Review of Normal Structures in Respiratory System

Purpose

Provides mechanisms for transporting O2 from air into the blood and
for removing CO2 from blood
Upper resp. tract
o Passageways that conduct air bet. atmosphere and lungs
Lower resp. tract
o Trachea
o Bronchial tree
o Lungs (gas exchange takes place)

Structures

I. Upper Respiratory Tract

When air is inhaled into the resp. system, it first enters the nasal
passages, passing over the conchae or turbinates
o
Air is warmed and moistened by highly vascular mucosa and
foreign material is filtered out by mucous secretions and
hairs

Opening off the nasal cavity through small canals are 4 pairs of
paranasal sinuses w/c are small cavities in skull bones
o
Reduces weight of facial bones
o
Add resonance to the voice
o
Named acc. to the bones in w/c they are located
- frontal
- ethmoid
- sphenoid
- maxillary

Sinuses
o
o
o
o
o

are lined by a continuation of Resp. mucosa

Consists of pseudostratified columnar epithelium
Includes mucus-secreting goblet cells and cilia
Mucus traps foreign particles and cilia sweep the mucus and
debris up and out of resp. tract
Excessive amt of mucus or particles stimulate a sneeze or
cough
Smoking impairs functions of cilia and irritation caused by
smoke leads to replacement of ciliated epithelium by
squamous cells

Airflow continues through Nasopharynx and Larynx into trachea

On the posterior wall of nasopharynx are located the pharyngeal

tonsils or adenoids
o
Consist of lymphoid tissue
o
If become enlarged owing to infection, they can obstruct
the flow of air through nasopharynx, leading to mouth
breathing
o
When air passes through mouth directly into resp. tract, it
is not warmed, moistened and filtered properly
o
Tissues of mouth become dry and irritated and there is a
risk of increase dental caries as normal salivary cleansing
function is lost
o
Palatine tonsil - lymphoid tissue located in posterior portion
of oral cavity

Opening off the nasopharynx are 2 auditory (Eustachian) tubes

o
Connect to the middle ear cavities
o
Continuation of resp. mucosa into sinuses and middle ear
creates a predisposition to the spread of infection from
upper resp. tract

Pharynx
o
o
o
o

Where the nasopharynx joins the oropharynx

Serves as a common passage for air and food
Descends to the point of separation of esophagus and
trachea
When infection is present, inflammation and swelling in
area causes sore throat and painful swallowing

Epiglottis
o Protects the opening into larynx by flipping up or down w/
swallowing or ventilation
Larynx/ voice box
o Consists of cartilages and their associate muscles
o Thyroid cartilage largest, forms the Adams apple
o 2 pairs of vocal cords
- upper or false pair
- lower or true pair (glottis)
o When air is expired through through larynx, true vocal cords
vibrate, producing sound of a voice
As inspired air is tracked downward through larynx, it flows into the
trachea or windpipe
o Composed of smooth muscle and elastic tissue in w/c are
located C-shaped rings of cartilage whose open side is on
posterior surface to allow for esophageal expansion
o Supports the wall of airway , preventing its collapse

II. Lower Respiratory tract

Bronchus
o
Right bronchus is larger and straighter and therefore is
the more likely destination for any aspirated material
o
Point @ w/c bronchus enters the lung is hilum
o
Primary bronchus - Secondary bronchi - Bronchioles
o
As the bronchi become smaller , cartilaginous rings
diminish in size, and smooth muscle increases
(contracts/relaxes)
o
Many elastic fibers are present , enabling expansion and
recoil of lungs during ventilation

Air in bronchioles then flows into alveolar ducts and alveoli

o
Formed by a single layer of simple squamous epithelial
tissue
o
Promotes diffusion of gases into the blood
o
End-point for inspired air
o
Resp. membrane is the combined alveolar and capillary
wall, a very thin membrane through w/c gas exchange
takes place
o
Contain macrophages, whose function is to remove any
foreign material
o
Inside surfaces are coated w/ surfactant (reduces
surface tension)

Lungs
o
o

o
o
o
o

Positioned on either side of heart

Mediastinum is the region in center of chest, contains the
ff :
- heart
- major blood vessels
- esophagus
- trachea
Diaphragm forms the inferior boundary
Right lung is divided into 3 lobes , Left lung is into 2 lobes
because of position of heart
Lung tissue is nourished by bronchial arteries w/c branch
from thoracic aorta
Pleural membrane
- visceral pleura (attached to outer surface of lung)
- parietal pleura (lines inside thoracic cavity, adhering to
chest wall and diaphragm)
- visceral lies closely against parietal pleura separated only
by very small amt of fluids in pleural cavity or space
(potential space)
- the slightly negative pressure (less than atmospheric
pressure) in pleural cavity also assists in holding pleura and
promoting lung expansion
- pleural fluid provides lubrication during resp. movements
and a force that provides cohesion or sticking together
(high surface tension) bet. 2 pleural layers during
inspiration

Thorax
o
o
o
o
o

Ribs, vertebrae, sternum (breastbone)

Upper 7 pairs of ribs (true ribs) articulate w/ vertebrae
and are attached to sternum by costal cartilage
3 pairs (false ribs) connected to costal cartilage of 7th ribs
, not directly to sternum
Last 2 ribs (false ribs) 11th and 12th pair, attached only to
vertebrae and are called floating ribs
Bet. ribs are located the external and internal intercostal
muscles w/c move the thoracic structures during
ventilation

Ventilation
Gas exchange/ External respiration

Flow of gases bet. alveolar air and blood in pulmonary circulation

Diffusion of O2 and CO2 in lungs depends on relative concentrations
or partial pressures of gases
Movement of each gas always occurs from a high pressure area to
low-pressure area
Partial pressure (PO2, PCO2) is the concentration of a gas in a
mixture
Partial pressure of O2 in arterial blood is expressed as PaO2
Each gas in a mixture moves or diffuses acc. to its own partial
pressure gradient and independent of other gases (Daltons law)
o
O2 diffuses from alveolar air, an area w/ a high
concentration of O2, to the blood in pulmonary capillary,
w/c has low concentration of O2 , until concentrations
become equal
o
CO2 diffuses out of pulmonary capillary into alveolar air
depending on its relative concentratins
Air contains O2, CO2, Nitrogen and H2O
Because air is not totally expired from alveoli during expiration and
has been humidified during its passage into lungs, alveolar air has
different concentrations of gases than either atmospheric air or
blood
The residual air in alveoli allows continuing gas exchange bet.
expiration and inspiration because blood continually flows through
pulmonary circulation

Pulmonary circulation is composed of :

Pulmonary arteries bring venous blood (dark blue-red color) from R

side of heart to be oxygenated
Pulmonary capillaries diffusion or gas exchange occurs
Pulmonary veins return oxygenated blood (bright red) to L side of
heart w/c then pumps it out into systemic circulation

Factors affecting Diffusion of Gases

Partial pressure gradient

Thickness of resp. membrane
o
When fluid accumulates in alveoli or interstitial tissue ,
diffusion , particularly O2 is greatly impaired
o
Normally, pressure in pulmonary circulation is very low ,
reducing risk of excessive fluid in interstitial space and
alveoli
o
Presence of extra fluid may also impede blood flow
through pulmonary capillaries and increase surface tension
in alveoli restricting expansion of lung
Surface area available for diffusion
o
Alveoli are the only structures that provide such a surface
area and both ventilation and perfusion must be adequate
for diffusion to occur
o
If part of alveolar wall is destroyed , as in emphysema , or
if fibrosis occurs in lungs, surface area is greatly reduced
o
If airflow into alveoli is obstructed or if capillaries are
damaged, involved surface area becomes nonfunctional

Imbalance in diffusion of gases can be measured by :

Ventilation-perfusion ration (Va/Q)

An autoregulatory mechanism in lungs can adjust ventilation and blood

flow
o
If PO2 is low because of poor ventilation in an area,
vasoconstriction occurs in pulmonary arterioles, shunting
blood to other areas of lungs where ventilation may be
better
o
If airflow is good, pulmonary arterioles dilate to maximize
gas exchange

Transport of O2 and CO2

Only about 1 % of total O2 is dissolved in plasma because O2 is
relatively insoluble to H2O

The dissolved form of gas is that w/c :

o
Diffuses from alveolar air into blood in pulmonary
capillaries
o
Diffuses into interstitial fluid and cells during process of
internal resp.
Oxygen

Most O2 is transported reversibly bound to Hgb by the iron molecules

(Oxyhemoglobin)
When all four heme molecules in Hgb have taken up O2 , the Hgb is
termed fully saturated (measurement expressed as SaO2)
As O2 diffuses out of blood into interstitial fluid and cells, Hgb
releases O2 to replace it, so dissolved O2 is always available in plasma
, ready to diffuse into cells
The rate @ w/c Hgb binds or releases O2 depends on factors :
o
PO2 (partial pressure of dissolved O2)
o
Temp.
o
Plasma pH
Normally, app. 25 % of bound O2 is released to cells for metabolism
during an RBCs trip through systemic circulation , leaving 75% of Hgb
in venous blood still saturated w/ O2

Carbon dioxide

Waste product from cell metabolism

Transported in several forms
App. 7 % is dissolved in plasma and can easily diffuse across
membrane
20 % is loosely and reversibly bound to Hgb, attached to an amino
group on globin portion (Carbaminoglobin)
Majority of CO2 resulting from cell metabolism diffuses into RBC
where under influence of enzyme carbonic anhydrase , it transitions
very briefly as carbonic acid , then is immediately converted into
bicarbonate ions

CO2 + H2O

H2CO3

H+ + HCO3-

The bicarbonate ions can diffuse back into plasma to function in

buffer pair
A ratio of 20 parts bicarbonate ion to 1 part carbonic acid maintains
blood pH @ 7.35
CO2 plays a major role in control of blood pH through the buffer
system

Diagnostic tests

Spirometry
Arterial blood gas determinations check O2, CO2 and HCO3- level
as well as serum pH
Oximeters measure O2 sat.
Exercise tolerance testing useful in pt w/ chronic pulmonary disease
for dx and monitoring of pts progress
Radiography for evaluating tumors or infections
Bronchocospy used in performing biopsy or in checking for site of
lesion or bleeding
Culture and sensitivity testing/ sputum specimens can identifiy
pathogens

General Manifestations of Resp. Disease

1. Sneezing

Reflex response to irritation in upper resp. tract

Assists in removing irritants
Associated w/ inflammation or foreign material in nasal passages

2. Coughing

May result from :

o Irritation due to a nasal discharge dripping into
oropharynx
o Inflammation or foreign material in lower resp. tract
o Inhaled irritants
Occasional cough is considered normal
Aspiration of food or fluid may cause spasm of coughing
Cough reflex is controlled by a center in medulla
o Inspire air then close glottis and vocal cords
o Followed by forceful expiration in w/c glottis is opened
and unwanted material is blown upward and out of mouth
Effectiveness of cough depends on strength of muscle action in
both inspiration and expiration
Constant dry/unproductive cough
o Fatiguing because it interferes w/ sleep
o Resp. muscles are excessively used
o A cough-suppressant med (eg. Codeine,
dextromethorphan) may be used @ night
Productive cough
o Secretions or inflammatory exudate accumulate in lungs
and removal of it is beneficial
o Management : Increased fluid intake, expectorant med
(eg. Guaifenesin) ,humidifier

3. Sputum or mucoid discharge

Yellowish-green, cloudy, thick

o Bacterial infection
Rusty /dark colored
o Pneumococcal pneumonia
Very large amt of purulent sputum w/ foul odor
o Bronchiectasis
Thick, tenacious (sticky)
o Asthma
o Cystic fibrosis
Blood tinged , frothy
o Pulmonary edema
o Chronic cough and irritation (causes rupture of
superficial capillaries)
o Tumor/TB

Absence of breath sounds

o Nonaeration or collapse of lung (atelectasis)

6. Dyspnea

Subjective feeling of discomfort

Person feels unable to inhale enough air

May be manifested as breathlessness or SOB, either w/ exertion

or @ rest

Severe dyspnea
o May be accompanied by flaring of nostrils , use of
accessory muscles, or retraction (pulling in) of muscles
bet. or above ribs

Orthopnea
o Occurs when a person is lying down
o Pulmonary congestion develops as more blood pools in
lungs when person lies down and also abdominal contents
push upward against lungs
o Raising the upper part of body w/ pillows facilitate
breathing

Paroxysmal nocturnal dyspnea

o Sudden acute type
o Common in pt w/ L sided CHF
o During sleep, body fluid is redistributed , leading to
pulmonary edema
o Person wakes up gasping for air and coughing
7. Cyanosis

Bluish discoloration of skin and mucous membrane

Results from large amounts of unoxygenated Hgb in blood
May develop in peripheral areas as a result of exertion or be
more generalized
May occur In pt w/ cv conditions as well as resp. disease
Not a reliable early indicator of hypoxia

8. Pleural pain

Results from inflammation or infection of parietal pleura

A cyclic pain that increases as the inflamed membrane is
stretched w/ inspiration or coughing

9. Friction rub

A soft sound produced as the rough membranes move against

each other
Pleural inflammation may be caused by lobar pneumonia or lung
infarction

10. Clubbed fingers

4. Breathing patterns
Eupnea
o
10-18 inspirations per min.
o
Regular and effortless

Kussmaul
o Deep rapid resp. or air hunger
o Acidosis
o May follow strenuous exercise

Labored
o Obstructon of airways

Wheezing
o Whistling sounds
o Obstruction of small airways

Stridor
o High pitched crowing noise
o Upper airway obstruction
5. Breath sounds

11. Changes in ABGs

Rales
o

Light bubbly or crackling sounds associated w/ serous

secretions

Rhonchi
o Deeper or harsher sounds resulting from thicker mucus

Result from chronic hypoxia associated w/ resp. or cv diseases

Painless, firm, fibrotic enlargement @ the end of digit

Hypoxemia is inadequate O2 in blood

Hypoxia or inadequate O2 supply to cells
Causes of hypoxia :
o
Deficit of RBC or Hgb levels
o
Circulatory impairment
o
Excessive release of O2
o
Impaired resp. function
o
Carbon monoxide poisoning
- carbon monoxide binds tightly to heme , displacing O2
- doesnt cause obvious signs of hypoxia or affect
ventilation
- can be fatal very quickly and quietly
Hypoxia affects cell metabolism leading to anaerobic metabolism
and development of metabolic acidosis
Brain is most susceptible to an O2 deficit because it has little
storage capacity for O2 and yet has a constant demand
Cerebral hypoxia initially stimulates the sympathetic NS
Decreased cell function is indicated by :

o
Fatigue
o
Lethargy
o
Muscle weakness
Extreme or prolonged hypoxia can result in cell death
Compensation mechanisms for hypoxia due to resp./cv impairment
o
Increased cv activity (tachycardia, increased BP)
o
Increased erythropoietin secretion , stimulating bone
marrow to produce addtl RBC (secondary polycythemia)
Resp. acidosis
o
Excess CO2
o
Increased H2CO3
o
Results from impaired expiration
Resp. alkalosis
o
RR is increased usually because of acute anxiety or
excessive intake of aspirin

Infectious Diseases

Sinusitis

Upper Respiratory Tract Infections

Common cold (infectious rhinitis)

Caused by a viral infection of the upper respiratory tract

Self limiting infection
Most Common pathogen: rhinovirus
May also be: adenovirus, parainfluenza virus, coronavirus
There are more than 100 possible causative organisms so it is
difficult for an individual to develop sufficient immunity to avoid all
colds
Mode of transmission : Respiratory droplets (either directly inhaled
or are spread by secretions on hands or contaminated objects)
Highly contagious because the virus is shed in large numbers from
the infected nasal mucosa during the first few days of infection and
can survive for several hrs outside the body
Signs :
o Nasal congestion
o Copious watery discharge (rhinorrhea, sneezing, watery eyes)
o Mouth breathing
o Change in the tone of voice
o Sore throat
o Headache
o Slight fever
o Malaise
o Cough may develop from the irritation of the secretions
dripping into the pharynx
o Stuffiness and irritation may also persists as the secretions
become more viscous
Infection and inflammation may spread to cause:
o Sore throat (pharyngitis)
o Hoarse voice (laryngitis)
o Cough (acute bronchitis)
Treatment : Symptomatic
o Acetaminophen for fever and headache
o Decongestants/vasoconstrictors to reduce edema and
congestion in the respiratory passages
o Antihistamines reduce secretions but may cause excessive
drying tissues and cough
o Humidifiers did in keeping the secretions liquid and easily
drained
o Vit. C remains controversial
o Antibiotics do not cure viral infection ; Usually reserved for
secondary bacterial infections or for prophylactic use in high
risk patients
To reduce risk of transmission :
o Proper handwashing
o Disposal of tissues
o Avoidance of crowded areas

A bacterial infection s/t a cold or an allergy that has obstructed the

drainage of one or more of the paranasal sinuses into the nasal cavity
Common causative agents:
o Pneumococci
o Streptococci
o Haemophilus influenzae
As the exudates accumulates, pressure builds up inside the sinus
cavity causing severe pain in the facial bone
Pain may be confused w/ : Headache (ethmoid sinus) or Toothache
(maxillary sinus)
Signs :
o Nasal congestion
o Fever
o Sore throat
Treatment
o Decongestants
o Analgesics
o Antibiotics
Diagnosis
o Radiograph
o Transillumination

Laryngotracheobronchitis (croup)

Viral infection particularly in children bet. 1 and 2 yrs of age

Common causative agents :
o Parainfluenza viruses
o Adenoviruses
Begin as an upper respiratory condition w/ Nasal congestion and
Cough
Larynx and subglottic area become inflamed w/ swelling and exudate
leading to obstruction and a characteristic :
o Barking sound
o Hoarse voice
o Inspiratory stridor
Becomes more severe at night
Treatment
o Moisturized air from a humidifier or shower or croup tent
Often relieves the obstruction
Prognosis
o Infection is self limited and full recovery occurs in several
days
o In some children w/ allergic tendencies , smooth muscle spasm
may exacerbate the obstruction requiring addtl treatment

Epiglotitis

An acute infection usually caused by bacterial organism, H. influenzae

type B
Common in children 3 to 7 yrs old
Causes swelling of the larynx, supraglottic area and epiglottis w/c
appears as a round, red ball obstructing the airway
Signs :

o
o
o
o
o
o
o
o

Onset is rapid
Fever
Sore throat
Child refuses to swallow
Drooling of saliva
Inspiratory stridor
Anxious /Pale
Child assumes sitting position/tripod position

Treatment
o Oxygen
o Antimicrobial therapy
o Intubation/ Tracheotomy if necessary

Influenza

Viral infection that may affect both the upper and lower respiratory
tracts
3 groups of influenza virus : Type A (the most prevalent pathogen) ,
Types B and C w/c mutate constantly preventing effective immune
defense
Incubation period : 1 to 4 days
Signs :
o Sudden, acute onset
o Fever
o Fatigue
o Aching pains in the body
May also cause viral pneumonia
Mild case can be complicated by secondary problems such as
bacterial pneumonia
Most deaths during flu epidemics result from pneumonia
Treatment : Symptomatic and Supportive unless bacterial infection
occurs
o Antiviral drugs : amantadine (Symmetrel, Endantadine)
o zanamivir (Relenza inhaler)
o oseltamivir (Tamiflu)
Vaccination is highly recommended
o If flu does develop following immunization, it is a mild
infection
o A period of 2 to 3 weeks after vaccination is required before
immunity develops

Pneumococcal pneumonias
- alveolar are inflamed and filled with exudate resulting in a
solid mass in a lobe
Epidemiologic data
o Nosocomial pneumonia
- affects those w/ less resistance , elderly , debilitated
,malnourished or immunesuppressed
- infection often results from gram-negative organisms
(Klebsiella pneumoniae, Pseudomonas aeruginosa)
o Community acquired pneumonia
- may be viral /bacterial
- can affect healthy persons such as ff influenza as well as
persons w/ underlying CV or Resp disease
o Aspiration pneumonia
- may be Nosocomial/community acquired
- involves aspiration of vomitus w/c is irritating to tissues or
nasopharyngeal secretions
- when periodontal disease is marked, it results from infection
by gram-negative microbes
o

Lower Respiratory Tract Infections

Bronchiolitis (RSV infection)

Common infection in young children 2 to 12 mos. of age

Caused by respiratory syncytial virus (RSV), a myxovirus
Mode of transmission : Oral droplet ; occurs more frequently in
winter months
Predisposing factors :
o Familial history of asthma
o Presence of cigarette smoke
Virus causes :
o Necrosis and inflammation in the small bronchi and bronchioles
o Edema
o Increased secretions
o Reflex bronchospasm
Signs :
o Wheezing
o Dyspnea
o Rapid shallow respiration
o Cough
o Rales
o Chest retraction
o Fever
o Malaise
There may be areas of :
o hyperinflation w/ air trapping due to partial obstruction or
o atelectasis or nonaeration resulting from total obstruction
Treatment : Symptomatic and Supportive
o Monitoring of blood gases

Pneumonia

May develop as a primary acute infection in the lungs or it may be

secondary to another respiratory or systemic condition in w/c tissue
resistance is reduced
A risk following any aspiration or inflammation in the lung when fluid
pool or defense mechanisms such as cilia are reduced
In most cases, organisms enter the lungs directly :
o by inhalation (virus)
o by resident bacteria spreading along the mucosa
o by aspiration in secretions
Occasionally it is bloodborne

Classification is based on :
Causative agent
o May be virus, bacterium or fungus
o May also involve multiple microbes ff aspiration
Anatomic location of infection
o May be diffuse or patchy throughout both lungs or lobar
(consolidated in one lobe)
Pathophysiologic changes
o Viral pneumonias
- changes occur primarily in interstitial tissue or alveolar
septae

Types :
1. Lobar pneumonia (pneumococcal pneumonia)
Usually caused by Streptococcus pneumoniae
Localized in one or more lobes
Congestion
First stage in the development process
Inflammation and vascular congestion develop in the alveolar wall and
exudate forms in the alveoli w/c interferes greatly w/ O2 diffusion
Consolidation
A solid mass in the lobe represented by accumulated neutrophils,
RBCs, and fibrin in the alveolar exudate
The presence of RBCs in the exudate produces the typical rusty
sputum
Pleurisy / pleuritis
Because a complete lobe is usually involved in the inflammatory
process , the adjacent pleurae are frequently involved producing
pleuritic pain at the affected site
Empyema
Infection may also be spread to pleural cavity
Can cause adhesions bet. the pleural membranes restricting
ventilation
- Manifestation
o Sudden onset
o Systemic signs of high fever w/ chills , marked fatigue, and
leukocytosis
o Dyspnea, tachypnea, tachycardia
o Pleuritic pain
o Rales heard initially over the affected lobe and then
disappearing as consolidation occurs
o productive cough w/ typical rusty-colored sputum
o confusion and disorientation

Treatment
o Antibacterial meds : penicillin
o Supportive measures such as : Fluids, drugs to reduce fever,
O2
o Pneumococcal vaccine (once in a life time immunization) is
recommended
Diagnosis
o Chest X-ray
o Sputum culture

2. Bronchopneumonia
Diffuse pattern of infection in both lungs more often in lower lobes
One or several microbes may cause the infection beginning in the
bronchial mucosa and spreading into the local alveoli

Inflammatory exudate forms in the alveoli interfering w/ O2

diffusion
Signs :
o Onset is insidious
o Moderate fever
o Cough
o Rales
Congestion causes a productive cough w/ purulent sputum (yellow /
green )
Hypostatic pneumonia
o Pooled secretions in the lungs become infected by organisms
draining from the upper passages
o Particularly in immobilized patients
Diagnosis
o Sputum culture
o Sensitivity tests

Severe Acute Respiratory Syndrome (SARS)

3. Legionnairess disease
Caused by gram-negative bacteria , Legionella pneumophila w/c
thrives in a warm, moist environment
Arises as a nosocomial infection
Microbe has been difficult to identify because it is found inside the
pulmonary macrophages and requires a special culture medium
If untreated, it can cause severe congestion and consolidation w/
necrosis in the lung and possibly fatal consequences
4. Primary atypical pneumonia (PAP)
Causative organisms : Mycoplasma or viral
o Mycoplasma pneumonia
Common in older children and young adults
Transmitted by aerosol but is not considered highly
contagious
Frequent cough is a prominent sign
Reponds to erythromycin or tetracycline
o Viral pneumonia
Often caused by influenza A or B
Also caused by : Adenoviruses and respiratory syncytial
virus (RSV)
Onset is insidious w/ inflammation in the mucosa of the
upper respiratory tract and then descend to involve the
lungs
The organisms produce inflammation that is diffuse and
interstitial w/ little exudate forming in the alveoli
therefore cough is unproductive and rales are not
pronounced
o Chlamydial pneumonia
Caused by Chlamydia pneumoniae
Often mild ; Sometimes not diagnosed

Signs of PAP
o Onset is often vague
o Nonproductive cough
o Hoarseness
o Sore throat
o Headache
o Mild fever
o Malaise

5. Pneumocystis carinii pneumonia (PCP)

Occurs as an opportunistic and often fatal infection in patients w/
AIDS
May also causes pneumonia in premature infants
The microbe was formerly classified as a protozoa , now it is
considered as a fungus
Microbe appears to be inhaled and attaches to alveolar cells causing
necrosis and diffuse interstitial inflammation then alveoli fill w/
exudate and fungi including the cystic form
Onset is marked by difficulty breathing and nonproductive cough
Prophylactic drugs : sulfamethoxazole- trimethroprim combination
or pentamidine aerosol are recommended for AIDS patients

Acute respiratory infection was first diagnosed in China in 2002

Causative microbe : Coronavirus, SARS-CoV (SARS-associated
coronavirus)
Mode of transmission : Respiratory droplets during close contac , Oral
fecal transmission
Incubation period : 2 to 7 days , ave. 4 to 6 days
First stage : Flu like syndrome , fever, headache, myalgia, chills,
anorexia, frequent diarrhea
Lymphopenia and Thrombocytopenia are often present
There is also An increased C-reactive protein levels and Elevated liver
enzymes resulting from liver damage by the virus
The nonspecific early manifestations and lack of a rapid diagnostic
test (antibodies are not present until 3 wks after onset) combine to
make identification of the infection difficult
Treatment
o Antiviral
o Ribavirin
o Glucocorticoid
o Methylprednisolone

Tuberculosis

Infection usually caused by Mycobacterium tuberculosis

Prevalence is difficult to estimate because of the large number of
latent cases /many are undiagnosed
Mycobacterium tuberculosis
o Affects primarily the lungs but it may invade the other organs
as well
o An acid fast, aerobic, slow-growing bacillus that is somewhat
resistant to drying and to many disinfectants
o Can survive in dried sputum for weeks
o Destroyed by UV light, heat, alcohol, glutaraldehyde and
formaldehyde
o Cell wall appears to protect them from destruction by normal
body defenses so that normal response by neutrophils PMNs to
infection and production of purulent exudate does not occur

Pathogenesis : 2 Stages
1. Primary or Latent Infection
Occurs when microorganisms first enter the lungs, are engulfed by
macrophages and cause a local inflammatory reaction usually on the
periphery of the upper lobe
Some bacilli migrate to the lymph nodes activating a type IV or cell
mediated hypersensitivity response
Granuloma
o Lymphocytes and macrophages cluster together at the site of
inflammation
o Contains bacilli, some of w/c remain alive forming a Tubercle
Caseation necrosis
o In the center of the tubercle forms a core of cheese-like
material consisting of dead macrophages and necrotic tissue
Ghon complexes
o A healthy person can resist the invasion, so the lesions remain
very small and become walled off by fibrous tissue ,eventually
to calcify
o The lesions in the lung and lymph nodes
o When calcified, the tubercle may be visible on a chest
radiograph
However, Bacilli may remain viable in a dormant state inside the
tubercle for years
As long as the persons resistance and immune responses remain high
the bacilli remain walled off w/in the tubercle
Person has been exposed to bacillus and infected but does not have
active disease and is asymptomatic
By about 6 to 8 wks the immune response is complete and is
considered primary /latent infection
2. Secondary or Reinfection
Stage of active infection

Often arises years after primary infection when the bacilli, hidden in
the tubercles are reactivated usually because of decreased host
resistance
Occasionally there is a new invasion of microbes, and as the organisms
multiply, tissue destruction occurs, forming a large area of necrosis
Cavitation
o Formation of a large open area in the lung and erosion into the
bronchi and blood vessels
o Hemoptysis is common as the blood vessels are eroded
o Spread of the organisms into the other parts of the lung is
promoted and bacilli are present in the sputum
Bacteria may be swallowed to infect the digestive tract
May also be spread into the pleural cavity causing pleuritis and
adhesions

Miliary tuberculosis
A rapidly progressive form in w/c multiple granulomas affect large
areas of lungs and rapidly disseminate into the circulation and to
other tissue
Does not respond to treatment
Mode of Transmission
o Oral droplets
o In some countries where milk is not pasteurized, TB may be
caused by = Mycobacterium bovis
o
Crowded areas
o Malnutrition
o Immunodeficiency
o Alcoholism
o Chronic diseases
o Genetic susceptibility
o Increased travel and immigration
o An increase in the homeless population
o Prevalence of infection in patients w/ AIDS
o Development of drug-resistant strains of the organisms

Histoplasmosis

Signs

Primary TB
o Asymptomatic

Secondary TB
o Onset is insidious
o Systemic signs often appear first :
- Anorexia
- Malaise
- Fatigue
- Weight loss
- Night sweats
- Afternoon grade fever
o Cough is prolonged and becomes more severe and as cavitation
develops, more productive
o Sputum becomes more purulent and often contains blood

Diagnosis
Tuberculin test

Used to detect exposure to bacillus

Several weeks after exposure, person has become hypersensitive and

will produce a positive skin reaction / large area of induration , a hard
raised, red area in response to administration of tuberculoprotein

Of no value if person has previously received the bacillus CalmetteGuerin (BCG) vaccine
Chest x-ray and Sputum culture

To determine whether active infection is present

Nucleic Acid amplification (NAA)

Newer technique to provide faster confirmation

Treatment

Long term treatment w/ a combination of drugs is recommended to

totally eradicate the microbes and to reduce the risk of resistant
bacteria
Length of treatment varies from 3 mos. to a year or longer depending
on the situation
Drugs of choice :
o isoniazid (INH)
o rifampin
o ethambutol
o pyrazinamide
o streptomycin
Sputum culture is usually negative after 1 to 2 mos. of treatment
It is recommended that contacts of the patient be given prophylactic
isoniazid for a year and receive tuberculin testing as well

Common in the Midwestern United States

Causative agent : fungus, Histoplasma capsulatum
The said fungus and its spores can be inhaled on dust particles
Occuring as an opportunistic infection common in persons w/ AIDS
where fungus tends to disseminate or spread easily through the body
Fungus is found as a parasite inside the macrophages
Effects are similar to those of TB :
o First stage is asymptomatic may be followed by ..
o Second stage of active infection w/c involves :
- granuloma formation
- necrosis and consolidation
Signs :
o Cough
o Fatigue
o Fever
o Night sweats
Diagnosis
o Skin test can differentiate histoplasmosis from TB
o Organisms can be also cultured to confirm diagnosis
Treatment
o Antifungal agent amphotericin B (Fungizone)

Sweat glands are also affected , producing sweat that is very high in
NaCl content
Usually not a serious problem unless hot weather or strenuous exercise
lead to excessive loss of electrolytes in sweat

In Reproductive system
Thick mucus obstructing the vas deferens in males or cervix in females
may lead to sterility or infertility
In some males, testes and duct do not develop normally
III. Etiology
The gene for cystic fibrosis is located on 7th chromosome
Transmitted as an autosomal recessive disorder
More common in whites from northern Europe

Obstructive Lung Disease

Cystic fibrosis (CF)

I. Definition
A common inherited disorder in children
Sometimes called Mucoviscidosis
A common genetic disorder
II. Pathophysiology

Gene has been identified and relates to a protein involved in chloride

ion transport in cell membrane
The defect in exocrine glands causes abnormally thick secretions such
as tenacious mucus
Primary effects of CF are seen in lungs and pancreas , where the sticky
mucus obstructs the passages
In the lungs
Mucus obstructs airflow in bronchioles and small bronchi causing air
trapping or atelectasis w/ permanent damage to bronchial walls
Because stagnant mucus is an excellent medium for bacterial growth,
infections are common and add to the progressive destruction of lung
tissue
Organisms commonly causing infection in pt w/ CF :
o P. aeruginosa
o S. aureus
Bronchiectasis and emphysematous changes are seen frequently as
fibrosis and obstructions advance
Eventually, respiratory failure or cor pulmonale (R-sided congestive
heart failure) develops
In the digestive tract
The first indication of abnormality may be meconium ileus in newborns
in w/c small intestine of neonate is blocked by mucus @ birth,
preventing the excretion of meconium shortly after birth
In the pancreas
Ducts of exocrine glands become blocked , leading to a deficit of
pancreatic digestive enzymes in intestine
Malabsorption and malnutrition result
Obstruction and backup of secretions eventually cause damage to the
pancreatic tissue including islets of Langerhans resulting in DM
In liver
Bile ducts of liver may be blocked by viscid mucus preventing bile from
reaching the duodenum and interfering w/ digestion and absorption of
fats and fat-soluble vit (ADEK) .
If obstruction is severe , backup of bile behind obstruction may cause
inflammation and permanent damage to liver in form of biliary cirrhosis
In Oral cavity
Salivary glands are often mildly affected ,w/ secretions that are
abnormally high in NaCl and mucus plugs that cause patchy fibrosis of
submaxillary and sublingual glands
In skin

IV. Signs and Symptoms

Meconium ileus may appear @ birth
Salty skin
Signs of malabsorption with the ff : (indicate lack of pancreatic
enzymes and bile)
o Steatorrhea
o Abdominal distention
o Failure to gain weight
Chronic cough and frequent respiratory infections
As lung damage proceeds, ff develop :
o Hypoxia
o Fatigue
o Exercise intolerance
Chest may be overinflated owing to air trapping
Rhonchi are audible
Failure to meet the normal growth milestones ,usually because of
chronic resp. problems
V. Diagnostic tests
Sweat is analyzed for abnormal electrolyte content
o May not be accurate until infant is @ least 2-3 weeks old
Stools may be checked for fat content and trypsin (pancreatic enzyme)
content
Lung involvement can be assessed w/ :
o X-rays
o Pulmonary function tests
o Blood gas analysis
VI. Treatment
In child, it requires a team or interdisciplinary approach because there
is multisystemic involvement w/ numerous complications for childs
growth and development
Replacement therapy for pancreatic enzymes (eg. pancrelipase
[Cotazym]) and if necessary , bile salt replacement can be administered
with meals and snacks to improve digestion and absorption
Diet high in CHON, low fat and vit.supplements
Avoid dehydration resulting from excessive losses in sweat or stool
because a fluid deficit may result in thicker and more tenacious resp.
mucus
Intensive chest physiotherapy to ensure removal of tenacious mucus
o Postural drainage
o Percussion
o Coughing techniques
Use of bronchodilators and humidifiers to promote drainage
Regular moderate aerobic exercise help remove secretions and promote
gen health
In pt with advanced lung disease, O2 therapy as well as medication for
CHF may be required

Lung Cancer
I. Definition
Lungs are a common site of both primary and secondary lung cancer
Benign lung tumors are rare
Metastatic cancer develops frequently in lungs because venous return
and lymphatics bring tumor cells from many distant sites in body to the
heart and then into pulmonary circulation w/c provides the first small
blood vessels and hospitable environment in w/c tumor cells can lodge
II. Pathophysiology
Types of Lung cancer :
Bronchogenic carcinoma
o Arising from the bronchial epithelium
o Most common type of malignant lung tumor
Squamous cell carcinoma
o Develops from epithelial lining of a bronchus near the hilum and
projects into the airway
Adenocarcinomas (from glands) and Bronchoalveolar cell carcinomas
o Usually found on periphery of lungs making them less
symptomatic and more difficult to detect in early stages
o Cells of adenocarcinomas may secrete mucin
Small-cell/ oat-cell carcinomas
o Rapidly growing type of lung cancer
o Often located near a major bronchus in central part of lung
o Tend to be invasive and metastasize very early in their
development
Large cell carcinomas
o Usually found in periphery
o Consist of undifferentiated large cells that have a rapid growth
rate and metastasize early
Changes in lungs
Metaplasia
o First change in lungs ; a change in epithelial tissue
o Associated w/ smoking or chronic irritation
o Reversible if irritation ceases
o Loss of normal protective, ciliated , pseudostratified epithelium
leaves the lung tissue more vulnerable to irritants and
inflammation from smoking
Dysplasia / Carcinoma in situ
o It then develops
o Difficult to detect
Stages of Lung cancer
Staged @ the time of dx based on tumor size-node involvementmetastases (TNM) classification
Stage I tumors localized
Stage III tumors disseminated
Common sites of metastases from lungs :
Brain
Bone
Liver
Effects of tumors in lungs :

Obstruction of airflow by tumor growth into a bronchus causes

abnormal breath sounds and dyspnea
Inflammation surrounding tumor stimulates cough and predisposes to
secondary infection ; frequent infections may occur because secretions
pool distal to the tumor
Pleural involvement is common w/ tumors located on lung periphery
owing to inflammation or erosion of pleural membrane
Paraneoplastic syndrome
o May accompany bronchogenic carcinoma when the tumor cells
secretes hormones or hormone-like substances such as ADH or
ACTH
o Endocrine effects may complicate both dx and treatment
o May include neuromuscular disturbances or hematologic
disorders such as DIC
Cause usual systemic effects of cancer

III. Etiology
Very high in women as well as in men
Cigarette smoking
o Major factor in the lung cancer development
o Second-hand smoke has been implicated in a significant # of
cases
o Risk of developing cancer is higher in persons who begin smoking
early , persist for many years and are considered heavy smokers
(smoke > 1 pack per day)
o In mucosa, it causes a change from ciliated columnar epithelium
to squamous cell epithelium
Genetic factor
o Influences cellular changes
Tumors may also develop in persons w/ COPD ,also associated w/
smoking
Occupational /Industrial exposure to carcinogens such as :
o Asbestos
o Silica
o Vinyl chloride
Any irritant such as smoke leads to chronic inflammation and frequent
infections in respiratory tract w/c in turn cause cellular changes
The alterations in resp. mucosa as it changes through metaplasia to
dysplasia demonstrate cell mutations caused by carcinogens and could
perhaps lead to earlier dx
III. Signs and Symptoms
Onset is insidious because early signs are often masked by signs of
predisposing factor such as smokers cough
4 possible categories of signs of lung cancer :
o Those r/t direct effects of tumor on resp. structures
o Those representing the systemic effects of cancer
o Those caused by associated paraneoplastic syndromes
o Those resulting from metastatic tumors @ other sites
Early signs r/t resp. involvement :
Persistent productive cough
Dyspnea
Wheezing
Detection on a CXR taken when a person develops pneumonia or other
complication
Hemoptysis, when tumors erode tissue
Pleural involvement w/c may lead to :
o Pleural effusion
o Pneumothorax
o Hemothorax
Chest pain , occurring w/ advanced tumors that involve pleura or
mediastinum
Hoarseness (laryngeal nerve compression)
Facial / arm edema and headache (compression of superior vena cava)
Dysphagia (compression of esophagus)
Atelectasis caused by large tumors or involved lymph nodes
Systemic signs :
Weight loss
Anemia
Fatigue

Paraneoplastic syndrome
Signs of endocrine disorder r/t specific hormone secreted

Signs of metastases depend on site

Metastatic bone cancer would be indicated on a bone scan and be
manifested by bone pain or pathologic fracture
IV. Diagnostic tests
Chest x-rays
o Demonstrate the lesion and complications such as atelectasis or
pleural effusion
CT scans and MRI
o Show more detail
Bronchoscopy
o Provides secretions containing malignant cells from central
lesions for definitive dx

Biopsy
o May be required for less accessible lesions
Mediastinoscopy
o Useful to check lymph nodes while bone scans are used to detect
metastasis
Pulmonary function tests
o Can clarify the effects of tumor on airflow

V. Treatment
Surgical resection or Lobectomy may be performed on localized lesions
Chemotherapy and radiation may be used in conjunction w/ surgery or
as palliative treatment, although many tumors are not responsive to
such therapy
Photodynamic therapy (a chemical is injected and migrates to tumor
cells , where it is activated by laser light and destroys the cancer cells)
is sometimes effective
VI. Prognosis
Poor unless tumor is in a very early stage of development

Aspiration
I. Definition
Passage of food or fluid, vomitus, drugs or other foreign material into
the trachea and lungs
R lower lung is often the destination of aspirated material because
anatomically the R branching bronchus tends to continue almost
straight down
Normally, a cough removes material from upper tract and vocal cords
and epiglottis prevent entry into lower tract
II. Pathophysiology
The characteristics of aspirate determine specific effects on
respiratory function
Object causes obstruction ; Irritating liquid causes inflammation and
swelling
Inflammation may interfere w/ gas exchange and predispose to
pneumonia
Effects of Aspirated solid objects :
Solid objects lodge in a passageway and totally obstruct airflow @ that
point ; A small obstruction may be asymptomatic
A large object may occlude the trachea and block all airflow . In such
cases , no sound can be made to alert others , consciousness is lost very
quickly as O2 supplies are depleted
Solid objects lodging in a bronchus lead to nonaeration and collapse of
area distal to obstacle
Sometimes solid objects create a ball-valve effect, in w/c air is able to
pass down the tract on inspiration but the passageway totally closes on
expiration , leading to buildup of air distal to obstruction
Foods such as dried beans may swell after aspiration and become more
firmly lodged
Sharp pointed objects such as bone fragments , also lodge in
passageway, although it does not totally occlude airway by itself, such

an object traumatizes the mucosa , causing an acute inflammatory

response that adds to barrier . Inflammatory response may stimulate
bronchoconstriction
Fatty / Irritating solids such as peanuts also cause inflammation around
the area , creating edema and further impeding airflow. If not
removed, a granuloma or fibrous tissue develops around such material

Effects of Aspirated liquids :

Irritating liquids tend to disperse into several bronchi
Causes severe inflammation leading to narrow airways and increased
secretions w/c make lungs more difficult to expand
Chemical / Aspiration pneumonia
o In some cases, Alveoli are involved in inflammation
o Gas diffusion is impaired

Other potential complications :

Respiratory distress syndrome may develop of inflammation is
widespread
Pulmonary abscess may develop if microbes are in the aspirate
Certain materials such as solvents, if aspirated in large amt may be
absorbed into blood and cause systemic effects
III. Etiology
Common problem in young children , they put most objects in their
mouth
Children w/ congenital anomalies (eg. cleft palate / tracheoesophageal
fistula ) are clinically @ risk for aspiration until repair takes place
Of any age , occurs when swallowing or gag reflex is depressed for any
reason . For an instance :
o Following anesthesia or stroke
o Pt with coma or neurologic damage
Individuals who drink or eat when lying down are also @ risk because
gravitational forces is of no value in moving food quickly
Adults combining eating with talking @ social events (caf coronary)
IV. Signs and Symptoms
Coughing and Choking w/ marked dyspnea
Stridor and hoarseness are characteristics of upper airway obstruction
Wheezing occurs w/ aspiration of liquids in lungs
Tachycardia and tachypnea are responses to resp. distress
Nasal flaring , chest retractions and marked hypoxia occur in pt with
severe resp. distress
Total obstruction @ larynx or trachea prevents any sounds or cough
from being produced ; person may reach for chest or neck area;
cardiac or resp. arrest quickly ensues
V. Treatment
Easier to prevent that to treat
Avoid talking or moving about when chewing and swallowing reduces the
risk
Small objects or fluid can frequently be coughed up

Asthma
I. Definition
Periodic episodes of severe but reversible bronchial obstruction in
persons w/ hypersensitive or hyperresponsive airways
Frequent repeated attacks of acute asthma may lead to irreversible
damage in lungs and development of chronic asthma (chronic
obstructive lung disease)
II. Pathophysiology
Classification :
o Acute - single episode
o Chronic long term
2 Basic types based on etiology and presence of a hypersensitivity
reaction :
o Extrinsic asthma
- acute episodes triggered by a type I hypersensitivity
reaction to an inhaled antigen

- frequently there is a familial hx of other allergic condition

(eg. allergic rhinitis, eczema)
- onset commonly occurs in children
- some pt are no longer subject to attacks after adolescence
- antigen reacts w/ immunoglobulin E (IgE) on previously
sensitized mast cells in resp.mucosa releasing chem. mediators
(histamine, kinins, prostaglandins, etc.) w/c then cause
inflammation, bronchospasm, edema and increased mucus
secretion
In 2nd stage of allergic response (few hours later..) :
- increased leukocyte particularly eosinophils , release addtl
chem. mediators such as leukotrienes resulting in prolonged
inflammation, bronchoconstriction and epithelial damage
Intrinsic asthma
- onset during adulthood
- other types of stimuli target hyperresponsive tissues in
airway ,initiating acute attack
- stimuli include : respiratory infections, exposure to cold,
exercise, drugs (eg. aspirin), stress, inhalation of irritants (eg.
cigarette smoke)
- tissues are hyperresponsive and an underlying chronic
inflammation or imbalance in autonomic innervations to tissues
is suspected
Bronchi and Bronchioles respond to stimuli w/ 3 changes :
o Inflammation of mucosa w/ edema
o Bronchoconstriction
o Increased secretion of thick mucus in passages
Those changes create partially or totally obstructed airways
interfering w/ airflow and o2 supply
o

Partial obstruction (di makalabas lhat ng hangin)

In small bronchi and bronchioles
Results in Air trapping w/ hyperinflation of lungs
Air passes into the areas distal to obstruction and alveoli but is only
partially expired
Because expiration is a passive process, less force if available to move
air out and force expiration often collapses bronchial wall , creating
further barrier to expiratory airflow
Residual volume increases
Result is it is difficult to inspired fresh air or to cough effectively to
remove mucus
Total obstruction
Results when mucus plugs completely block the flow of air in already
narrowed passage
Leads to atelectasis or nonaeration of tissue distal to obstruction
Air in the distal section diffuses out and is not replaced resulting in
collapse of that section of lung
Both partial and total airway obstruction lead to marked hypoxia
Status asthmaticus
A persistent severe attack
Does not respond to therapy
Often r/t inadequate medical treatment
May be fatal owing to severe hypoxia and acidosis leading to cardiac
arrhythmias or CNS depression

IV. Signs and Symptoms

Cough
Marked dyspnea
A tight feeling in chest
Agitation
Unable to talk
Wheezing as air passes through narrowed bronchioles
Rapid and Labored breathing w/ use of accessory muscles and possible
chest retractions
Thick and tenacious /sticky mucus is coughed up
Tachycardia
Pulsus paradoxus pulse differs on inspiration and expiration
Paradoxical pulse
o Observe when BP measurement is taken during an asthma attack
o Sounds registering systolic pressure are heard first during
expiration
o There is a gap of 10 mm Hg or more before sounds of both
inspiration and expiration are eard
Hypoxia
Resp. alkalosis develops initially because of hyperventilation
Resp. acidosis develops in time due to air trapping and marked fatigue
causes decreased resp. effort w/ weaker cough
Severe resp. distress
Hypoventilation leads to increasing hypoxemia and resp. acidosis
Resp. failure is indicated by :
o Decreasing responsiveness
o Cyanosis
o ABG : PaO2 of below 50 mm Hg or PaCO2 of above 50 mm Hg
V. Treatment
General Measures :
o Skin tests for allergic reactions to determine specific stimuli to
be avoided
o Avoidance of common triggering factors including airborne
irritants or drugs such as aspirin
o Good ventilation
o Regular swimming sessions are of great benefit particularly to
affected children to strengthen chest muscles and improve cv
fitness as well as to reduce stress
o Walking and swimming are recommended for adults
o Prophylactic medication be given as children return in school or
@ first sign of a cold
Acute attacks :
o Inhalers so that person can self administer a bronchodilator
such as albuterol (Ventolin)
o Controlled breathing techniques and Reduction in anxiety
o Glucocorticoids such as beclomethasone (Beclovent)

Chronic asthma/ chronic obstructive lung disease

May develop from irreversible damage in lungs when frequent and
severe acute asthmatic attacks form a pattern
Bronchial walls become thickened
Fibrous tissue resulting from frequent infections that follow attacks
develops in atelectatic areas
Because it is impossible to remove all tiny mucus plugs in small passages,
complications are common ff frequent episodes of asthma
III. Etiology
Familial hx of ff is common :
o Hay fever
o Asthma
o Eczema

Viral upper resp. infections frequently precipitate attacks

Contributing factors :
o Increase in sedentary lifestyles
o Increased exposure to allergens
o Poor ventilation
o Increased air pollution

Status asthmaticus :
o Hosp. care is essential when a pt does not respond to
bronchodilator
Prophylaxis and treatment of chronic asthma :
o Leukotriene receptor antagonists
- zafirlukast (Accolate) and montelukast (Singulair)
- block inflammatory responses in presence of stimuli
- taken orally on regular basis to prevent attacks due to
allergens , exercise and aspirin
- not effective in treatment of acute attacks
o Cromolyn sodium
- a prophylactic med that is administered by inhalation on a
regular daily basis
- inhibits release of chem. mediators from sensitized mast cells
in resp. passages and decreases # of eosinophils
- useful for athletes and sports enthusiasts
- of no value during an acute attack

o
o
o

Chronic Obstructive Pulmonary Disease

Also called Chronic obstructive lung disease (COLD)

Group of common chronic resp. disorders that are characterized by
progressive tissue degeneration and obstruction in airways of lungs
Debilitating conditions that affect persons ability to work and function
independently
Causes irreversible and progressive damage to the lungs
Eventually , resp. failure may result because of severe hypoxia or
hypercapnia
In many pt, it leads to development of cor pulmonale, a R-sided CHF
due to lung disease

II. Etiology

Emphysema
Airsacs lose their flexibility making it harder for them to expand and
contract
I. Pathophysiology

The significant change is the destruction of alveolar walls and septae,

leading to a large, permanently inflated alveolar air spaces
(overinflated alveoli)
May be further classified by specific location of changes :
o Distal alveoli (panacinar)
o Bronchiolar (centrilobular)

Breakdown of alveolar wall results in :

o Loss of surface area for gas exchange
o Loss of pulmonary capillaries, affecting perfusion and diffusion
of gases
o Loss of elastic fibers, affecting ability of lung to recoil on
expiration
o Altered ventilation-perfusion ratio as various changes occur in
alveoli
o Decreased support for other structures such as small bronchi
w/c often leads to collapse of walls and additional obstruction
of airflow during expiration
Fibrosis and thickening of bronchial walls have resulted from chronic
irritation and frequent infections associated w/ smoking and increased
mucus production. These conditions lead to :
o Narrowed airways
o Weakened walls
o Interference w/ passive expiratory airflow
Progressive difficulty w/ expiration leads :
o Air trapping and increased residual volume
o Overinflation of lungs
o Fixation of ribs in an inspiratory position and increased AP
diameter of thorax (barrel chest)
o Diaphragm appears flattened on x-rays
W/ advanced emphysema , and significant loss of tissue :
o Adjacent damaged alveoli coalesce forming very large air
spaces. Normally the uninflated lung appears to be a solid
mass. W/ emphysema, lung appears to have many large holes in

Cigarette smoking is implicated in most cases

o
Increases both the number of neutrophils in alveoli and
the release and activity of elastase but decreases the
effect of alpha1- antitrypsin, thus greatly contributing to
breakdown of alveolar structures
Genetic factor
o
In some person, there is a genetic deficiency of alpha1antitrypsin , a protein normally present in tissues and
body fluids that inhibits activity of proteases, w/c are
destructive enzymes released by neutrophils during an
inflammatory response
o
An ex. of protease is elastase w/c breaks down elastic
fibers
Exposure to other air pollutants

III. Signs and Symptoms

Changes in lung tissue have many effects on lung function

it. Sometimes one can see through the scraps of remaining

tissue from one side to the other. These air-filled spaces are
called blebs or bullae
Tissue and pleural membrane surrounding large blebs near the
surface of lung may rupture, resulting in pneumothorax
Hypercapnia becomes marked
Hypoxic drive for inspiration develops as the pts resp. contool
adapts to chronic elevation of CO2 levels and hypoxia becomes
the driving force for resp.
Infections develop frequently because secretions are more
difficult to remove past obstructions and airway defenses are
impaired
Pulmonary HTN and cor pulmonale may develop in a late stage
as pulmonary blood vessels are destroyed and hypoxia causes
pulmonary vasoconstriction. The increased pressure in
pulmonary circulation increases resistance to R ventricle and
eventually ventricle fails. Many pt w/ resp. disease manifest
signs of HF

Pink puffer of emphysema (maintain O2 in emphysema)

o
Dyspnea occurs first on exertion and then progresses until
it is marked even at rest
o
Hyperventilation (maintains adequate O2 levels until later
stages) w/ a prolonged expiratory phase
o
Use of accessory muscles
o
Hyperinflation leading to barrel chest
Typical posture is a sitting position, leaning forward (tripod
position) to facilitate breathing
Hyperresonant lung sound
Anorexia and Fatigue
Clubbed fingers
Secondary polycythemia

IV. Diagnostic tests

CXR and pulmonary function tests
o
Indicate presence of increased residual volume and total
lung capacity as well as decreased forced expiratory
volume and vital capacity
V. Treatment

Avoidance of resp. irritants and sources of resp. infections

Cessation of smoking
Immunization against influenza and pneumonia
Learning app. Breathing techniques
Maintenance of adequate nutrition and hydration
Bronchodilators, antibiotics and O2 theray
Lung reduction surgery has proved helpful. By removing part of
lung , air trapping can be reduced and expiration improved

Chronic Bronchitis

I. Pathophysiology

There is a significant changes in bronchi

Effects are irreversible and progressive

Inflammation and obstruction, repeated infection and chronic coughing

characterize bronchitis as ff occur :
Mucosa is inflamed and swollen
There is hypertrophy and hyperplasia of mucous glands and
increased secretions are produced. Number of goblet cells is
increased and there is a decreased ciliated epithelium
Chronic irritation and inflammation lead to fibrosis and thickening
of bronchial wall and further obstruction. Secretions pool distal to
obstructions and are difficult to remove

Blue bloater of bronchitis (typical clinical presentation of low O2

levels)
o
Cyanosis
o
Edema
Severe dyspnea and fatigue interfere w/ daily activities leading to
gen. debilitation
Pulmonary HTN and cor pulmonale are common

III. Signs and Symptoms

II. Etiology

Cigarette smoking
Heavy exposure to inhaled irritants
Asthma is an associated condition in some cases

III. Signs and Symptoms

Constant productive cough significant indicator

Tachypnea
Shortness of breath
Frequently secretions are thick and purulent
Cough and ronchi are usually more severe in morning because
secretions have pooled during sleep
Airway obstruction leads to hypoxia and eventually to cyanosis as
well as to hypercapnia
Secondary polycythemia
Severe weight loss
Signs of cor pulmonale (systemic edema) as vascular damage and
pulmonary HTN progresses

IV. Treatment

Reducing exposure to irritants

Influenza and pneumonia vaccines provide useful prophylaxis as will
antimicrobials when app.
Expectorants
Bronchodilators
Chest therapy : postural drainage and percussion
Low-flow O2
Nutritional supplements

Bronchiectasis
I. Definition

Usually a secondary problem, rather than a primary one

Develops in pt w/ conditions such as cystic fibrosis or COPD
Some cases result from ff :
o Childhood infection
o Aspiration of foreign bodies
o Congenital weakness in bronchial wall
Depending on cause, it may be localized in one lobe or more often it
is diffuse in both lungs

II. Pathophysiology

It is an irreversible abnormal dilation or widening , primarily of

medium-sized bronchi
Dilations may be saccular or elongated (fusiform)

Arise from recurrent inflammation and infection in airways leading

to :
o Obstruction in airways
o Weakening of muscle and elastic fibers in bronchial wall
o Combination of both
Fibrous adhesions may pull the wall of bronchus outward, dilating it
In dilated or ballooning areas :
o Large amt of fluid constantly collect and become infected
o Infecting organisms are usually mixed and include
streptococci, staphylococci, pneumococci and H. inflenzae
o These infections then cause loss of cilia and metaplasia in
epithelium , additional fibrosis and progressive obstruction
o Obstructions and loss of cilia interfere w/ removal of
fluids, continuing cycle of events

Chronic cough
Production of copious amt of purulent sputum (1-2 cups per day)
Cough may be paroxysm (sudden , uncontrollable attack) in morning
as the purulent sputum shifts in lungs w/ changes in body position,
stimulating cough reflex
Rales and Ronchi
Foul breath
Dyspnea
Hemoptysis
Weight loss
Anemia
Fatigue

IV. Treatment

Antibiotics
Bronchodilators
Chest physiotherapy
Treatment of primary condition

Restrictive Lung Disorder

Vascular Disorders

Pneumoconioses

Pulmonary Edema
I. Definition
Fluid collecting in alveoli and interstitial area
II. Pathophysiology
Accumulation of fluid reduces amt of O2 diffusing into blood and
interferes w/ lung expansion
Excess fluid in alveolar tissue may develop when :
o Inflammation is present in the lungs, increasing capillary
permeability
o Plasma protein levels are low , decreasing plasma osmotic
pressure
o Pulmonary HTN develops
Normally , pressure in pulmonary capillaries is very low and there is
minimal fluid in air passages and alveoli
When hydrostatic pressure in pulmonary capillaries becomes high (eg. in
CHF) this leads to a shift in fluid out of capillaries into alveoli
Excessive amt of fluid in interstitial areas and alveoli may interfere w/:
o Diffusion of O2 , causing severe hypoxemia
o Action of surfactant , leading to difficulty in expanding lungs
w/c ultimately collapse
Capillaries may rupture causing blood-streaked sputum
There is an increased risk of pneumonia developing after an episode of
pulmonary edema because of residual secretions
III. Etiology
Can result from many primary conditions
o L sided CHF backup of blood from failing L ventricle causes
high pressure in pulmonary circulation
Hypoproteinemia due to kidney/liver disease in w/c serum albumin
levels are low
Inhalation of toxic gases or in association w/ tumors result in
inflammation in lungs w/ increased capillary permeability
Blocked lymphatic drainage due to tumors or fibrosis in lungs may cause
edema
IV. Signs and Symptoms
Mild
Cough
Orthopnea
Rales
As congestion increases ..
Hemoptysis
Sputum is frothy owing to air mixed w/ secretions and blood-tinged
owing to ruptured capillaries in lungs
Labored breathing
Difficulty expanding lungs
Person feels as if he /she is drowning
Hypoxemia increases
Cyanosis
Paroxysmal nocturnal dyspnea (in CHF)

V. Treatment
Causative factors must be treated
Supportive care such as O2 is offered
Positive-pressure mechanical ventilation may be necessary in severe
cases
Positioning w/ upper body elevated

Pulmonary Embolus
I. Definition
A blood clot or a mass of other material that obstructs pulmonary
artery or a branch of it, blocking the flow of blood through lung tissue
Most emboli are thrombi or blood clots originating from the leg veins
An embolus to the lungs travels from its source through larger and
larger veins until it reaches the heart and pulmonary artery
Emboli then lodges as soon it reaches a smaller artery in lungs through
w/c it cannot pass
II. Pathophysiology
Effects depend somewhat on material but largely on size and therefore
on location of obstruction in pulmonary circulation
Because lung tissue is supplied w/ O2 and nutrients by bronchial
circulation . infarction does not follow obstruction of pulmonary
circulation unless gen. circulation is compromised
Infarction usually involves a segment of lung and pleural membrane in
area
Small pulmonary emboli
o Frequently silent or asymptomatic
Emboli that block moderate-sized arteries
o Usually cause resp. impairment because fluid and blood fill the
alveoli of involved area
o Reflex vasoconstriction often occurs in area, further
increasing pressure in blood vessels
Large emboli
o Usually those involving > 60 % of lung tissue
o Affected the CV system causing R-sided heart failure and
decreased CO (shock)
o Sudden death often results
o Involve greatly increased resistance in pulmonary arteries
because of embolus plus reflex vasoconstriction due to
released chem. mediators (eg. serotonin , histamine)
o The resistance to the output from R ventricle causes acute cor
pulmonale
o There is much less blood returning from lungs to the L
ventricle and then to systemic circulation (decreased CO)
III. Etiology
90 % have originated from deep veins , primarily in the legs as result of
phlebothrombosis or thrombophlebitis
Risk factors for emboli :
o Immobility
o Trauma to the legs
o Childbirth
o CHF
o Dehydration
o Increased coagulability of blood
o Cancer
o Sitting for a long time period
Thrombi tend to break off w/ sudden muscle action or massage. trauma
or changes in blood flow
Other types :
Fat emboli from bone marrow resulting from fracture of a large bone
Vegetations resulting from endocarditis in R side of heart
Amniotic fluid emboli from placental tears occurring during labor and
delivery
Tumor cell emboli that break away from a malignant mass
Air embolus injected into a vein
IV. Signs and Symptoms

Small emboli (often unnoticed but can be significant because it may be a

warning of more emboli developing)
Transient chest pain
Cough
Dyspnea
Large emboli
Chest pain that increases w/ coughing or deep breathing
Tachypnea
Dyspnea
Hemoptysis
Fever
Hypoxia stimulates sympathetic response (anxiety, restlessness,
pallor, tachycardia)
Massive emboli
Severe crushing chest pain
Low BP
Rapid, weak pulse
Loss of consciousness
Fat emboli
Acute resp. distress
Petechial rash on trunk
Neurologic signs (confusion and disorientation)
V. Dx
MRI
X-ray
Lung scan
Pulmonary angiography
VI. Treatment
Postoperative risk can be reduced by early ambulation or use of TEDS
(thromboembolic) stockings
Filter can be inserted in inferior vena cava to remove blood clots
W/ prolonged bed rest , compression stockings are helpful
In pt w/ pulmonary embolus due to thrombus , O2 is administered and
usually heparin or a fibrinolytic agent
Mechanical ventilation may be necessary
Embolectomy is performed in some cases

Expansion Disorders

Atelectasis
I. Definition
Nonaeration or collapse of a lung or part of a lung leading to decreased
gas exchange and hypoxia
Occurs as a complication of many primary conditions
II. Pathophysiology
When alveoli become airless , they shrivel up as the natural elasticity
of tissues dominates
o Interferes w/ blood flow through lung
o Both ventilation and perfusion are altered affecting O2
diffusion
o Unless a very large proportion of lungs is affected, increased RR
can control CO2 levels because this gas diffuses easily
If lungs are not reinflated quickly , lung tissue can become necrotic and
infected and permanent lung damage results
III. Etiology
Obstructive / Resorption atelectasis
o When total obstruction of airway due to mucus or tumor leads to
diffusion into the tissue of air distal to obstruction ; this air is
not replaced
Compression atelectasis
o When a mass such as a tumor exerts pressure on a part of lung
and prevents air from entering that section of lung
o Alternatively , when pressure in pleural cavity is increased , as
w/ increased fluid or air, and adhesion bet pleural membranes is
destroyed , lung cannot expand
Increased surface tension in alveoli
o Occurs w/ pulmonary edema or resp. distress syndrome ,
preventing expansion of lung
Fibrotic tissue in lungs /pleura (contraction atelectasis)
o May restrict expansion and lead to collapse
Postoperative atelectasis
o Commonly occurs 24-72 h ff surgery , particularly abd.surgery
o A number of factors are implicated :
- restricted ventilation due to pain /abdl distention
- slow, shallow resp. due to anesthetics and analgesics
- increased secretions due to supine position
- decreased cough effort
IV. Signs and Symptoms
Small areas
Asymptomatic
Large areas
Dyspnea
Increased HR and RR
Chest pain
Abnormal or symmetrical chest expansion depending on cause
o Obstructive atelectasis
leads to potential low pressure gap or space on affected side
- therefore mediastinum shifts toward it and other lung
compensates by overinflating
o Compression atelectasis
- mediastinum may shift toward the other unaffected side

Pleural Effusion
I. Definition

Presence of excessive fluid in pleural cavity

Normally , a very small amt of fluid is present to provide lubrication

for the membranes

Both lungs may be involved , but more often only one is affected
because each lung is enclosed in a separate pleural membrane
Pleurisy / Pleuritis

May follow pleural effusion or occur independently

Pleural membranes are inflamed , swollen and rough , often in

association w/ lobar pneumonia
II. Pathophysiology

Small amts of fluid are drained from the pleural cavity by lymphatics
and have little effect on resp. function

Large amts of fluid

o First increase the pressure in pleural cavity and then cause
separation of pleural membranes , preventing their cohesion
during inspiration
o These effects prevent expansion of lung leading to atelectasis
, particularly when fluid accumulates rapidly
o Causes atelectasis on affected side and a shift of mediastinal
contents toward unaffected lung , limiting its expansion also ;
Tracheal deviation indicates the shift
o Venous return in inferior vena cava and cardiac filling may be
impaired because large effusions increase pressure in
mediastinum
III. Etiology
Types of fluid
Exudative effusions
o Response to inflammation , perhaps from a tumor , in w/c
increased capillary permeability allows fluid containing
protein and WBC to leak into pleural cavity
Transudates
o Watery effusions
o Sometimes called hydrothorax
o Result from increased hydrostatic pressure or decreased
osmotic pressure in blood vessels leading to a shift of fluid
out of blood vessels into potential space in pleural cavity
o May occur s/t liver/kidney disease
Hemothorax
o Fluid is blood
o Result from trauma, cancer or surgery
Empyema
o Fluid is purulent as a result on infection . often r/t
pneumonia
IV. Signs and Symptoms
Dyspnea
Chest pain
Increased RR and HR
Dullness in percussion
Absence of breath sounds over the affected area because air no
longer flows through passages
Tracheal deviation and hypotension indicate a massive effusion that
interferes w/ both respiratory and circulatory function
Pleurisy :
o Manifested by cyclic pleuritic pain and friction rub as the
rough ,swollen membranes move against each other during
respiratory movements
V. Treatment
Fluid may have to be analyzed to confirm the cause

Chest drainage tubes may be used to assist inflation

Thoracocentesis
o Needle aspiration
o If large quantity of fluid forms
o Required to remove fluid and relieve pressure

Pneumothorax
I. Definition
Air in the pleural cavity
Prevent expansion of lung by the ff :
o Presence of air @ atmospheric pressure in pleural cavity
o Separation of pleural membranes by air
When caused by a malignant tumor or trauma, fluid or blood may
also be present in cavity
o Hydropneumothorax - Fluid in the more dependent area and
air above it
II. Types
Closed pneumothorax
o Air can enter pleural cavity through an opening directly from
internal airways
o There is no opening in chestwall
o Can be a simple / spontaneous pneumothorax or can be s/t
another disease
Simple / Spontaneous pneumothorax
o A tear on surface of lung allows air to escape from inside
lung through bronchus and visceral pleura into pleural cavity
o As lung tissue collapses , it seals off the leak
o Often occurs in young men who have no prior lung disease
but perhaps an idiopathic bleb or defect on lung surface
o Following collapse, mediastinum can shift toward the
affected lung. allowing other lung to expand more
Secondary pneumothorax
o Associated w/ underlying resp. disease
o Resulting from rupture of an emphysematous bleb on
surface of lung or erosion by a tumor or tubercular
cavitation through visceral pleura
o Lets inspired air pass into pleural cavity
Open pneumothorax
o Atmospheric air entering pleural cavity through an opening in
chest wall
o Could result from trauma or surgery
o Sucking wound a large opening in chest wall in w/c sound of
air moving in and out makes a typical sucking sound
o Air enters pleural cavity through opening in chest wall and
parietal pleura causing immediate atelectasis on affected
side
o Because more air enters pleural cavity during inspiration,
mediastinum pushes against unaffected lung, limiting its
expansion
o Subsequently, on expiration , as air is pushed out of pleural
cavity through opening, mediastinal contents shift back
toward affected side
o Those abnormal movements occur as the pressure changes
w/ rib movements on inspiration and expiration (Mediastinal
flutter / to-and-fro motion)
Tension pneumothorax
o Most serious form
o May result from :
- an opening through chest wall and parietal pleura (open
pneumothorax)
- tear in lung tissue and visceral pleura (closed
pneumothorax)
o The particular pattern of damage creates a flap of tissue or
a one-way valve effect , whereby opening enlarges in
inspiration promoting airflow into pleural cavity
o However, on expiration , opening is sealed off, preventing
removal of air from pleural cavity
o Pressure increases on affected side eventually push the
mediastinal contents against the other lung , compressing
other lung and inferior vena cava

Severe hypoxia and resp. distress develop quickly if source

of valve effect and increasing intrapleural pressure is not
removed

III. Signs and Symptoms

Atelectasis
Dyspnea
Cough
Chest pain
Breath sounds are reduced over atelectasis area
Unequal chest expansion
Mediastinal shift vary w/ type
Hypoxia leads to sympathetic response : anxiety, tachycardia, and
pallor
Interference w/ venous return leads to hypotension

II. Pathophysiology

Flail chest
I. Definition
Result from fractures of the thorax , usually fractures of 3-6 ribs in
2 places or fracture of sternum and a number of consecutive ribs
There is often contusion w/ edema and some bleeding in lung tissue
adjacent to the flail section
Atelectasis
o Does not occur as a direct result of trauma
o May ff as a complication if a broken rib punctures the pleura
Paradoxical (opposite) movement
o Chest wall rigidity is lost resulting in this movement during
inspiration and expiration
Hypoxia results from :
o Limited expansion
o Decreased inspiratory volume of flail lung
o Shunting of stale air bet. lungs
o Decreased venous return
During inspiration - Air from affected lung flow to unaffected lung
There is usual decrease in pressure inside lungs then :
o The flail or broken section of ribs moves inward rather than
outward as intrathoracic pressure is decreased
o The inward movement of ribs prevents expansion of affected
lung
o A large flail section can compress the adjacent lung tissue
,pushing the air out of that section and up the bronchus.
Because air is flowing down the trachea and into the other lung,
the stale air from damaged lung crosses into other lung,
allowing w/ newly inspired air
On expiration Air from unaffected lung flow into affected lung
The unstable flail section is pushed outward by increasing
intrathoracic pressure
If the flail section is large, the paradoxical movement of ribs alters
airflow during expiration
Air from unaffected lung moves across into affected lung as outward
movement of ribs decreases pressure in affected lung
II. Treatment
Abnormal movement is obvious and therefore first aid measures
include stabilizing flail section w/ a flat, heavy object , thus limiting
the outward paradoxical movement of thorax until surgical repair can
be performed

Infant Respiratory Distress Syndrome

Adult or Acute Respiratory Distress Syndrome (ARDS)
I. Definition

Also known as :
o Shock lung
o Wet lung
o Stiff lung

o Postperfusion lung
Considered to be a restrictive disorder
Onset of resp. distress usually occurs 1-2 days after an injury or
other precipitating event
Associated w/ multiple organ dysfunction or failure s/t a severe
insult to the body , in many cases

Basic changes in lungs result from injury to alveolar wall and capillary
membrane leading to :
o Release of chemical mediators
o Increased permeability of alveolar capillary membranes
o Increased fluid and protein in interstitial area and alveoli
o Damage to surfactant-producing cells
The above changes result in :
o Decreased diffusion of O2
o Reduced blood flow to the lungs
o Difficulty in expanding lungs
o Diffuse atelectasis
Reduction in tidal volume (The amount of air breathed in or out during
normal respiration) and vital capacity (the maximum amount of air
that can be exhaled after a maximum inhalation) occur
Damage to lung tissue progresses as increased numbers of neutrophils
migrate to the lungs, releasing proteases and other mediators
Hyaline membranes form from protein-rich fluid in alveoli and platelet
aggregation and microthrombi develop in pulmonary circulation,
causing stiffness and decreased compliance
If pt survives, diffuse necrosis and fibrosis are apparent throughout
lungs
Excess fluid in lungs predisposes to pneumonia as a complication
CHF may develop

III. Etiology

Severe or prolonged shock because of ischemic damage to lung tissue

Inflammation in lungs arises directly from ff :
o Inhalation of toxic chemicals or smoke
o Excessive O2 concentration in inspired air
o Severe viral infections in lungs
o Toxins from systemic infection
o Fat emboli
o Explosions
o Aspiration of highly acidic gastric contents
o Lung trauma
DIC
Cancer
Acute pancreatitis
Uremia

IV. Signs and Symptoms

Early signs may be masked by effects of primary problem

Onset is usually marked by :

o Dyspnea
o Restlessness
o Rapid, shallow respirations
o Increased heart rate

ABG measurements indicate a significant decrease in PaO2

As lung congestion increases :

o The accessory muscle are used
o Rales can be heard
o Productive cough w/ frothy sputum may be evident
o Cyanosis and lethargy w/ confusion develop

A combination of respiratory and metabolic acidosis evolves as

diffusion is impaired and anerobic metabolism is required
V. Treatment

Underlying cause must be treated

Supportive resp. therapy such as :

o O2 therapy
o Mechanical ventilation

Administration of fluid may be limited to minimize alveolar edema

VI. Prognosis

Generally poor

Mortality rate of 30-40 % but does depend on underlying problem

With infection, mortality rate is 80-90%

Acute Resp. Failure

I. Pathophysiology

Can be the end result of many pulmonary disorders

Indicated when :
o PaO2 is less than 50 mm Hg (severe hypoxemia)
o PaCO2 is greater than 50 mm Hg (hypercapnia)
o Serum pH is decreasing (less than 7.3)

Normal values :
o Oxygen 80 to 100 mm Hg
o CO2 35 to 45 mm Hg

Respiratory insufficiency
o An interim state where blood gases are abnormal but cell
function can continue

Respiratory arrest
o Cessation of respiratory activity
II. Etiology
May result from acute or chronic disorders :

Chronic conditions such as emphysema may lead to resp. failure if

degenerative tissue changes progress to the point where ventilation
and gas exchange are minimal

A combination of chronic w/ an acute disorder

Acute resp. disorders such as chest trauma (flail chest or tension

pneumothorax), pulmonary embolus or acute asthma

Neuromuscular diseases (eg. Myasthenia gravis, amyotrophic lateral

sclerosis, muscular dystrophy)
III. Signs and Symptoms

May be masked or altered by the primary problem

Rapid, shallow, often labored respirations

Gen.signs of hypoxia and hypercapnia

o Headache
o Tachycardia
o Lethargy
o Confusion
IV. Treatment

Primary problem must be resolved

Supportive treatment to maintain resp. function