Power point pulmonary pathophysiology - v.1

Suggested HW: Complete the end of
chapter questions for:
• CH 11-30
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QUESTIONS

Educational Objectives
• List the etiology and risk factors, clinical manifestations,
pathological changes, and diagnostic results for:
– Bronchitis
– Pulmonary emphysema
– Asthma
– Bronchiectasis
– Pulmonary infections
– Acute respiratory distress syndrome (ARDS)
– Interstitial lung disease (ILD)
– Lung cancer
– Pulmonary Vascular Disorders
– Neuromuscular Disorders
– Pleural Diseases (including pneumothorax)

Educational Objectives
• Differentiate and define obstructive pulmonary
disease and restrictive pulmonary disease

Classification of Pulmonary Disorders
• Obstructive disease
– Causes a decrease in the rate of airflow in the
conducting airways
• Restrictive disease
– Causes a decrease in the volume of lung, especially
the inspiratory capacity and vital capacity

Obstructive Diseases
Airway
Obstruction
Enlarged
submucosal
gland
Hyperinflated
alveoli
Mucus Plug
Inflammation of
epithelium

Chronic Obstructive Pulmonary Disease
• A group of disorders characterized by progressive
limitations in predominantly expiratory airflow that
are partially reversible by bronchodilator or anti-inflammatory
therapy

Definitions
• FVC Forced vital capacity: the determination of the vital
capacity from a maximally forced expiratory effort
• FEV1 Volume that has been exhaled at the end of the
first second of forced expiration
• PEF The highest forced expiratory flow measured with a
peak flow meter
• MVV Maximal voluntary ventilation: volume of air
expired in a specified period during repetitive maximal
effort
• MIP: Maximum inspiration (IC), used to assess
diaphragm strength

Forced Vital Capacity
• Vital capacity is the maximum amount of air a person can expel from
the lungs after a maximum inspiration. It is equal to the inspiratory
reserve volume plus VT plus the expiratory reserve volume.
• A person's vital capacity can be measured by a spirometer
• In combination with other physiological measurements, the vital
capacity can help make a diagnosis of underlying lung disease. The
unit that is used to determine this vital capacity is the millilitre (mL).
• A normal adult has a vital capacity between 3 and 5 litres.
Predicted normal values for VC depend on age, sex, height,
weight and ethnicity

Overall Classification of Pulmonary
Disorders
• Obstructive Disease (COPD)
– Causes a decrease in the rate of airflow in the conducting
airways, causes an increase in residual volume due to air
trapping
FEV1 , FVC , FEV1/FVC < 70% of predicted, TLC > 120% of predicted,
RV > 120% of predicted, MMV , DLCO < 80% of predicted, PEF

Disorders
• In obstructive lung disease, the FEV1 is reduced due to
obstruction to air escape. Thus, the FEV1/FVC ratio will
be reduced.
• More specifically, the diagnosis of COPD is made when
the FEV1/FVC ratio is less than 70%.
• The Global Initiative for Obstructive Lung Disease
(GOLD) criteria also require that values are after
bronchodilator medication has been given to make the
diagnosis
• Dx: Pre-post bronchodilator testing with Spriomtery
testing. In Emphysema/Bronchitis small change less
than 5%; Asthma typically changes >12% or 200 mL

Disorders
• Restrictive Disease (everything besides COPD)
– Causes a decrease in the volume of lung, especially the
inspiratory capacity and vital capacity
FEV1 , FVC , FEV1/FVC or normal, TLC < 80% of predicted,
RV < 80% of predicted, MVV , DLCO > 120-140% of predicted,
PEF normal or increased

Disorders
• In restrictive lung disease, the FEV1 and FVC are
equally reduced due to fibrosis or other lung pathology
(not obstructive pathology).
• Thus, the FEV1/FVC ratio should be approximately
normal, or even increased due to an increased FEV1
value (because of the decreased compliance associated
with the presence of fibrosis in some pathological
conditions).

Spirogram Capacities and Volumes
• TLC Total lung capacity: the volume in the lungs at
maximal inflation
• RV Residual volume: the volume of air remaining in the
lungs after a maximal exhalation
• ERV Expiratory reserve volume: the maximal volume of
air that can be exhaled from the end-expiratory position
• IRV Inspiratory reserve volume: the maximal volume
that can be inhaled from the end-inspiratory level

Spirogram Capacities and Volumes
• IC Inspiratory capacity: the sum of IRV and TV
• IVC Inspiratory vital capacity: the maximum volume of
air inhaled from the point of maximum expiration
• VC Vital capacity: the volume equal to TLC − RV
• VT Tidal volume: that volume of air moved into or out of
the lungs during quiet breathing
• FRC Functional residual capacity: the volume in the
lungs at the end-expiratory position RV/TLC% Residual
volume expressed as percent of TLC

FEV1/FVC ratio
• The FEV1/FVC ratio, also called Tiffeneau index, is a calculated ratio
used in the diagnosis of obstructive and restrictive lung disease
• It represents the proportion of the forced vital capacity exhaled in the
first second
• Normal values are approximately 80% of predicted
• Predicted normal values are calculated based on age, sex, height,
weight and ethnicity, sometimes smoking
• A derived value of FEV1% is FEV1% predicted, which is defined as
FEV1% of the patient divided by the average FEV1% in the population
for any person of similar age, sex and body composition.

DLCO
• DLCO test is performed by having the test subject blow out all of the
air that they can to reach residual volume.
• The person then takes a full vital capacity inhalation of a test gas
mixture that contains a small amount of carbon monoxide (usually
0.3%) and some helium or other non-absorbed tracer gas.
• The test gas is held in the lung for about 10 seconds and then is
exhaled from the lung. The first part of the expired gas is discarded
and the next portion which represents gas from the alveoli is collected.
• By analyzing the concentrations of carbon monoxide and helium in the
inspired gas and in the exhaled gas, it is possible to calculate how
much carbon monoxide was taken up during the breath hold, and what
the partial pressure of carbon monoxide was during the breath hold.
This method is known as the single-breath diffusing capacity
test.

DLCO
• Values between 75% and 125% of average diffusion
capacity in the healthy population are considered
normal.
• The diffusing capacity (DLCO) is a test of the integrity of
the alveolar-capillary surface area for gas transfer. It
may be reduced in disorders that damage the alveolar
walls (septa) such as emphysema, which leads to a loss
of effective surface area. The DLCO is also reduced in
disorders that thicken or damage the alveolar walls such
as pulmonary fibrosis.
• Lung Volumes and DLCo

Chronic Obstructive Pulmonary
Disease
• May be preventable and treatable. Disease state
characterized by airflow limitation that is not fully responsive
to bronchodilator therapy. The airflow limitation is
progressive and associated with an abnormal inflammatory
response of the airway.
• Primary cause is cigarette smoking
• A significant response to the bronchodilator is considered by
an increase in the FEV1 by 12% AND an increase in VC by
200 mL.

Epidemiology
• Some 16 Million Americans are affected
• COPD is the 3rd leading cause of death in the U.S.
• COPD caused 726,000 hospitalizations in 2000
• Total health expenditure of $32.1 Billion in 2000
• Most common form of COPD is Chronic Bronchitis

Risk Factors for COPD
1. Cigarette smoking/passive smoking
2. Pollution
3. Occupational exposure to dust and
fumes
4. Recurrent lung infections
5. Hereditary factors
6. Allergies
7. Socioeconomic factors
8. Alcohol ingestion
9. Age

Disease
• Smoking
– #1 cause of COPD
– Increased mucous production
– Inhibition of mucociliary clearance
– Toxicity of inhaled gases and particulates
– Bronchospasm
– Decrease in macrophage activity
– Disruption of the alveolar wall and capillary endothelium

General Manifestations of COPD
1. Small airways ( < 2mm) are most susceptible to airway obstruction in COPD
2. Diagnosed by PFT, clinical signs and symptoms
3. Early to middle manifestations of COPD include:
I. Changes in pulmonary function testing
II. Shortness of breath with exertion
III. Changes in CXR
IV. Increases in sputum production
V. Cough
VI. Recurrent pulmonary infections
VII.Wheezing
4. Late manifestations of COPD include:
I. Accessory muscle usage
II. Edema from Cor Pulmonale
III. Mental status changes from chronic hypoxia/hypercapnea
IV. Clubbing of fingers
V. Barrel Chest or Increased A-P Diameter

Disease
• ystic Fibrosis
• ronchitis – Chronic
• sthma
• ronchiectasis
• mphysema
• ronchiolitis

What is Emphysema?
 Loss of elastic recoil
 This loss of recoil leads to an
increased compliance and
inability to expel gas out of the
alveoli
 Leading to trapped air in the
lung
 Alveoli cluster together forming
“blebs”
 Understanding COPD
 Emphysema

What is Emphysema Cont…
 Damage occurs to the tiny airways in the lungs called
bronchioles. Bronchioles are joined to alveoli, tiny
grape-like clusters of sacs in the lungs where oxygen
from the air is exchanged for carbon dioxide from the
body. The elastic properties of the lung reside in the
tissue around the alveoli
 Because the lungs lose elasticity they become less
able to contract.
 This prevents the alveoli from deflating completely,
and the person has difficulty exhaling.

Emphysema Cont…
• Hence, the next breath is started with more air in the
lungs.
• The trapped "old" air takes up space, so the alveoli are
unable to fill with enough fresh air to supply the body
with needed oxygen.

Pulmonary Emphysema
• Centrilobular emphysema
– Abnormal weakening and
enlargement of the respiratory
bronchioles in the proximal
portion of the acinus
– Primary changes occur in
upper lobes
– High correlation with smoking

Pulmonary Emphysema
• Bullous emphysema
– Changes seen at
both respiratory
bronchiole and
alveolar levels
– Prominent bullae
formation (air
spaces greater
than 1 cm in
diameter)

Emphysema Cont…
 A person with emphysema may feel short of breath
during exertion and, as the disease progresses, even
while at rest.
 Emphysema is one of several irreversible lung diseases
that diminish the ability to exhale. This group of diseases
is called chronic obstructive pulmonary disease
(COPD). The two major diseases in this category are
emphysema and chronic bronchitis, which often
develop together.

Emphysema
 Typically, symptoms of emphysema appear only after 30
to 50 percent of lung tissue is lost.
 Emphysema rates are highest for men age 65 and older.
 More people in the Midwest have emphysema than in
any other region in the country.
 Emphysema is an irreversible disease that can be
slowed but not reversed or stopped.

Causes
• Generally, lungs become damaged because of
reactions to irritants entering the airways and alveoli.
Researchers continue to investigate the factors that
may make some people more susceptible to
emphysema than others. But there are some clear
causes for emphysema:
• Cigarette smoking
• Alpha-1 antitrypsin deficiency

Other Cause
Alpha-1 Antitrypsin Deficiency
• People who a deficiency of a protein called alpha-1
antitrypsin (AAT) are at a higher risk of developing
severe emphysema. Alpha-1 antitrypsin deficiency (AAT
deficiency) is an inherited condition and occurs in
varying degrees

AAT
• AAT is thought to protect against some of the damage
caused by macrophages. In AAT deficiency-related
emphysema, the walls of the bronchial tubes and the
alveoli are both damaged, often leading to severe
disease.
• About 2 out of every 1,000 people have an alpha-1
antitrypsin deficiency. People who smoke and have AAT
deficiency are almost certain to develop emphysema.

Causes
 Cigarette smoking is the major cause of emphysema.
When exposed to cigarette smoke, the air sacs of the
lungs produce defensive cells, called macrophages,
which "eat" the inhaled particles. But macrophages are
stimulated to release materials which can destroy the
proteins that let the lungs expand and contract, called
elastin and collagen.
 Cigarette smoke also damages the cilia, tiny hair-like
projections in the bronchi that "sweep" foreign bodies
and bacteria out of the lungs

Symptoms
The first sign of emphysema is shortness of breath during exertion.
Eventually, this shortness of breath occurs while at rest. As the
disease progresses, the following symptoms which are related to one
of the other major lung diseases also caused by smoking - bronchitis
- may occur:
• Difficulty breathing (dyspnea)
• Coughing (with or without sputum)
• Wheezing (this can also be caused by emphysema itself)
• Excess mucus production
• A bluish tint to the skin (cyanosis)
• Hypoxemia
• Tachycardia
• Polycythemia

More Symptoms
• Clubbed fingers (chronic hypoxia)
• Right Heart Failure
• Stained yellow fingers, teeth

Diagnosis
History And Physical Examination
 Smoking history (calculate pack years, # packs
smoked times # years smoked)
 Working environment- breathing in any harmful
chemicals?
 A physical examination will include an examination of
your chest and breathing patterns; prolonged
expiratory times
 Nasal flaring, accessory muscle usage (due to loss of
diaphragm recoil from air trapping)

Diagnosis Continued
X-Ray and/or CT of the Chest
 Chest x-rays are a very useful tool to evaluate anatomy of
the lung. In emphysema, there is evidence of increased air
in the chest and destruction of some of the lung tissue.
Bronchitis can be suspected on a chest x-ray by presence
of thickening of the tissue around the large airways
(bronchi). Chest x-rays are also useful as screening for
lung cancer and heart disease.
 Computerized axial tomography or CAT scans indicate
lung anatomy in greater detail. In some cases, this
information is needed to fully evaluate lung disease.

Lung Function Tests
• Routine lung function tests can help define the
kind and amount of damage to the lungs. The
following tests can identify various stages of
emphysema:
• Spirometry measures breathing capacity. A
common measure of breathing capacity is the
forced expiratory volume in one second (FEV1),
or the amount of air that can be forced out of the
lungs in one second. This is a common way to
determine the amount of airway obstruction.

Lung Function Tests
• Frequently, your physician will ask that spirometry and
body plethysmography be repeated after administration
of an inhaled bronchodilator
• This test will help your physician determine if there is an
asthmatic component present
• Lung Volumes measures the amount of air in the
lungs. This increases markedly in emphysema.

Lung Function Tests
• Diffusing Capacity measures the ability of the lung to
transfer the gases from the air to the blood and vice
versa. Decrease in diffusing capacity allow fairly
accurate estimation of amount of emphysema.
• Body Plethysmography is a rapid way of evaluating
both degree and type of obstruction and lung volumes. It
is a useful adjunct to understanding the mechanism of
airway obstruction - e.g., asthma vs emphysema.
• Arterial blood gases (ABG) analyzes blood from an
artery for amounts of carbon dioxide and oxygen. This
test is often used in more advanced stages of
emphysema to help determine if a person needs
supplemental oxygen.

Arterial Blood Gas
• Patient’s with emphysema have chronic CO2 retention
due to the inability to expel gas. Their blood reflects
higher levels of CO2 than normal people; CO2 is acidic
in nature.
• Over time their body compensates for this higher CO2
by creating more buffer in the blood in the form of
HCO- from the kidneys.
3

Emphysema Diagnosis Cont…
Tests For Alpha-1 Antitrypsin Deficiency
 The symptoms of alpha-1 antitrypsin deficiency-related
emphysema tend to appear between the ages of 30 and
40. The symptoms and diagnostic tests are basically the
same in any kind of emphysema except that, in this
disease, emphysematous changes are greatest in the
lower lung. However, if AAT deficiency is suspected, a
special blood test can confirm the diagnosis.

Treatment for Emphysema
• There is no cure for emphysema. The goal of
treatment is to slow the development of disabling
symptoms. The most important step to take is to stop
smoking.
• Treatments for emphysema caused by smoking
include medication, breathing retraining, and surgery.
• People with inherited emphysema due to alpha-1
antitrypsin deficiency can receive alpha 1-proteinase
inhibitor (A1PI), which slows lung tissue destruction.

Breathing Techniques
Diaphragmatic Breathing
• The diaphragm is a major muscle used in breathing and is
located beneath the lowest two ribs. At rest, the diaphragm
muscle is bell shaped. During inspiration, it lowers and flattens
out.
• Optimizing the use of the diaphragm is beneficial because it
pulls air into the lower lobes of the lungs where more gas
exchange takes place. Not only is the diaphragm the most
efficient of all respiratory muscles, but using it tends to be very
relaxing and calming.
• Along with our diaphragm, we use intercostal and abdominal
muscles in the work of breathing. The intercostals (muscles
between the ribs) pull to lift the rib cage up and out. This
causes the lungs to open in all directions and air can be pulled
down the airways. To exhale, the muscles that have been
pulling relax and air is forced out.
• The diaphragm tenses, pulling air in; and relaxes, letting the
spring of the ribs push the air out again.

Breathing Techniques
Diaphragmatic Breathing
Pursed Lip Breathing
How:
• Breathe in through your nose.
• Purse lips slightly as if to whistle.
• Breathe out slowly through pursed lips.
• Do not force the air out.
• Pursed Lip Exercise

Medications Used
Medications To Treat Emphysema
 Emphysema cannot be cured and, except for oxygen, does
not reverse with any medication. However, emphysema is
frequently associated with bronchitis and asthma and the
symptoms associated with these processes often can be
alleviated with medication (hence, you can see the value of
pulmonary function and other tests designed to discover if
there is asthmatic component present:
 Bronchodilator medication
 Corticosteroids
 Supplemental oxygen

Medications Used
Bronchodilator Medication
• Bronchodilator medication may be prescribed for airway
tightness. Bronchodilators react similar to norepinephrine
through the sympathetic nervous system
• The most commonly prescribed bronchodilators are
beta2 agonists, the anti-cholinergic drug ipatropium
bromide, and theophylline.
• Anti-cholinergics block musacaric receptors which
normally respond to acetylcholine and cause
bronchoconstriction

Medications Used
Corticosteroids
• The potent anti-inflammatory medications known as
corticosteroids - commonly called steroids - may be
used to help lessen the inflammation that often
accompanies emphysema. These may be taken by
mouth or inhaled.

Oxygen
• Due to the chronic state of increased CO2 in the blood
(hypercapnia), the patient has adapted a breathing
regulation in the brain that responds to changes in O2
and not CO2 like most people
• If you give a patient with COPD more than 30% oxygen
they will slow their breathing
• Give low flow oxygen at 2 LPM by NC
• Or high flow oxygen with a venturi mask at 22-30%
• What Would Happen If The World Lost Oxygen For 5
Seconds?
• Home Oxygen Therapy, What To Expect

Surgical Interventions
• Surgical treatments for emphysema remain experimental
and are not covered by insurance. Most people with
emphysema are not candidates for surgery.
• Two types of surgery for people with emphysema are:
• Lung Reduction
• Lung Transplantation
• History of lung volume reduction surgery

Lung Reduction
 A surgical procedure called lung reduction may improve
symptoms for people with certain types of emphysema.
During the procedure, part of the lung is cut out, giving
healthy lung tissue more room to expand.
 Lung reduction may eliminate the need for supplemental
oxygen and make it much easier for the person to breathe.
Early studies show that it reduces the volume of the over-inflated
lungs. This improves the ability of the lung and
chest wall to spring back during exhalation. This more-elastic
lung appears to be the biggest reason that
emphysema sufferers experience relief.

Conclusion
 Emphysema is a chronic disease that takes years to
progress; usually as a result of heavy cigarette smoking
but also can be caused by inherited Alpha-1 antitrypsin
deficiency
 It destroys the stability of the alveoli and bronchioles
leaving them over compliant
 This leads to air trapping and an accumulation of CO2 and
decrease in O2
 The air trapping leads to dyspnea
 Diagnose with symptoms, ABG, CXR, PFT and history
 Treatment consists of stop smoking, medications and lung
reduction surgery or transplant

Cystic Fibrosis
(Mucoviscidosis)

Cystic Fibrosis
• Hereditary Disease
• Most common lethal genetic disease among Caucasian
Americans
• Affects 30,000 persons in the U.S.
• Mean life expectancy – +/-(5 years) 38 yrs.
• Caused by a genetic mutation of the gene coding for a
large protein that controls the movement of chloride ions
through the cell membrane.
• Movement of chloride is vital to the proper production
and regulation of secretions in the lungs, pancreas,
sweat glands and others.

Introduction
• CF is an inherited disease of your mucus and sweat
glands
• It affects mostly the lungs, pancreas, liver, intestines,
sinuses and sex organs
• An abnormal gene causes mucus to become extra
thick and sticky
• This gene makes a protein that controls the movement
of salt and water not work properly (retaining salt=thick
secretions)
• This leads to mucus plugs

Introduction Continued
• Mucus plugs lead to
collapsed lungs
(atlectasis)
• Increased mucus in the
lungs also allows for
more bacterial growth
which leads to frequent
pneumonia
• Constant infections lead
to inflammation in the
lung

Introduction Continued
Cystic fibrosis is the most common cause of chronic
genetic lung disease in children and young adults,
and the most common fatal hereditary disorder
affecting Caucasians in the US.
CF is a multi-system disorder of exocrine glands causing
the formation of a thick mucus substance that affects
the lungs, intestines, pancreas, and liver. The
standard test for diagnosis is a sweat test which
evaluates the level of chloride excreted by the body.

Cystic Fibrosis
• Chloride levels in sweat is elevated due to lack of
normal removal, as a result CF patients are vulnerable
to dehydration. A sweat chloride test is used for the
diagnosis of the disease (> 60mEq/L in infants and > 80
in adults)
• Pancreatic insufficiency reduces the number of
digestive enzymes. These patients experience
malnutrition, diarrhea, vitamin deficiency and
undigested fat in the stool.

Diagnosis
The sweat chloride test is performed to determine the amount of
chloride that is excreted in sweat from the body during a certain
period of time. The test may be performed on infants to determine if
cystic fibrosis is present. Children with cystic fibrosis have
increased sodium and chloride concentrations in their sweat.
Normal Sweat
18 mEq/L
Positive Test
60 mEq/L

Diagnosis
• Often the first sign of CF
begins after birth, the
mother kisses the baby
and they taste salty.
• Poor feeding occurs from
blocked bile ducts (bile
released from pancreas
helps digest food)

Diagnosis
• Cystic Fibrosis: Early Intervention
• Genetic Carrier Testing — More than 10 million Americans are
symptomless carriers of the defective CF gene. This blood test can
help detect carriers, who could pass CF onto their children. To have
cystic fibrosis, a child must inherit one copy of the defective CF gene
from each parent.
• Each time two carriers of the CF gene have a child, the chances are:
• 25% (1 in 4) the child will have CF;
• 50% (1 in 2) the child will carry the CF gene but not have CF; and
• 25% (1 in 4) the child will not carry the gene and not have CF

Diagnosis Continued
• Detailed medical history is obtained (CF is Hereditary)
• Chest X-RAY to show scarring from frequent
inflammation
• Sinus X-RAY
• Pulmonary Function Test (CF is a COPD); used only
with individuals old enough to comply > 8years old
usually
• Sputum Cultures to determine certain bacteria growth
• Blood tests to find abnormal CF gene

Symptoms
• Increased WOB from plugged airways and air trapping
• Tenacious Secretions
• Frequent productive cough
• Frequent bouts of bronchitis and pneumonia
• Dehydration and malnutrition despite huge appetite;
failure to thrive
• Infertility (mostly in men)
• Ongoing diarrhea and stomach pain

Cystic Fibrosis
Finger Clubbing

Cystic Fibrosis
Radiologic Findings:
1. Translucent (dark) lung
fields
2. Depressed or flattened
diaphragms
3. Right ventricular
enlargement
4. Areas of atelectasis
and fibrosis
Occasionally:
1. Abscess formation
2. Pneumothorax

CF leads to…
• Sinusitis: the sinuses have mucus build up leading to
headaches, ear and equilibrium problems.
• Bronchiectasis: damaged lungs become overly
stretched and retain secretions and gas.
• Pancreatitis: Leads to inability to digest food, leading
to bowel obstruction and sepsis.
• Liver Disease, Diabetes, Gallstones and low bone
density from lack of Vitamin D.

CF leads to Respiratory failure
• The mucus plugs the airways causing collapse of
the alveoli and increased WOB
• Increased PaCO2, decreased PaO2 and eventual
death if not treated.
• Infections lead to inflamed and damaged lung lining
• Blocked pancreas leads to vitamin deficiencies
• There is no cure for CF only treatments; average life
span is 38 years

Treatments for CF
• Chest physiotherapy (CPT) is the
traditional means of airway clearance in CF.
It uses postural drainage in various
positions, percussion, vibration, deep
breathing, and coughing to loosen and
move secretions out of the lungs. The
treatment time including an aerosol before
is about 45 minutes. Done so by using
manual percussion with hand, pneumatic
precursor with device or by Vest.

Cystic Fibrosis Physical Therapy of Toddler

Treatment for CF
Chest Physical Therapy:
Using the “Vest” or manual
precursor. Helps loosen
secretions with percusion

Treatment Continued
• PEP is a technique that uses a hand held device
which can be used with a nebulizer attached. It
has a restricted orifice. When exhaled into, this
creates pressure in the lungs. This pressure
allows air to enter behind areas of mucus
obstruction and keeps the airways open during
exhalation. As you exhale, mucus moves
towards the larger airways, so it can be more
easily coughed up with the huff technique. PEP
can be taught to children as young as 5 years,
and can be passively given to infants via a
mask. The treatment time is about 20 minutes.

Treatment Continued
• Vibratory Positive Expiratory Pressure (Flutter®,
Acapella®)
Vibratory positive expiratory pressure is a hand held
device. Exhaling into this device results in oscillations
of pressure and airflow which vibrate the airway walls
(loosening mucus), helps hold the airway open (which
allows air to get behind secretions and keeps the
airways open during exhalation). It speeds up airflow
helping mucus move up to the larger airways where it
can be more easily coughed up. Vibratory PEP can
be taught to children as young as 2 years old by
mask, and to ages 5 and up via mouthpiece.
Treatment time is about 20 minutes.

Treatment Continued…
Intrapulmonary Percussive Ventilation.
The IPV is a pneumatic (air driven) device that
delivers both continuous airway pressure and mini
bursts of air. At the same time the IPV delivers a
dense aerosol.
The combination allows air to
enter behind mucus blockage,
and vibration to dislodge mucus
from the airway walls so it can
be more easily coughed up.
IPV

Treatment Continued
• Active Cycle of Breathing
Active cycle of breathing is a series of breathing
techniques, consisting of thoracic expansion
exercises (deep breathing), breathing control
(using the diaphragm), and the forced expiration
technique (huff). These breathing cycles are
performed in various positions of drainage
similar to CPT positions but without the
percussion. This can be taught at about the age
of 8 years. Treatment time, including an aerosol
before, is about 45 minutes.

Treatments
• Autogenic Drainage is a breathing technique
which involves 3 phases of breathing levels:
• Phase One is the unsticking phase which is
inhalation and exhalation of small amounts of air.
• Phase Two is the collection phase where medium
sized breaths are inhaled and exhaled.
• Phase Three is the evacuation phase where large
amounts of air are inhaled and exhaled.

Treatments
• Hand Held Nebulizers are used in
conjunction with PEP, IPV, CPT and
breathing techniques
• The nebulizer will nebulize medications
that bronchodilate and help break up
mucus
• Antibiotics can also be used in a
nebulizer

Medications Used
• Antibiotics: Tobramycin and Azithromycin to fight
bacterial infection. Given by aerosol in nebulizer
or by IV
• Anti-Inflammatory Drugs: Steroids given inhaled
or by IV; also Ibuprofen is given
• Bronchodilators: Albuterol/Xopenex given to
relax smooth muscle
• Mucolytics: Given with bronchodilators to break
up thick secretions. Main one is Dornase Alfa
(Pulmozyne) made specifically for CF patients

More Treatments
• Oxygen Therapy at low concentrations.
• Lung Transplantation; depends on severity of illness
and health of participate
• Nutritional therapy; oral pancreatic enzymes to digest
fats and proteins and absorb vitamins.
• Vitamin supplements of A, D, E and K
• Feeding tube at night (G-Tube)
• Enemas and stomach meds to control acid

Conclusion
• CF is a deadly hereditary disease that is
treatable but not curable
• CF causes abnormally thick mucus which
blocks bile ducts and plugs up the lung
and sinus
• May lead to respiratory failure, malnutrition
and frequent occurrences of pneumonia
• Treatment includes methods to remove
and thin mucus and medications to treat
digestive problems, and infections

Chronic Bronchitis
• Presence of cough and sputum production for three or
more months in two successive years
• Etiology
– Smoking
– Air pollution
– Chronic infections
– Chronic Bronchitis Symptoms

Chronic Bronchitis
• 14 million Americans are affected
• Most common causes are smoking/pollution
• Repeated lung infections, especially in childhood increase
risk
• Common pathogens include Haemophilus influenzae and
Streptococcus pneumoniae
• Gastroesophageal reflux disease (GERD) can lead to
pneumonias from aspiration of stomach contents

Chronic Bronchitis – Pathophysiology
• Most changes in the lungs occur in the conducting
airways
• Airway changes occur from:
– Chronic inflammation and swelling
– Excessive mucus production and accumulation
– Partial or total mucus plugging
– Hyperinflation of alveoli
– Smooth muscle constriction of airways

• Changes in mucus glands
– Increase in number of mucus secreting glands; goblet
cells increase, causing decrease in ciliated columnar
cells; submucosal glands hypertrophy
• Smooth muscle hypertrophy in bronchial airways
• Diminished airway radius

• Increase in sputum production
• Accumulation of secretions
• Loss of ciliated cells
• Impairment of mucociliary escalator
• Decreased flow rates, VC, FVC, FEV1, MVV
• Increased RV, FRC, TLC

Chronic Bronchitis
Radiologic Findings
1.Hyperinflation of the Lungs
2.Flattened Hemidiaphram
3.Peripheral Pulmonary
Vasculature may be Prominent
4.Pulmonary Vascular
Engorgement
5.Long and narrow heart (pulled
down by the diaphragms)
6.Enlarged heart

Chronic Bronchitis – Clinical Findings
• Typical appearance is of the “Blue Bloater”
– Stocky build
– Cyanotic
– Increased A-P diameter
– Jugular vein distension
– Edema

• Cough
– Smoker’s cough
– Morning cough
– Continual cough
• Sputum production
– Volume increases slowly leading to abnormal production but
typically less than a cup/day
– Thick, gray, mucoid in nature
– Mucopurulent infections leading to yellow or green sputum

• Increase in respiratory rate
– Stimulation of peripheral chemoreceptors secondary to hypoxemia
and chronic CO2 retention
– Decrease in lung compliance
– Anxiety
• Increase in heart rate
• Dyspnea, especially on exertion
• Use of accessory muscles
• BS: rhonchi, crackles, wheezing and decreased BS
• Breath Sounds

• Pursed lip breathing
• Increase in A-P diameter of the chest (barrel chest)
secondary to hyperinflation
• Clubbing
• Increased sputum production
• ABG results
– Fully compensated pH unless in an acute exacerbation
– Increase in PaCO2
– Decrease in PaO2

CXR Interpretation for COPD
• Chest x-ray interpretation --COPD and Emphysema

Pink Puffer Vs. Blue Bloater
• A "pink puffer" is a person where emphysema is the
primary underlying pathology. As you recall,
emphysema results from destruction of the airways
distal to the terminal bronchiole--which also includes the
gradual destruction of the pulmonary capillary bed and
thus decreased inability to oxygenate the blood. So, not
only is there less surface area for gas exchange, there
is also less vascular bed for gas exchange--but less
ventilation-perfusion mismatch than blue bloaters. The
body then has to compensate by hyperventilation (the
"puffer" part).

• Pink Puffers: Their arterial blood gases (ABGs) actually
are relatively normal because of this compensatory
hyperventilation. Eventually, because of the low cardiac
output, people afflicted with this disease develop muscle
wasting and weight loss. They actually have less
hypoxemia (compared to blue bloaters) and appear to
have a "pink" complexion and hence "pink
puffer". Some of the pink appearance may also be due
to the work (use of neck and chest muscles) these folks
put into just drawing a breath.

• A "blue bloater" is a person where the primary
underlying lung pathology is chronic bronchitis. Just a
reminder, chronic bronchitis is caused by excessive
mucus production with airway obstruction resulting from
hyperplasia of mucus-producing glands, goblet cell
metaplasia, and chronic inflammation around
bronchi. Unlike emphysema, the pulmonary capillary
bed is undamaged. Instead, the body responds to the
increased obstruction by decreasing ventilation and
increasing cardiac output.

• There is a dreadful ventilation to perfusion mismatch
leading to hypoxemia and polycythemia. In addition,
they also have increased carbon dioxide retention
(hypercapnia). Because of increasing obstruction, their
residual lung volume gradually increases (the "bloating"
part). They are hypoxemic/cyanotic because they
actually have worse hypoxemia than pink puffers and
this manifests as bluish lips and faces--the "blue" part.

Asthma
Watch an Asthma Attack

Asthma
• A disease of the airway “characterized by an
increased responsiveness of the trachea and
bronchi to various stimuli and is manifested by
widespread narrowing of the airways that change
in severity either spontaneously or as a result of
treatment” (ATS)

Asthma
• Airway constriction may be partially or completely
reversible either spontaneously or with treatment
• Affects more than 15 million Americans
• Recognized more than 2000 years ago
• More than 5,000 die per year - Teen dies of asthma
• The most common chronic illness of childhood
• May develop in adulthood with increased mortality
• May disappear at puberty

Asthma
• Allergic or Extrinsic Asthma
– Results from an antigen-antibody reaction on mast cells
causing a release of histamine, bradykinins, and other
chemicals
• Idiopathic or Intrinsic Asthma
– Cannot be linked to a specific antigen
– Results from an imbalance of the autonomic nervous system
• Non-specific Asthma
– Results from an unknown cause, possibly viral, emotional, or
exercise

Asthma
• From your text page 189:
• Occupational Sensitizers (box 12-1)
• Seen predominantly in adults, more than 300
substances contribute to it.
• Sensitive work environments include:
– Farming
– Agricultural
– Painting
– Cleaning work
– Plastic manufacturing

Immunologic Mechanism (from your
text, page 188)
• When exposed to specific antigens, lymphoid tissue
forms specific IgE antibodies
• The IgE antibodies attach themselves to surface of
mast cells in the bronchial wall
• Re-exposure to the same antigen creates antigen-antibody
reaction on the surface of the mast cell,
causes mast cell to degranulate and release chemical
mediators:
– Histamine
– Eosinophil/neutrophil chemotactic factors
– Leukotrienes
– Prostglandins and platelet activating factor
– Allergies

Mast Cell Degranulation
Exposed to antigen, form
antibodies, attach to mast cells
Re-exposure to antigen causes
the degranulation of mast cell
and release of inflammatory
cells

Mast Cell Degranulation
Following an Asthma attack; the patient will have congestion
and increased sputum production for several days

Inflammatory cell release (page 189)
• Release of chemical mediators from mast cell stimulates
parasympathetic nerve endings in the bronchial airways
leading to reflex bronchoconstriction and mucous hyper-secretion
• The mediators also increase permeability of capillaries
causing dilation of blood vessels and tissue edema
Early vs. late response (after steroids and bronchodilators
have worn off)

Mast Cell inhibitors for asthma
treatment
• Cromolyn sodium (Intal) and nedocromil (Tilade) are used to prevent
allergic symptoms like runny nose, itchy eyes, and asthma. The response is
not as potent as that of corticosteroid inhalers.
How mast cell inhibitors work
• These drugs prevent the release of histamine and other chemicals from mast
cells that cause asthma symptoms when you come into contact with an
allergen (for example, pollen). The drug is not effective until four to seven
days after you begin taking it.
Who should Use it
• Patients with extrinsic asthma, with known allergies
• Frequent dosing is necessary, since the effects last only six to eight hours.
Mast cell inhibitors are available as a liquid to be used with a nebulizer, a
capsule that is placed in a device that releases the capsule powder to inhale,
and handheld inhalers

Intal and Tilade
Both drugs are used only for prophylaxis of asthma, not for
treatment of the acute exacerbation or for the symptomatic
patient

Anti- Leukotriens
• Do not prevent mast cell degranulation, as do Intal and
Tilade
• They stop the inflammatory mediators once the mast
cells is degranulated
• Leukotrienes are proinflammatory mediators with
special significance in asthma. Released by numerous
cell types, particularly after exposure to allergens,
leukotrienes cause a potent contraction of bronchial
smooth muscle, resulting in reduced airway caliber.
Further, they cause plasma to leak from the vessels,
resulting in edema, and enhance the secretion of mucus

Anti-leukotriene drugs
• ORAL ONLY. First drug of this type (Nov 1996) is the
leukotriene-receptor antagonist Zafirlukast [Accolate],
20 mg bid. The 2nd approved anti-leukotriene (Jan 1997)
is the leukotriene-synthesis inhibitor Zileuton [Zyflo],
with a 600 mg QID dosage schedule. Both are approved
only for asthma, and for patients 12 years or older. The
3rd approved anti-leukotriene, Montelukast (Singulair),
10 mg qd, is also approved for ages 6-14 in a 5 mg QD
dose. All anti-leukotrienes have some bronchodilator as
well as anti-inflammatory activity.

Asthma
• Etiology
– Heredity – one or more parents with disease
– Allergies, especially if onset between ages five and fifteen
– Inhaled irritants
• Pollen
• Dust mites
• Grasses
• Pollution
• Animal dander
• Chemicals

The Role of Heredity in
Asthma
• Heredity. To some extent, asthma seems to run in families. People
whose brothers, sisters or parents have asthma are more likely to
develop the illness themselves.
• Atopy. A person is said to have atopy (or to be atopic) when he or
she is prone to have allergies. For reasons that are not fully known,
some people seem to inherit a tendency to develop allergies. This is
not to say that a parent can pass on a specific type of allergy to a
child. In other words, it doesn't mean that if your mother is allergic to
bananas, you will be too. But you may develop allergies to something
else, like pollen or mold.
• In addition, several factors must be present for asthma symptoms to
develop:
• Specific genes must be acquired from parents.
• Exposure to allergens or triggers to which you have a genetically
programmed response.
• Environmental factors such as quality of air, exposure to irritants,
behavioral factors such as smoking, etc.

Asthma Risk Factors (page 190)
• Obesity: Certain mediators such as leptins may have an
effect on airway function that can lead to development of
asthma
• Gender: Males up to 14, have a higher prevalence, due to
possible lung size of boys vs. girls, after 14, girls have a
higher prevalence
• Infections: upper viral infections and bacterial infections
contribute to asthma. Commonly seen in children after
RSV, parainfluenza, rhinovirus.
• Exercise induced: heat loss, water loss, increased
osmolority increase inflammatory release

• Outdoor/indoor air pollution: increases in asthma
incidences occur in heavily polluted areas. Smoke, gas
fumes, biomass fuels for heating, molds and cockroach
droppings contribute to asthma
• Drugs/foods/preservatives: Aspirin sensitivity, and other
non-steroidals (NSAIDS), beta-blocking agents to treat
hypertension and tachycardia, tartazine (food coloring),
and preservatives for restaurant food
• GERD: regurgitation and aspiration, may lead to asthma
or exacerbate it

• Emotional Distress: psychological factors can induce
tachypnea and stress the lung contributing to asthma
exacerbation
• Perimenstrual asthma: symptoms worsen 2-3 days
before menstruation

Allergy Test
• Skin test - numerous known substances are placed on
the skin, reactions are noted and allergens are then
determined

Allergy Test
• Besides the skin allergy test they also do blood tests.
The RAST test measures the levels of the allergy
antibody IgE that is produced when your blood is mixed
with a series of allergens
• in a laboratory.

Causes
• Substances that cause allergies (allergens) such as dust
mites, pollens, molds, pet dander, and even cockroach droppings. In
many people with asthma, the same substances that cause allergy
symptoms can also trigger an asthma episode. These allergens may
be things that you inhale, such as pollen or dust, or things that you
eat, such as shellfish. It is best to avoid or limit your exposure to
known allergens in order to prevent asthma symptoms.
• Irritants in the air, including smoke from cigarettes, wood fires, or
charcoal grills. Also, strong fumes or odors like household sprays,
paint, gasoline, perfumes, and scented soaps. Although people are
not actually allergic to these particles, they can aggravate inflamed,
sensitive airways. Today most people are aware that smoking can
lead to cancer and heart disease. Smoking is also a risk factor for
asthma in children, and a common trigger of asthma symptoms for all
ages

Causes
• Respiratory infections such as colds, flu, sore throats, and
sinus infections. These are the number one asthma trigger in
children
• GERD: Gastric esophageal reflux disease, stomach acid can be
aspirated and inflame the airway
• Exercise and other activities that make you breathe harder.
Exercise—especially in cold air—is a frequent asthma trigger. A
form of asthma called exercise-induced asthma is triggered by
physical activity. Symptoms of this kind of asthma may not appear
until after several minutes of sustained exercise. (When symptoms
appear sooner than this, it usually means that the person needs to
adjust his or her treatment.) The kind of physical activities that can
bring on asthma symptoms include not only exercise, but also
laughing, crying, holding one's breath, and hyperventilating (rapid,
shallow breathing). The symptoms of exercise-induced asthma
usually go away within a few hours
Exercise Induced Asthma Attack

More Causes…
• Weather such as dry wind, cold air, or sudden changes in
weather can sometimes bring on an asthma episode.
• Expressing strong emotions like anger, fear or
excitement. When you experience strong emotions, your
breathing changes -- even if you don’t have asthma. When
a person with asthma laughs, yells, or cries hard, natural
airway changes may cause wheezing or other asthma
symptoms.
• Some medications like aspirin can also be related
to episodes in adults who are sensitive to aspirin. Irritants
in the environment can also bring on an asthma episode.
These irritants may include paint fumes, smog, aerosol
sprays and even perfume.

Why Does My Asthma Act Up at
Night?
• For reasons we don't fully understand, uncontrolled
asthma -- with its underlying inflammation -- often acts
up at night. It probably has to do with natural body
rhythms and changes in your body’s hormones, as
well as the fact that some symptoms appear hours
after you come in contact with a trigger.
• Also during sleep you release less norepinephrine
(adrenaline) which acts as your bodies natural
bronchodilator
• A Tragic Asthma Attack Story

Asthma – Pathophysiology
• Airway Inflammation
– Acute Phase Response – triggered by activation of mast
cells and the release of intracellular mediators
• Bronchospasm
• Increase in secretions
• Mucosal edema
• Significant reduction in airflow

– Subacute phase
• Continuous inflammatory pattern
• Significant airflow limitation
• Can continue for days to weeks

– Chronic inflammation
• Present between episodes of exacerbation
• Controlled by corticosteroids, mast cell modifiers, or
leukotriene modifiers

• Airway Hyperresponsiveness
– Usually most evident in acute phase
– Increased sensitivity to both specific and non-specific
causes
– Release of immunoglobulin E (IgE) mediators into the
cellular tissue causing bronchoconstriciton of the smooth
muscle of the airway, degranulation of mast cells releasing
histamines, leukotrienes, certain interleukins, prostaglandins
and others
– Treated with beta2 agonists

Degranulation of the mast cell
Smooth muscle contraction
Mucous accumulation
Mucous plugging
Hyperinflation of alveoli

Asthma – Classification
• Classifications of Asthma
– Mild intermittent asthma
• Symptoms < 2/week or < 2 times/month at night
• Little effect on day to day activities
• Expiratory flow ≥ 80% of predicted

– Mild Persistent Asthma
• Symptoms > 2/week but less than 1/day; < 2
times/month at night
• Exacerbations may affect activity
• Expiratory flow ≥ 80% of predicted

– Moderate persistent asthma
• Symptoms daily; > 1/week at night
• Limitations ≥ 2/week; may last days
• Expiratory flow > 60% but < 80% of predicted

– Severe persistent asthma
• Symptoms continually with frequent symptoms at night
• Frequent exacerbations which limit activity
• Expiratory flow < 60% of predicted

Asthma – Pulmonary Function
Results
• May have normal results when asymptomatic
• Airway obstruction
– Decrease in FEV1
– Decrease in FEV1/FVC ratio
– Demonstrate reversibility of obstruction following
bronchodilator administration (↑ in FEV1 of at least 12% and
an increase in VC of 200mL or more)
– Decrease in expiratory flow rates: peak flows are used to
monitor asthmatic events in the home.

Asthma – Pulmonary Function
Results
• Bronchoprovocation Testing
– Administration of Methacholine
– Causes decrease in FEV1 by 20% or more in
hyperresponsive airways
• Diagnostic test used in the evaluation of suspected asthma. The methacholine
challenge is also used for research purposes to study airway hyperreactivity.
Under special circumstances it plays a role in the clinical arena. Cold-air
exercise tests are another example of a bronchoprovocation test.
• A bronchoprovocation test might be ordered in the evaluation of suspected
asthma. It is not considered a “routine” test. Usually, the patient describes
subtle symptoms suggestive of asthma. Spirometry and other pulmonary
function testing are entirely normal.

Methacholine
• Methacholine (Provocholine) is a synthetic choline
ester that acts as a non-selective muscarinic receptor
agonist in the parasympathetic nervous system

Using a Peak Flow
• A Peak Flow device is a assessment tool used to
measure the effectiveness of fast acting
bronchodilators.
• Given during the attack, before and after treatments
• It is a handheld device that the patient exhales forcibly
on; as the airway opens and improves, the value
increases

Peak Flow Continued…
• Peak Flow Meter Demo

Asthma – Clinical Findings
• Auscultation – episodic wheezing
– Absence of wheezing does not preclude asthma
– Not all wheezing is asthma
– Breath sounds may get worse but patient could be improving
• Shortness of breath
• Tachypnea
• Tachycardia
• Use of accessory muscles
• Pursed-lip breathing
• Anxiety
• Hypoxia
• Altered LOC
• Full Arrest
• BS – wheezes, crackles, rhonchi, decreased BS

Asthma – Clinical Findings
• Blood Gas Results
– In mild to moderate episode:
pH PCO2 HCO3 slightly PaO2
– In moderate to severe episode:
• pH PCO2 HCO3 slightly PaO2

Status Asthmaticus
• A severe asthma attack not responsive to bronchodilators
• Typically requires intubation and mechanical ventilation due to
respiratory failure
• Typically, patients present a few days after the onset of a viral
respiratory illness, following exposure to a potent allergen or irritant, or
after exercise in a cold environment. Frequently, patients have
underused or have been under prescribed anti-inflammatory therapy.
Illicit drug use may play a role in poor adherence to anti-inflammatory
therapy. Patients report chest tightness, rapidly progressive shortness
of breath, dry cough, and wheezing and may have increased their
beta-agonist intake (either inhaled or nebulized) to as often as every
few minutes.

Early and Late
Asthmatic Response
• Late response is usually more severe and longer
lasting.

Mosby items and derived items ©
2009 by Mosby, Inc., an affiliate of
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Pharmacotherapy
Corticosteroids
– Most effective mediation in treatment of asthma
• Reduces symptoms and mortality
– Use of inhaled steroids for long-term treatment preferred
• Use spacer and rinse mouth to eliminate or minimize
side effects
– Long-term use of oral steroids should be restricted to
patients with asthma refractory to other treatment.
– Short-term oral steroid use during exacerbation reduces
severity, duration, and mortality.

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Pharmacotherapy
Inhaled Corticosteroids (page 194)
• Beclomethasone (QVAR); 40 or 80 ug/puff BID
• Flunisolide (Aerobid); 250 ug/puff; BID
• Fluticosone (Flovent); 44, 110, or 220 ug/puff, BID
• Budesonide (Pulmicort); SVN 0.25 or 0.5 mg, BID
• Momestone furoate (Asmanex twisthaler) DPI 220 ug QD

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Pharmacotherapy
Systemic Steroids Corticosteroids (page 194)
• Prednisone (short term use following an acute attack)
usually 3-5 days, BID
• Methylpredinsone (Solu-Medrol); Typically an IV potent
systemic steroid, given during and after acute attacks

HHN Delivery
• Delivery of the a small volume nebulizer takes practice
and in fact the way the medication is delivered to a
patient can dictate the hazards. Below is a link of the
proper way to give a nebulizer treatment, granted it is
from another RT program, I think it shows the proper
components of neb delivery
You Tube- Neb Delivery

MDI Delivery
• Delivering an MDI to a patient takes some practice.
Below are three videos, one for an MDI using a closed
mouth technique, one showing an open mouth
technique and one showing an MDI with a holding
chamber (Aerochamber). You should encourage MDI
use with a holding chamber
1. You Tube- closed mouth
2. You Tube- open mouth
3. You Tube- holding chamber

Pharmacotherapy (cont.)
Cromolyn (NSAID) non-steroidal anti-inflammatory drug
– Protective against allergens, cold air, exercise
– Administered prophylactically, CANNOT be used during an
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acute asthma attack
– Of limited use in adults
– Drug of choice for atopic children with asthma
Nedocromil (NSAID)
– Similar to Cromolyn, it is 4–10 times more potent in
preventing acute allergic bronchospasm.

DOSAGES AND FREQUENCIES:
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Cromolyn (NSAID)
• SVN 20 mg QID
• MDI 2 puffs 800 ug QID
Nedocromil (NSAID)
– Similar to Cromolyn, it is 4–10 times more potent in
preventing acute allergic bronchospasm.
– MDI only, 2 puffs 1.75 mg/puff QID

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Leukotriene inhibitors
– Leukotrienes mediate inflammation and bronchospasms.
– Modestly effective to control mild to moderate asthma
– Accolate, Singular, Zyflo
Inhaled steroids remain the anti-inflammatory drug of
choice for the treatment of asthma.
Methyxanthines (use is controversial)
– Oral or IV use if admitted for acute asthma attack
– Theophylline

2-Adrenergic agonists Short Acting
– Most rapid and effective bronchodilator
– Drug of choice for exercise-induced asthma and emergency
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relief of bronchospasms
• Should be used PRN
– Improves symptoms not underlying inflammation
• Regular use may worsen asthma control and increase
risk of death.
• Albuterol (Proventil, Ventolin); SVN UD 0.5% Soln, or 2.5
mg (0.5 ml) give TID, QID, Q4, Q6 or PRN
• Levalbuterol (Xopenex), SVN 0.31, 0.63, or 1.25 mg

2-Adrenergic agonists Short Acting
Albuterol MDI = Pro Air/ Ventolin 90 ug: 2 puffs TID/QID
Xopenex MDI = Xopenex HFA 45 ug/puff x 2 puffs Q4-6
Combivent: MDI of Albuterol and Atrovent
DuoNeb: SVN of Albuterol and Atrovent
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2-Adrenergic agonists Ultra Short Acting
• Epinephrine (Epinephrine Mist, Primatene mist): SVN
1% soln (1:100), 0.25-0.5 ml QID; MDI 0.22 mg/puff
• Racemic Epinephrine; (Micronephrine, Nephrone); SVN
2.25% soln, 0.25-0.5 ml QID
Last about 90 minutes, Racemic has a strong Beta and
Alpha response, used for upper airway swelling
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2-Adrenergic agonists Long Acting and Combination
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drugs
Salmeterol (Serevent); DPI 50 ug/inhalation; 50 ug BID
Formoterol (Foradil) DPI, 12 ug, BID
Arformoterol (Brovona) SVN 15 ug/2ml, BID (some fast
acting response)

2-Adrenergic agonists Long Acting and Combination
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drugs
Advair (fluticosone and Serevent); DPI; 3 doses; 500/50,
250/50 and 100/50; the fluctuating dose is the steroid
Also comes in a MDI
Symbicort (Pulmicort and Foradil); MDI 80 and 160 ug
• DULERA mometasone furoate and a long acting
beta2-agonist medicine (LABA) called formoterol
fumarate
Arcapta (indacaterol maleate inhalation powder)

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Anticholinergics
– Can be used as adjunct to first-line bronchodilators if there is an
inadequate response
– Has an additive affect to 2-agonists
– Blocks musacarenic receptors (Acetycholine)
– Ipatropium Bromide (Atrovent); SVN 0.5 mg, 0.02% solution
– MDI 18 ug/puff; dose TID, Q6
– Tiotropium (Spiriva), used through a handi-haler, QD

Asthma and Environmental Control
• Recognized relationship between asthma and allergy
– 75–85% asthma patients react to inhaled allergens
• Environmental control is aimed at reducing exposure to allergens.
– Avoid outdoor allergens by remaining inside, windows closed, AC
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on
– Indoor allergens are combated by
• Air purifiers and no pets
• Dust mites: airtight covers on bed and pillow, no carpets in
bedroom, chemical agents to kill mites

Special Considerations in Asthma
Management (cont.)
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• Nocturnal asthma
– Present in two-thirds of poorly controlled asthmatics
– May be due to diurnal decrease in airway tone or gastric reflux
– Treatment should include:
• Steroid treatment targeted to relieve night symptoms
• Sustained release theophylline
• New long-acting 2-agonists
• Antacids for reflux

Management (cont.)
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• Aspirin sensitivity
– 5% of adult asthmatics will have severe, life-threatening asthma
attacks after taking NSAIDs.
– All asthmatics should avoid; suggest Tylenol use.
• Asthma during pregnancy
– A third of asthmatics have worse control at this time.
– Much higher fetal risk associated with uncontrolled asthma than
that of asthma medications
– Theophyllines, 2-agonists, and steroids can be used without
significant risk of fetal abnormalities.

Management (cont.)
• Sinusitis may cause asthma exacerbation.
– CT of sinuses will diagnosis problem.
– Treat: 2–3 weeks antibiotics, nasal decongestants, and nasal
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inhaled steroids
• Surgery
– Asthmatics at higher risk for respiratory complications
• Arrest during induction
• Hypoxemia with/without hypercarbia
• Impaired cough, atelectasis, pneumonia
– Optimize lung function preoperatively.
– Use steroids during procedure.

Review
• Emphysema:
– Low expiratory flows (FVC, FEV1 less than 80%), FEV1/FVC less
than 70%
– Decreased DLCO
– Increased Lung Volumes
– Main cause smoking, also caused by genetic alpha anti-trypson
disorder, environmental
– Chronic hypercapnia, hypoxemia, barrel chest, clubbing of fingers,
hyperinflated lungs on CXR (hyperlucent with flattened
diaphragms), accessory muscle use, SOB at rest...
– Damage occurs primarily in upper lobes
– Persistent irritants overwhelm lungs natural macrophage and
neutrophil removal, causing loss of elastin creating bullae

Review
• Emphysema:
– Treatments include breathing exercises, diaphragmatic
breathing, pursed lip breathing; low supplemental oxygen
less than 30% to avoid knocking out hypoxic drive;
bronchodilators, and steroids. Bronchial hygiene, Possible
lung transplant, smoking cessation
– Increased pressure in alveoli causes: decreased VA,
increased VD/VT, decreased in PaO2, PAO2, CaO2, SaO2,
increase in A-a gradient, CO2, Hb
– Get frequent pneumonia, bronchitis…

Review
• Cystic Fibrosis
– Heredity based
– Disease of tenacious mucus, blocks bile ducts, lungs and
sinuses.

Bronchiectasis
An Amazing Story
Bronchiectasis

Bronchiectasis
• Bronchiectasis is characterized by chronic dilation and
distortion of one or more bronchi as a result of extensive
inflammation and destruction of the bronchial wall
cartilage, blood vessels, elastic tissue, and smooth
muscle components
• Can affect one or both lungs
• Commonly limited to a lobe or segment
• Most frequently found in the lower lobes
• The smaller bronchi, with less supporting cartilage are
predominantly affected

Bronchiectasis
• Three forms or anatomic varieties of bronchiectasis
have been described:
– Varicose or fusiform
– Cylindrical or tubular
– Saccular or cystic

Bronchiectasis
• Etiology
– Not as common today because of increased use of antibiotics
for lower respiratory infections
– May be acquired or congenital but not thoroughly understood
– Acquired bronchiectasis is thought to occur by repeated and
prolonged respiratory infections, bronchial obstruction from a
foreign body, tumor or enlarged hilar lymph nodes
– People with cystic fibrosis have a much higher incidence of
bronchiectasis due to the chronic airway obstruction

Bronchiectasis
• Etiology
– Congenital Bronchiectasis
• Kartagener’s Syndrome responsible for 20% of all
bronchiectasis. Consists of a triad of Bronchiectasis,
dextracardia (heart on right side of chest), and
pansinusitus
• Hypogammaglobulinemia: An inherited immune deficiency
disorder that leaves the lung vulnerable to infection

Bronchiectasis
• Fusiform or Varicose
– Bronchial walls are dilated and constricted in an irregular
fashion similar to varicose veins ultimately ending in a
distorted bulbous shape ending in nonfunctional respiratory
units
– Evidence of bronchitis or bronchiolitis often present

Bronchiectasis
• Cylindrical
– Bronchial walls dilated with regular outlines.
– Least severe form

Bronchiectasis
• Saccular
– Complete destruction of bronchial walls
– Normal tissue replaced by fibrous tissue
– Most severe form with poorest prognosis

Bronchiectasis
• Pathophysiology
– Loss of ciliated epithelium and respiratory units
– Chronic inflammation
– Sloughing of mucosa with ulceration and possible abscess formation
– Reduced volume of distal lung and adjacent lung secondary to scarring
and bronchial obstruction
– Excessive production of sputum (greater than 1 cup/day)
– Sputum is foul-smelling and hemoptysis is common
– Hyperinflation of alveoli
– Atelectasis, consolidation and parenchymal fibrosis

Bronchiectasis
• Radiologic Findings
– Bronchograms have been largely replaced by thin slice CT
imagery
– May show multiple cysts
– May show cor pulmonale

Bronchiectasis
• PFT Findings
– FVC , FEV1 , FLOWS , VC , FRC , TLC
 Bronchiectasis is obstructive in nature when in a non acute
phase
 When in an acute phase, can be restrictive due to
bronchial filling and subsequent alveolar atelectasis and
collapse

Bronchiectasis – Clinical Findings
• Chronic loose cough exacerbated by change of position
• Recurrent infections
• Increased sputum production: tri-layer sputum
– Top layer – thin, frothy
– Middle layer – mucopurulent
– Bottom layer – opaque, mucopurulent or purulent with
mucus plugs, foul-smelling

Bronchiectasis – Clinical Findings
• Halitosis (bad
breath)
• Hemoptysis
• Severe V/Q
abnormalities
• Clubbing
• BS- rhonchi,
crackles,
diminished

Bronchiolitis
Sick with Bronchiolitis

Bronchiolitis
• Also called pneumonitis
• Caused primarily by the respiratory syncytial virus
(RSV)
• RSV is the most common viral respiratory pathogen
seen in infancy and early childhood but can be acquired
at any age
• Outbreaks are usually seasonal in fall and winter
• Most children under 6 months of age require
hospitalization.
• Spread by aerosol/droplets from coughs and sneezes
• Bronchiolitis Boy
• Baby with Bronchiolitis and seconday complications

Old Treatment for RSV- Ribavirin
• Ribavirin (Virazole) is an anti-viral drug indicated for
severe RSV infection. Ribavirin is active against a
number of DNA and RNA viruses. It is a member of the
nucleoside antimetabolite drugs that interfere with
duplication of viral genetic material. Ribavirin is active
against influenzas, flaviviruses and agents of many viral
hemorrhagic fevers.
• Side effects:
– Teratogenic effects
– Anemia
RSV - what is it?
RSV preventions

Bronchiolitis
• Pathophysiology –
– Inflammation and swelling of the peripheral airways
– Excessive airway and nasal secretions
– Sloughing of necrotic airway epithelium
– Partial airway obstruction and alveolar hyperinflation
– Complete airway obstruction and atelectasis
– Consolidation

Bronchiolitis
• Diagnosis made by:
– Obtaining a nasal swab or
nasopharyngeal aspirate
– Immunofluorescense staining
– Results available within 2-6
hours
– X-ray results show streaky
peribronchial opacities
associated with air trapping,
hyperinflation, and lobar
pneumonic consolidation

Bronchiolitis
• Clinical Manifestations
– Excessive nasal, oral and bronchial secretions
– BS: wheezes, crackles, rhonchi, expiratory grunting
– Increased RR, HR, BP, CO
– Apnea
– Intercostal/Substernal retractions
– Cyanosis
– Nasal flaring

Percussive Vest Therapy
Vest Percussion Therapy

Pulmonary Infections
• Infections occur more frequently in the respiratory tract
than in any other organ, yet this might be anticipated
when one considers the heavy and constant
environmental exposure to which the lung is subjected
by breathing.
• Although most of these infections are in the upper
airways, various types of microbial agents also injure
the lung. In the upper airways, viral infections
predominate.

• Pneumonia is the commonest type of lung infection and
accounts for 8.5-10% of hospitalizations in the US, as well
as for 3% of deaths in the population .
• PNA is the 4th leading cause of death in the population over
75 yrs. of age, and is a common autopsy finding, often
representing the "immediate cause of death." 80% of AIDS
patients die of respiratory failure and over 60% of these
have a pulmonary infection . Pneumonia has a morphologic
spectrum which traditionally includes bronchopneumonia,
lobar pneumonia, and interstitial pneumonia. In addition,
there is a category of infectious granulomas, due primarily
to tuberculosis and a variety of fungi.
• A Patient's Story

Bacterial infections typically cause lobar or
bronchopneumonia both of which are characterized
histologically by neutrophilic intra-alveolar exudates. Viral
pneumonias generally manifest as interstitial inflammatory
processes, while fungal and mycrobacterial infections are
granulomatous. Other infectious lesions are an abscess
and empyema (infection of the pleura).
• Atypical pneumonia is a clinical term applied to patients
with an acute febrile respiratory presentation and patchy
interstitial infiltrates without alveolar exudates. The most
common agents are mycoplasma and legionella.
• Mycoplasma Pneumonia Rap

The lung is normally a sterile environment. Infection
results when there is alteration in normal host defense
mechanisms or diminution in the general immune status
of an individual, or when an immunocompetent
individual is exposed to a virulent organism which
overwhelms the host defenses

Entry of Microorganisms
Inhalation
• Most microbes can be inhaled but in most cases this exposure is without
untoward effects on the host. Infection by inhalation depends in some
instances on the virulence of the organism i.e. tuberculosis, and in other
situations on the dosage of exposure i.e. Histoplasma from bat droppings in
caves or the Hantavirus from rodent droppings. Bacteria & viruses are small
enough to reside on aerosolized droplets that can be inhaled. Mechanisms
which trap particles in the airways are more effective against dry materials
than against liquid droplets.
• The Hantavirus Diseases
• Hoarder's Hanta Virus
• Yosemite Hanta Virus Outbreak

Entry of Microorganisms
• Aspiration
• Aspiration, particularly at night, is a common event and
may include small amounts of the bacterial and fungal
flora which resides normally in our mouths. Nocturnal or
similar aspiration is not usually a problem as our normal
defense mechanisms can eliminate these small
dosages. Sometimes, however, these microbes lodge in
the upper airways and form larger colonies which when
aspirated result in infection.

• Pneumonia – Inflammatory process of the lung parenchyma, usually
infectious in origin
• 6th leading cause of death in the United States and the most common
cause of infection-related mortality
• Classifications of Pneumonia
– Community Acquired: Acute
• Typical: Streptococcus Pneumoniae, Hemophilus Influenzae,
Staphylococcus Aureus
• Atypical: Legionella Pneumophila, Chlamydophila
Pneumoniae, Mycoplasma Pneumoniae, Viruses

Streptococcus Pneumoniae
• Gram-positive, A significant human pathogenic
bacterium, S. pneumoniae was recognized as a major
cause of pneumonia in the late 19th century.
• The organism causes many types of pneumococcal
infections other than pneumonia. These invasive
pneumococcal diseases include acute sinusitis, otitis
media, meningitis, bacteremia, sepsis, osteomyelitis,
septic arthritis, endocarditis, peritonitis, pericarditis,
cellulitis, and brain abscess
• S. pneumoniae is one of the most common causes of
bacterial meningitis

Streptococcus Pneumoniae
• A vaccine against Streptococcus pneumoniae exists,
recommended for the elderly or those with chronic lung
disease.
• S. pneumoniae is part of the normal upper respiratory
tract flora, but, as with many natural flora, it can become
pathogenic under the right conditions (e.g., if the
immune system of the host is suppressed). Invasins,
such as pneumolysin, an antiphagocytic capsule,
various adhesins and immunogenic cell wall
components are all major virulence factors.

Hemophilus Influenzae
• Gram-negative, rod-shaped bacterium first described in
1892 during an influenza pandemic.
• it is generally aerobic, but can grow as a facultative
anaerobe
• H. influenzae was mistakenly considered to be the
cause of influenza until 1933, when the viral etiology of
the flu became apparent. Still, H. influenzae is
responsible for a wide range of clinical diseases;

Hemophilus Influenzae
• Most strains of H. influenzae are opportunistic
pathogens; that is, they usually live in their host without
causing disease, but cause problems only when other
factors (such as a viral infection, reduced immune
function or chronically inflamed tissues, e.g. from
allergies) create an opportunity.
• In infants and young children, H. influenzae type b (Hib)
causes bacteremia, pneumonia, and acute bacterial
meningitis AND Epiglotttis
• Due to routine use of the Hib conjugate vaccine the
incidence of invasive Hib disease has declined

• Gram-positive coccal bacterium. It is frequently found as part of the
normal skin flora on the skin and nasal passages.
• It is estimated that 20% of the human population are long-term
carriers of S. aureus. S. aureus is the most common species of
staphylococci to cause Staph infections. The reasons S. aureus is a
successful pathogen are a combination of bacterial immuno-evasive
strategies. One of these strategies is the production of carotenoid
pigment staphyloxanthin which is responsible for the characteristic
golden color of S. aureus colonies.
• This pigment acts as a virulence factor, primarily being a bacterial
antioxidant which helps the microbe evade the hosts immune system
in the form of reactive oxygen species which the host uses to kill
pathogens

• S. aureus can cause a range of illnesses from minor skin infections, such
as pimples, impetigo, boils (furuncles), cellulitis folliculitis, carbuncles,
scalded skin syndrome, and abscesses; to life-threatening diseases such
as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock
syndrome (TSS), bacteremia, and sepsis.
• It is still one of the five most common causes of nosocomial infections,
often causing postsurgical wound infections. Each year, some 500,000
patients in American hospitals contract a staphylococcal infection.
• Methicillin-resistant S. aureus, abbreviated MRSA and often pronounced
"mer-sa" is one of a number of greatly-feared strains of S. aureus which
have become resistant to most antibiotics.
• Map
• Pimple/Boil
• Meningitis - Meningoccal

• MRSA strains are most often found associated with
institutions such as hospitals, but are becoming
increasingly prevalent in community-acquired infections.
• The treatment of choice for S. aureus infection is
Penicillin; in most countries, though, Penicillin
resistance is extremely common, and first-line therapy is
most commonly a penicillinase-resistant β-lactam
antibiotic (for example, Oxacillin or Fucloxacillin).
Combination therapy with Gentamicin may be used to
treat serious infections, such as endocarditis, but its use
is controversial because of the high risk of damage to
the kidneys. The duration of treatment depends on the
site of infection and on severity.

Legionella Pneumophila
• Aerobic, non-spore forming, Gram-negative bacterium
• the primary human pathogenic bacterium in this group
and is the causative agent of Legionellosis or
Legionnaires' disease.
• In humans, L. pneumophila invades and replicates in
macrophages. The internalization of the bacteria can be
enhanced by the presence of antibody and complement,
but is not absolutely required. A pseudopod coils around
the bacterium in this unique form of phagocytosis
• Primary source of infection = water supply
• Azithromycin or Moxifloxacin are the standard treatment

Chlamydophila Pneumoniae
• C. pneumoniae is a common cause of pneumonia
around the world. C. pneumoniae is typically acquired
by otherwise healthy people and is a form of
community-acquired pneumonia. Because treatment
and diagnosis are different from historically recognized
causes such as Streptococcus pneumoniae, pneumonia
caused by C. pneumoniae is categorized as an "atypical
pneumonia.“
• This atypical bacterium commonly causes pharyngitis,
bronchitis and atypical pneumonia

Mycoplasma Pneumoniae
• the causative agent of human primary atypical
pneumonia (PAP) or "walking pneumonia.“
• Mycoplasma pneumoniae is a very small bacterium
• Antibiotics with activity against these organisms include
certain macrolides (Erythromycin, Azithromycin,
Clarithromycin), fluoroquinolones and their derivatives
(e.g., Ciprofloxacin, Levofloxacin), and Tetracyclines
(e.g., Doxycycline)

Viral Pneumonia
• Viral pneumonia is a pneumonia caused by a virus
• Viruses are one of the two major causes of pneumonia,
the other being bacteria; less common causes are fungi
and parasites. Viruses are the most common cause of
pneumonia in children, while in adults bacteria are a
more common cause.
• Symptoms of viral pneumonia include fever, non-productive
cough, runny nose, and systemic symptoms
(e.g. myalgia, headache). Different viruses cause
different symptoms.

Viral Pneumonia
• Common causes of viral pneumonia are:
• Influenza virus A and B
• Respiratory syncytial virus (RSV)
• Human parainfluenza viruses (in children)
• Rarer viruses that commonly result in pneumonia include:
• Adenoviruses (in military recruits)
• Metapneumovirus
• Severe acute respiratory syndrome virus (SARS, coronavirus)
• Viruses that primarily cause other diseases, but sometimes cause
pneumonia include:
• Herpes simplex virus (HSV), mainly in newborns
• Varicella-zoster virus (VZV) – chickenpox, shingles
• Measles virus
• Rubella virus
• Cytomegalovirus (CMV), mainly in people with immune system problems

Pneumonia
• Sixth leading cause of death in the U.S.
• 3 million suffer each year
• 40,000 die each year
• 5 million die each year worldwide
• Causes include
– Bacteria
– Viruses
– Fungi
– Tuberculosis
– Anaerobic organisms
– Aspiration
– Inhalation of irritating chemicals

Pneumonia
• Pneumonia or pneumonitis with consolidation is the
result of an inflammatory process that primarily affects
the gas exchange area of the lung.
• In response to the inflammation, blood serum and some
RBC’s from the adjacent capillaries pour into the alveoli
• Leukocytes move into the infected area to engulf and kill
the invading bacteria
• Increased numbers of macrophages appear to remove
cellular and bacterial debris
• If all this material fills the alveoli, they are said to be
“consolidated”

Pneumonia
• Pathologic and structural changes associated with
pneumonia are:
– Inflammation of the alveoli
– Alveolar consolidation
– Atelectasis
– Primarily obstructive in nature

Pneumonia– Etiology
• Inhalation of aerosolized infectious particles – aerosol
particles generated by coughing
• Aspiration of organisms colonizing the oropharynx
– Occurs in all individuals, especially during sleep
– Impairment of the gag reflex allows large volume aspiration
• Direct inoculation of organisms into the lower airway –
suction catheters, ET tubes

Pneumonia – Etiology
• Spread of infection to the lungs from adjacent structures
– Infrequent source of infection
– Liver abscesses
• Spread of infection to the lungs through the blood
– Hematogenous dissemination (septic spread)
– Right-sided bacterial endocarditis

Pneumonia – Etiology
• Reactivation of latent infection, usually resulting from
immunosuppression but may occur spontaneously
• There are four stages of progression in pneumonia:
– Inflammatory Stage
– Red hepatization stage
– Grey hepatization stage
– Resolution stage

Pneumonia
• Inflammatory Stage
– Inflammatory pulmonary edema
– Engorgement of the pulmonary capillaries
– Exudation of serous fluid
– This stage is localized to the areas of infection

Pneumonia
• Red Hepatization Stage
– Onset 24 to 48 Hours Post Infection
– Alveolar spaces filled with coagulated exudate
• Fibrin
• Red blood cells
• Polymorphonuclear leukocytes
• Bacteria
– Red liver-like appearance of lung tissue

Pneumonia
• Gray Hepatization Stage
– Occurs 4 to 5 days post infection
– Alveolar spaces filled with many polymorphonuclear
leukocytes and few red blood cells
– Yellow-gray appearance of lung tissue

Pneumonia
• Resolution Stage
– Healing stage
– Exudate liquefied by enzymes of leukocytes
– Phagocytes reabsorb the liquid
– Areas of atelectasis begin to re-inflate

Pneumonia
• Types of pneumonia
– Lobar pneumonia: affects a large and continuous area of the
lobe of a lung
– Bronchial pneumonia: the acute inflammation of the walls of
the bronchioles. It is a type of pneumonia characterized by
multiple foci of isolated, acute consolidation, affecting one or
more pulmonary lobules.

Pneumonia
• Classification of Pneumonia
– Community acquired: acute and chronic
• Acute: rapid onset of symptoms
• Chronic: slower onset with gradually escalating symptoms
– Health care associated pneumonia (HCAP) [previously known
as nosocomial infections]
• Defined as pneumonia occurring in any pt. hospitalized for
2 or more days in the past 90 days in an acute care setting
or who, in the past 30 days resided in a LTC or SNF

• Classifications of Pneumonia
– Ventilator associated pneumonia (VAP)
• A lower respiratory tract infection that develops more
than 48 – 72 hrs after endotracheal intubation.
• VAP Busters

Pneumonia
• Causative agents
– Gram positive organisms
– Gram negative organisms
– Atypical organisms
– Anaerobic bacterial infections
– Viral causes
– Other causes

Pneumonia
• Gram Positive Bacteria
– Streptococcus pneumoniae
• Accounts for 80% of all bacterial pneumonias
• Found singly, in pairs, and in short chains
• Transmitted by aerosol via cough or sneeze
• Generally an acute community acquired organism
• Sputum is usually yellow in color

Pneumonia
• Gram Positive Bacteria (cont)
– Clostridium difficile (C-diff)
• Anaerobic spore-forming organisms of drumstick or
spindle shape
• Hospital acquired in patients on antibiotic therapy
• Replaces normal flora causing severe gastric instability
and diarrhea mimicking flu and colitis
• Fast becoming antibiotic resistant
• Hands MUST be washed with soap and water before and
after entering patient room

Pneumonia
• Gram Positive Bacteria (cont)
– Staphylococcus aureus
• Responsible for “Staph infections” in humans
• Found singly, in pairs and in irregular clusters
• Transmitted by aerosol from a cough or sneeze and via
fomites
• Common cause of hospital acquired pneumonia and is
becoming extremely resistant to antibiotics thus the
abbreviation: MDRSA – multiple drug-resistant S. Aureus
• Sputum is usually yellow in color and foul smelling

Pneumonia
• Gram Negative Bacteria
– Rod shaped Bacilli
– Haemophilus influenzae
• Common pharyngeal organism
• Infections most often seen in children between 1 month to 6 yrs
of age
• Almost always the cause of acute epiglotitis
• Usually community acquired
• Transmitted via aerosol, contact, fomites
• Sensitive to cold and does not survive long
• Picmonic – Epiglotitis
• Clinical Symptoms - Stridor,Wheezing and Croup Cough
• Epiglotitis Explained and Illustrated

Pneumonia
• Gram Negative Bacteria (cont)
– Klebsiella pneumoniae
• Associated with lobar pneumonia
• Found singly, pairs and chains
• A normal inhabitant of the GI tract
• Transmitted by aerosol or fomites – especially the hands
of healthcare workers
• Usually a hospital acquired infection
• Mortality is high because septicemia is a frequent
complication

Pneumonia
– Pseudomonas aeruginosa
• Water loving organism
• Leading cause of hospital acquired pneumonia
• Normally colonizes in the GI tract
• Frequently found in burns, the respiratory tract of
intubated or trached respiratory patients, catheters,
respiratory therapy equipment
• Transmitted via aerosol or contact with fomites
• Sputum infected is usually sweet smelling and green

Pneumonia
– Escherichia coli or E.coli
• Normal GI inhabitant
• Usually hospital acquired pneumonia
– Moraxella catarrhalis
• Naturally inhabits the pharynx
• Third most common cause of acute exacerbation of
chronic bronchitis
• Usually hospital acquired

Pneumonia
– Serratia Species
• Very water loving species
• Usually hospital acquired
• Lives well on fomites, under sinks, rampant spread in
respiratory equipment
• Multi Drug Resistant Infections

Pneumonia
• Atypical Organisms
– Mycoplasma pneumoniae
• Common cause of mild pneumonia (walking pneumonia)
• Smaller than bacteria but larger than viruses
• Described as Primary Atypical Pneumonia because the
organism escapes ID by standard bacteriologic tests
• Most frequently seen in people younger than 40
• Spreads easily where people congregate
• Usually community acquired

Pneumonia
• Atypical Organisms (cont)
– Legionella pneumophila
• Discovered in 1976 during an outbreak of severe
pneumonia-like disease at an American Legion
convention
• Gram negative bacillus
• Transmitted via aerosol
• Thought to have colonized in the AC units of the
convention hall
• Community acquired

Pneumonia
• Viral Causes
– Influenza Virus
• Several subtypes in which A and B are the most common
causes of viral respiratory tract infections
• Commonly occur in epidemics
• Children, young adults and the elderly are most at risk
• Transmitted via aerosol
• Survives well in conditions of low moisture and humidity
• Found also in swine, horses and birds

Pneumonia
• Viral Causes (cont)
– Respiratory Syncytial Virus (RSV)
• Member of the paramyxovirus group along with
parainfluenza, mumps and rubella viruses
• Most often seen in children under the age of 6
• Transmitted via aerosol and direct contact
– Parainfluenza Virus
• Member of the paramyxovirus group
• Type 1 is considered a “croup” type virus seen in the young
• Type 2 and 3 present as a severe type of infection
• Transmitted via aerosol and direct contact

Pneumonia
– Adenoviruses
• More than 30 subgroups
• Transmitted by aerosol
• Generally seasonal outbreaks

Pneumonia
– Severe Acute Respiratory Syndrome (SARS)
• First reported in China in 2002
• Newly recognized Coronavirus
• Transmitted via droplet and aerosol and possibly
contaminated objects
• Incubation is 2-7 days
• 10-20% require mechanical ventilation

Pneumonia
• Other Causes
– Aspiration Pneumonitis
• Caused by aspiration of stomach contents
• Major cause of anaerobic lung infections
• May progress into ARDS
– Varicella (chickenpox)
– Rubella (Measles)
– Rickettsiae
• Intracellular parasites
• Most well known: Rocky Mountain Spotted Fever

Pneumonia
• Other Causes
– Yeast pneumonias occur, some of the pathogens include:
• Candida albicans,
• Cryptococcus neoformans
• Aspergillus
– Fungal Infections
• Most fungi are aerobes thus making lungs prime targets
• Fungal pathogens include:
– Histoplasma capsulatum
– Coccidioides immitis
– Blastomyces dermatitidis

Tuberculosis
Tuberculosis Today CDC - TB statistics

Tuberculosis
• TB is a chronic bacterial infection that primarily affects the lungs but can involve
almost any part of the body
• It is one of the oldest diseases known to man and remains one of the most
widespread diseases in the world. Chapter 1 - TB
• Called “consumption, Captain of the men of death and the White plague
• 10 – 15 million infected in the U.S.
• 17,000 new infections per year
• WHO estimates that between the years 2000 and 2020 35 million people
worldwide will die from TB
• Chapter 2 - TB

Tuberculosis
• Caused by the Mycobacterium
tuberculosis organism
• Transmission from person to
person by inhalation of
organisms suspended in
aerosolized drops of saliva,
respiratory secretions, or other
fluids

Tuberculosis
• Pathophysiology
– Highly aerobic organism
– Multiplies more rapidly in the presence of higher partial
pressures of oxygen, especially in lung apices
– Primary TB follows the patients first exposure to the organism
– Upon inhalation, the bacterium is implanted into the alveoli
and begin to multiply
– The initial inflammation causes an influx of macrophages and
leukocytes which engulf but do not kill the organism

Tuberculosis
• Pathophysiology
– This causes the pulmonary capillary bed to dilate, the
interstitium to fill with fluid, and the alveolar epithelium to
swell from the edema
– The alveoli become consolidated and at this point the TB
skin test becomes positive
– In approx. 2-10 weeks, the lung tissue surrounding the
infection slowly produces a protective cell wall around the
infection called a tubercle or granuloma

Tuberculosis
• Pathophysiology
– After the formation of the tubercle, the center of the mass
breaks down and fills with necrotic tissue. At this point the
tubercle is called a caseous lesion or caseous granuloma
– As the infection becomes controlled by the immune system
or medication, fibrosis and calcification of the lung
parenchyma replaces the tubercle.
– As a result of the fibrosis and calcification, the lung retracts,
becomes scarred, and can cause dilation of the bronchi and
bronchiectasis
– Chapter 3 - TB

Tuberculosis
• Post primary tuberculosis
– Also called secondary or reinfection TB
• A term used to describe the reactivation of TB months or
even years after the initial infection has been controlled
• Tubercle bacilli can remain dormant for decades
• At any time, TB can reactivate; especially in patients with
weakened immunity

Tuberculosis
• If the infection is uncontrolled, cavitation of the tubercle
develops
• In severe cases a deep tuberculous cavity may rupture and
allow air and infected material to flow into the pleural space
or the tracheobronchial tree
• Pneumothoracies and pleural disease are common
complications of TB

Tuberculosis
• Diagnostic Testing:
– CXR may show cavitation or nodule
– Intradermal (mantoux) skin testing which contains a purified
protein derivative (PPD) of the bacillus. An induration of
10mm is positive
– Acid-fast stain with sputum culture

Tuberculosis
• Radiologic findings
• Increased opacity
• Cavity formation
• Calcification & fibrosis
• Pleural effusions

Tuberculosis
• Clinical Findings
– Fatigue
– Fever
– Night sweats
– Weight loss
– Chronic cough
– Sputum production/hemoptiysis

Tuberculosis
• Clinical Findings
– Auscultation
• Crackles
• Wheezes
• Bronchial breath sounds

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