions may occur, as in chronic bronchitis.
• Vasomotor/vasoconstriction may occur in alveolar hypoxia (blood is shunted to more
functional alveoli) which leads to pulmonary hypertension.

Cor Pulmonale
Enlargement of the right ventricle secondary to diseases of the lung, thorax or pulmonary
circulation. Pulmonary hypertension is usually a pre-existing condition of cor pulmonale.
• The most common cause is COPD
 • Any disorder of the lungs can cause cor pulmonale
• Signs/symptoms are:
• Dyspnea
• Chronic productive cough
• Wheezing respirations
• Retrosternal or substernal pain
• Fatigue
• Polycythemia, increased total blood volume and viscosity of blood
• If heart failure is present…
o Peripheral edema
o Weight gain
o Distended neck veins
o Full, bounding pulse
o Enlarged liver
Treat underlying problem, plus…
• Long-term, low-flow oxygen
• Reduce vasoconstriction
• Diuretics
• Low sodium diet
• Bronchodilators
• Digitalis if left-sided heart failure
• Treat pulmonary hypertension: Vasodilator, calcium channel blockers and
anticoagulants
• Theophylline may reduce dyspnea
• Lung transplantation when all else fails.
OBSTRUCTIVE PULMONARY DISEASES Chapter 28

Obstructive Pulmonary Disease

The most common chronic lung diseases and are characterized by increased resistance to airflow as a result of airway
obstruction or airway narrowing.

Includes four conditions:

o Asthma (allergic reaction)
o Emphysema (COPD)
o Chronic Bronchitis (COPD)
o Cystic Fibrosis (genetic disorder)

Asthma

Definition: An obstructive pulmonary disease characterized by airway inflammation, and non-specific hyperirritability
or hyper-responsiveness of the tracheobronchial tree (bronchospasm). The hyper-responsiveness seen
in asthma is caused by bronchoconstriction in response to physical, chemical and pharmacological
agents.
High morbidity is associated with asthma.
Asthma affects blacks more than whites in hospitalizations and deaths.
Cause: Allergens
• Exaggerated allergic response (IgE) to environmental factors (dust, pollen, grass, mites, roaches,
mold, dander, etc.).
Exercise
• “Exercise-Induced Asthma”
• Occurs within several minutes of vigorous exercise
• Bronchospasm, shortness of breath, cough, wheezing

• Cromolyn (Intal)/nedocromil (Tilade) and B2-adrenergic agonists (salmeterol/Severent) maintain

bronchodilation during exercise when inhaled 10-20 minutes before activity

• Prevent attacks with pre-medication, 2-3 minutes of stretching/warm-up and avoid exercise in
cold weather
Respiratory Infections
• Most common precipitating factor of an acute asthma attack.

• Bacterial infections cause inflammatory changes in tracheobronchial system and alter

mucociliary mechanism thereby increasing hyperresponsiveness of the bronchial system (for 2 to
8 weeks following infection).
• Avoid people with colds and flu! Get vaccinated for flu.
Nose, Sinuses and Drugs/Food Additives
• “Asthma-Triad”….Nasal polyps, asthma, sensitivity to aspirin and NSAIDS
• Nose and Sinus Problems
o Allergic rhinitis (seasonal or perennial) and nasal polyps contribute to asthma problems
o Treat/prevent sinusitis and remove large nasal polyps
• Drug Allergies

o Exposure to ASA/NSAIDS = wheezing within 2 hours

o Avoid Beta blockers (propranolol, timolol, other “-olol” drugs) because they prevent
bronchodilation.
o Avoid ACE inhibitors; they cause coughs and trigger asthma symptoms.
• Food Allergies
o Avoid exposure to Tartrazine (yellow dye #5 found in many foods)
o Avoid vitamins
o Avoid sodium metabisulfite (food preservative in fruit, beer/wine and salad bars). They
interfere with prostaglandins and increase production of leukotrienes
(bronchoconstrictors).
o Symptoms occur in 15 minutes to 3 hours
o Causes profuse rhinorrhea, nausea, vomiting, intestinal cramps and diarrhea.
o Do NOT use corticosteroids or cromolyn. Use EPINEPHRINE after onset of symptoms.
o Avoidance diets may be needed to prevent asthma.
Gastroesophageal Reflux Disese (GERD)
• Theory is that reflux of stomach acid gets aspirated and causes reflex bronchoconstriction.
• GERD is primarily involved in nocturnal asthma.
• Patients with hiatal hernia, excessive stress and prior history of reflux or ulcer may have GERD
as an asthma trigger.
• Diagnose by monitoring esophageal pH simultaneously with peak expiratory flow rate (PEFR)
Emotional Stress
• Psychological or emotional stress may be a trigger
 • Panic and anxiety during an attack may exacerbate and prolong the attack
Signs/Symptoms: Early-Phase Response

 Characterized by bronchospasm triggered by allergen or irritant, increased mucus secretion,

edema formation and increased amounts of tenacious sputum.
 Involves release of histamine, bradykinin, leukotrienes, prostaglandins, platelet-activating factor,
chemotactic factors and cytokines, which bring about inflammatory response.
 Immediate response that peaks within 30 to 60 minutes of exposure to the trigger.
 Symptoms: wheezing, chest tightness, dyspnea and cough.
Late-Phase Response

 Characterized by inflammation, constriction of bronchioles and excess mucus when

eosinophils and neutrophils (WBCs) infiltrate the airways.
 Late-phase response peaks 5 to 6 hours after exposure and may last for days.
 WBC infiltration release mediators that sustain the inflammation cycle and bring lymphocytes and
monocytes to the area.
 This activity increases airway reactivity which worsens the symptoms of future attacks, and makes
them easier to trigger.
 Inflammation, constriction of bronchioles and excess mucus leads to reduction in airway diameter
and increase in airway resistance which result in air trapping in the alveoli and increased work of
breathing.

 If untreated, inflammation leads to progressive, irreversible lung damage and structural changes in
the airway, known as airway remodeling.
Clinical Manifestations of asthma:
• Recurrent episodes of wheezing, breathlessness, dyspnea, chest tightness and cough (particularly
at night and in the early morning) after exposure to a trigger
• Characterized by prolonged expiration (wheezing upon expiration, air trapping and hyperinflation).
• Diminished or absent breath sounds during attack is an ominous sign and may indicate atelectasis
or pneumothorax.
• Person may sit upright or slightly bent forward using the accessory muscles of respiration to try to
get enough air.
• Attacks may last a few minutes to several hours.
• Symptoms of hypoxia occur: restlessness, anxiety, inappropriate behavior, increased pulse and
blood pressure, significantly increased respiratory rate (>30 breaths per minute) with use of
accessory muscles.
Classification: Mild Intermittent
• Symptoms < twice per week; nighttime < twice per month
• Asymptomatic with normal PEFR between attacks
• Exacerbations brief (hours to days)
• Intensity of exacerbations varies
• Treated with short-acting beta-agonist inhaler (may be combined with long-acting meds)
Mild Persistent
• Symptoms > twice per week but < once per day; nighttime > twice per month
• Exacerbations may affect activity
• Treated with anti-inflammatory inhaler
Moderate Persistent
 • Daily symptoms; nighttime > once per week
• Daily use of inhaled short-acting beta agonist
• Exacerbations affect activity
• Exacerbations at least twice weekly and may last for days
• Treated with anti-inflammatory inhaler plus medium-dose corticosteroid inhaler.
Severe Persistent
• Continual symptoms; nighttime = frequent
• Limited physical activity
• Frequent exacerbations
• Treated with anti-inflammatory inhaler plus long-acting bronchodilator plus oral corticosteroid.
Status Asthmaticus
• Severe, life-threatening attack that does not respond to usual treatment.
• “The longer it lasts, the worse it gets and the worse it gets, the longer it lasts.”
• Caused by viruses; aspirin/NSAIDS; stress; environmental pollutants; allergens; abrupt
discontinuation of drug therapy (corticosteroids); abuse of aerosol medication; use of beta-
blockers.
• Symptoms same as asthma, but more severe and more prolonged with extreme anxiety, fear of
suffocation, diaphoresis and severely increased work of breathing.
• Chest remains in hyperinflated state; hypertension, sinus tachycardia and ventricular arrhythmias
may occur (related to hypoxemia).
Complications: Rib fractures, pneumothorax, pneumomediastinum, atelectasis, pneumonia and status asthmaticus.
Diagnosis: Asthma presents with same symptoms as other respiratory diseases. To diagnose asthma:
• History and physical examination
• Pulmonary function studies including response to bronchodilator therapy
• Peak expiratory flow monitoring
• Chest X-Ray
• Measurement of ABGs or Oximetry
• Allergy skin testing (if indicated)
• Blood level of eosinophils and IgE.
Treatment: Successful treatment depends on active partnership with patient.
• Mild Intermittent/Persistent Asthma: avoid triggers of attacks; pre-medicate before exercise

• Mild/Exercise-Induced: use inhaled B2-agonists/bronchodilators or anti-inflammatory drugs

(cromlyn/Intal or nedocromil/Tilade) before activity or exposure to triggers

• Moderate Persistent: regular/maintenance use of inhaled anti-inflammatory meds

(corticosteroids) used at lowest effective dose, plus B2-agonists/bronchdilators.

• Severe Persistent: inhaled or oral corticosteroids, inhaled or oral B2-agonists and theophylline.

o If patient requires continuous oral corticosteroids, use at lowest dose possible and
administer on alternate days to reduce systemic side effects.
• Acute Episode:
o Oxygen therapy immediately with pulse oximetry and ABGs

o Inhaled B2-agonists by metered-dose inhaler (MDI) with spacer or nebulizer every 20

 minutes to 4 hours as necessary.
o If no response in 30 to 60 minutes, use oral corticosteroids, or if severe—IV
corticosteroids. IV aminophylline may be considered, but effectiveness is questionable.
o Continue treatment until patient breathes comfortably, wheezing has stopped and
pulmonary function results are near baselines.
• Status Asthmaticus:
o Correct hypoxemia and improve ventilation

o Same interventions as for acute asthma (above), but may need to increase the
frequency and dose of inhaled bronchodilators to 2 to 6 puffs every 5 to 20 minutes
(depending upon medication).
o Continuous monitoring of patient is critical.

o If B2-agonists do not work, use IV corticosteroids (methylprednisolone) every 4 to 6

hours (peaks in 12 hours).
o IV mag sulfate and subcutaneous epinephrine may act as bronchodilators. If
administered, monitor BP and EKG closely.
o Oxygen therapy and IV fluids (for hydration) are usually required.
o Severe, non-responsive attacks may require mechanical ventilation.
• Even after bronchospasm resolves, inflammation, edema, and viscous mucus plugs remain for
several days.
• Drug classifications
o Two categories:
 Long-term control (achieve/maintain control of persistent asthma)
• Coricosteroids (anti-inflammatory)
 Quick-relief (treat symptoms and exacerbations)
• Mast cell stailizers (cromolyn, nedocromil)
• Bronchodilators

o B2-agonists (albuterol)

o Anticholinergics (Atrovent)
o methylxanthine derivatives (theophylline)
o Because inflammation is considered an early and persistent component of asthma, drug
therapy must be directed toward long-term suppression of the inflammation process.
o Anti-inflammatory Drugs
 Corticosteroids
• Used in the long-term control of asthma
• Block the late-phase response, but not the immediate, early-phase, of
the attack.
• Onset is 3 to 6 hours after administration
• Inhaled corticosteroids:
o Must be used for 4 to 5 days before therapeutic effect
o Adverse effects: oropharyngeal candidiases, hoarseness
and dry cough (use a spacer and gargle with water after
each use to reduce side effects)
o Little risk of systemic effects (immune suppression)
 • Oral corticosteroids
o Used for acute exacerbations
o Side effects include insomnia, heartburn, mood swings,
blurry vision, headache, increased appetite, weight gain.
o Maintenance doses should be used every other day to
minimize side effects.
o Post-menopausal women should increase calcium, vit D and
weight-bearing activities while on oral corticosteroids.
 Mast Cell Stabilizers
• Cromolyn and Nedocromil
• Used in early-phase and prevent late-phase

• Effective in seasonal asthma and very effective in exercise-induced

asthma when used 10 to 20 minutes before activity.
• Teach patient when and how to use these drugs!
 Leukotriene Modifiers
• Accolate and Singulair
• Prevent bronchoconstriction and inflammation caused by leukotrienes
• Not to be used in acute attacks or as sole therapy.
o Bronchodilators
 Beta-adrenergic agonists; methylxanthine derivatives and anticholinergics

 Beta agonists (B2-agonist)

• Albuterol, Alupent, Tornalate, Maxair
• Act within minutes and effective for 4 to 8 hours
• Used for acute exacerbations
• Prevent bronchospasm in exercise and other triggers because they
prevent mast cell activity (inflammation)
• Do not use in late-phase response (they’re not effective)
• Side effects: tremors, anxiety, tachycardia, palpitations and nausea.
Can cause rebound bronchoconstriction (especially albuterol).
• Avoid contact between med and tongue to reduce side effects.

• Use longer-acting Severent (8 to 12 or 24 hours) to reduce side

effects of frequent/prolonged use of beta-agonists.
• Combo therapy with inhaled corticosteroid is recommended for better
control of asthma and improved lung functioning (Advair Diskus is a
combo drug).
 Methylxanthines (theophylline)
• Not as effective as Beta-agonists
• May have synergistic effect with Beta-agonists (used together)
• Must be used orally or by IV
• Effective in early phase as a bronchodilator but not on bronchial
hyperresponsiveness.
• Use at bedtime to control nocturnal asthma.
 • Side effects: nausea, headache, insomnia, GI distress, tachycardia,
arrhythmias, seizures.
 Anticholinergics
• Parasympathetic effects include increased mucus secretion and
bronchoconstriction. Anticholinergics block this response.
• Atrovent is an example
• Not as effective as beta-agonists and are used in combo with other
drugs.
• Slower to act than beta-agonists: peak in 1 hour and last longer (4 to
6 hours)
• Poorly absorbed, so few side effects
 Monoclonal Antibody to IgE
• Omalizumab/Xolair
• Decreases circulating IgE levels and prevents IgE from attaching to
mast cells thereby preventing the allergy/inflammation response.
Role of Nurse: Interventions
• Administer oxygen
• Administer bronchodilators
• Perform chest physiotherapy
• Administer medications as ordered
• Continuously monitor patient’s condition
• Monitor effectiveness of treatments
• Decrease the patient’s sense of panic; encourage slow breathing using pursed lips for prolonged
exhalation
• Provide rest and a quiet, calm environment for the patient
Information to teach patient with asthma:
• Drugs: Name, dosage, method of administration, schedule (meals/ADLs), purpose, side effects,
appropriate action for side effects, consequences of improper use, importance of refilling the
prescription before the medication runs out.
• Inhalation is better than oral because they’re faster, a lower dose is needed and systemic side
effects are reduced.
• MDI (metered-dose); DPI (dry powder) and nebulizers all deliver inhaled medication. Teach
proper use of each.
• Nebulizers deliver a larger dose and are used for severe asthma.
• Patient may have multiple inhalers with different drugs. Teach patient to use beta-agonist first
and inhaled corticosteroid last.
• Teach patient to rinse mouth immediately after using inhaled corticosteroid to prevent yeast
infections.
• Poor adherence to long-term drug therapy is a major challenge. Patients will use the beta-
agonists because immediate relief is provided, but long-term therapy is not followed because no
immediate benefit is seen. Explain importance of adhering to long-term, preventive therapy.
• Explain that maximum improvement may take more than 1 week to achieve with long-term
therapy.
• Tell patient NOT to use OTC bronchospasm drugs (Primatene spray). They are dangerous for
patients with underlying cardiac conditions and contain epinephrine, theophylline and/or
ephedrine.
 • Teach patient to measure his/her peak flow rate (PEFR) daily.
o PEFR provides good, objective measurement of asthma condition
o Green zone (80 – 100%) = remain on usual medications
o Yellow zone (50 – 80%) = caution. Increase dose of corticosteroid inhaler one third to
one half, depending on management plan, until PEFR is back to green zone.
o Red zone (<50%) = serious problem. Increase use of beta-agonist inhaler and oral
corticosteroids. See health care provider!
• Teach relaxation techniques (yoga, meditation, guided imagery, breathing techniques, etc.)

COPD (Emphysema and Chronic Bronchitis)

Definition: Group of diseases with the major characteristic of airflow obstruction and hyper-reactivity of airway.
Symptoms include difficulty with exhalation caused by airway obstruction from edema or excessive mucus
production. Lung hyperinflation causes alveolar air trapping and leads to frequent pulmonary infections.
Symptoms are usually progressive and irreversible.
Emphysema: an abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls and without obvious fibrosis.
Chronic Bronchitis: the presence of a chronic productive cough for 3 months in each of 2 successive
years in a patient in whom other causes of chronic cough have been excluded.
Cause: Cigarette Smoking…
• Causes hyperplasia of cells, including goblet cells, which results in increased production of
mucus and reduction of airway diameter
• Reduces the ciliary activity and may cause actual loss of ciliated cells
• Produces abnormal dilation of the distal air space with destruction of alveolar walls
• Creates cells with large, atypical nuclei—a precancerous condition.
• Creates CO (carbon monoxide) which binds more readily with hemoglobin than oxygen, thereby
reducing the smoker’s oxygen-carrying capacity.

• Reduces amount of O2 inhaled, thereby reducing the amount of O2 available to the body.

• Affects non-smokers when they are exposed to second-hand/side-stream smoke from cigarettes.
Infection
• Recurring respiratory tract infections impair normal defense mechanisms making alveoli more
susceptible to injury

• Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis are common

bacteria in infections
• Retained secretions create growth medium
Heredity
• Alpha-1 Antitrypsin (AAT) deficiency is the only known genetic abnormality that leads to COPD
• Accounts for less than 1% of cases
Aging
• Some degree of emphysema is common in elderly (even nonsmokers)
• Gradual loss of the elastic recoil of the lungs
• Lungs become more rounded and smaller, and number of functional alveoli diminishes
• Alveolar walls thin out, decreasing alveolar tissue and capillaries which results in less gas
exchange
 • Changes in thoracic cage result from osteoporosis and calcification of the costal cartilages (chest
becomes stiff, rigid and less pliable).
• Increased functional residual capacity (retained air in lungs) causes chest expansion and
rounding (barrel chest) resulting in increased work of breathing.
Signs/Symptoms: Emphysema:
• Hyperinflation of alveoli
• Destruction of alveolar walls
• Destruction of alveolar capillary walls
• Narrowed, tortuous, small airways
• Loss of lung elasticity (like blowing into a paper bag…air goes in, but does not come out)
• Two types…but may overlap in some patients
o Centrilobular

 Involves central part of the lobule

 Bronchioles enlarge, walls are destroyed and bronchioles become confluent
(merge together)
o Panlobular

 Involves distention and destruction of the whole lobule.

 Bronchioles, alveolar ducts and sacs, and alveoli are affected
 Progressive loss of lung tissue and decreased alveolar-capillary surface area
results
Symptoms
• Early symptom: dyspnea on exertion which gets progressively worse to dyspnea at rest
• Minimal coughing
• Scanty, mucoid sputum
• Quiet or diminished breath sounds; limited chest excursion
• Barrel chest; patient becomes chest breather with intercostal and accessory muscle
involvement
• Underweight (possibly in a hypermetabolic state with increased energy requirements R/T
increased work of breathing); protein-calorie malnutrition with loss of lean muscle mass
and subcutaneous fat
• Hypoxemia (early sign) and hypercapnia (late sign)
Chronic Bronchitis
• Hyperplasia of mucus-secreting glands in the trachea and bronchi
• Increase in goblet cells
• Disappearance of cilia
• Chronic inflammatory changes and narrowing of small airways
• Altered function of alveolar macrophages, leading to increased bronchial infections
• High colonization with microorganisms = increased infection risks
• Chronic inflammation causes narrowing of the airway lumen = diminished airflow
• Hypoxemia and hypercapnia develop more frequently than in emphysema

• Diminished respiratory drive (hypoventilation and retention of CO2)

Symptoms
 • Frequent, productive cough during winter
• Bronchospasm at end of paroxysms of coughing
• Frequent respiratory tract infections
• Dyspnea on exertion
• Copious, mucopurulent sputum
• Scattered crackles, rhonchi, wheezing
• History of cigarette smoking
• Normal weight or obese with a ruddy appearance
• Increased production of RBCs = polycythemia, resulting from body’s attempt to compensate
for chronic hypoxemia
• Cyanosis = circulating unoxygenated hemoglobin
Complications: Cor Pulmonale: Hypertrophy of the right side of the heart, with or without heart failure, resulting from
pulmonary hypertension.
Acute Exacerbation of Chronic Bronchitis: Worsened cough, hemoptysis, wheezing, shortness of breath,
changes in sputum. Usually results from bacterial infection and treated with antibiotics, bronchdilators,
corticosteroids, humidifiers and postural drainage.
Acute Respiratory Failure: Usually precipitated by acute, viral respiratory tract infection or acute
bronchitis; Avoid sedatives/narcotics in patients who retain CO2 because they may suppress ventilatory
drive and lead to respiratory failure.
Peptic Ulcer/GERD: There is a close association between PUD/GERD and COPD. Which is the cause
and which is the effect is unknown.
Pneumonia: Bacterial or viral; manifested as purulent sputum. Fever, chills and leukocytosis may not be
present.
Diagnosis: H & P; chest x-ray; pulmonary function tests; sputum specimens for culturing; ABGs; EKGs; exercise
testing with oximetry; cardiac nuclear scans
Treatment: Goals:
• Improve ventilation
• Promote secretion removal
• Prevent complications and progression of symptoms
• Promote patient comfort and participation in care
• Improve quality of life as much as possible
• Avoid environmental pollutants
• Treat infections immediately
• Stop smoking
Drug therapy:
• Bronchodilators (as a maintenance therapy, not for acute symptoms)

o Beta-2 agonists are commonly used

o MDI or nebulizer
o Anticholinergics are more effective in emphysema
• Oxygen therapy

o Raises the partial pressure of O2 in inspired air to treat hypoxemia

o Delivery

 Nasal Cannula
  Masks
• Simple (35 – 50% O2)

• Venturi (High air flow; flex tube; mixture is 100% O2)

• Partial or Non-Rebreathing: (Uses a reservoir bag; 100% O2, but

actual percentage depends on respiration)
 Oxygen Concentrator
 Positive Airway Pressure Devices
• CPAP Mask
o Continuous positive airway pressure
• BIPAP Mask
o Bilevel positive airway positive pressure device
 Transtracheal catheter (pg 251 L)
• Immature or mature tract
 Tracheostomy tube
 Endotracheal tube

• Often via ventilator

• Or by T-bar

 Manual Breathing
• with bag
• with mouth in CPR (w/barrier)
o Humidification and nebulizers

 O2 is dry and irritating and must be humidified before delivery

o Complications of O2 Therapy

 Combustion (“No Smoking”!)

 CO2 Narcosis (“Oxygen-Drive” for breathing may get eliminated if oxygen is

administered)

 O2 Toxicity (from prolonged exposure to O2; may inactivate pulmonary

surfactant and lead to ARDS (acute respiratory distress syndrome).
• Cough
• Substernal chest pain
• Nausea and vomiting
• Paresthesia
• Nasal stuffiness
• Sore throat
• Malaise
• Progressive fibrosis of the lungs

• Levels >50% for more than 24 hours is considered toxic

 Absorption atelectasis
 • Nitrogen from room air is usually retained in alveoli (not absorbed into
blood stream) to prevent atelectasis

• O2 therapy replaces nitrogen with oxygen, which all gets absorbed,

leading to collapse
 Infection (humidity encourages growth of bacteria in lungs)
Surgery
• Lung volume reduction surgery (LVRS): removal of diseased part of lungs to reduce airway
obstruction and provide more room for normal alveoli to expand
• Lung transplantation: prolongs life, improves functional capacity and enhances quality of life;
rejection and effects of immunosuppressive therapy remain a problem.
Respiratory Therapy
• Breathing retraining (pursed lip breathing; diaphragmatic/abdominal; practice 8 -10 reps; 3-4 x
per day )
• Effective coughing techniques (conserve energy; reduce fatigue; facilitate removal of secretions)
• Chest physiotherapy (percussion, vibration and postural drainage to clear secretions…
complications include fractured ribs, bruising, hypoxemia and discomfort; flutter mucus clearance
device may be used instead of CPT)
• Aerosol-nebulization therapy (methods of delivering inhaled medications)
• Exercise; pulmonary conditioning; smoking cessation and COPD support groups
Nutritional Therapy
• Maintain weight
• Rest for 30 minutes before eating
• Use bronchodilator before meals
• Eat five to six small meals (avoid bloating which puts pressure on diaphragm)
• Liquid/pureed diets may be helpful
• Avoid foods that require a lot of chewing
• Avoid exercise within 1 hour of eating
• Bloating/early satiety may be related to swallowing air, position of diaphragm or side effects of
meds
• High calorie/high protein recommended for emphysema

• High carbs metabolize into high CO2, and should be avoided

• Fluid intake should be at least 3 L per day unless contraindicated, and between meals rather
than with meals
Role of Nurse: Interventions:
• Pneumonia, cor pulmonale, acute respiratory failure need medical intervention
• Pulmonary rehab (control and alleviate symptoms as possible; teach patient to achieve optimal
capability for ADLs; overall goal is improved quality of life)

• Activity considerations (Upper extremity work outs may improve function and reduce dyspnea;
teach to use O2 during ADLs; encourage walking with slow, pursed-lip breathing; allow 5-minute
recovery period from activity before using medication: keep a diary of exercises to record
progress)
• Teach client how to modify sexual activity to accommodate COPD (plan sexual activity during
time when beathing best; use slow pursed-lip breathing; refrain from sex after eating or other
strenuous activity; do not assume a dominant position; do not prolong foreplay)
 • Teach client that adequate sleep is extremely important.
• Consider psychosocial aspects of patient’s life (coping; lifestyle changes; decreased energy for
socialization; depression; guilt)

Cystic Fibrosis
Definition: An autosomal recessive, multisystem disease characterized by altered function of the exocrine glands
involving the lungs, pancreas and sweat glands. Abnormally thick, abundant secretions from mucus
glands can lead to a chronic, diffuse, obstructive pulmonary disorder in almost all patients. Exocrine
pancreatic insufficiency is associated with most cases of CF; sweat glands excrete increased amounts of
sodium and chloride.
Cause: Mutations in a gene located on chromosome 7. (CFTR: Cystic Fibrosis Transmembrane Regulator).
Primary defect in CF is abnormally regulated chloride channel activity; manifestation is obstruction of the
ducts of exocrine glands with thick, viscous secretions that adhere to the lumen of the ducts; the glands
distal to the duct eventually undergo fibrosis.
Affects both upper and lower respiratory tracts.
Signs/Symptoms: Upper respiratory:
• Chronic sinusitis; nasal polyps
Lower respiratory:
• Progresses from small airway obstruction to larger airway obstruction and finally causes
destruction of lung tissue;
• Thick secretions obstruct bronchioles and lead to air trapping/hyperinflation of the lungs.
• Stasis of mucus provides excellent growth medium for bacteria = chronic airway infection
• Progressive loss of lung tissue results from inflammation and scarring and leads to chronic
hypoxia and pulmonary hypertension/cor pulmonale
• Hemoptysis (possibly fatal) and pneumothorax may be complications of CF
• CF is first obstructive (with mucus); later it becomes restrictive (fibrosis; lung destruction; thoracic
wall changes)
• Death from CF is a result of loss of pulmonary function.
• Pancreatic insufficiency leads to inability to absorb nutrients and diabetes mellitus
• GI problems; GERD and distal intestinal obstructive syndrome; constipation
Clinical manifestations
• In children: meconium ileus in newborn; failure to grow; clubbing; persistent cough with mucus
production; tachypnea; large, frequent bowel movements; large, protuberant abdomen with
emaciated limbs
• In adults: cough that becomes persistent and produces thick, purulent, often green sputum
• Recurring lung infections
• Weight loss
• Increased sputum
• Decreased pulmonary function
• Right, lower quadrant pain (abdomen)
• Loss of appetite, emesis, palpable abdominal mass
• Insufficient pancreatic enzyme release causes protein/fat malabsorption with frequent, bulky,
foul-smelling stools.
• Male sterility (but not impotent)
• Delayed menarche in females; diminished fertility (but can become pregnant)
Diagnosis: Sweat chloride test: >65 mEq/L suggest CF
 Other tests:
• Chest x-ray
• Pulmonary function tests
• Fecal analysis for fat
• Duodenoscopy for quantitative determination of pancreatic enzymes
• DNA analysis can only confirm a diagnosis not be sole test (too many CF mutations)
Treatment: Goals:
• Promote clearance of secretions
• Control infection in the lungs
• Provide adequate nutrition
Airway clearance
• Draining of thick secretions
• DNase (Pulmozyme) decreases sputum viscosity and increases airflow
• Bronchodilators and mucolytics may be used
• CPT; postural drainage; positive expiratory pressure (PEP) breathing; aerobic exercise
Lung infections
• Antimicrobial treatment for infection
• Antibiotics specific to microorganism
• Home oxygen may be required for patients with cor pulmonale or hypoxemia
• Lung transplantation
• Surgical pleural abrasion or pleural stripping for recurrent pneumothorax
Pancreatic insufficiency
• Pancreatic enzyme replacement (lipase, protease, amylase) before each meal
• High calorie/high protein diet and multivitamins recommended
• Add salt when sweating is excessive (hot weather, fever, physical activity)
Gene Therapy (experimental)