OT SEM 2 REHABILITATION OF PULMONARY DYSFUNCTION
Rehabilitation of Pulmonary Dysfunction
 To live is to breath
 Respiration
o The human body must receive oxygen and give up carbon
dioxide in order for life to continue
o Accomplished through the interrelationship of several systems
o Action of breathing
o A physiologic process of gas exchange within the lungs,
however, there is also respiration in the biological sense at the
cellular level where oxygen is utilized in oxidative tissue
metabolism and carbon dioxide is expelled as waste product in
the process
 Ventilation
o A process to cause air to enter and circulate freely into the lungs
o A process of transport in moving mass movement of oxygen
from air to the alveoli and removing carbon dioxide from the
alveoli
Review of Anatomy and Physiology
 The respiratory system is divided into the upper and lower respiratory
tracts
o Upper tract begins with the nose, pharynx, and larynx
o Lower tract consists of the trachea, the bifurcation (carina)
between the right and left main bronchi, then subdivide into
several branches of 16 generations until they end up to the
terminal bronchiole, before continuing to the respiratory
bronchiole down the alveolar ducts and terminate into the alveoli
 Upper tract prepares inspired air for entry into the lungs through
filtration, humidification, and heat supply
o Particles of dust, viruses, and bacteria are filtrated within
these nasal passages wherein ciliary activity, mucus
secretion, alveolar macrophages, lymphatics, cough and
airway reflexes act as the first line of defense.
 Lower tract is primarily a midline structure composed of smooth
muscles with regularly patterned cartilaginous rings that are
horseshoe shaped and incomplete posteriorly, having a
membranous sheath that forms a flat, posterior portion of the
trachea lying close to the esophagus
o At the end of the trachea is the carina or bifurcation which
divides into the right and left bronchi, wherein the right
bronchus extends as shorter, wider, and almost vertical tube
compared to the left bronchus which is longer and narrower
and extends out in a much sharper angle
o The significance of the difference of the two main bronchi is
that most of the mistaken or accidental insertion of the
endotracheal tube and aspiration of foreign bodies commonly
occur in the right bronchus
o The bronchi further divide into lobar bronchi, and repeatedly
bifurcate continuously through the segmental bronchi,
bronchioles, and several generations until distally terminate in
the alveoli
 Patency of the bronchi all throughout are maintained by smooth
muscles and incomplete cartilaginous rings and segmental
cartilaginous structures down the distal segments of the tree
o The inner lining of the bronchi is composed of
psuedostratified ciliated epithelium that is rich in mucus-
secreting goblet cells that serve to protect the lungs from
dust, virus, bacteria, and other particulate deposits
o Below this epithelial layer is composed of two structures, a
basement membrane and the membrane propria which is
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composed of loose fibrous tissue that has a rich capillary
blood supply
o There are also bands of longitudinal and circular elastic
fibers in the membrane that help to maintain the patency of
the segmental bronchi and bronchioles
 Terminal bronchi divide into bronchioles, which further divide into
terminal bronchioles, then with respiratory bronchioles
o These continue to subdivide to finally into alveolar ducts,
alveolar sacs, and the alveoli
o Bronchioles may be distinguished from bronchi because they
lack cartilage and their lining epithelium is a single layer, the
terminal bronchioles do not have mucus-secreting goblet
cells and cilia, and it’s epithelium is flattened
o Terminal bronchioles are the last purely conducting portions
of the bronchial tree where no gas exchange occurs.
o Distal to these are the respiratory bronchioles, alveolar
ducts, alveolar sacs, and alveoli which all make up gas-
exchanging lung units and are also called acinar gas-
exchanging unit
 Alveolar-lining membrane is also known as the alveolar-capillary
membrane which has five layers, namely; 1) a continuous lining
of squamous epithelium, 2) a fine basement membrane made up
elastic fibers and collagen, 3) the basement membrane of the
pulmonary capillary, 4) a ground substance, 5) the endothelial
lining of the pulmonary capillaries
o A thin layer of interstitial fluid bathes these membranous
layers
o There are three types of alveolar cells: type I, type II, and
alveolar macrophages
o Type I form the first lining of the alveolar-capillary membrane
while type II are larger and are highly active metabolically
and contain mitochondria, and are responsible for the
production of the substance, surfactant, which is responsible
for reducing alveolar surface tension
o Alveolar macrophages are the lung’s garbage disposal uniy
in preventing infection in the lungs.
 Located in the lung is an important group of granular cells
known as mast cells which lye beneath the bronchial epithelium
near smooth muscle and blood vessels, and their role is
releasing histamine in response to an antigen-antibody response,
such as seen in asthma
Pulmonary Mechanics
 For gas exchange to occur, this requires a muscular effort to
overcome the elastic recoil of the lungs and thoracic cage
 For an active inspiration to occur, respiratory muscles provide
the necessary force to accomplish this process
 Expiration is a passive action and does not need muscle effort
 Diaphragm is the chief respiratory muscle
 Other chest wall muscles include the intercostal muscles,
scalene and sternocleidomastoid muscles, and the abdominal
muscles
 During inspiration, the chest wall expands to increase volume by
virtue of: the dome of the diaphragm becomes flattened during
contraction, the external intercostal muscles and scalene
muscles elevate the anterior portion of the thorax and ribs, and
because of their adherence to the pleura, the lungs are pulled
outward with the chest wall
 During expiration, a normal quiet breathing occurs with the
normal elastic recoil of the lungs and chest wall that bring back
 OT SEM 2 REHABILITATION OF PULMONARY DYSFUNCTION
the chest to its normal resting position, which is all passive.
However, during forced expiration or labored breathing during
exercise, or due to disease, the internal intercostal muscles
draw the ribs and sternum downward, and contraction of the
abdominal muscles elevate the diaphragm which eventually
squeeze out the thoracic contents and forcing actively air out of
the lungs
I. Disturbances in Respiratory Function:
o The Effort or Cost of Ventilation depends on the following:
a) Elastic properties of the lungs, thorax, diaphragm,
abdominal complex, accessory muscles
b) The resistance to flow through the multiple air passages
between the outside and alveoli
Causes of Disorder
a) Muscle weakness or inefficiency, or, increasing stiffness of
elastic components
b) Increased resistance to air flow through the Tracheo-bronchial
tree (either Obstructive or Resistive)
c) Increased thickness of or decrease in area of the alveolar
diffusing membrane – usually associated with a restrictive
disorder leading to the decrease in Oxygen tension in the
arterial blood without Carbon Dioxide retention
d) Alveolar Hypoventilation wherein arterial Pco2 (Pulmonary Carbon
Dioxide pressure) increases above the normal 37-43 mmHg and
chronic hypoventilation syndrome Paco2 (Pulmonary arterial
Carbon Dioxide pressure) at 50-80 mmHg
e) Increased energy requirement to overcome elastic recoil of lung
or chest structures at any given ventilation, usually involves
disease that stiffens at the costovertebral, sternocostal
connections, fibrosis of the respiratory, abdominal, or shoulder
girdle, and lung fibrosis
f) Loss of muscle or loss of nerves that innervate the muscles of
respiration
g) Vital capacity is reduced by a decrease in inspiratory and
expiratory reserve volume
 Two major patterns of abnormal ventilatory functions are the
Obstructive and Restrictive:
1) In OBSTRUCTIVE PATTERN:
a) Hallmark is decrease in expiratory flow rate, i.e. Forced
Expiratory Volume (FEV)
b) Ratio FEV/FVC is reduced
c) TLC is normal or increased
d) RV is elevated due to trapping of air during expiration,
Obstructive Lung Diseases
a) Chronic Bronchitis - Expiratory airflow is obstructed by excessive
mucus secretion and pathologic changes seen in the airways
b) Pulmonary Emphysema - Air “trapped” in overdistended alveoli;
collapse of respiratory bronchioles on expiration causing
prolongation of expiratory airflow
c) Bronchial Asthma - Obstruction of expiratory airflow due to
pathologic changes in airways, mucus plugs, and spasms of
smooth muscles
d) Bronchiectasis - Inflammation, degradation, infection of the
bronchial wall causing obstruction to airway flow
e) Bronchiolitis - inflammation and / or infection of bronchiolar
surface causing obstruction to airway flow
f) Mucoviscidosis (Cystic Fibrosis) - Airways obstruction on
expiration due to secretions and exudates
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g) Coal Miner’s Pneumoconiosis - Excessive bronchial secretions
resulting in obstructed expiratory airflow
 Chronic Obstructive Lung Disease (COLD) is a general term
used for diseases involved in the disruption of normal
ventilation of air to and from the lungs
o It is a chronic expiratory airflow obstruction due primarily to
emphysema, often exacerbated by airways inflammation and
bronchospasm. Inevitably, it becomes progressive due to
loss of lung elastic tissue due to a normal part of aging.
 The three most commonly seen in clinical practice are: 1)
Chronic Bronchitis, 2) Pulmonary Emphysema, and 3) Bronchial
Asthma
 Although these three are separate and distinct diseases, in
practice, most patients may have bronchitis with emphysema,
and / or with a concomitant bronchial asthma, further complicated
with cor pulmonale
 However, there may be purely bronchitis or purely emphysema,
but mostly a combination of both is very common, and
sometimes the term Bronchitis-Emphysema has developed
 Although there are studies that determine and separate these
pathologic entities, certain predisposing factors seem to appear
to be common in both bronchitis and emphysema, namely:
1) Smoking: most common and well-established cause of
many lung diseases
2) Climate: a combination of cold and dampness that
contribute and trigger recurrence of chronic bronchitis
3) Atmospheric pollution: such pollutants coming from
industrial smoke or engine exhaust emissions
4) Occupation: exposure to dust particles such as in carpentry,
or in mining with exposure to high concentration of nitrous
oxide and sulfur dioxide, silicosis, asbestosis, and
pneumoconiosis
5) Aging: changes and reduction in the elastic qualities of
lung tissue and thoracic cage, kyphotic spine
A. Chronic Bronchitis
o Defined as excessive tracheobronchial mucus secretion
sufficient to cause cough with expectoration for at least 3
months of the year for 2 consecutive years
o It could be classified as simple chronic with mucoid sputum
production, chronic mucopurulent bronchitis by purulent
sputum in the absence of localized suppurative disease such
as bronchiectasis, chronic asthmatic bronchitis with cough
and mucus hypersecretion associated with dyspnea and
wheezing with acute respiratory infection or exposure to
inhaled irritants
o There is goblet hyperplasia and hypertrophy of submucosal
mucus glands, mucosal edema and inflammation, increased
smooth muscle in small airways, with loss of ciliary function
o Medical consultation is usually sought due to shortness of
breath associated with wheezes, usually preceded by a
recent respiratory infection
o Due to the presence of hypoxemia resulting in cyanosis in
the nail beds and tendency to edema in some joints, the
description is noted to be “blue and bloated” (Blue Bloaters)
o There may be coarse rhonchi and wheezes upon
auscultation
o Arterial blood gases are severely deranged and maximal
expiratory flow rates are reduced, residual volume is
OT SEM 2 REHABILITATION OF PULMONARY DYSFUNCTION
moderately elevated, and diffusing capacity is normal or
slightly decreased
o There may be episodes of respiratory failure but recovery is
usually good with therapy
B. Emphysema
o Described by a French physician Laennec in 1820 and
defined as distention of air sacs distal to the terminal
bronchioles with disruption of alveolar septa
o A degenerative and destructive disease involving the gas-
exchanging areas of the lungs
o Pathologic changes seen in Emphysema have four distinctive
features namely:
1) Alveolar walls degenerate into lacy patterns made up of
thin strands of collagen fibers, as the disease progress
2) Progression to destruction of alveolar tissue walls and
septa
3) Destruction of pulmonary capillaries of affected alveoli;
4) Development of air spaces
o Alveoli are hyperinflated as the elastic integrity is gradually
lost which retention or trapping of air along the alveoli. The
resulting patterns contribute to the four classification of
emphysema:
1) Centrilobular (Centriacinar): occurs anatomically in the
central portion of the lobule close to the respiratory
bronchioles; is the most common of the four; seen in
40-50 years old patients, more in men than in women;
frequently associated with bronchitis;
2) Bulla: progressive destruction of the whole lobule
occurs from the center outward until whole lobule
becomes a big air space, or “bulla”;
3) Panlobular (Panacinar): a more generalized pattern
which occurs in the acinar units with destruction of
alveolar septa and walls; usually common in 60-70
year olds;
4) In Chronic Bronchitis : wherein destruction of the
pulmonary capillary bed accompanies alveolar
destruction.
o Emphysema is an insidious disease wherein the progressive
destructed effect will only be seen with dyspnea upon
exertion.
o Usually seen in older and emaciated male with muscle
wasting, and having a characteristic barrel-chested
appearance, with elevated shoulder girdle, has to use all
muscles of respiration in order to breath
o Prolonged expiratory phase through slow pursed lips is
beneficial because the minute respiratory and terminal
bronchioles tend to collapse during normal phase / speed of
breathing, and thus help complete expiration
o In the presence of severe disease, emphysematous patients
maintain a normal gas exchange with an elevated hematocrit
value, which shows a patient with a “pink and puffy” (pink
puffers) appearance compared to a cyanotic appearance in
chronic bronchitis
C. Bronchial Asthma
o Defined as increased responsiveness of lower airways to
multiple stimuli
o Episodic and with reversible obstruction; may range in
severity from mild without limitation of patients activity to
severe and life-threatening
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o Unresponsive to conventional therapy which constitute life-
threatening situation is known to called “status asthmaticus”
o Basic abnormality is airway hyperresponsiveness to both
specific and non-specific stimuli, with enhanced
bronchoconstriction in response to inhalation of methacholine
or histamine
o Some classification of asthma may be the following:
1) Allergic Asthma
 Worsening or exacerbation of signs and symptoms due
to exposure to allergens or pollens
 Characteristically fall into the influence of a personal
or family history of allergies such as rhinitis, urticaria,
and eczema; positive skin test to allergens
 Increased serum IgE
2) Idiosyncratic Asthma: with negative skin tests for
allergens; bronchospasms occur after an upper
respiratory tract infection;
3) Exercise Asthma: due to exercise whether short or
prolonged
4) Cold Air or Occupational Asthma: exposure to sudden
changes in temperature especially from hot to cold;
5) Emotional Stress Asthma: due to fatigue, stress
 Common denominator in asthma is the non-specific
hyperirritability of the tracheobronchial tree
 With unknown etiology, however, airway inflammation plays a
fundamental role in the etiology; occlusion of bronchi and
bronchioles with thick, tenacious plugs; inflamed and thickened
basement membrane; spasms of smooth muscle cells causing
constriction of the tracheobronchial tree; as clogging occurs, air
in the alveoli distal to the occlusion can not escape and
eventually absorbed in the blood, resulting in atelectasis of the
affected alveoli
 Two Major Etiologic Theories in Asthma have had extensive
investigation, namely
1) Antigen-Antibody Theory
o An invasion of a foreign body (antigen) causes the
immune system to produce from mast cells IgE which
attaches to the antigen and as a consequence there
is a release of histamine and slow-reactive substance
of anaphylaxis (SRS-A) or other chemical mediators
such as bradykinin, acetylcholine, serotonin, and certain
prostaglandins that may be theorized to be involved in
the reaction in asthma
2) Role of the Autonomic nervous system in the regulation of
bronchial smooth muscle activity
o In 1948, Dr. R.P. Ahlquist discovered that there two types of
adrenergic receptors, alpha and beta, found in the glands,
smooth muscles, and mucosal vessels of the
tracheobronchial tree
o In 1960s, beta receptors were divided further into beta 1 and
beta 2, and, it was discovered that stimulation of the
adrenergic beta 2 receptors resulted in bronchodilatation
 The significance of this theory of beta 2 receptor led
to the consideration of pharmacological research in
selecting a drug with direct and specific beta 2
stimulation for the treatment of asthma
 Usually attacks are at nighttime, symptoms may be in the form
of wheezes, dyspnea, cough, fever, sputum production, or other
allergic disorders
OT SEM 2 REHABILITATION OF PULMONARY DYSFUNCTION
 Symptoms include tachypnea, tachycardia, use of accessory
respiratory muscles, cyanosis, pulsus paradoxus (accessory
muscle use and paradoxus correlate with severity of
obstruction); adequate lung aeration with symmetry of breath
sounds, wheezes, hyperinflation, and prolonged phase of
expiration to help almost full expiration with evidence of
congestive heart failure (CHF) or enlarged heart; evidence of
allergic nasal, sinus, or skin disease
 Differential Diagnosis
o Not all with wheezes are due to Asthma
o Wheezes can be found in congestive heart failure (CHF);
Bronchitis/Emphysema; Upper airway obstruction due to
foreign body; Tumors; Laryngeal Edema; Carcinoid Tumors
(usually associated with stridor, not wheezing); Recurrent
Pulmonary Emboli; Eosinophilic Pneumonia; Vocal Cord
Dysfunction; Systemic Vasculitis with Pulmonary involvement.
2) In Restrictive Pattern
a) Hallmark is decreased in TLC (Total Lung Capacity)
b) May be caused by pulmonary parenchymal disease or
extrapulmonary (neuromuscular such as myasthenia
gravis or chest wall such as kyphoscoliosis);
c) Prenchymal disease usually occur with a reduced RV ,
but extra-parenchymal disease (with expiratory
dysfunction) occur with an increased RV
Restrictive Diseases
1) Parenchymal Disorders
a) Restriction to lung and/or Alveolar expansion -
Pneumonia, Pneumothorax, Pleural Effusion, Pulmonary
Fibrosis, Pulmonary Edema, Atelectasis, Sarcoidosis,
Pneumoconiosis, Idiopathic pulmonary Fibrosis, Drug-
or Radiation-induced interstitial lung disease;
b) Infiltrative - Tuberculosis, Carcinoma;
2) Extra-parechymal Disorders
a) Neuromuscular disorders - Myasthenia Gravis, Muscular
Dystrophy, Cervical Spine Surgery, Poliomyelitis,
Guilain-Barre syndrome, Diaphragmatic weakness /
paralysis;
b) Thoracic deformity - Kyphoscoliosis, Pectus Excavatum;
c) Obesity - Pickwickian Syndrome, Abdominal Ascites
 Restrictive Lung Disorders
o In spite of varying causes, restrictive function is a result of
reduced vital capacity and other ventilatory function.
o An overall reduction in compliance of the thorax and/or lung
tissue resulting in loss of chest expansion and therefore a
reduction in the volume of air inspired and expired
a) Pneumonia
 The most common acute respiratory infection caused
by bacteria or viruses, but may include aspiration
pneumonia and hypostatic pneumonia
 The lung parenchyma becomes consolidated because
of inflammation of the lung tissue wherein the alveoli
are filled with exudates
 Several organisms can cause pneumonia:
pneumococci, staphylococci, streptococci, gram negative
bacilli, viruses, fungi, and others; primary pneumonia
is commonly produced by Diplococcus Pneumonea
while the secondary pneumonia is caused by
Staphylococcus Aureus
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
Another secondary pneumonia is the dreaded gram
negative Pseudomonas bacillus infection
 Signs and symptoms include fever, chills,
productive coughs, and general malaise;
Influenza vaccines may be found to be
effective in the prevention of pneumonia
infection
b) Restriction to lung and alveolar expansion
 A result from compression of the lung from within the
thorax, by fluid, pus or air, collection of fluid at the
alveolar level, or collapsed alveoli as in atelectasis
 These manifestations are seen in: Spontaneous
Pneumothorax, Pleural Effusion, Hydrothorax,
Hemothorax, Fibrothorax
c) Infiltrative disease
 Include damage to healthy lung tissue through invasion
of the respiratory system by bacteria, irritants, or
malignant cells
 All resulting in chronically inflamed lung tissue,
resulting to scarring, loss of lung compliance, and
impairment of respiratory function
 Usually seen in tuberculosis and malignant carcinoma
d) Pneumoconiosis
 Both a restrictive and obstructive lung disease wherein
it is most commonly found in coal miners where they
are exposed to coal dust
 The dust is black that when the patient coughs it
exhibits black sputum, called “Black Lung”
e) Asbestosis
 The asbestos found in workers as pipe laggers in
shipyards, industrial plumbers, mechanics on brake
lining, in hair dryers, irons, and kitchenware, all may
cause lung fibrosis upon prolonged exposure and may
cause bronchial carcinoma or mesothelioma, a tumor
of the pleural cavity causing pleural effusion with
extremely poor prognosis
f) Thoracic deformity
 May cause decreased lung volume due to restriction
as seen Kyphoscoliosis and Pectus Excavatum;
g) Nerve defects may cause restrictive type of lung
disease as seen in paralysis due to PNI, SCI,
infections involving the nerve as in Poliomyelitis, auto-
immune disease causing Guillaine-Barre Syndrome,
h) Neuromuscular junction defect as in post-synaptic cleft
disease in Myasthenia Gravis resulting to weakness of
the respiratory nerves
i) Muscle defects as seen in Muscle Dystrophies and
other hereditary muscle diseases;
j) Obesity
 Restriction is a result of overdistended belly pushing
abdominal contents upward against the diaphragm and
limiting its descent causing decreased expiratory
reserve volume
 A term seen in obese people called “Pickwickian
Syndrome” which applies to a certain group of
severely obese people, described by Charles Dickens,
showing clinical features as extremely obese,
somnolence, twitching, cyanosis, periodic respiration,
polycythemia, right ventricular hypertrophy, and right
ventricular failure, associated with alveolar
OT SEM 2 REHABILITATION OF PULMONARY DYSFUNCTION
hypoventilation with increased arterial Pco2 and
decreased arterial Po2
 Somnolence and fatigue are the main reason why
these patients would want medical consultation and/or
hospital admission
 Patients will fall asleep sitting or even standing and it
can occur during the middle of a conversation or
some other light activity which eventually become a
source of embarrassment to the patient
 With dramatic weight reduction, Pickwickian Syndrome
is treated with most impressive return of the patient to
normal pulmonary status
Review the different Lung Volumes and Graph by Spirograph
Tracing:
 Tidal Volume (TV)
o Amount of air that can be inhaled or exhaled during one
respiratory cycle
 Vital Capacity (VC)
o Total amount of air exhaled after maximal inhalation
 Residual Volume (RV)
o The volume of air remaining in the lungs after maximal exhalation
 Inspiratory Residual Volume (IRV)
o Amount of air that can be forcibly inhaled after a normal tidal
volume
 Expiratory Residual Volume (ERV)
o The volume of air that can be exhaled forcibly after exhalation of
normal tidal volume
 Functional Residual Capacity (FRC)
o The amount of air remaining in the lungs at the end of a normal
exhalation
 Inspiratory Capacity (IC)
o The maximum volume of air the lungs can accommodate or sum
of all volume compartments or volume of air in lungs after
maximum inspiration
 Total Lung Capacity (TLC)
o The maximum volume of air the lungs can accommodate or sum
of all volume compartments or volume of air in lungs after
maximum inspiration
Disturbance in Pulmonary Circulation
 Pulmonary circulation reflects the residual volume (RV) output,
which at low pulmonary pressure, it is approximately 5L/min, of
which perfusion of lung is greatest
 In assessing this, it requires measuring pulmonary vascular
pressure and cardiac output to determine pulmonary vascular
resistance
 Hypoxia, intraluminal thrombi, scarring, or lessened or loss of
alveolar beds would cause increase in pulmonary vascular
resistance or hypertension.
 All respiratory diseases causing hypoxia are capable of causing
pulmonary hypertension, more so on those patients having
hypoxemia due to chronic obstructive pulmonary disease
(COPDs), interstitial lung disease, chest wall disease, and
obesity-hypoventilation sleep apnea
1) Pulmonary Embolism
 Immediate result is obstruction of pulmonary blood flow
to the distal lung, with consequence of: a) wasted
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ventilation or no perfusion of air ventilated, b)
atelectasis occurs following 2-24 hours after episode of
embolism, and c) widespread alveolar-arterial Po2
gradient usually with arterial hypoxemia
 As a result of these there is pulmonary hypertension,
acute residual volume failure, and decline in cardiac
output
 Signs and symptoms are sudden onset of dyspnea
(most common), chest pain, hemoptysis accompany
infarction of the lung, syncope indicating massive
embolism
 Common also is tachypnea and tachycardia; residual
volume gallop; loud P2 and prominent jugular alpha
waves suggestive of right ventricular failure;
temperature is >39 degrees centigrade; hypotension
suggest massive pulmonary embolism
 Treatment is IV Heparin by continuous infusion;
surgery to extract the embolus is optional
2) Primary Pulmonary Hypertension
 An uncommon condition with typical female patient
with hyperventilation, chest discomfort, anxiety,
weakness, fatigue, and later, dyspnea with precordial
pain on exertion; effort syncope occurs very late and
signifies ominous prognosis
 Prominent alpha waves in jugular venous pulse, right
ventricular heave, narrowly split S1 with accentuated
P2; right-sided heart failure with right Atrial and
ventricular enlargement and tricuspid regurgitation
 Treatment is palliative, where there is progressive
deterioration
 Main focus in treatment is vasodilatation with
use of drugs with the goal of lowering
pulmonary artery pressure and pulmonary
vascular resistance while preserving systemic
pressure; massive doses of calcium channel
antagonists may reduce pulmonary pressure
and resistance, however, less than 50%
respond well with this regimen;
anticoagulation drugs may be recommended
for all patients; but if medical therapy fails,
heart transplant is recommended
Disturbance in Pulmonary Gas Exchange
 Defined as impedance to the primary function of the lungs to
remove CO2 and provide O2, with normal tidal volume of about
500ml, and with normal frequency is 15 breaths/min for a total
ventilation of 7.5 L/min., however, because of the dead space
the total ventilation is only 5 L/min
 Gas exchange is critically dependent on proper matching of
ventilation and perfusion; assessment of gas exchange requires
measurement of arterial blood gases
 The actual content of O2 in blood is determined by both Po2
and Hemoglobin; adequate CO2 removal is reflected in the
partial pressure of CO2 in arterial blood
 The pulse oximeter measures oxygen saturation Sa02 (Systemic
O2) rather than Pa02 (Pulmonary O2); ability of gas to diffuse
across the alveolar-capillary membrane is assessed by the
diffusing capacity of the lung (DLco)
OT SEM 2 REHABILITATION OF PULMONARY DYSFUNCTION
 Value depends on alveolar-capillary surface area, pulmonary
capillary blood volume, degree of ventilation-perfusion (V/Q)
mismatching, and thickness of alveolar-capillary membrane
Four basic mechanisms of hypoxemia
1) Decreased inspired Po2
2) Hypoventilation
3) Shunt
4) V/Q mismatch
Potential contributing factors in the development of hypercapnia
1) Increased CO2 production
2) Decreased ventilatory drive
3) Malfunction of the respiratory pump or increased airway
resistance
4) Inefficiency of gas exchange (increased dead space or V/Q
mismatch) necessitating a compensatory increase in overall
minute ventilation
RESPIRATORY FAILURE
 Defined as the inability of the respiratory apparatus to maintain
adequate oxygenation of the blood, with or without carbon
dioxide retention
 Main factors of respiratory failure are of two aspects, namely:
1) Hypoxemic Respiratory Failure with reduction in arterial Po2
(60 mmHg or below) and a normal or slight decreased
arterial Pco2
2) Hypoventilatory Respiratory Failure characterized by both
hypoxemia and an elevated arterial Pco2 (>50 mmHg) or
hypercapnia;
RESPIRATORY CARE
 In order to have a high quality respiratory care unit, efforts from
a skilled medical team must be available
 Such a team is composed of a physician director,
pulmonologists, anesthesiologists, physiotherapists, respiratory
therapists, nurses and auxiliary personnel
PULMONARY REHABILITATION
 “ The art of the medical practice wherein an individually tailored,
multidisciplinary program is formulated which through accurate
diagnosis, therapy, emotional support, and education, stabilizes
or reverses both the physio- and psychopathology of pulmonary
diseases and attempts to return the patient to the highest
possible functional capacity allowed by his pulmonary handicap
and overall life situation.” , by John R. Bach,M.D. (De Lisa)
 Pulmonary Rehabilitation goals are the following:
1) Improve cardiopulmonary function
2) Prevent and treat complications
3) Recognize and treat stress and depression, which often
interfere with coping mechanisms and independence
4) Facilitate coping mechanisms to overcome any sense of
loss (e.g. control of personal and social relationships, self-
esteem, sense of self-worth)
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5) Promote increasing patient responsibility for his or her own
care and well-being, including acceptance of and
compliance with optimum medical care with the goal of
reducing numbers of exacerbations, emergency room visits,
and hospitalization
6) Increase understanding of the disease process so that the
patient and family can confront it realistically
7) Return to a more active, productive, and emotionally
satisfying life, and possibly to work
 Essential Elements of Pulmonary Rehabilitation:
a) Careful initial evaluation
b) Educational content
c) Exercise program
d) Psychological session
e) Tailored chest physiotherapy and respiratory therapy
f) Evaluation post-program
g) Provision for post-program maintenance of the patient
 Careful initial evaluation: history and physical examination is
essential, laboratory and pulmonary function test and exercise
testing are required here to determine the level or degree of
disability, level of exercise tolerance, cardiovascular status, and
prognosis for improvement
 Educational content: this is a very important element in the
rehabilitation program, any oral instruction must also be made
available with reading manuals
 Exercise program: this is the hallmark of increased physical
conditioning because of an increase in muscular and
cardiovascular tone
 Psychological session: it is very important to have psychology
sessions with the patient and his family members with clinical
psychologist and rehabilitation counselor; also this helps cope
with the guilt of past bad habits or the frustrations involved in
patient’s situation, and also an excellent time to teach patient
stress reduction and relaxation techniques
 Tailored chest physiotherapy and respiratory therapy:
individualized instruction on postural drainage techniques that
can be done at home on a regular basis or as necessary when
secretions are increased is very essential, as is careful
demonstration of the use, cleaning, and maintenance of
respiratory equipment for the home; coughing technique,
rebreathing technique, and use of good body mechanics when
performing activities of daily living are also very essential to the
rehabilitation process for the care and recovery of the patient
 Evaluation post-program: this is feedback to evaluate what
content of knowledge the oral and manual materials have been
retained by the patient; also evaluates the increase in exercise
tolerance, the degree of which dyspnea has been reduced
during exercise, and the level of improvement in performance of
activities of daily living
 Provision for post-program maintenance of the patient: there
must be continuous care and follow-up evaluations of patients
on a post-program quarterly basis not only for data collection
but for group get-togethers
Foundations of respiratory care:
a) Oxygen therapy
o It is important to understand the essential use in correcting
compromised oxygen-deprived (hypoxemia) patients and it’s
potential damage it may cause when it is used
inappropriately on the respiratory patient
b) Humidification and nebulization
OT SEM 2 REHABILITATION OF PULMONARY DYSFUNCTION RESPICIO 5OT
o Conditioning of inspired air is essential to mucus production,
ciliary activity, and a healthy respiratory tract
o Adding moisture to the respiratory tract must be undertaken
when normal function is compromised in respiratory patients
o Humidification is one method is to help in a dry gas (oxygen)
during administration, or when a nasopharynx is bypassed by
endotracheal intubation or tracheostomy, or the presence of
thick, tenacious secretions, and, in the relief of croup or
tracheitis
o Nebulization adds moisture to the inspired air by additional
water droplets of varying sizes and compose the general
term of aerosol
c) Chest physiotherapy
o Usually applied to patients immobilized who are at risk of
developing pulmonary secretions that may compromise
breathing, atelectasis, as well as the eventual development
of pulmonary infection seen in pneumonia; this may
compose of regular proper turning technique as in postural
drainage, chest percussion and vibration, rocking, and
assisted coughing, deep breathing exercises
d) Adequate ventilation
o For compromised respiratory patients it is highly indicated to
apply mechanical ventilators to correct the inadequacy of
ventilation; mechanical ventilators come into place that are
available and their use should be appropriate according to
the necessary need of the patient
o Some such devices are the pressure-set and volume-set
ventilators; assisted ventilators; controlled ventilators; positive
end expiratory pressure (PEEP) ventilator; continuous
positive airway pressure (CPAP) ventilator; intermittent
mandatory ventilation (IVM); synchronous intermittent
mandatory ventilation (SIMV)
e) Drugs
o Antibiotics to correct infections
o Liquefaction of secretions which are generally termed
mucolytics
o For relief of bronchospasm are the sympathomimetics;
selective beta-2 stimulants; corticosteroids to control
inflammation; drugs used to stimulate respiration; drugs used
in treatment of acid-base disturbances
f) Hydration
o Pulmonary patients should be adequately hydrated for normal
fluid and electrolyte balance, avoidance of
hematoconcentration, avoidance of urine concentration;
however, there is danger also in too much hydration