Responses to Altered

Ventilatory Function
• It share responsibility with
cardiovascular system for
supplying the body with
oxygen and disposing of
carbon dioxide.
• It oversee the gas exchange
that occur between the blood
and external environment.
NOSE
• pug- or ski jump in shape, is the only
externally visible part of the
respiratory system.
• The air enter the nose through the
nostrils or nares.
• The interior of the nose consist of the
nasal cavity, divided by nasal septum.
• Olfactory receptor for the sense of smell are
located in the mucosa in the slit like superior
part of the nasal cavity just beneath the
ethmoid.
• Respiratory mucosa, rests on a rich network of
thinned walled veins that warms the air as it
flows past.
• Mucosa’s gland moistens the air and traps
incoming bacteria and other foreign debris and
lysosome enzyme destroy bacteria chemically.
• The ciliated cells of the nasal mucosa
create a gentle current that moves the
sheet of contaminated mucous
posteriorly toward the throat
• Conchae- are found in the lateral walls
of nasal cavity which greatly increase
the surface area of the mucosa exposed
to the air. It also increase air turbulence
in the nasal cavity
• Palate – separates nasal cavity
from oral cavity. The hard
palate is the anterior palate
which is supported by bones
and soft palate is the
unsupported posterior part of
the palate
• Paranasal sinuses it lightens the skull
and act as resonance chambers of
speech. It is located in the frontal,
sphenoid, ethmoid and maxillary. the
blowing of nose helps drain the sinuses.
• The nasolacrimal ducts, which drain
tears from the eyes also empty into the
nasal cavity.
PHARYNX
• Is a muscular passageway that vaguely
resembles a short length garden hose.
• Commonly called throat
• It is continuous with the nasal cavity
anteriorly via the posterior nasal aperture
• The air enters the superior portion,
the nasopharynx and then descends
the oropharynx and
laryngopharynx to enter the larynx
below.
• The pharyngotympanic tubes, which
drain the middle ear open into
nasopharynx
• The pharyngeal tonsils are often
called adenoid which is located high
in nasopharynx.
• The palatine tonsils are in the
oropharynx at the end of soft
palate.
• Lingual tonsils which lie at the base
of the tongue.
LARYNX
• Or voice box, routes air and food
into the proper channels and plays a
role in speech.
• Epiglottis contains an eight rigid
hyaline cartilages and spoon-shaped
flap of elastic cartilage. Sometime
called the guardian of the airway.
• Thyroid cartilage is the largest of the
hyaline cartilage which protrudes
anteriorly and is commonly called Adams
apple.
• Vocal Folds or true vocal cords – part of
the mucus membrane in the larynx which
vibrate with expelled air- allow us to
speak.
• Glottis is a slitlike passageway between
the vocal folds
TRACHEA
• Or the windpipe
• Is a rigid which reinforced with C-shaped rings
of hyaline cartilage.
• The open parts of the rings about the
esophagus and allow it to expand anteriorly
when we swallow a large piece of food
• The solid portion support the tracheal walls
and keep it patent, in spite of the pressure
changes that occur during breathing.
MAIN BRONCHI
• The right and left main bronchi are
formed by the division of trachea
• The right bronchus is wider, shorter
and straighter than the left. The most
common site for an inhaled foreign
object to become dislodged
LUNGS
• Occupy the entire thoracic cavity
• The narrow superior of the
lungs, the apex, is just deep to
the clavicle. The broad lung area
resting on the diaphragm is the
base
• Each lung is divided into lobes by
fissures, the left lung has two lobes
and the right lung has three lobes
• The surface of the lung is covered
with a visceral pleura
• The thoracic cavity is lined by
parietal pleura
• The pleural membranes produce
pleural fluid, a slippery serous
secretion which allow lungs to
glide easily over the thorax wall
during breathing movements
and causes the pleural layers to
cling together.
BRONCHIOLES
• Small conducting passageway of air
entering the lungs

RESPIRATORY TREE
• The network that is formed from the
branching and rebranching of the
respiratory passageways within the lungs
ALVEOLI
• Air sacs

RESPIRATORY ZONES
• Includes the respiratory bronchioles,
alveolar ducts and alveolar sacs and
the alveoli
RESPIRATORY MEMBRANE
• Air-blood barrier
• Membranes that fused capillary walls and
alveoli
• It has gas flowing past on one side and
the blood flowing past on the other side
• The gas exchange occur by simple
diffusion through the respiratory
membrane
Respiratory Physiology
RESPIRATIONS
Four distinct events must occur:
• PULMONARY VENTILATION
• EXTERNAL RESPIRATION
• RESPIRATORY GAS TRANSPORT
• INTERNAL RESPIRATION
PULMONARY VENTILATION
• Commonly breathing
• Air must move into and out of the
lungs so that gases in the air sacs of
the lungs continuously refreshed
• Two phases include inspiration and
expiration
Mechanics of Breathing
Is a completely mechanical process
that depends on volume changes
occurring in the thoracic cavity
Volume changes leads to pressure
changes, which lead to the flow of
gases to equalize the pressure
inspiration
• when air is flowing into the lungs
• Occurs when contraction of respiratory
muscles cause an increase in thoracic
volume, with expansion of lungs and a
decrease in intrathoracic and
intrapulmonic pressure.
expiration
• When air is leaving the lungs
• It follows passively as thoracic volume
decreases and intrapulmonic pressure
rises above atmospheric, with the
recoil of the rib cage and contraction
of the lungs
 EXTERNAL RESPIRATION
• Gas exchange (oxygen loading and
carbon dioxide unloading) between
the pulmonary blood and alveoli
must takes place.
• gas exchange are being made
between the blood and the body
exterior
 RESPIRATORY GAS TRANSPORT

• Oxygen and carbon dioxide must be

transported to and from the lungs
and tissue cells of the body via
bloodstream
• Of the oxygen transported in the
blood, only small amount is dissolved
in the plasma.
• More than 99% of the oxygen is
carried by hemoglobin molecules in
the red blood cells
• Carbon dioxide carried in the blood
is mostly converted to bicarbonate
ions in the red blood cells and
released into the plasma
• More than 99% of the oxygen is
carried by hemoglobin molecules in
the red blood cells
• Carbon dioxide carried in the blood
is mostly converted to bicarbonate
ions in the red blood cells and
released into the plasma
 INTERNAL RESPIRATION

• Gas exchange between the blood and

cells inside the body
ASSESSMENT
DIAGNOSTIC
ASSESSMENT
An arterial blood gas test usually includes the following measurements:

Oxygen content (O2CT): This measures the amount of oxygen in your blood.

Hemoglobin: This measures the amount of hemoglobin, the protein responsible for carrying
oxygen to your cells, in your blood.

Oxygen saturation (O2Sat): This measures how much hemoglobin in your blood is carrying
oxygen. Hemoglobin is a protein in your red blood cells that carries oxygen from your lungs
to the rest of your body.

Partial pressure of oxygen (PaO2): This measures the pressure of oxygen dissolved in your
blood. It helps show how well oxygen moves from your lungs to your bloodstream.

Partial pressure of carbon dioxide (PaCO2): This measures the amount of carbon dioxide in
your blood and how well carbon dioxide can move out of your body.

pH: This measures the balance of acids and bases in your blood, known as your blood pH
level. The pH of blood is usually between 7.35 and 7.45. If it’s lower than that, your blood
is considered too acidic. If it’s higher than that range, your blood is considered too basic
(alkaline).

Bicarbonate (HCO3): This is calculated using the measured values of pH and PaCO2 to
determine the amount of the basic compound made from carbon dioxide (CO2.)
PULMONARY CAPILLARY WEDGE PRESSURE
• is an integrated measurement of the compliance of the left side
of the heart and the pulmonary circulation. The measurement of
PCWP can be useful in several diagnostic settings.
• It is frequently used to assess left ventricular filling, represent
left atrial pressure, and assess mitral valve function. It
is measured by inserting a balloon-tipped, multi-lumen catheter
(Swan-Ganz catheter) into a central vein and advancing the
catheter into a branch of the pulmonary artery. The balloon is
then inflated, which occludes the branch of the pulmonary
artery and then provides a pressure reading that is equivalent
to the pressure of the left atrium.
ALTERATIONS IN
VENTILATION
Acute and Chronic
Obstructive
Pulmonary Disease
• Obstructive pulmonary disease,
the most common chronic lung
disease, is characterized by
increased resistance to airflow
as a result of airway obstruction
or airway narrowing.
Types of Obstructive Lung diseases
• Asthma
• COPD
• cystic fibrosis (CF),
• bronchiectasis
Asthma
• is a chronic inflammatory lung disease that
results in variable episodes of airflow
obstruction, but it is usually reversible.
• The chronic inflammation leads to recurrent
episodes of wheezing, breathlessness, chest
tightness, and cough, particularly at night or
in the early morning
Risk Factors for Asthma and Triggers of Asthma Attacks

Genetics-
Atopy, the genetic predisposition to develop an
allergic (immunoglobulin E [IgE]–mediated)
response to common allergens, is a major risk
factor for asthma.
Immune Response.
Allergens.
Occupational Factors.
Risk Factors for Asthma and Triggers of Asthma Attacks

Respiratory Tract Infections.

Nose and Sinus Problems.
Drugs and Food Additives.
Gastroesophageal Reflux Disease.
Psychologic Factors
Pathophysiology
Clinical Manifestations
wheezing,
cough,
dyspnea, and chest tightness
Expiration may be prolonged. Instead of a
normal inspiratory-expiratory ratio of 1:2, it
may be prolonged to 1:3 or 1:4.
Complications
Severe and Life-Threatening Asthma
Exacerbations.
occur when the patient is dyspneic at rest and the patient
speaks in words, not sentences, because of the difficulty of
breathing.
The patient is usually sitting forward to maximize the
diaphragmatic movement with prominent wheezing, a
respiratory rate higher than 30 breaths/minute, and pulse
greater than 120 beats/minute.
Accessory muscles in the neck are straining to lift the chest wall,
and the patient is often agitated.
Complications
SAFETY ALERT
• If the patient has been wheezing and then there
is an absence of a wheeze (i.e., silent chest) and
the patient is obviously struggling, this is a life-
threatening situation that may require mechanical
ventilation
Diagnostic Studies
A detailed history
clinical manifestations
 peak flow variability or spirometry
Pulmonary function tests (PFTs) can be used to determine the
reversibility of bronchoconstriction (using bronchodilators) and
thus establish the diagnosis of asthma
The peak expiratory flow rate (PEFR) measured by the peak
flow meter is an aid to diagnose and monitor asthma.
chest x-ray
Measurement of oximetry •
Allergy skin testing (if indicated) •
Blood level of eosinophils and IgE (if indicated)
Collaborative Care
Intermittent and Persistent Asthma
Identification and avoidance or elimination of triggers
Patient and caregiver teaching
Drug therapy
Asthma action plan
Desensitization (immunotherapy) if indicated
Assess for control (e.g., Asthma Control Test [ACT])
Collaborative Care
Acute Asthma Exacerbations.
usually the symptoms are relieved at home promptly with an
SABA such as albuterol delivered via a nebulizer or metered-
dose inhaler (MDI) with a spacer. For any classification of
asthma in a “rescue plan,” patients are instructed to take 2 to 4
puffs of albuterol every 20 minutes three times to gain rapid
control of symptoms.
Occasionally a short course of oral corticosteroids is needed to
decrease airway inflammation
Relief is provided with the SABA delivered as in the mild
exacerbation, and oral corticosteroids are needed. Oral routes
are usually as effective as IV routes
Collaborative Care
Acute Asthma Exacerbations.
usually the symptoms are relieved at home promptly with an
SABA such as albuterol delivered via a nebulizer or metered-
dose inhaler (MDI) with a spacer. For any classification of
asthma in a “rescue plan,” patients are instructed to take 2 to 4
puffs of albuterol every 20 minutes three times to gain rapid
control of symptoms.
Occasionally a short course of oral corticosteroids is needed to
decrease airway inflammation
Relief is provided with the SABA delivered as in the mild
exacerbation, and oral corticosteroids are needed. Oral routes
are usually as effective as IV routes
Collaborative Care
Severe and Life-Threatening Asthma
Exacerbations.
SaO2 monitoring •
ABGs •
 Inhaled β2-adrenergic agonists •
Inhaled anticholinergic agents (only in the initial treatment) •
O2 by mask or nasal prongs •
 IV or oral corticosteroids •
IV fluids •
 IV magnesium and/or heliox •
Intubation and assisted ventilation
DRUG THERAPY
Medications are divided into two
general classifications: (1) quick-relief
or rescue medications to treat
symptoms and exacerbations, such
as SABAs; and (2) long-term control
medications to achieve and maintain
control of persistent asthma, such as
ICSs
DRUG ALERT: β2-Adrenergic Agonists
• Use with caution in patients with cardiac
disorders, since both SABAs and LABAs may
cause elevated BP and heart rate, central
nervous system stimulation or excitation, and
increased risk of dysrhythmias.
• Overuse of SABAs may cause rebound
bronchospasms
DRUG ALERT: Long-Acting β2-Adrenergic
Agonists (LABAs)
• Should not be the first medicine used to treat asthma.
• Should never be used as the only medication to treat
asthma but should be added to the treatment plan only
if other controller medicines do not control asthma.
• Should not be used to treat wheezing that is getting
worse.
• Always use a SABA to treat sudden wheezing
DRUG ALERT: Theophylline
• Instruct patient to report signs of toxicity:
nausea, vomiting, seizures, insomnia.
• Avoid caffeine to prevent intensifying
adverse effects.
Types of Obstructive Lung diseases
Cystic fibrosis
another form of obstructive pulmonary
disease
is a genetic disorder that produces
airway obstruction because of changes
in exocrine glandular secretions,
resulting in increased mucus production
is an autosomal recessive, multisystem
disease characterized by altered
transport of sodium and chloride ions in
and out of epithelial cells.
 This defect primarily affects the lungs,
gastrointestinal tract (pancreas and
biliary tract), and reproductive tract.
CF was first described in 1938 when
autopsies of young children revealed
multiple cysts in the pancreas, so the
disease was called “cystic fibrosis of the
pancreas.”
Etiology and Pathophysiology
The CF gene is located on chromosome 7 and
produces a protein called CF transmembrane
regulator (CFTR).
The CFTR protein localizes to the epithelial
surface of the airways, gastrointestinal tract, and
ducts of the liver, pancreas, and sweat glands.
CFTR regulates sodium and chloride channels.
 Mutations in the CF gene alter this protein in
such a way that the channels are blocked.
As a result, cells that line the passageways
of the lungs, pancreas, intestines, and other
organs produce secretions that are low in
sodium chloride content (thus low in water
content), making mucus abnormally thick
and sticky
This mucus fills (plugs up) the glands in
these organs and causes the glands to
atrophy, ultimately resulting in organ failure
The hallmark of respiratory involvement in CF is
its effect on the airways. The disease progresses from
being a disease of the small airways (chronic
bronchiolitis) to involvement of the larger airways, and
finally causes destruction of lung tissue.
The mucus becomes dehydrated and tenacious due to
the defect in the chloride secretion and excess sodium
absorption. Cilia motility is decreased, thus allowing
mucus to adhere to the airways. The bronchioles become
obstructed with thick mucus, leading to air trapping and
hyperinflation of the lungs.
The hallmark of respiratory involvement in CF is
its effect on the airways. The disease progresses from
being a disease of the small airways (chronic
bronchiolitis) to involvement of the larger airways, and
finally causes destruction of lung tissue.
The mucus becomes dehydrated and tenacious due to
the defect in the chloride secretion and excess sodium
absorption. Cilia motility is decreased, thus allowing
mucus to adhere to the airways. The bronchioles become
obstructed with thick mucus, leading to air trapping and
hyperinflation of the lungs.
Clinical Manifestations
An initial finding of meconium ileus in the newborn
infant prompts the diagnosis in 20% of people with
CF.
acute or persistent respiratory symptoms
(wheezing, coughing, frequent pneumonia), failure
to thrive or malnutrition, steatorrhea (large, oily,
frequent bowel movements), and family history.
Without treatment, a large, protuberant abdomen
may develop with an emaciated appearance of the
extremities.
Clinical Manifestations
One of the most common symptoms of CF in
the adult is frequent cough. With time, the
cough becomes persistent and produces
viscous, purulent, often yellow or greenish
sputum.
Clinical Manifestations
If the patient with CF develops DIOS (Distal
Intestinal Obstruction Syndrome), he or she may
have right lower quadrant pain (the area of the
ileocecal valve), loss of appetite, nausea, emesis,
and often a palpable mass.
 Insufficient pancreatic enzyme release causes
the typical pattern of protein and fat
malabsorption with a person being thin with a
low body mass index (BMI) and frequent, bulky,
foul-smelling stools.
Clinical Manifestations
Both males and females have delayed puberty
Some women with CF have difficulty conceiving;
the cervical mucus is thought to be thickened.
During exacerbations, menstrual irregularities
and secondary amenorrhea are common
Complications
Complications in CF include CFRD (cystic fibrosis-
related diabetes), bone disease, sinus disease,
and liver disease.
Pneumothorax, a relatively uncommon but
serious complication, is caused by the formation
of bullae and blebs.
A small amount of blood in sputum is common in
the CF patient because of chronic lung infection.
Diagnostic Studies
The diagnostic criteria for CF include a combination of clinical
presentation, family history, laboratory testing, and genetic
testing.
The sweat chloride test is considered the gold standard for the
diagnosis of CF
The sweat chloride test is performed with the pilocarpine iontophoresis
method. Pilocarpine is placed on the skin and carried by a small electric
current to stimulate sweat production. This part of the process takes
about 5 minutes, and the patient feels a slight tingling or warmth. The
sweat is collected on filter paper or gauze and then analyzed for sweat
chloride concentrations. The test takes approximately 1 hour. Sweat
chloride values above 60 mmol/L are considered positive for the
diagnosis of CF. Usually a second sweat chloride test is obtained at the
same time (one test in each arm) to confirm the diagnosis
Diagnostic Studies
A blood sample or cells taken inside the cheek
(buccal smear) are sent to a laboratory that
specializes in genetic testing. Most laboratories
test for only the most common mutations of the
CF gene
Collaborative Care
aerosol and nebulization treatments of medications used
to dilate the airways, liquefy mucus, and facilitate
clearance.
Agents that degrade the DNA in CF sputum (e.g., dornase
alfa [Pulmozyme]) increase airflow and reduce the
number of acute pulmonary exacerbations.
Inhaled hypertonic saline (7%) is effective in clearing
mucus and also decreases the frequency of exacerbations.
Bronchodilators (e.g., β2-adrenergic agonists) may be
used to control bronchospasm, but the long-term benefit is
not proven.
Collaborative Care
CPT (including postural drainage with percussion and vibration)
Standard treatment of infections includes antibiotics for
exacerbations and may include chronic suppressive therapy in
conjunction with airway clearance.
The management of pancreatic insufficiency includes pancreatic
enzyme replacement of lipase, protease, and amylase (e.g.,
pancrelipase [Pancreaze, Creon, Ultresa, Viokase, Zenpep])
administered before each meal and snack. Adequate intake of
fat, calories, protein, and vitamins is important. Fat-soluble
vitamins (A, D, E, and K) must be supplemented, since they are
malabsorbed. Use of caloric supplements improves nutritional
Collaborative Care
If the patient develops DIOS with complete
bowel obstruction, gastric decompression may
be needed
Ivacaftor (Kalydeco) is used to treat patients
who have a specific G551D mutation in the CFTR
gene.
Aerobic exercise is effective in clearing the
airways
Types of Obstructive Lung diseases
Bronchiectasis is an obstructive
disease characterized by dilated
bronchioles. It most frequently results
from untreated or poorly treated
pulmonary infections that cause an
increase in sputum production.
characterized by permanent, abnormal
dilation of medium-sized bronchi that is a
result of inflammatory changes that destroy
elastic and muscular structures supporting
the bronchial wall.
Infection is the primary reason for the
continuing cycle of inflammation, airway
damage, and remodeling
Airways can become colonized with
microorganisms (e.g., Pseudomonas
species), which cause the bronchial
walls to weaken, and pockets of
infection begin to form
Pathophysiology
 -Cystic Fibrosis
-Bacterial Infections

-mucociliary mechanism is
damaged

bacteria and mucus to

accumulate within the pockets

reduced ability to clear mucus

from the lungs and decreased
expiratory airflow
Clinical Manifestations
The hallmark of bronchiectasis is persistent
cough with consistent production of thick,
tenacious, purulent sputum.
Recurrent infections injure blood vessels,
and hemoptysis occurs.
pleuritic chest pain, dyspnea, wheezing,
clubbing of digits, weight loss, and anemia
Diagnostic Studies
An individual with a chronic productive cough
with copious purulent sputum (which may be
blood streaked) should be suspected of having
bronchiectasis.
Chest x-rays may show some nonspecific
abnormalities.
A high-resolution CT (HRCT) scan of the chest is
the preferred method for diagnosing
bronchiectasis.
Diagnostic Assessment
chronic productive cough with copious
purulent sputum (which may be blood
streaked)
Chest X-ray
CT scan in the chest
Sputum examination
Collaborative Care
. Antibiotics are the mainstay of treatment and are
often given empirically, but attempts are made to
culture the sputum.
 Long-term suppressive therapy with antibiotics is
reserved for those patients who have symptoms that
recur a few days after stopping antibiotics.
Concurrent bronchodilator therapy with LABAs, SABAs,
or anticholinergics is given to prevent bronchospasm
and stimulate mucociliary clearance
Collaborative Care
Maintaining good hydration is important to liquefy
secretions.
CPT and other airway clearance techniques are
important to facilitate expectoration of sputum.
Teach the patient to reduce exposure to excessive air
pollutants and irritants, avoid cigarette smoking, and
obtain pneumococcal and influenza vaccinations.
Collaborative Management
Therapy is aimed at treating acute flare-ups and
preventing a decline in lung function.
Antibiotic therapy
Bronchodilators
Hypertonic agents
Hydration and CPT
Teach the patient to reduce exposure to excessive air pollutants
and irritants, avoid cigarette smoking, and obtain
pneumococcal and influenza vaccinations
Types of Obstructive Lung diseases

COPD is an obstructive pulmonary

disease with progressive limitation in
airflow that is not fully reversible
is a preventable and treatable disease
characterized by persistent airflow
limitation that is slowly progressive.
Previous definitions of COPD
encompassed two types of obstructive
airway diseases: chronic bronchitis and
emphysema
Emphysema is an abnormal
permanent enlargement of the
air spaces distal to the terminal
bronchioles, accompanied by
destruction of their walls and
without obvious fibrosis.
Chronic bronchitis is the
presence of chronic productive
cough for 3 months in each of 2
consecutive years in a patient in
whom other causes of chronic
cough have been excluded
Inflammation and eventual
scarring of the lining of bronchial
tubes. This restricts airflow to
and from the lungs, which
produces heavy mucus and
phlegm.
The mucus-lined tubes are an
ideal breeding place for
bacterial infections.
Blue bloaters often take deeper
breaths but can’t take in the
right amount of oxygen.
ETIOLOGY
Cigarette Smoking.
Occupational Chemicals and Dusts
Air Pollution.
Infection
Genetics
α1-Antitrypsin (AAT) Deficiency. α1-Antitrypsin
(AAT) deficiency is an autosomal recessive
disorder that may affect the lungs or liver
aging
Clinical Manifestations
A chronic intermittent cough, which is often the first symptom to
develop.
dyspnea is progressive, usually occurs with exertion, and is
present every day.
Patients may complain of not being able to take a deep breath,
heaviness in the chest, gasping, increased effort to breathe, and
air hunger.
In late stages of COPD, dyspnea may be present at rest
Wheezing and chest tightness may be present, but may vary by
time of the day or from day to day, especially in patients with
more severe disease.
The person with advanced COPD frequently
experiences fatigue, weight loss, and anorexia.
The anteroposterior diameter of the chest is increased
(“barrel chest”) from the chronic air trapping.
The patient may sit upright with arms supported on a
fixed surface such as an overbed table (tripod position).
The patient may naturally purse lips on expiration
(pursed-lip breathing)
Edema in the ankles may be the only clue to right-
sided heart involvement (cor pulmonale).
Classification
Complications
Cor pulmonale results from pulmonary hypertension,
which is caused by diseases affecting the lungs or pulmonary
blood vessels
In COPD, pulmonary hypertension is caused primarily by
constriction of the pulmonary vessels in response to alveolar
hypoxia, with acidosis further potentiating the vasoconstriction.
Chronic alveolar hypoxia causes vascular remodeling. Chronic
hypoxia also stimulates erythropoiesis, which causes
polycythemia. This results in increased viscosity of the blood. An
anatomic reduction of the pulmonary vascular bed, as seen in
emphysema with bullae, may occur.
Dyspnea is the most common symptom of chronic cor
pulmonale.
Lung sounds are normal, or crackles may be heard in
the bases of the lungs bilaterally.
 Heart sound changes occur but are usually masked by
the underlying lung disease.
Other manifestations of right-sided heart failure may
develop, including distended neck veins (jugular
venous distention), hepatomegaly with right upper
quadrant tenderness, peripheral edema, and weight
gain.
COPD exacerbation is an acute event in
the natural course of the disease. The
primary causes of exacerbations are
bacterial or viral infections.
Exacerbations are signaled by an acute
change in the patient’s usual dyspnea,
cough, and/or sputum (i.e., something
different from the usual daily patterns)
Be alert for signs of severity such as
use of accessory muscles, central
cyanosis, edema in the lower
extremities, unstable BP, right-sided
heart failure, and altered alertness.
Short-acting bronchodilators, oral systemic
corticosteroids, and antibiotics are the
typical therapies for exacerbations. SABAs
with or without short-acting anticholinergics
are preferred for those who are breathless.
the presence of green or purulent sputum
(as opposed to white sputum) is one of the
best ways to determine if antibiotics are
needed
Patients with severe COPD who have
exacerbations are at risk for respiratory
failure.
Discontinuing bronchodilator or
corticosteroid medication may also
precipitate respiratory failure
Chronic treatment with β-blockers may
improve survival and reduce the risk of
exacerbations of COPD.1
Many patients with COPD experience
depression and anxiety
Help the patient with muscle relaxation
exercises that can reduce anxiety
Cognitive and behavioral therapy along
with COPD teaching may improve the
quality of life.
Buspirone (BuSpar), which is used to treat
anxiety, has few if any respiratory
depression effects
Diagnostic Studies
Spirometry confirms the presence of airflow
obstruction and determines the severity of COPD
Chest x-rays- hyperinflation
Ct scan – emphysema
6-minute walk test
The BODE index can be used to assess not only the risk
of death from COPD, but also the pulmonary and
systemic manifestations
COPD Assessment Test (CAT) and modified Medical
Research Council (mMRC) Dyspnea Scale
Collaborative Care
Smoking Cessation.
Drug Therapy
Bronchodilators (Beta adrenergic agonist)
Anticholinergic
Methyxanthines
Roflumilast (Daliresp) is an oral medication used to decrease
the frequency of exacerbations in severe COPD. This drug is a
phosphodiesterase inhibitor, which is an antiinflammatory
drug that suppresses the release of cytokines and other
inflammatory mediators, and inhibits the production of
reactive oxygen radicals
Oxygen Therapy
 Breathing Retraining
 The purpose of pursed-lip breathing (PLB) is to prolong exhalation and thereby
prevent bronchiolar collapse and air trapping. PLB is simple and easy to teach
and learn, and it gives the patient more control over breathing, especially
during exercise and periods of dyspnea
 Diaphragmatic (abdominal) breathing focuses on using the diaphragm instead of
the accessory muscles of the chest to (1) achieve maximum inhalation and (2)
slow the respiratory rate.
 Airway Clearance Techniques- loosen mucus and secretions so they can be cleared by coughing
 Effective Coughing. Huff coughing is an effective forced expiratory technique that you can easily teach the patient
Breathing Retraining
 The pursed-lip breathing (PLB) is to prolong
exhalation and thereby prevent bronchiolar
collapse and air trapping. PLB is simple and easy
to teach and learn, and it gives the patient more
control over breathing, especially during exercise
and periods of dyspnea
Diaphragmatic (abdominal) breathing focuses on
using the diaphragm instead of the accessory
muscles of the chest to (1) achieve maximum
inhalation and (2) slow the respiratory rate.
Effective Coughing.
Huff coughing is an effective forced expiratory
technique

Chest Physiotherapy. Chest physiotherapy (CPT) is

primarily used for patients with excessive bronchial
secretions who have difficulty clearing them
Percussion and vibration are manual or mechanical
techniques used to augment postural drainage. These
techniques are used after the patient has assumed a
postural drainage position to assist in loosening the
mobilized secretions
Effective Coughing.
Huff coughing is an effective forced expiratory
technique
Chest Physiotherapy. Chest physiotherapy (CPT) is
primarily used for patients with excessive bronchial
secretions who have difficulty clearing them
Percussion and vibration are manual or mechanical
techniques used to augment postural drainage. These
techniques are used after the patient has assumed a
postural drainage position to assist in loosening the
mobilized secretions
CPT consists of postural drainage, percussion, and
vibration
Postural drainage is the use of positioning
techniques that drain secretions from specific
segments of the lungs and bronchi into the
trachea.
The purpose of various positions in postural
drainage is to drain each segment toward the
larger airways. A side-lying position can be
used for the patient who cannot tolerate a
headdown position
Percussion is performed in the appropriate
postural drainage position with the hands in
a cuplike position, with the fingers and
thumbs closed
Vibration is accomplished by tensing the
hand and arm muscles repeatedly and
pressing mildly with the flat of the hand on
the affected area while the patient slowly
exhales a deep breath
Percussion is performed in the appropriate
postural drainage position with the hands in
a cuplike position, with the fingers and
thumbs closed
Vibration is accomplished by tensing the
hand and arm muscles repeatedly and
pressing mildly with the flat of the hand on
the affected area while the patient slowly
exhales a deep breath
Nutritional Therapy
Surgical Therapy for COPD
Lung volume reduction surgery (LVRS). The
goal of this surgery is to reduce the size of
the lungs by removing the most diseased lung
tissue so the remaining healthy lung tissue
can perform better.
The second surgical procedure is bullectomy.
This procedure is used for carefully selected
patients with emphysematous COPD who
have large bullae (larger than 1 cm).
Surgical Therapy for COPD
Lung volume reduction surgery (LVRS). The
goal of this surgery is to reduce the size of
the lungs by removing the most diseased lung
tissue so the remaining healthy lung tissue
can perform better.
The second surgical procedure is bullectomy.
This procedure is used for carefully selected
patients with emphysematous COPD who
have large bullae (larger than 1 cm).
Surgical Therapy for COPD
The third surgical procedure is lung transplantation,
which benefits carefully selected patients with
advanced COPD. Although single-lung transplant is
the most commonly used technique because of a
shortage of donors, bilateral transplantation can be
performed
Airway bypass is a bronchoscopic procedure
currently under evaluation to determine if creating
small extra-anatomic openings between the diseased
lung and the distal bronchi can reduce hyperinflation