PART 2- OBSTRUCTIVE PULMONARY
DISEASES
ASTHMA
• Is one type of a obstructive airway disorder,
this is due to increase resistance to air flow,
so as we know the bronchial asthma is a
chronic inflammatory disorder that mark by
increase responsiveness of the airway to the
various stimuli which may manifest by
airway smooth muscle contraction,
hypersecretion of mucus and inflammation.
• So as we all know there is a bronchial
hypersensitivity mark by reversible airway
of bronchospasm caused by: increased
mucosal edema, there’s a wrong constriction
of the bronchial smooth muscles, increase
production of viscous mucus which
eventually may lead to increase mucus plugs,
bronchial airway obstruction and over
distention of the lungs
Types
a) Extrinsic (atopic) asthma- caused by external
agents such as dust, food (chocolate), pollens,
sports
• This is due to allergic reaction to specific
allergen
b) Intrinsic (idiopathic) asthma- we cannot
identify specific cause that triggered
asthmatic attack, but there are many
situations that precipitate asthmatic attack
such as upper respiratory tract infection,
patients may have common colds or exercise
Both of these extrinsic and intrinsic type of
asthma it can be trigger by changes in the
environmental temperature, strong odor,
stress, emotion, exercise. Especially for
intrinsic type, stimulation of PNS that may
cause the release of acetylcholine that may
result to bronchoconstriction whereas SNS is
stimulated it may cause the release of these
muscle that may result to
bronchoconstriction.
c) Mixed asthma- sometimes this is the
complications of the bronchial asthma,
they call it as the “Status Asthmaticus”
• This is a severe asthmatic attack
which does not respond to any
pharmacological treatment in a few
hours, so this is a life threatening
Causes of Asthma Attack
1. Allergens – dust mite, pollens
• Inhalation of these allergens
• usually occur in childhood or
adolescence or patients who have
family history
2. Respiratory tract infections- this is the
most common precipitating factors of an
acute asthmatic attack.
• The infection may cause
inflammatory changes in the
tracheobronchial system which may
alter the mucociliary mechanism.
3. Exercise-induced asthma (EIA) – due to
patients may develop asthma after several
minutes of vigorous exercise.
• Climbing stairs, walking gristly, so it
make characterize by bronchospasm
patients may have shortness of
breath, cough, and wheezing.
• As we know during exercise,
bronchospasm may be cause by the
loss of heat and water from the
tracheobronchial tree because of the
need for conditioning the large
volume of air, so it may be
exaggerated when exercise in a cold
environment.
• That’s why it is recommended to
those patients who have history of
asthma wearing a mask to prevent or
to minimize attack.
• Cromolyn Na, ß-adrenergic agonist is
given prior to exercise- in order to
maintain a bronchodilation during
exercise. This is usually engulfed 10
to 20 minutes before exercise
• Stretching prior to exercise may also
help the likelihood to develop
symptoms.

Nose and Sinus Problems- because of the
altered mucociliary mechanism
4. Inhaled irritants –fumes, epoxy
Because this irritants may induced
bronchospasm through vagal reflex
5. Drugs – asthma triad (nasal polyps, rhinitis,
asthma and sensitivity to aspirin and
NSAIDs)
• beta adrenergic blockers that may trigger
asthmatic attack, adrenergic stimulation
try to inhibit the bronchioles and prevent
bronchodilation, that’s why patients taking
beta adrenergic blockers the doctor have to
be very cautious in prescribing these
medications to have history of asthma
the muscles so the tendency it may activate the
muscle to release granules, these are the
chemical mediators that may cause bronchial
smooth muscle constriction. So it may cause
bronchospasm.
Patients may also increase in
mucosecretions because of the edema
formation and likewise it may also
increase amount of tenacious sputum
(sticky sputum)
Then the late phase that is the
inflammation, this usually peaks about
5-6 hours characterized by inflammation.
So these eosinophils, neutrophils that
may infiltrate the airway so the tendency
the lymphocytes
Pathophysiology

6. Chemicals or food additives – tartrazine

(Wherein it may provoke asthmatic attack)
7. Emotional factors and changes in hormone
levels- because of the cholinergic response that
may cause bronchoconstriction through vagal
pathway so it may trigger an increase airway
responsiveness to other factors through non
inflammatory mechanism
8. Gastroesophageal reflux- the reflux may act
as bronchospastic factors that may cause the
vagal stimulation reflex that may result to
bronchoconstriction.
Airway Response of Asthma
• Triggers are the extrinsic and intrinsic
• The whole mark of the asthma is the airway
factors, the responsiveness of the IgE
inflammation.
cells which may release chemical
S – Spasm of bronchial smooth muscle mediators from the muscles, then if there
• because of this granules that is released is a release of this chemical mediator it
from the muscle may cause increase in muscle
hypertrophy that may cause thickening
E – Edema
of the membrane and when the goblet
• because of vasodilation and increased
cells is being stimulated that may cause
permeability that may cause edema
hypersecretions of the mucus.
formation
• There’s an increase in vasodilation
A – Accumulation of tenacious secretions permeability that may cause mucosal
• because of the hyperactive of the goblet inflammation not only that it may also
cells that may cause increase secretions of secrete excess mucus that may cause a
the mucus plugging that will decrease the diameter
of the airway that may increase the
So during the early stage as we know that the
airway resistance. And because of the
muscles found beneath the basement membrane
chemical mediators it has an effect on the
of the bronchial wall, if there’s an allergen it may
bronchus that may cause
attach to the immunoglobulin E receptors and
bronchoconstriction or bronchospasm.
 • If there’s an increase in airway resistance 4. Non-productive coughing
there’s a hyperinflation of the alveoli 5. Hypoxemia
wherein the air is being trap in the 6. Restlessness
alveoli so the patient may have increase 7. Tachycardia
work of breathing and at the same time 8. Increased PR and BP
alter in the respiratory muscle function.
• If there’s an increase mucus patients may
have cough and the secretions would be a
white gelatinous and sticky secretions.
• Increase work of breathing- patients may also
have dyspnea because of decrease in airway
diameter so that’s why have asthma have the
expiratory wheezes, prolonged expiration
because the air is being trapped in the alveoli

• During respiration you will observe nasal

flaring and retractions of the intercostal
space during physical examination if it is
severe.
• Productive cough with thick gelatinous
sputum
• Shortness of breath because of
inflammatory process occur in the
tracheobronchial tree
• Expiratory wheezes because the air is
trapped in the alveoli so there will be
• Because of the PNS response that may carbon dioxide retention
stimulate the sensory nerve ending that may
• Patients may have prolonged expiration-
result to the release of acetylcholine which
prone to develop respiratory acidosis if no
may cause bronchoconstriction and
medication or treatment done
production of chemical mediator that may
immediately.
result to bronchoconstriction.
• Hypoxia that may result to increase HR
• Whereas in SNS response due to stimulation
and RR patient may also be restless
of the alpha adrenergic receptors that may
cause the release of chemical mediators by Diagnostic Studies
the muscles that may also result to
1. Pulmonary function test
bronchoconstriction and may manifest
• especially during the initial visit to
dyspnea, cough and wheezes.
their physician
• And there’s a bronchial wall responsiveness
• ↓ Peak Expiratory Flow Rate, ↓ Force
because of the increase of vasodilation with
Expiratory V volume (because of the
mucosal edema that may result to
air that is being trapped in the alveoli)
permeability and increase secretions and
• ↑Functional Residual Capacity,
smooth muscle contractions
↑Residual Volume (because there’s a
Clinical Manifestation problem in the outflow of air)

1. Chest constriction 2. Arterial Blood Gases (ABGs)

2. Wheezes • can be done to patients because of the
3. Thick, tenacious, white gelatinous retention especially you can see this in
mucus severe asthma or status asthmaticus
 wherein patients retention of partial2. Pulsus Paradoxus – dropping of systolic
arterial carbon dioxide so patients pressure
may have respiratory acidosis • Normally during inspiration the systolic
• mild stage you expect slightly blood pressure may decrease <10mmHg
elevation of PaO2 and the pulse rate goes up slightly
• If the patients develop acidosis there because of the intrathoracic pressure
is significantly increase in the PCO2 become more negative
• But in pulsus Paradoxus, there’s a fall on
arterial BP of >10mmHg during
3. CXR- in order for us to refill hyperinflation inspiration

4. Radioallergosorbent test (RAST) - in order to3. Acute Cor Pulmonale – hypertrophy of the
identify the cause of allergy, through this we right side of the heart
can could identify IgE antibodies. • With or without heart failure resulting
from pulmonary hypertension.
5. CBC- to check for eosinophil
• If there’s a chronic alveolar hypoxia
6. C & S of sputum- to check for any bacterial
then it may cause muscle hypertrophy
infection
it may stimulate erythropoiesis that
7. ECG – for patients with status asthmaticus, if may cause polycythemia and increase
there’s a complication on the heart in viscosity of the blood

Complications 4. Pneumothorax- because of the rapid

accumulation of air in the pleural space
1. Status asthmaticus – it is a severe life
that may cause an increase an
threatening complication of asthma
intrapleural space that may cause
• It is common that the patient may
tension on the heart and great vessels
experience respiratory arrest as status
asthamaticus is not responsive to Management
medication so it may result severe
1. Maintain patent airway to relieve
bronchospasm, inflammation and mucus
bronchospasm and we want to clear the
plugging and there’s a force exhalation
excess secretions
that may result to increase thoracic
• Bronchodilator
pressure that may transmitted in the
• ß-adrenergic agonist drugs- which
great vessels, the heart, may also cause
may produce bronchodilation and
pulmonary hypertension, sinus
increase mucociliary clearance
tachycardia, ventricular arrhythmias
(albuterol, salbutamol)
and all of these conditions is related to
• sometimes magnesium sulfate may
hypoxemia
also be given to act as bronchodilator
• Signs and symptoms would be: extreme
• methylxanthines- through IV like
anxiety or sweating or diaphoresis,
aminophylline but aminophyllines is
wheezing, tachycardia, chest tightness,
not being given through oral but this
dry cough as we know because there is a
is given through parenteral by
reduction in the diameter of the airway
incorporating this in a IV fluids.
because if the inflammation and the air
is being trapped inside even the
• Antihistamine – diphenhydramine- this
tenacious secretion or mucus is being
is the common wherein it try to compete
trapped in the alveoli.
with the histamine in the receptor
• The patient may also manifest extreme
orthopnea and obviously there is an • Anti-inflammatory- Anti- inflammatory
increase work of breathing that may agent it works energetically with beta
develop adrenergic agonist to decrease mucus
secretion like Solu Cortef that is being
administered parenterally
 • Corticosteroids- in order to relieve • Low CHO- because the metabolism of
inflammation and edema. It block the carbohydrate it may yield more carbon
late phase response. dioxide
Betamethasone, prednisone, • Avoid gas-forming foods or carbonated
• Cromolyn (mast cell stabilizers) this drinks- it may limit the movement of
is given before or its not use during diaphragm it may hamper abdominal
acute attack, this is to prevent the breathing
release of histamine. • Very hot or cold foods- which may
• Leukotriene (Singulair) Montelukast induce cough spasm
- block the action of leukotriene, one
of the chemical mediator. This is
Effective Ways of Using MDI or DPI
given before exercise, do not inhibit
late phase it means it is only effective Tilt head back slightly and breathe out. DO
prior to the release of muscle, prior to NOT breathe into your inhaler
inflammation Close your lips lightly around the
• Anticholinergic – inhibits mouthpiece of the inhaler
bronchoconstriction Breathe in deeply and quickly
• It blocks the acetylcholine in order to Hold your breath for 10 seconds
have effect on the bronchus to cause Do not put the inhaler directly to the
bronchodilation (Atrovent, Combivent) mouth it should be held 2 fingers width
1
or about 12 inches then after that then
2. Maintain supplemental gas exchange – O2 gargle
supplement
• For severe like status asthamaticus they Metered-dose inhaler (MDI)
are hook to mechanical ventilation
through endotracheal intubation to
improve gas exchange
3. Sodium Bicarbonate – treat respiratory
acidosis
4. Nebulization – decrease airway resistance
5. Preventing complications – acute respiratory Dry Powder Inhaler
failure and status asthmaticus (may cause
respiratory arrest)
6. Alleviate anxiety- the patients may become
restless during asthmatic attack
Patient Teaching
1. Adaptive breathing techniques- to decrease
the work of breathing and facilitate
exhalation of carbon dioxide Etiology of COPD
2. Relaxation technique- to reduce their panic
Chronic airway limitation or chronic
and anxiety
obstructive lung disease- there’s a presence
3. Proper positioning- to facilitate breathing
of airway obstruction
4. Increase fluid intake- in order to liquefy the
tenacious secretion 1. Cigarette smoking – it may cause
5. CPT- after nebulization to facilitate loosening hyperplasia of the goblet cells that may
and bubbling of the secretions result to increase production of mucus
6. Diet • If there’s a production or a lot of
• High protein- to support immune system secretion in the bronchial area there
will be a reduction in airway diameter
 so patients may have difficulty inflating
the secretions
• Benzopyrene- it may damage the
ciliary it more dangerous than other
component in the cigarette it may
cause abnormal dilation of the distal
air space
2. Infection – it may impair normal defense
mechanism so the retained secretion may
be a medium for their proliferation
recurrent RTI
3. Heredity – alpha-1-antitrypsin deficiency-
premature emphysema that is seen in
patient with emphysema. It may cause the
lysis of the lung tissue from neutrophils
and macrophage may inhibit the action of
this enzyme.
• more common in emphysema because
it is a genetic abnormality that may
lead to COPD

Aging – changes in the lung structure, as

person age there’s a gradual loss of elastic
recall of the lungs so the number of
functional alveoli is also reduced as a result Chronic Bronchitis
of loss of alveolar supporting structure
• Thoracic cage- as the patient age it
becomes thick and rigid and the ribs are
less mobile. So the shape of the ribs is
gradually increased or
• changed may also increase the functional
residual capacity therefore, there’s a
reduction in the compliance of the chest
wall with the work of breathing
• Acute bronchitis- inflammation of the
Types of Obstructive Airway Disease bronchial area so acute is self- limiting ,
just have adequate intake of fluids , bed
1. Chronic bronchitis – affect the small
rest, anti- inflammatory agents, cough
airways; also known as the “blue bloater”
suppressant or bronchodilators as per
• Usually this is secondary to severe
doctor’s order
hypoxemia because of the excess
• Chronic bronchitis- may obstruct the
production of mucus in the bronchi and
small airway that may cause a severe
persistent coughing so there’s some
hypoxia that why they call it as the “blue
changes or hyperplasia of the leuko
bloaters”
secreting gland that is your goblet and
• There’s a mismatching of ventilation
there’s a reduction in ciliary activity
and perfusion
2. Emphysema – permanent over distention of • Normal bronchus: the diameter is wide,
the air spaces; also known as “pink puffers” there’s no problem with the inflow and
• The elasticity of the alveoli it loss their outflow of air
function so it cannot recall anymore, so • With bronchitis: there’s an
remain dilated inflammatory process occur in the
bronchial area and there’s a plugging of
 mucus because the cilia is also damaged 8. Feeling of epigastric fullness
so it may affect the small airway 9. Distended neck vein
10. Ankle edema
Pathologic Changes in Chronic Bronchitis
11. Clubbing fingers
1. Hyperplasia of mucous-secreting in the 12. Pulmonary HPN
trachea and bronchi
Diagnostic- taking the history of the patient so
2. Increase goblet cells
we’ll identify the different factors and do the
3. Disappearance of cilia- because of the
physical examination through the IPPA
damage
technique
4. Chronic inflammatory changes and
Chest x-ray- usually done to patient with
narrowing of small airways
respiratory problem
5. Altered function of Alveolar
Blood test

Treatment of Chronic Bronchitis

1. STOP smoking- the only way is to stop
smoking, the only measure if the reason is
due to smoking
2. Immunization- vaccinations become effective
after 10-14 days after administration.
• You can encourage patients especially to
those elderly
3. Wearing a cold-weather mask- to decrease or
relieve spasm
macrophage it may lead to bronchial
4. Antibiotics- because of the excessive mucus
infection
accumulation in the lungs then to prevent
• Accumulation of secretion- not only
infection.
because there is a small airway but it
• If the patients have bacterial infection
affects the cilia with increase production of
already
mucus.
• Coughing- one of the defense mechanism 5. Diet - Small frequent feeding- to reduce
• CO2 retention- that is why patient is at the work of breathing, less effort of
risk to develop acidosis breathing
• Bronchial infection- because of the • ↓ CHO- it may yield to more carbon
proliferation of this bacteria in the dioxide
secretions 6. Medications
• anticholinergic- may produce
Clinical Manifestations of Chronic Bronchitis
bronchodilation by blocking the PNS
1. Shortness of breath with progressive • theophylline- improve respiratory
decrease in exercise tolerance function and increase mucociliary
2. Labored breathing even at rest clearance
3. Hypoxemia- reduction in oxygen level in the 7. O2 therapy- may have difficulty of
blood which may also stimulate the breathing, hypoxia (to supplement oxygen)
production of RBC that may result to 8. Surgery – if there’s a distended areas of
polycythemia (there’s an increase in blood the lungs- lung volume reduction surgery
viscosity) (LVRS), Lung transplantation
4. Expiratory wheezes and crackles
5. Hypercapnia
Complications of Chronic Bronchitis
6. Right-sided heart failure with peripheral
edema- because of cor pulmonale 1. Cor Pulmonale – hypertrophy of right side
7. Productive cough in the morning of the heart resulting from pulmonary
 HPN because of the pressure on the proteases have the ability to breakdown the
pulmonary vasculature elastase and lung tissue
• Management: oxygen therapy, diet,
3. Respiratory tract infections- decrease level of
reduce from intake of sodium,
anti-alpha 1 antitrypsin level
diuretics
2. Acute Exacerbation of Chronic Bronchitis 4. Inhaled irritants
- colonized with strepto pneumonia and
5. Aging
H. Influenza
• Which are non- pathogenic in this 6. Allergic factors
patients
4,5,6- will be contributing to the
• Signs and symptoms: Cough may
development of emphysema
worsen, presence of hemoptysis.,
wheezes, SOB, viscosity of mucus
become thick Pathogenesis of Emphysema
• Management: Antibiotic, increase of
1. Inflammation
bronchodilator agents, corticosteroid,
humidification, postural drainage 2. Fibrosis of bronchial wall
3. Acute Respiratory Failure
3. Hypertrophy of the submucosal
4. Peptic Ulcer and GERD- side effect from
glandsHypersecretion of mucus
the long term use of bronchodilators and
corticosteroid 4. Loss of elasticity of the lung fibers and
5. Pneumonia- very common alveolar tissue
Emphysema L – loss of elastic recoil (remain distended)
• enlargement of air spaces andA – air trapping
destruction of lung tissue
T – thoracic overdistention (barrel chest
• there is an abnormal permanent
appearance)
enlargement of the airspace in the
thermal bronchioles and alveoli S – sputum over production (↑ introduction of
• destruction of the lung tissue it may mucus)
cause increase in lung compliance,
Types of Emphysema
decrease in the diffusing capacity and
even increase in the airway size during 1. Centrilobular – changes in the upper parts of
inspiration and it may cause collapse of the lungs
the airway during exhalation • Dominantly it affects the male smoker
• there will be a reduction in the lung • It affects the bronchioles in the central
function part of the respiratory lobules with
initial preservations of the alveolar duct
and sac
2. 2. Panlobular – lower parts of the lungs
• It’s not only respiratory bronchioles is
affected but, alveolar duct and sac are
affected
• Common in patients with alpha 1 anti-
trypsin deficiency and also found in
smoker
Etiology of Emphysema
1. Smoking- caused by lung decrease
2. Inherited deficiency of α 1-antitrypsin- which
protect against proteases, and these
 dioxide because the patient may seem to be
adequate of oxygen that’s why they call it as
the pink puffer a type of disorder unlike in
bronchitis because of hypoxemia.
• Eventually because of the air that is being
trapped in the alveolar or distal area or air
spaces and cannot recoil there’s a coalesce so
there’s a united of these alveoli which may
form bleb wherein as you know the alveoli
there’s a form of proper distribution of air in
the different alveoli so there’s a decrease in
oxygen diffusion and bleb will be form
(cough) small fluids or air that may filled in
the lungs
• Due to coalesce there’s a decrease in the
proper gas distribution so in the late stage
Pathophysiology
the patient may have hypoxemia
• Decrease in oxygen diffusion there will be a
retention, the distal air spaces become
permanently open so enlargement and
destruction of this alveoli and they cannot
recoil so there’s a difficulty in the removal of
oxygen then patients may have hypercapnia,
retention of these carbon dioxide may lead
patients to respiratory acidosis
• And decrease in oxygen diffusion expect that
the patient may develop an increase work in
breathing result to fatigue
• RR may also increase due to hypercapnia

• Because of irritants it may lead to increase

production of neutrophil and macrophage
and this will release proteolytic enzyme
that will destroy the alveolar tissue so
causing derangement of elastase due to
decrease of level of alpha 1 anti-trypsin .
So the elastin, collagen will destroy the
lungs then it will cause enlargement or
destruction of the alveoli.
• So once there’s a destruction the air will • There’s an hyperinflation of the alveoli
become trapped then it will cause impaired and destruction of the alveolar wall
in the gas exchange, because of the inability • Narrow airway, loss of lung elasticity
to recoil the air will be trapped. • Easy fatigue- increase work of breathing
• Due to the destruction of alveoli there will be • Frequent respiratory infection- because
some changes in the chest of the patient, of accumulation of secretions in the distal
usually may appear barrel chest. area
• Due to air trap there will be hyperinflation • Use of accessory muscle to facilitate
and over distention so there is too much of breathing- patients may have an
oxygen that enters the lungs that they have orthopneic in order to breath easily,
inability or they cannot remove the carbon sometimes the patient may have tripod
 position to ease breathing, they may also4.
have pursed lip breathing, in order to
exhale the air out of the lungs
• Barrel chest and digital clubbing- one of
the characteristic in patients with
emphysema
Lip Pursing
Diagnostic Studies for Emphysema
1. ABG – elevated pCO2; decreased pO2
• To check for any respiratory acidosis,
if there’s a changes in the pH of the
patient and partial arterial oxygen
and carbon dioxide
2. Serum electrolyte – potassium depletion • Bronchodilator
(Due to diuretic administration)
3. Pulmonary function test - ↓ FEV, ↓ FVC,
↑ TLC , ↑ RV (due to decrease in the
elastic recoil)
4. CXR – flattened diaphragm and increase
in the anterior posterior diameter and
the intercostal space become widen and
bulla is present
Collaborative Management of Emphysema
1. Avoid causative factors- like cigarette have this deficiency
smoking, alcohol intake, environmental
pollutants this inhibits mucociliary function
2. Bedrest- in order to reduce the oxygen demand
of the tissue
3. Increase oral fluid intake- in order to liquefy
the secretions
Oral care- hygiene, in order to improve the
well-being of the patient and prevent infection
because of the too much secretions that is
being expectorate by coughing it may reduce
the bacterial infection
5. Diet – high calorie, high protein, low CHO
(carbon dioxide may be yield in the products of
carbohydrates which may result to carbon
dioxide accumulation)
6. O2 therapy
7. Intubation and Mechanical ventilation- if the
patient have a problem to give supplemental
oxygen or the patient cannot maintain partial
arterial oxygen above 40mmHg
8. CPT and nebulization- aerosol inhalation-
bronchial hygiene measures
9. Medications
• Expectorants (Guaifenesin)
• Mucolytic
• Antitussive (methorphan)- observe for
drowsiness, avoid activities that involve
mental alertness (driving, operating
electrical machine) , it may cause
constipation (increase fiber intake of the
patients
(aminophylline,
salbutamol, terbutaline, prexanil) to treat
bronchospasm
• Metaproterenol- observe for tachycardia
• Anti histamine- but observe for
drowsiness
• Steroids- anti-inflammatory affect
• Anti microbial- to treat bacterial infection
10. Intravenous augmentation therapy – therapy
for those who have deficiency of alpha 1 anti-
trypsin protein, by administering or obtaining
a blood plasma of alpha 1 anti-trypsin protein
of a healthy human donor to increase the
alpha 1 level circulating blood in patients who
• Goal of this is to increase the level of
alpha 1 in the lungs to protect the lungs
from destructive effect of the neutrophil
and elastase ad which these enzyme are
released from our body by WBC as its
response to inflammatory or infection
• Primary goal: limit or slow down the
progression of the lung destructive by
replacing the deficient protein
11. Surgery • avoid smoke (may trigger cough which
• Bullectomy- involve the removal of may affect mucociliary activity and
large emphysematous bulla that mechanism) avoid abrupt changes in
compress the adjacent lung tissue that temperature
causes dyspnea
c. Avoidance of inhaled irritants- stay
• Lung volume reduction surgery
indoor if the pollutions are high or use air
(LVRS)- reducing the size of hyper
conditions with high efficiency particulate
inflated emphysematous lung and
air filter to remover particles from the air
decrease airways obstruction,
• Lung transplant- to improve functional4. Avoidance and diet
capacity • high calories diet- may provide high source
of energy
Nursing Interventions for Emphysema
• high protein to help maintain integrity of
1. Improve ventilation- place the patient in
your alveolar wall low
semi high fowler’s position or sometimes
• Carbohydrate- to limit carbon dioxide
in a tripod position
production
• Encourage the use of diaphragmatic
muscles breath or even you need to
encourage productive coughing after
every treatment by splinting the
abdomen to help reduce more expulsive
cough
• Purse lips breathing technique- slow
relax expiration against pursed lips as
this may increase the resistant to
outflow of air
• Oxygen therapy as order- do not give
high concentration of oxygen so about 1-
3L/min but the safest is placing the
oxygen at least 2L/min
2. Facilitate removal of secretions- through
increase of oral fluid intake of the patient
in order to liquefy the mucus or may RESTRICTIVE
do RESPIRATORY DISORDERS
CPT, Coughing and deep breathing and
Restrictive-decrease in the compliance of the
even the use of nebulizer, postural
lungs or chest wall
drainage, suctioning
• Provide oral hygiene after expectorating Pneumonia
of sputum to prevent infection or
bacterial infection • An inflammatory of lung parenchyma in
which consolidation of the affected part and
3. Patient teaching a filling of the alveolar air spaces with
a. Prevention of recurrent infections- exudate, inflammatory cells, and fibrin
avoid over crowd areas, avoid individual usually associated with a marked increase in
with known infection, receive interstitial alveolar fluid.
immunization from influenza and • Pneumonitis – a non-infectious bronchial and
pneumonia and report for worsening of alveolar inflammation.
symptoms
b. Control environment- use of cold Predisposing factors: Smoking, COPD
humidifier (30-50% of humidity) wear Deficiency in immune system, the use of
scarf over nose and mouth during cold alcohol or old age
weather to prevent bronchospasm Routes of Bacteria Reach the Lung
 • The bacteria associated with pneumonia decrease in compliance in the vital capacity
like and may cause hypoxia.
Gram positive and streptococcal • Invasion of respiratory system- loss of cough
pneumonia that is the most common reflex or damage of the ciliated endothelium
type of bacterial pneumonia or that line the respiratory tract or impaired
staphylococcus aureus. immune defenses that may predispose to
Gram negative- haemophilus colonization or infection of lower respiratory
influenza, pseudomonas aeruginosa, tract, may cause activation of the immune
klebsiella pneumonia response and may develop cough and because
virus: influenza or parainfluenza of the production of mucus, the immune
Opportunistic organism: amoebiasis or response become ineffective may cause
even pneumocytsis carinii pneumonia infection with may invade the lung
(seen in patients with AIDS) parenchyma
1. Inhalation- one route for the bacteria to • Hypoxemia- due to inflammation
reach the lungs because of the ambient air
2. Aspiration- which is previously colonized
in the upper airway
• Usually seen in patients with altered
consciousness, depressed cough and
epiglottis reflex which allow
aspiration or may result to aspiration
3. Direct spread from contagious infected
sites- hematogenous spread
4. Critical ill patient – may require organism
to colonize ET, NGT
• 90% of the cases of pneumonia is due to bacterial
• Patients with NGT or ET, It may
pneumonia this is result from the inflammation
interfere with the normal cough
or exudations of fluid in the air space of the
reflex and mucociliary escalator
alveoli.
mechanism which may pass air
✓ Streptococcus pneumonia- usually seen in
pressure and humidification in the
infant, elderly or patients who have CAD,
upper airway
alcoholism, sickle cell disease or diabetes.
✓ May occur as a result of decrease bacterial
Pathophysiology
ability of the alveolar macrophage because of
the extreme virulence of the bacteria or even
the susceptibility of the host against
infection
• Viral- it may produce patchy inflammatory
changes that are confined in the alveolar septum
and interstitium of the lungs. There are less
striking symptoms and physical finding than
bacterial.
Cardinal Signs of Pneumonia
1. Cough
2. Sputum production
3. Pleuritic chest pain
4. Shaking chills
• Common features of all type of pneumonia is5. Fever- bacterial (90%) of that may have
an inflammatory pulmonary response to any bacterial fever
organism, may lead to lungs to be stiff,
 Diagnostic Assessment
1. CBC and WBC- increase number of WBC
2. Erythrocytes sedimentation rate (ESR)
3. CXR- any diffuse patches in the lungs or
consolidated in the lobe
4. ABG analysis- to assess for the need of oxygen
5. Sputum studies – gram stain and culture
• to identify the organism. To know if
staphylococcal, streptococcal or klebsiella.
Phases Occur in the Alveoli
6. CT scan-
1. Engorgement / Congestion / Hyperemia7. Blood culture- to assess systemic spread,
(1st 4 – 12 hours)- due to the engorgement leukocytosis for bacterial infection
of the alveolar space with fluid and
Management
hemorrhagic exudate. It is a rich medium
corporation and rapid spread of organism 1. Antibiotic therapy
through the lobe. • Macrolide (zithromax, azithromycin) - if
• The alveoli is edematous, presence of they are allergic to macrolides doctor may
serous fluid, infection may spread the prescribe doxycycline in the form of
entire lungs Vibramycin.
• Streptomycin may be prescribed but avoid
2. Red hepatization (next 48 hours)-
using these antibiotics because for
hepatization )because the lungs appear
featuring minor viral infection because it
liver like) there’s a dilation of the
may result to upper airway colonization
capillaries and the alveolar is filled with
with antibiotic resistant bacteria
organism, neutrophils, RBC and fibrin
• monotherapy to those not know resistant:
3. Gray hepatization (3 - 8 days)- decrease Ceftriaxone, Sulbactam, Levofloxacin
in blood flow, leukocytes, fibrins • Multi drug resistant: Septacidin,
consolidate in the affected part of the Vancomycin, piperacillin or Tazobactam
lungs. 2. Measure to alleviate symptoms-
4. Resolution (7 – 11 days)- wherein the • humidification,
exudate is light and reabsorbed by • prescribe antipyretics (fever)
macrophage so restoring the tissue to its • Prescribe analgesic (myalgia)
original structure • mucolytic or expectorant (productive
cough),
Healing occur when there is no • bronchodilator (difficulty of breathing due
complication to bronchospasm)
2nd and 3rd Phase of Pneumonia 3. Client Education- coughing and deep breathing
and increase oral fluid intake
4. Oxygenation- via nasal cannula
Different Types of Pneumonia
1. Community Acquired Pneumonia- “CAP” even
if it is viral or bacterial
 • The patient may develop infection within there’s an abnormal collection of fluid in
48 hours after admission to the hospital the pleural space resulting from excess
• Organisms: streptococcal, pneumococcal fluid production or decreased absorption
or both
2. Hospital Acquired Pneumonia- “Nosocomial
• Usually secondary to other diseases
Pneumonia”
• Pleural effusion may be a complication of
• as the lower respiratory tract infection
heart failure, TB, pneumonia, pulmonary
that was not present or intubating so the
infections (particularly viral infections),
infection occur after 48hours upon
nephrotic syndrome, connective tissue
admission
disease, pulmonary embolus, and
• The usual organism present in hospital:
neoplastic tumors
pseudomonas, Enterobacter species,
Klebsiella, E. coli. They are different
from those responsible for community
acquired pneumonia
• The risk are those who are hook to
mechanical ventilator or patient who
have chronic lung disease or airway
instrumentation (ET, Tracheostomy)
3. Aspiration Pneumonia
• Occur as a result of aspirated gastric
content
• In patient with altered state of
consciousness due to seizure, alcohol or
anesthesia
There’s an accumulation of fluid in the base of the
• It may occur when the anatomy is
lungs
altered by esophageal stricture or
patient who have tracheostomy or NGTMechanism of Pleural Effusion
• Usually in this type of pneumonia it’s a
1. Increase capillary pressure- increase in the
poor prognosis even with antibiotic
hydrostatic pressure that can see in patients
therapy it may cause extensive lung
with lung cancer, Heart failure due to blockage
damage resulting in lung abscess or
of the lymphatic drainage system and change
emphysema
in osmotic pressure
• May also lead to exudation or severe
2. Increase permeability- occur in patients with
case of acute respiratory distress
inflammatory conditions or neoplastic effusion
syndrome
3. Increase negative intrapleural pressure
4. Legionnaires Disease 4. Decrease colloidal osmotic pressure- patients
• A form of bronchopneumonia, the may have a decrease in alkaline content. May
causative agent is legionella agent occur in patients with liver diseases
which is frequently found in water5. Impaired lymphatic drainage- result to have
particularly, warm standing water obstruction process such as mediastinal
• 2-10 days after infection carcinoma
• Immunization may protect the patient
Classification of Pleural Effusion
about5 years
Pleural Effusion
• Pleurisy or pleuritis- due to
inflammation of visceral and parietal
pleura
• The pleural fluid is about less than 10-
20ml that separates the two layers so
• Transudate- due to non- inflammatory 2. Dyspnea- common
conditions that there’s an imbalance of • when the fluid compresses the lungs
hydrostatic pressure and oncotic pressure. That may result decrease in ventilation
means there’s an elevation of hydrostatic
3. Decrease breath sounds, dull, flat sound
pressure and reduction on oncotic pressure.
upon percussion, decreased fremitus
✓ There’s a disturbance in the flow of protein in
the pleural space 4. Tachycardia
5. Cough
• Exudate- result from the disease of the pleural
6. Fatigue
surface or any obstruction of the lymphatic
system this prevent the drainage of protein so 7. Tracheal deviation from affected side-
because of this accumulation of fluid and cells pressure try to pull the trachea on the
in the area of inflammation that increase affected side
capillary permeability that is a characteristic of
inflammatory condition (Cancer) Diagnostic Evaluation &Treatment
1. CXR- determine the side to recheck the structure
of lungs
2. CT scan
3. Physical exam - IPPA
4. Thoracentesis- aspirate the fluid to categorize if
it is a transudate or exudate
5. Pleural biopsy- to get sample of this specimen
especially to patients with bronchogenic CA
6. Pleurodesis- there’s an instillation of sclerosing
agent (tetracycline, bleomycin, talc) into the
pleural space.
• This is to remove the pleural space by forming
Pathophysiology adhesions between the visceral and parietal
pleura
• Done in bed side, assist the doctor and
reposition the patient every 15 mins for equal
distribution of the agent
• This is a palliative method use for the
treatment of pleural effusion caused by
malignancy
7. Open surgical drainage
8. VATS – video assisted thoracotomy surgery
9. Tube drainage or water seal drainage

• Percussion- dullness due to accumulated Nursing Intervention

fluid
1.Consent for thoracentesis
• Auscultate- diminished or decrease on
breath sounds Check if the px needs to undergo
• Pleural pain- Friction between the visceral surgery,throracentesis, or even
and parietal space pleurodesys and then

Clinical Manifestations 2.Positioning –place in high fowler’s

position to promote ventilation and
1. Sharp pleuritic pain-abrupt, unilateral optimize diaphgramatic contraction.
and usually localize in the lower lateral
part of the chest. 3.Emotional support- to know the
• May become worsen during movement causative factor
of the chest during deep breathing or 4.Coughing and deep breathing exercises-
coughing due to the changes in to promote lung expansion and to avoid
pressure lung atelectasis
5.Splint chest-to reduce pain during
coughing
6.O2 therapy- given as ordered to improve
gas exchange and to reduce the work of
breathing
7.Incentive spirometry- teach the px about
incentive spirometry
8.Antibiotic therapy- if it is brought by
infection
Pneumothorax
Presence of air in the pleural space.
As the air enters the pleural space from an
opening to the chest wall or the lung itself
Types of Pneumothorax
1.Closed – no external wound,
spontaneous pneumothorax
a) perforation of the esophagus
b) injury from broken ribs
c) ruptured blebs or bullae
In the image there is shifting of the
mediastinum, as the air enters the
chestwall it pushes the mediastinum
towards the unaffected area unlike in
atelectasis the tracheal??? shifting
towards the affected site
2. Open – air enters the pleural space thru
an opening to the chestwall
such as gunshot wound or surgical
thoracotomy.
3. Tension - mechanical ventilation and
resuscitative efforts
Gun tensions due to the rapid
accumulations of air in the pleural space
caused by high intrapleural pressures that
may result to tensions in the heart and
great vessels
increase intrapleural pressure may lead to
lung collapse so shifting of the spinum? in
the unaffected site
Causes of Pneumothorax
1. Traumatic pneumothorax- there’s
an Injury that maybe cause by
penetrationg or non penetrating
injuries like fracture ribs or
multiple rib fracture
Flail chest – multiple rib fracture
• usually a complication from a flat
chest trauma that may cause free
floating of the rib segment,
• px may have hypoxemia and
compromised gas exchange,
• respiratory acidosis as a result of
carbon dioxide retension
Paradoxic chest movement- during
inspiration the affected portion sucked in
and it bulge during exhalation
-you may expect increase in dead space
-Reduce in lung compliance and reduce in
alveolar ventilation
Prevents adequate ventilation in the lungs
in the injured area
2. Spontaneous pneumothorax- no
apparent cause, no injury
• Rupture of a blebs on the visceral
space- cause of bleb is unknown so
the blister in the lungs surface that
it rupture and allow atmospheric
air from the airway to enter the
pleural space then is divided in
primary and secondary.
• Primary, secondary
• Primary- occurs in healthy persons
or young people. Common in young
men and tall boys age from 10-30 y/o
bc of dif pressure from top and
bottom of the lungs that may
contribute to the devt of bleb or even
if they’re smoking
 • - change in atsmopheric pressure bc
of exposure to loud music that may
cause spontaneous pneumothorax
• Secondary- people with lung
diseases like asthma,tb, or px w
bronchogenic cancer
• Expect px to have hypoxemia,
sinosis?, hypercapnia or even
confusion or coma
3. Iatrogenic pneumothorax – after
medical treatment
Flail Chest
-Results from multiple rib fractures
causing instability of the chest wall
-Manifests with rapid, shallow respiration
and tachycardia.
-Crepitus of the rib
-Asymmetric chest expansion means
unilateral chest expansion (one is
expanding and one is not)
-Dx assessment: serial of CXR, ABG to
check for any respiratory acidosis
especially px due to traumatic
pneumothorax
CBC and O2 sat can also be done
FLAIL CHEST PARADOXICAL
BREATHING
A patient with a blunt chest injury may
develop flail chest, in which a portion of
the chest “caves in”. this results in
paradoxical breathing.
Inhalation
• Injured chest wall collapses in
• Uninjured chest wall moves out
Exhalation
• Injured chestwall moves out
• Uninjured chest wall moves in
Interventions for Flail Chest
1.Humidified O2 therapy
2.Crystalloid IV solution-by infusion
3.Definitive therapy: intubation and
ventilation
4.Positive end-expiratory pressure (PEEP)
with mechanical ventilation to prevent
atelectasis
Clinical Manifestations of Pneumothorax
1.Mild tachycardia and dyspnea – mild
2.Respiratory distress – severe
3.Shallow, rapid respiration, dyspnea and
air hunger
4.Chest pain
5.Cough with or without hemoptysis
6.No breath sounds over the affected area
7.Hyperresonance may be present
8.Mediastinal shift – tension
pneumothorax
Tension pneumothorax pathophysiology
Inspiration
Air enters pleural cavity through lung
wound or ruptured bleb(or occasionally via
penetrating chest wound) with valvelike
opening. Ipsilateral lung collapses and
mediastinum shifts to opposite side,
compressing contralateral lung and
impairing its ventilating capacity.
Expiration
Intrapleural pressure rises, closing
valvelike opening, thus preventing escape
of pleural air. Pressure is thus
progressively increased with each breath.
Mediastinal and tracheal shifts are
augmented, diaphragm is depressed and
venous return is impaired by increased
pressure and vena caval distortion.
Management
*Definitive therapy: chest tube insertion
or Heimlich valve is used to remove air out
of the pleural space
*Repeated spontaneous pneumothorax –
partial pleurectomy, stapling or
pleurodesis
Maybe thoracentesis as a rule of thumb
the chest wound is open surgically for
thoracotomy so the doctor cand perform
thoracentesis or chest tube output
continuously at greater of 200 mL
Mechanical ventilation for flail chest if
needed
Pulmonary Embolism (PE)
-thrombus formation that maybe arise
from the peripheral line?? Diko
maintindihan… maybe bcs of the air, fats
and blood clots. Or accidentally been
injected during IV infusion for embolism,
if fat has been mobilized in the broncho
after a fracture or even Amniotic fluid that
enters the maternal circulation after the
ruptured membrane at the time of
delivery
Common site: Deep vein of the legs 90%
Predisposing Factors
Bearchow or bearkow triad, nonactive
exteremities(seen in px w prolong bedrest)
1.Venous stasis – dysfunctional valves
2.Endothelial damage – by trauma or
external pressure- fibrinolytic
properties predispose to the devt of
thrombus like surgery or injury on the
legs, pelvis abdomen or thorax
3.Increased blood coagulability
hematological disorders- from
severe anemia, polycythemia vera, px who
have malignancy or have been taking
contraceptives that are high in estrogen
4.Disease – chronic lung disease, heart
and history or vascular surgery,
diabetes mellitus and infection
Pathophysiology of pulmonary embolism
Serotonin is a mediator that has an effect
to the bronchus.
In Pulmonary embolism Black blood? from
the peripheral area may travel or dislodge
the site of origin that may cause blockage
or obstruction in the pulmonary arteries
Clinical Manifestations
1.Chest pain
2. Dyspnea – 1st symptom accompanied by
pleuritic pain- common that they may
perceive as chest pain
3.Tachypnea and tachycardia
4.Hypoxemia – result to change in mental
status bc of carbon dioxide retension as a
result of impair gas exchange.
5.Productive cough of blood-streaked
sputum
6.Low BP, distended neck vein
7.Cyanotic and diaphoretic skin
–
Diagnostic Studies
1.CXR- helpful to include other possible
causes but not a diagnostic test unless
presence of infarction of about 50% and
note for pleural effusion or any unilateral
diaphragm elevation so it may show if
there is a infiltrate or atelectasis
2.Lung scan- to assess the history of the
lesions and evaluate the effectiveness of
therapy. Also to know the perfusion and
ventilation ratio
3.CT scan- pwede CT angiography bc it
about pulmonary artery. Bc not only ct
scan it involves angiography
4.UTZ- 97% of the lower lung progression? embolus without interruption in the blood
flow” note recommended for initial
5.Pulmonary angiography- most definite
treatment for px w pulmonary embolism”
test but risk of allergies kaya need check
bawal px na umiinom anticoagulant),
creatinine result or findings of px before
any angiography. *pulmonary embolectomy( removing
embolus from the pulmo artery before the
6.ECG-done when right heart of the px is
introductions of any procedure” a rare
affected bc if there is an increase in the
procedure bc of high mortality”)
pulmonary vasculature or pressure it will
increase the work of heart that will cause
right heart strain. Patient may have
sinustachycardia or segment and p-wave
abnormalities
7.Blood test – LDH- for acute or chronic
lung or tissue damage
8.ABG- to check for any acidosis bc it can
cause retension that may result to respi
acidosis
Nursing Interventions
9.D-dimer assay test (N - <500 ug/L)- to
measure for any thrombotic or Minimize the risk of embolism particularly
thrombolytic effect. Expect to have the conditions that predisposing to a
eleveation if there is pulmonary embolism slowing venous return.
1.Observe rate, depth of respirations,
determine the adequacy of gas xchange,
Treatment dyspnea, diaphoresis and air hunger
1.O2 therapy-to relieve hypoxemia,respi 2. Assess LOC – hypoxia
distress, and presence of cyanosis
3. Auscultate lungs for rhonchi, crackles
2.Endotracheal intubation to mech vent- and wheezes
3.Turning, coughing and deep breathing- 4. Elevate head to semi-Fowler’s
to facilitate gas flow to and from the alveoli
5. Use relaxation technique if px is
4.Medications – Heparin (drug of conscious to relieve anxiety
choice)and warfarin (Coumadin-usually
given 3 days before heparin is being stop. 6. Administer oxygen if px has hypoxia
This is to be maintained for 3-6 months hypoxemia
and take note drug food interaction when 7. Assist coughing or by suctioning to
taking warfarin. It may inhibit action of facilitate gas flow
digitalis, corticosteroid and vitmin K.
8. Physical activity – NEVER massage the
Food that antagonize warfarin are legs vigorously it may promote thrombus
spinach, lettuce- antidote vit k ) as formation
anticoagulant ; tPA
Leg pumping exercise may increase
Activated thromboplastin time can be venous return to increase flow if
measured and the use of thrombolytic ambulatory perform ROM or isometric
therapy to reestablish blood flow from the
blockage of artery to prevent dead cells Possible complications

5.Surgery – pulmonary infarction (death of lung

tissue) due to alveolar necrosis and
*venous ligation(prevent embolus from hemorrhage
travelling the lungs),
Pulmonary HTN- May compromise the
*vena caval plication( to insert a filter then capillaries
permit the flow of blood by trapping the
Pulmonary Edema-restrictive typr of respi
disorder
Accumulation of fluid in the lung tissue,
the alveolar space or both.
• May result of increased
microvascular pressure from
abnormal cardiac function. It could
be cardiac in origin or non cardiac
cause
• Hypervolemia or a sudden increase
in the intravascular pressure in the
lung. e.g. “flash” pulmonary edema
– can be seen in px who has
Pneumonectomy or re-expansion –
result from a rapid reinflation of the
lung after removal of air or fluid
from the lungs
• Pulmo edema caused by the
decreased ability of the lungs to
oxygenate blood and the
haemoglobin leaves the pulmo
circulation w/o being fully
oxygenated that can be cardiogenic
or noncardiogenic
Types of Pulmonary Edema
1.Cardiogenic – cardiac in origin-
underlying cardiac dx bc of the left
ventricle pulling the fluid back or increase
pressure into the Left atrium to the PV
and capillaries
2.Noncardiogenic –
a. Increased capillary permeability-
damaged to the capillary endothelium,
b. Lymphatic insufficiency- there is a
blockage of the lymphatic vessel can be
seen in px w cancer or silicosis?.
c. Decreased interstitial pressure- bc of the
rapid removal of the pleural effusion or
pneumothorax even hyperinflation.
d. Decreased colloid osmotic pressure-bc of
overtransfusion or hypoproteinemia
e.Unknown etiology- can be bc of high
altitude , neurogenic causes or usenof
heroin
In normal there is pressure in the capillary
of the lung structure, no obstruction the
lymphatic fluid whreas pulmonary edema
fluid and distance between the capillaries
and alveoli is altered.
Cardio-wide distance of the capillary and
the alveoli that cause impairment of gas
exchange and increase hydrostatic
pressure
• Increase fluid filtration but the
endothelium of the alveoli is intact
unlike px w
noncardiogenic pulmo edema
increase in permeability
- Disruption in the endothelial
barrier
- - presence of neutrophils that
invade the alveoli but there is a
normal hydrostatic pressure and bc
of permeability of fluid there will be
accumulation of fluid in this
lymphatic system therefore there
should be increase in the lymphatic
drainage
Stages of Pulmonary Edema
1.Interstitial edema – involvement of
lymphatics system to decreased the fluid-
there is increase hydrostatic pressure and
decrease in oncotic pressure
Effect will be fluid leaving the pulmonary
capillaries and entering the interstitial
space this stage is interstitial edema
Lymphatic- the lymph channels or vessels
attempt to reduce this fluid by widening
this lumina anc increasing the rate of flow
A wide distance between the alveoli and
pulmonary capillaries but has little effect
on gaseous exchange on the early stage
2.Alveolar edema – dilution of surfactant
and the fluid- lymphatic system drains
away excess fluid
Lymphatic system usually drain away the
excess fluid , if the fluid continuos to leak
from the pulmonary capillaries it enters
the alveoli that’s why its called alveolar
edema
Hydrostatic is high that it pushes the fluid
into the alveoli as seen on pic since the
fluid enters the alveoli it dilute the
surfactant with the incoming fluid it may
cause reduction in the surface tension in
the alveoli and then may predispose to
collapse
Pathophysiology
May have cold clammy skin bc of natrigges
SNS
If there is gas exchange impairment then
it may cause unoxygenated blood back to
the system that may cause cyanosis
Clinical Manifestations of Pulmonary
Edema
Monitor vs and pe
1.Rapid pulse and tachycardia-
2.Lips and nailbeds are cyanotic-
3.Air hunger-
4.Moist and cool skin-
5.Nasal flarings-
6.Orthopnea-
7.Hypotension-
8.Productive cough – frothy sputum-
Collaborative Care
1.Monitor vital signs
2.Semi to high fowler’s
3.O2 administration- to increase o2
content in blood. Pwede nasal o2 via nasal
cannula
4.Treat underlying condition (CHF)-
usually from ventricular failure ang
cardiac failure
5.Cardiac monitoring and oximetry
6.Weigh daily
7.Diet – low in sodium
8.Drug therapy
Medications
1.Morphine sulfate- reduce venous return
and reduce anxiety
2.Diuretics- such as furosemide to
decrease the fluid congestion
3.Inotropic drugs – improve cardiac
contractility that may cause increase
cardiac output reduce the left ventricular
diastole pressure
4.Bronchodilators- use of digitalis,
adrenergic agonist like dopamine if there
is hypotension
Acute Respiratory Distress Syndrome
(ARDS)
It is characterized by inflammation of the
lung parenchyma leading to impaired gas
exchange cause by inflammation,
hypoxemia and frequently resulting in
multiple organ failure
Increase in capillary permeability causing
the lungs to become wet ,heavy, congested
even hemorrhagic and lungs become thic
unable to diffused o2 that may result to
pulmo edema or respi failure secondary to
increase capillary permeability
Also known as post traumatic pulmonary
insufficiency (WW I); Wet lung (WW II);
Da Nang Lung (Vietnam War), Hyaline
Membrane Disease
Causes of ARDS (ARD-direct cause)
A – aspiration ( gastric aspiration, even
bacterial pneumonia or chest trauma or
embolism, inhalation of toxic substance, o2
toxicity
R – radiation
D – drug overdose, DIC, diffuse lung
disease/drowning (additional acute
pancreatitis)
S – shock/sepsis/smoke (indirect cause)
Major problem occurs in ARDS
1.Reduction in the functional vital
capacity
2. Bronchovascular edema- reduction in
the interstitial negative pressure , there is
a distal atelectasis
3. Decreased lung compliance- there is a
congestion and the lung become stiff may
result to decreased lung residual capacity
4. Hypoxia- imapaired gas exchange bc of
increase capillary permeability
5. Increased O2 consumption- bc of
resistance which the px attempt to
increase breathing
Ang may ards need ventialition bc of
impaired gas echange at baka congested
ang lungs
Signs and Symptoms
1.Tachypnea and dyspnea-
2.Central cyanosis
3.Alteration in LOC
4.Decreased PO2 and increased in PCO2
5.Retractions
6.Dry cough and fine crackles
Stages of ARDS
1.Exudation phase – 1 – 7 days (injury
phase)
Usually 24-48 hrs after initial lung injury
Neutrophils adhere to the microcirculation
causing damage to the vascular
endothelium and increase capillary
permeability therefore lungs become stiff
bcs the alveoli is filled with proteinacious
exudate? That has leaked up in the
damaged pulmonary capillaries
Stiff lungs is manifested by reduced in
compliance and then the cause of this
interstitial edema of the alveoli fill w
fluids and blood there’s a problem w the
oxygenation
The alveolar cells the type 1and 2 is
damged by these ARDS
Type 1 for gas exchange
Type 2 production of surfactant
Therefore decrease in the synthesis of the
surfactant and inactivation of these
surfactant that may cause the alveoli to
become unstable that may result to
collapse or further decrease lung
compliance
Gas exchange will be compromised that
will contribute to hypoxemia
* Interstitial and alveolar edema,
atelectasis, hypoxemia, and stiff lungs
2.Proliferative – 1 – 2 weeks (reparative
stage)
* Dense fibrous tissue, increased
pulmonary vascular resistance and
pulmonary HTN occurs
It begins 1-2 weeks after injury, injury has
regenerative capacity after lung injury can
be characterized by dense fibrous tissue,
as well it may increase the pulmonary
vascular resiatnce and pulmo HTn may
occur in this stage bcs of fibroblast and
the inflammatory cells destroyed the
pulmonary vasculature
As the lung compliance decreased as the
result of interstitial fibrosis then the
hypoxemia may worsen bcs of thickened
alveolar membrane causing limitations in
diffusion
This stage wherein the hyaline membrane
will be form kaya called adult hyaline
membrane
3.Fibrotic – 2 to 3 weeks (chronic or late
phase of ards)
* Diffuse scarring and fibrosis, decreased
surface area, decreased compliance and
pulmonary HTN
Wherein lungs is completely remodeled by
collagainous or fibrous tissues. There is a
diffuse scarring and fibrosis may be form
that will result in decrease lung
compliance
In addition of that the surface area of the
gas exchange is reduced bcs of fibrotic
interstitium and hypoxemia may continue
Then pulmo HTN may result from pulmo
vasculature or vascular destruction and
fibrosis
Pag di niremodel lungs mamumuo parin
fibrous keme that may lead to death kasi
it affects residual and vital lung capacity
Pathophysiology
Diagnostic Studies
1. Pulmonary function test- check for vital
capacity, you expect there is reduction in
the vital and residual lung capacity
because the decreased in lung compliance
and lung volume particularly the residual
lung capacity
2. ABG - ↓ PaO2, ↑ PaCO2, ↓ HCO3
- to determine hypoxemia and rsoiratory alkalosis caused by
ventilation
in the beginning there will be elevations and risk in pH but if
the ARDS worsens then it may result to respi acidosis wherein
pH may reduced or there is a decresed in pH
3. CXR-to determine any scatterd
insterstitial infiltration
-edema cant be shown in cxr unless there
is 30% increase content in the lungs so the
cxr is term as the white out lungs because
of this consolidated and coalescing?
infiltration throughout the lungs leaving
few noticeable spaces
4. Lactic acid levels – due to lack of O2
expect elevation of lactic acid
Interventions for ARDS
1.Adequate oxygenation- mech ventilation
to reverse hypoxemia and expand distal
gas xchange to prevent alveolar lung
collapse
2.Fluids and electrolytes - to determine
excessive intravascular fluid that may
result to cardiogenic edema
px w capillary damaged are susceptible to
fluid leakage into the alveolar space and
px who have??/ ano daw 35.22
All px should have crystalloid fluid tht
means all administration have IV fluid
3.ECG monitoring-
4.Measure intake and output- pag
increase intake to monitor and balance the
diuretics. Urine ouput every hr
5.Alimentation- thru tube feeding or small
feeding. Could be enteral or parenteral
feeding
1cause by edema, cellular exudate or
6.Drug therapy – fibrosis and it may increase the lung
inotropic agents(if heart is affected), stiffness that may result to reduce lung
compliance that may cause exertional
antacid & H2 blockers( to maintain gastric dyspnea
pH above 4),
Palliative care only sa may ILd bcs its not
morphine, corticosteroids(reducing pulmo curable
edema and stabilizing the pulmo
membrane), Signs and Symptoms

heparin – to combat microvascular Fever

emboli, Sweating
diuretics- as per order to keep px dry Anorexia
7.Positioning Weight loss
Interstitial Lung Disease Fatigue
Also a restrictive type of respi disorder Myalgia
wherein may produce various degree of
inflammation, fibrosis and disability and Nonproductive cough
changes in the interstitium
Exertional Dyspnea
It may cause the lung to become stiff and
Hemoptysis
difficult to inflate
Sputum production
Causes
1.Exposure to occupational hazards –
asbestos, silicosis, talc, coal… or even Important s/sx
aiconditoner that has bacteria that may
1.Dyspnea
affect the lungs
2.Hypoxia
3.CXR – diffuse infiltration
2.Environmental inhalants – gases,
fumes, aerosols.. those that contain
chlorine, ammonia
Management
Chemotherapeuyic drugs also included
like leomycin, amniodarone these 1.Oxygen therapy- to main the functional
drugs may cuse interstitial lung dx … status and improve the quality of life of the
TB , radiation px as possible
2.Mechanical ventilation – depending on
the severity of interstitial lung dx
3. Unknown – sarcoidosis(connective
tissue disorder), idiopathic pulmonary 3.ABG analysis- monitor
fibrosis, systematic lucus 4.Lung transplant

Etiologic Determinants of Occupational
Lung Disease
1. Nature of the exposure
2. Duration and intensity of the exposure
3. Particle size and water solubility
4. Smoking history
5. Presence of underlying pulmonary
disease
TUBERCULOSIS- from the inhalation of
the bacterium
Chronic respiratory disease affecting the
lungs characterized by formation of
tubercles in the → caseation → necrosis →
calcification.
It affects the upper part of the lower lobe
of the lungs then ventilation is greatest
Not highly contagious and required
frequent and prolonged exposure
AKA: Phthisis, Consumption, Koch’s,
Immigrant’s disease
Etiologic agent: Mycobacterium(outer
waxy structure that make it more
resistant to destruction, often known as
the acid fast bacilli) tuberculosis
Incubation period: 2 – 10 weeks.
Period of communicability: all throughout
the life if not treated
MOT: Airborne
Sources of infection: Sputum, blood, nasal
discharge, saliva
Classification of Tuberculosis
Quantitative
Minimal – slight lesion
Moderately advanced – not exceed 4 cm
Far advanced – more extensive than # 2
Clinical
Inactive – asymptomatic, sputum is (-), no
cavity on chest X ray
Active – (+) CXR, S/S are present, sputum
(+) smear
Classification Scheme
Class 0: no exposure; no infection
Class 1: exposure; no evidence of infection
Class 2: latent infection; no disease (e.g,
positive PPD reaction but no clinical
evidence of active TB)
Class 3: disease; clinically active
Class 4: disease; not clinically active
Class 5: suspected disease; diagnosis
pending
Clinical Manifestations of TB
1.Primary Complex: TB in children: non
contagious, children swallow phlegm,
fever, cough, anorexia, weight loss, easy
fatigability
Pag primary sa adult no manifestations,
no symptoms. Di madetect sa cxr at – acid
fast test
2.Adult TB
afternoon rise in temperature about 38-39
celsius
night sweats
weight loss
sometimes amenorrhea for women
cough dry to productive
Hemoptysis- if there is ulceration or
cavity px may develop this
sputum AFB (+)
3. Miliary TB - very ill, with exogenous TB
like Pott’s disease
This is where tiny size of a lesion may
spread or go through the blood vessels and
may spread to other body organs such as
kidney, meniges, liver.
 3.Improve nutritional status
Management
DOTS
1 6 months of RIPE..
2 Respiratory isolation,..
3 Take medicines religiously –
prevent resistance
4. Stop smoking
5. Plenty of rest
6. Nutritious and balance meals,
increase CHON, Vit. A, C
Diagnostic’ 7. Regular follow-up
Tuberculin test
Cxr- common
Sputum studies for Acid fast bacilli
Sputum culture- not a standard but may
be done to px
Git expert? Ha ano daw

PRIMARY ANTI TUBERCULAR

AGENTS
R – Rifampicin
I – Isoniazid
P – Pyrazinamide
E – Ethambutol
S – Streptomycin

Pathophysiology 52
Pharmacologic Management
1.Isoniazid – 6 to 12 months, inhibit
growth of dormant organisms.. latest now
up to 9 months
2.Rifampicin – inhibit bacterial RNA
synthesis orange-colored urine- cautious
sa may liver problems, check muna
creatinine and BON test? And even liver
enzyme test
3. Vitamin B6 – to prevent peripheral
neuritis especially of taking INH
(isoniazid)
Prevention
4.Ethambutol – caution with renal
1.BCG vaccination disease, may affect optic nerve
2.Avoid overcrowding
5.Streptomycin – inhibit CHON synthesis
and bactericidal; CNS toxicity
6.Pyrazinamide – bacteriostatic and
bacteriocidal

DOTS – Direct Observed Treatment

Short-Course

NURSING CARE for TB

Respiratory precautions: 2-4 weeks
Needs well ventilated private room
Mask to all visitors and staff, discard mask after use
Strict hand washing after each contact with patient
Small frequent meals with supplements
Activity as tolerated
Take medications as prescribed
Multi-Drug Resistance Tuberculosis (MDR-TB)