PATHOPHYSIOLOGY OF
RESPIRATORY SYSTEM
DISEASES
Mehtap KAÇAR KOÇAK M.D. PhD
Yeditepe University Medicine School,
Pathophysiology
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1
General Introduction

Respiratory diseases is often
classified as acute or chronic,
obstructive or restrictive, and
infectious or noninfectious.
2
Reduction of Pulmonary Function
1.
2.
Inadequate blood flow to the lungs –
hypoperfusion
Inadequate air flow to the alveoli hypoventilation
3
Signs and Symptoms of
Pulmonary Disease
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Dyspnea,
Abnormal breathing patterns,
Hypoventilation and hyperventilation,
Cough,
Hemoptysis,
Cyanosis,
Pain,
Clubbing,
Abnormal sputum.
4
Dyspnea
Dyspnea – subjective sensation of
uncomfortable breathing, feeling “short of
breath”
 Ranges from mild discomfort after
exertion to extreme difficulty breathing at
rest.
 Usually caused by diffuse and extensive
rather than focal pulmonary disease.

5
Dyspnea

Due to:
Airway obstruction
• Greater force needed to provide
adequate ventilation
• Wheezing sound due to air being
forced through airways narrowed due to
constriction or fluid accumulation
 Decreased compliance of lung tissue

6
Signs of dyspnea:
Flaring nostrils
 Use of accessory muscles in breathing
 Retraction (pulling back) of intercostal
spaces
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7
Types of dyspnea
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Orthopnea; is caused by the horizontal position,
which redistributes body water, causes the
abdominal contents to exert pressure on the
diaphragm, and decreases the efficiency of the
respiratory muscles.
Some individuals with left ventricular failure wake up
at night gasping for air and must sit up or stand to
relieve the dispnea, this type of positional dyspnea
is termed Paroxysmal nocturnal dyspnea (PND)
PND results from fluid in the lungs caused by the
redistribution of of body water while the individual is
recumbent.
8
Abnormal breathing patterns
Normal breathing (eupnea) is rhythmic and
effortless. Ventilatory rate is 8 to 16
breaths per minute, and tidal volume
ranges from 400 to 800 ml.
 The rate, depht, regulatory and effort of
breathing undergo characteristic alterations
in response to physiologic and
pathophysiologic conditions…..

9
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Kussmaul respiration (hyperpnea); is
characterized by
→a slightly increased ventilatory rate,
→ very large tidal volume,
→ no expiration pause.
Strenous exercise or metabolic acidosis induces
Kussmaul respiration.
Labored or obstructed breathing consists of slow
ventilatory rate, large tidal volume, increased effort,
and prolonged inspiration or expiration, depending
on the site of obstruction.
Audible wheezing (whistling sounds) and stridor
(high-pitched sounds made during inspiration) is
often present.
10
Restricted breathing is characterized by
small tidal volumes and rapid ventilatory rate
(tachypnea).
 Restricted breathing is commonly caused by
disorders such as pulmonary fibrosis that
stiffen the lungs or chest wall and decrease
compliance.
 Panting occurs with exercise.
 Shock and severe cerebral hypoxia
contribute to gasping respirations that
consist of irregular, quick inspirations with an
expiratory pause.
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11
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Sighing respirations consists of irregular
breathing characterized by frequent, deep sighing
inspirations. Sighing respirations are caused by
anxiety.
Cheyne-Stokes respirations are characterized by
alternating periods of deep and shallow breathing.
Apnea lasting 15 to 60 seconds is followed by
ventilations that increase in volume until a peak is
reached, after which ventilation (tidal volume)
decreases again to apnea.
This respirations results from any condition that
slows the blood flow to the brain stem, which in turn
slows impulses sending information to the
respiratory centers of the brain stem.
12
Hypoventilation and hyperventilation
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Hypoventilation is inadequate alveolar ventilation
in relation to metabolic demands. It is caused by
alterations in pulmonary mechanics or in the
neurologic control of breathing.
With hypoventilation, CO2 removal does not keep
up with CO2 production and PaCO2 increases,
causing hypercapnia (PaCO2>44 mmHg).
This results in respiratory acidosis, which can
affect the function of many tissues throughout the
body. (somnolence or disorientation)
13
Hyperventilation is alveolar ventilation that
exceeds metabolic demands. The lungs
remove CO2 at a faster rate than it is produced
by cellular metabolism, resulting in decreased
PaCO2 or hypocapnia (PaCO2<36 mmHg).
 Hyperventilation results in a respiratory
alkalosis that also can interfere with tissue
function.
 Hyperventilation commonly occurs with severe
anxiety, acute head injury, and conditions that
cause insufficient oxygenation of the blood.
 Hypoventilation and hyperventilation can be
determined only by arterial blood gas analysis.

14
Blood Gas Analysis
 Factors
Connected with blood gas
measurements
 Abnormalities
of respiratory control
 Gas
exchange
 Respiratory mechanics
 Circulation
15
Blood Gas Analysis
 Blood
gas values
pH : 7.35—7.45
 PaO2: 80—100mmHg(10.6~13.3kpa)
 SaO2: 91—97.7%
 PaCO2: 35—45mmHg(4.67~6.0kpa)

16
Cough
Attempt to clear the lower respiratory
passages by abrupt and forceful
expulsion of air
 Most common when fluid accumulates in
lower airways
 Most coughs are initiated in the larynx
and in the tracheabronchial tree by both
mechanical and chemical irritant receptor
stimulation.
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17
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Other cough receptors are located:
The external auditory canal,
Diaphragm,
Pericardium,
Pleura,
Stomach,
The most distal bronchioli and the alveoli (a
few).
Stimulation of cough receptors is transmitted
centrally through the vagus nerve. (this way is
inhibited by opiates and serotoninergic agents)
18
Acute cough:
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It is cough that resolves within 2 to 3 weeks of
the onset of illness or resolves with treatment
of the underlying condition.
It is commonly the result of;
Upper respiratory infections,
Allergic rhinitis,
Acute bronchitis,
Pneumonia,
Congestive heart failure,
Pulmonary embolus,
Aspiration.
19
Chronic cough:

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It is defined as cough that has persisted for more
than 3 weeks.
In nonsmokers, chronic cough is almost always
caused by
postnasal drainage syndrome,
Asthma,
Gastroesophageal reflux disease.
In smokers, chronic bronchitis is the most
common cause of chronic cough.
20
Hemoptysis:

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Hemoptysis is the coughing up of blood or
bloody secretion.
Hemoptysis is sometimes confused with
hematemesis, which is the vomiting of blood.
Blood that is coughed up is usually bright red,
has an alkaline pH, and is mixed frothy
sputum, whereas blood that is vomited is
dark, has an acidic pH, and is mixed with food
particles.
21

Hemoptysis results from damage to the
lung parenchyma with rupture of
pulmonary vessels or from inflammation,
injury, or cancer of the bronchial tree.
22
The most common causes of
hemoptysis are:
Tuberculosis,
 Bronchiectasis,
 Lung cancer,
 Bronchitis,
 Pneumonia.

23
Cyanosis
Cyanosis is bluish discoloration of the
skin and mucous membranes caused by
increasing amounts of desaturated or
reduced hemoglobin (which is bluish) in
the blood.
 Cyanosis generally develops when 5 g of
hemoglobin is desaturated, regardless of
hemoglobin concentration.

24
Cyanosis can be caused by decreased
arterial oxygenation (low PaO2), pulmonary
or cardiac right-to-left shunts, decreased
cardiac output, cold environments, or anxiety.
 Lack of cyanosis does not necessarily
indicate that oxygenation is normal. For
example, severe anemia and CO poisoning
can cause inadequate oxygenation of tissues
without causing cyanosis.

25
Most cases arise as a result of peripheral
vasoconstriction – result is reduced blood
flow, which allows hemoglobin to give up
more of its oxygen to tissues- peripheral
cyanosis.
 Best seen in nail beds
 Due to cold environment, anxiety, etc.

26

Central cyanosis can be due to :
Abnormalities of the respiratory membrane
 Mismatch between air flow and blood flow
 Expressed as a ratio of change in ventilation
(V) to perfusion (Q) : V/Q ratio
• Pulmonary thromboembolus - reduced
blood flow
• Airway obstruction – reduced ventilation

 In
persons with dark skin can be seen
in the whites of the eyes and mucous
membranes.
27
Pain

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Pain caused by pulmonary disorders originates
in the pleurae, airways or chest wall.
Pleural pain is the most common pain caused
by pulmonary disease and is usually sharp or
stabbing in character. (infection and
inflammation)
Pleural pain is also common with pulmonary
infarction caused by pulmonary embolism.
28
Pulmonary pain is central chest pain that
is pronounced after coughing and occurs
in individulas with infection and
inflammation of the trachea or bronchi. (it
is differentiated from cardiac pain).
 Pain in the chest wall is muscle pain or rib
pain. (excessive coughing,
costochondritis)

29
Clubbing

Clubbing is the selective bulbous
enlargement of the end (distal segment)
of a digit (finger or toe), whose severity
can be graded from 1 to 5 based on the
extend of nail bed hypertrophy and the
amount of changes in the nails
themselves.
30
31
Clubbing is commonly associated with
diseases that interfere with oxygenation,
such as bronchiectasis, cystic fibrosis,
pulmonary fibrosis, lung abscess and
congenital heart disease.
 Lung cancer is sometimes associated
with clubbing even in the absence of
significant hypoxemia.
 This syndrome is called hypertrophic
osteoarthropathy (HOA) and its
pathogenesis is unknown.

32
Abnormal sputum

The color, consistency, odor and amount
of sputum vary different pulmonary
disorders.
33
Conditions Caused by
Pulmonary Disease or Injury
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Hypercapnia,
Hypoxemia,
Acute respiratory failure,
Pulmonary edema,
Aspiration,
Atelectasis,
Bronchiectasis,
Bronchiolitis,
Pleural abnormalities (pneumothorax,
pleural effusion, empyema)
Abscess formation and cavitation,
Pulmonary fibrosis
34
Hypercapnia
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Hypercapnia or increased CO2 in the arterial blood
is caused by hypoventilation of the alveoli.
Causes include;
* depression of the respiratory center by drug,
* infection of CNS or trauma,
* spinal cord disruption or poliomyelitis,
* diseases of the neuromuscular junction (MG, MD)
* chest injury,
* large airway obstruction.
Hypercapnia and the associated respiratory
acidosis can result in several important clinical
manifestations. (dysrythmia, coma, somnolence)
35
Hypoxemia
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Hypoxemia or reduced oxygenation of arterial blood is
caused by respiratory alterations.
The five causes of hypoxemia are;
* decreased oxygen content in inspired gas (high altitude),
* hypoventilation (drug overdose, neurologic damage),
* diffusion abnormalities (emphysema, fibrosis, edema),
* abnormal ventilation-perfusion ratios (asthma, chronic
bronchitis, ARDS),
* pulmonary right-to-left shunt (congenital heart defects).
Hypoxemia is often associated with a compensatory
hyperventilation and resultant respiratory alkalosis.
Hypoxemia result in widwspread tissue dysfunction and
when severe can lead to organ infarction.
36
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Adult Respiratory Pathophysiology
W. Rose
Acute respiratory failure
Respiratory failure is defined as
inadequate gas exchange, that is
hypoxemia, where
 PaO2 is ≤50 mmHg
 PaCO2 is ≥50mmHg, (hypercapnia)
 pH ≤7.25.
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38
Pulmonary edema
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Pulmonary edema is excess water in the lung.
The normal lung contains very little water or
fluid.
It is kept dry by lymphatic drainage and a
balance among capillary hydrostatic pressure,
capillary oncotic pressure and capillary
permeability.
The most common cause of pulmonary edema
is heart disease.
39
Pulmonary Circulation:
• Consists of:
• Pulmonary artery & its branches
• Thin-walled, easily distensible
Pulmonary
capillaries
• Pulmonary venous system
• Left Atrium
• Low pressure
• Low resistance to blood flow
• Accepts all blood from right heart
40
PA pressure:
Sys: 20 – 30 mm Hg
Dias: 8 – 12 mmHg.
12 – 15 mm Hg mean
Normal L.A.Pr: 8 mm Hg with an
Upper limit of 15 mm Hg
Blood vol: About 1 litre.
More than 100 ml in capillaries.
41
Pulmonary Circulation
Pul cap pr.: about 10 mm Hg
 Oncotic pressure: 25 mm Hg
 Inward gradient: 15 mm Hg
 Pul congestion and oedema result
when the pul cap pr is >25 mm Hg
(“backward failure”)

42
Pulmonary Arterial Pressure rises
during:
 Negative
pressure breathing
 Supine position
 Systemic venous congestion from
any cause
 Overtransfusion
 Left ventricular failure
43
Pulmonary Arterial Pressure falls
during:
Positive pressure breathing
 Upright position
 Valsalva manuevre
 After haemorrhage
 Systemic vasodilatation from any
cause.
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44
PULMONARY EDEMA
Classified into:
Cardiogenic: Otherwise
called as Hydrostatic or
Transudative.
Non-Cardiogenic: Other-wise
called as Permeability or
Exudative.
45
Cardiogenic
Pulmonary
Edema


Increased
pulmonary
vascular
pressure
Transudation of
fluid across
endothelium into
pulmonary
interstitium and
then into the
alveolar space.
Noncardiogenic
Pulmonary
Edema


Low pressure
pulmonary edema
Injured
microvascular
endothelium
allows protein-rich
fluid to enter the
extravascular
spaces.
46
Noncardiogenic
Pulmonary
Edema Causes:
Cardiogenic
Pulmonary
Edema Causes:
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Left ventricular
failure
Volume overload
Mechanical
obstruction of left
outflow tract e.g.
Mitral stenosis
Other valvular
diseases like Mitral
stenosis, PDA,
Aortic valvular
diseases & also in
congestive failure
and hypertension.
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
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Toxins: eg. Smoke,
ozone, phosgene,
Nitrogen dioxide,
Emboli: Air,
thrombotic, amniotic
fluid
Trauma and burns
Aspiration of gastric
contents
Acute radiation
Pneumonitis
D.I.C.
47
PULMONARY EDEMA MIXED
PATHOGENESIS
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Incompletely understood:
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High altitude pulmonary edema
Neurogenic: midbrain lesions, Middle/Posterior
cranial fossa surgeries
Reperfusion pulmonary edema
Narcotic overdose
Tocolytic therapy
Uraemia
Negative pressure pulmonary edema.
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PUL EDEMA – SIGNS & SYMPTOMS
Symptoms:
Acute Dyspnea
Cough, Pink frothy sputum
Signs:
Tachycardia
Blood Pressure: variable
Lung crepitations
50
PUL EDEMA – SIGNS & SYMPTOMS

Other signs of congestion:
Increased JVP
 Peripheral edema

 Cardiac
enlargement -- apex beat
displaced
 S3 Gallop – apical 3rd heart sound
51
Atelectasis
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Atelectasis is the collaps of lung tissues. The two
types of atelectasis:
1- Compression atelectasis is caused by the
external pressure exerted by a tumor in the lung,
or by fluid or air in the pleural space.
2- Absorption atelectasis results from gradual
absorption of air from obstructed or hypoventilated
alveoli or from inhalation of concentrated oxygen
or anesthetic agent.
.
52
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Clinical manifestations of atelectasis
are dyspnea, cough, fever and
leukocytosis.
Atelectasis tends to occur after surgery.
Prevention and treatment of
postoperative atelectasis usually
include deep breathing. (open pore of
Kohn)
53
54
Bronchiectasis

Bronchiectasis is
persistent
abnormal dilatation
of the bronchi.
55
56
Pathophysiology
It results from two causes:

Infectious insult

Impairment of drainage, airway
obstruction, and/or a defect in host
defense.
57
Infection:
Bacterial, mycobacterial,  central airway bronchiectasis

Airway obstruction:
intraluminal tumor, foreign body, lymph nodes, COPD

Immunodeficiency:
ciliary dyskinesia, HIV, hypogammaglobulinemia, cystic
fibrosis (obstruction and immunodef.)

58
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Bronchial dilatation may be;
Clindrical bronchiectasis, (with symmetrically
dilated airways as is commonly seen after
pneumonia and is reversible)
Saccular bronchiectasis (in which the bronchi
become large and balloon-like),
Varicose bronchiectasis (in which
constrictions and dilations deform the
bronchi).
59
60
Clinical manifestations of
bronchiectasis:
Cough (90 %)
 Daily sputum production (76%)
 Dyspnea (72%)
 Hemoptysis (56%)
 Recurrent pleurisy

61
62
63
Bronchiectasis

If wide spread 

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Dyspnea
Clubbing of the
fingers
 h pulmonary
blood pressure 
Cor pulmonale
64
Pneumothorax

Pneumothorax is the presence of air or
gas in the pleural space caused by a
rupture in the visceral pleura or parietal
pleura and chest wall.
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PULMONARY DISORDERS
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Acute Respiratory Distress Syndrome (ARDS)
Obstructive Pulmonary Diseases :
*Chronic obstructive pulmonary diseases
(Chronic bronchitis and Emphysema)
*Asthma
Respiratory Tract Infections (Tuberculosis)
Pulmonary Vascular Disease (Pulmonary
Embolism and Pulmonary Hypertension)
67
Acute Respiratory Distress Syndrome :
 Acute
Respiratory Distress Syndrome
(or Adult Respiratory Distress Syndrome)
• Rapid and severe onset of respiratory
failure characterized by acute lung
inflammation and diffuse injury to the
respiratory membrane with
noncardiogenic edema.
68
ARDS
Identified in last 25 years
 Affects 200 -250 thousand people each
year in U.S.
 Mortality in persons < 60 is 40% (↓ 67%)
 Those over 65 and immuno compromised
still have mortality over 60 %
 Most survivors have almost normal lung
function 1 year after acute illness.

69
Pathophysiology of ARDS

All disorders causing ARDS acutely injure
the respiratory membrane and produce
severe pulmonary edema, shunting, and
hypoxemia.

Shunting: blow flow is normal, but gas
exchanged is decreased. V/Q ratio changes:
the same effect as if blood were shunting or
bypassing the lungs.
70
Damage can occur directly:
 Aspiration of acidic gastric contents
 Inhalation of toxic gases
 Or indirectly:
 Chemical mediators from systemic
disorders

71
Result is massive inflammatory
response by lungs
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Initial injury damages the pulmonary capillary
epithelium, causing platelet aggregation and
intravascular thrombus formation.
Platelets release substances that attract and
activate neutrophils.
Damage also activates the complement cascade
which also activates neutrophils and the
inflammatory response.
72
Role of neutrophils is central to the
development of ARDS.
 Neutrophils release inflammatory mediators:

Proteolytic enzymes
 Toxic oxygen products
 Prostaglandins and leukotrienes
 Platelet activating factors


These damage the respiratory membrane and
increase capillary permeability, allowing fluids,
proteins, and blood cells to leak into alveoli →
pulmonary edema and hemorrhage
73
Reduces pulmonary ventilation and
compliance
 Neutrophils and macrophages release
mediators that cause pulmonary
vasoconstriction → pulmonary hypertension
 Type II alveolar cells also damaged, see
decreased surfactant production
 Alveoli fill with fluid or collapse.
 Lungs become less compliant, and
ventilation decreases.

74
After 24 – 48 hours hyaline membranes
form
 After about 7 days, fibrosis progressively
obliterates the alveoli, respiratory
bronchioles and interstitium
 Result is acute respiratory failure

75
In addition, chemical mediators often
cause widespread inflammation,
endothelial damage and increased
capillary permeability throughout the body
 This leads to systemic inflammatory
response syndrome, which leads to
multiple organ dysfunction syndrome
(MODS)
 Death may not be caused by ARDS alone,
but by MODS

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McCance & Heuther 32.09
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Clinical manifestations:

Symptoms develop progressively:
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Hyperventilation→
respiratory alkalosis→
dyspnea and hypoxemia→
metabolic acidosis→
respiratory acidosis →
further hypoxemia →
hypotension →
decreased cardiac output →
death
79
Evaluation and Treatment

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Diagnosis based on physical examination, blood
gases and imaging
Treatment is based on early detection,
supportive therapy and prevention of
complications, esp. infection
Often requires mechanical ventilation
Many studies underway for treatment:

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Prophylactic immunotherapy
Antibodies against endotoxins
Inhibition of inflammatory mediators
Inhalation of nitric oxide to reduce pulmonary
hypertension
Surfactant replacement
80
Obstructive and Inflammatory
Lung Disease
Chronic Bronchitis
 Emphysema
 Asthma

Christine Hooper, Ed.D., RN
Spring 2006
81
A- Normal lung, B- Emphysema, C- Chronic bronchitis, D- Asthma
NURSING 621
W. Rose
Chronic Obstructive
Pulmonary Disease: COPD
Disease of airflow obstruction
that is not totally reversible
Chronic
Bronchitis
Emphysema
83
Risk Factors for COPD
Nutrition
Infections
Socio-economic status
Aging Populations
84
COPD: Etiology
Cigarette smoking #1
 Recurrent respiratory infection
 Alpha 1-antitrypsin deficiency
 Aging

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Adult Respiratory Pathophysiology
W. Rose
Mucous plug
McCance & Heuther 32.12
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Adult Respiratory Pathophysiology
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McCance & Heuther 32.13
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Adult Respiratory Pathophysiology
W. Rose
Chronic Bronchitis
Recurrent or chronic productive cough for
a minimum of 3 months for 2 consecutive
years.
 Risk factors

Cigarette smoke
 Air pollution

89
Chronic Bronchitis
Pathophysiology




Chronic inflammation
Hypertrophy &
hyperplasia of
bronchial glands that
secrete mucus
Increase number of
goblet cells
Cilia are destroyed
90
Chronic Bronchitis
Pathophysiology

Narrowing of airway
Starting w/ bronchi 
smaller airways
airflow resistance
work of breathing
Hypoventilation & CO2
retention  hypoxemia &
hypercapnea


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91
Chronic Bronchitis
Pathophysiology
Bronchospasm often occurs
 End result

Hypoxemia
 Hypercapnea
 Polycythemia (increase RBCs)
 Cyanosis
 Cor pulmonale (enlargement of right side of heart)

92
Chronic Bronchitis:
Clinical Manifestations

In early stages


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Clients may not recognize early symptoms
Symptoms progress slowly
May not be diagnosed until severe episode with a
cold or flu
Productive cough
• Especially in the morning
• Typically referred to as “cigarette cough”


Bronchospasm
Frequent respiratory infections
93
Chronic Bronchitis:
Clinical Manifestations

Advanced stages
Dyspnea on exertion Dyspnea at rest
 Hypoxemia & hypercapnea
 Polycythemia
 Cyanosis
 Bluish-red skin color
 Pulmonary hypertension Cor pulmonale

94
Chronic Bronchitis:
Diagnostic Tests

PFTs

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ABGs



FVC:  Forced vital capacity
FEV1:  Forcible exhale in 1 second
FEV1/FVC = <70%
 PaCO2
 PaO2
CBC

 Hct
95
Emphysema


Abnormal distension
of air spaces
Actual cause is
unknown
96
Emphysema: Pathophysiology

Structural changes




Hyperinflamation of alveoli
Destruction of alveolar &
alveolar-capillary walls
Small airways narrow
Lung elasticity decreases
97
Emphysema: Pathophysiology

Mechanisms of
structural change

Obstruction of small
bronchioles
Proteolytic enzymes destroy
alveolar tissue
Elastin & collagen are
destroyed




Support structure is destroyed
“paper bag” lungs
98
Emphysema: Pathophysiology






The end result:
Alveoli lose elastic recoil,
then distend, &
eventually blow out.
Small airways collapse or
narrow
Air trapping
Hyperinflation
Decreased surface area
for ventilation
99
Healthy Lung
elastic
 clean
 many alveoli with
large surface
areas
 healthy capillaries
 clear airways

100
Emphysema Lung





loss of elasticity
filled with toxins
from tobacco smoke
fewer alveoli with
smaller surface
areas
destroyed
capillaries
blocked airways
101

Types: according to distribution within the
acinus

Panacinar:


Uniform involvement of the acinus
Associated with α1-antitrypsin deficiency

Centriacinar:

Enlargement of central parts of the acinus
(respiratory bronchioles and alveolar duct),
sparing the peripheral alveoli (distal alveoli)
More common and more severe in apical
segments of upper lobes
In heavy smokers and often associated with
Chronic bronchitis



102
A- Centriacinar emphysema, B- Panacinar emphysema
NURSING 621
W. Rose
Emphysema:
Clinical Manifestations

Early stages




Dyspnea
Non productive cough
Diaphragm flattens
A-P diameter increases
• “Barrel chest”

Hypoxemia may occur
• Increased respiratory rate
• Respiratory alkalosis

Prolonged expiratory phase
104
Emphysema:
Clinical Manifestations

Later stages




Hypercapnea
Purse-lip breathing
Use of accessory muscles
to breathe
Underweight
• No appetite & increase
breathing workload

Lung sounds diminished
105
Emphysema: Examination

Pulmonary function
•  residual volume,  lung capacity, DECREASED FEV1,
vital capacity maybe normal

Arterial blood gases




Normal in moderate disease
May develop respiratory alkalosis
Later: hypercapnia and respiratory acidosis
Chest x-ray


Flattened diaphragm
hyperinflation
106
Goals of Treatment: Emphysema
& Chronic Bronchitis
Improved ventilation
 Remove secretions
 Prevent complications
 Slow progression of signs & symptoms
 Promote patient comfort and participation
in treatment

107
Asthma



Asthma is defined as
A chronic inflammatory disorder of the airways in
which many cells and cellular elements play a role,
in particular mast cells, eosinophils, T
lymphocytes, macrophages, neutrophils, and
epithelial cellls.
In susceptible individuals, this inflammation causes
recurrent episodes of wheezing, breathlessness,
chest tightness, and coughing, particulary at night
or in the early morning.
108
Asthma





Reversible
inflammation &
obstruction
Intermittent attacks
Sudden onset
Varies from person to
person
Severity can vary from
shortness of breath to
death

Triggers






Allergens
Exercise
Respiratory infections
Drugs and food
additives
Nose and sinus
problems
Emotional stress
109
Asthma: Pathophysiology


Swelling of mucus membranes (edema)
Spasm of smooth muscle in bronchioles


Increased airway resistance
Increased mucus gland secretion
110
Asthma: Pathophysiology

Early phase response: 30 – 60 minutes

Allergen or irritant activates mast cells

Inflammatory mediators are released
• histamine, bradykinin, leukotrienes, prostaglandins, plateletactivating-factor, chemotactic factors, cytokines

Intense inflammation occurs
• Bronchial smooth muscle constricts
• Increased vasodilation and permeability
• Epithelial damage

Bronchospasm
• Increased mucus secretion
• Edema
111
112
Asthma: Pathophysiology

Late phase response: 5 – 6 hours

Characterized by inflammation

Eosinophils and neutrophils infiltrate
Mediators are released
mast cells release
histamine and additional mediators
Self-perpetuating cycle
Lymphocytes and monocytes invade as well
Future attacks may be worse because of increased
airway reactivity that results from late phase
response




• Individual becomes hyperresponsive to specific allergens
and non-specific irritants such as cold air and dust
• Specific triggers can be difficult to identify and less
stimulation is required to produce a reaction
113
Asthma: Early Clinical
Manifestations








Expiratory & inspiratory wheezing
Dry or moist non-productive cough
Chest tightness
Dyspnea
Anxious &Agitated
Prolonged expiratory phase
Increased respiratory & heart rate
Decreased PEFR
114
Asthma: Early Clinical
Manifestations

Wheezing

Chest tightness
Dyspnea
 Cough
 Prolonged expiratory phase [1:3 or 1:4]

115
Asthma: Severe Clinical
Manifestations








Hypoxia
Confusion
Increased heart rate & blood pressure
Respiratory rate up to 40/minute & pursed lip
breathing
Use of accessory muscles
Diaphoresis & pallor
Cyanotic nail beds
Flaring nostrils
116
Classifications of Asthma

Mild intermittent
Mild persistent
 Moderate persistent
 Severe persistent

117
Asthma: Diagnostic Tests

Pulmonary Function Tests

FEV1 decreased
• Increase of 12% - 15% after bronchodilator indicative of asthma



PEFR decreased
Symptomatic patient

eosinophils > 5% of total WBC

Increased serum IgE

Chest x-ray shows hyperinflation
ABGs

Early: respiratory alkalosis, PaO2 normal or near-normal

severe: respiratory acidosis, increased PaCO2,
118
Asthma: Collaborative Care

Mild intermittent

Avoid triggers
Premedicate before exercising
 May not need daily medication


Mild persistent asthma

Avoid triggers
Premedicate before exercising
 Low-dose inhaled corticosteroids

119
Asthma: Collaborative Care

Moderate persistent asthma

Low-medium dose inhaled corticosteroids

Long-acting beta2-agonists
Can increase doses or use theophylline or
leukotriene-modifier [singulair, accolate, zyflo]


Severe persistent asthma

High-dose inhaled corticosteroids

Long-acting inhaled beta2-agonists
Corticosteroids if needed

120
Asthma: Collaborative Care

Acute episode

FEV1, PEFR, pulse oximetry compared to baseline

O2 therapy
Beta2-adrenergic agonist

• via MDI w/spacer or nebulizer
• Q20 minutes – 4 hours prn

Corticosteroids if initial response insufficient
• Severity of attack determines po or IV
• If poor response, consider IV aminophylline
121
Asthma: Client Teaching


Correct use of medications
Signs & symptoms of an attack





Dyspnea, anxiety, tight chest, wheezing, cough
Relaxation techniques
When to call for help, seek treatment
Environmental control
Cough & postural drainage techniques
122
COPD
Complications
Cor pulmonale
 Pulmonary hypertension
 Acidosis
 Polycythemia

123
COPD
Complications

Right side of the heart must increase to
push blood into the lungs
• Right-sided heart failure develops
• Subsequent intravascular volume
expansion
• Systemic venous congestion
124
Pathophysiology of Cor Pulmonale
125
Cor pulmonale signs&symptoms
Heart sound changes to the second heart sound,
right-sided ventricular diastolic S3 gallop, and
early ejection click along left sternal border
 Distended neck veins
 Hepatomegaly with upper quadrant tenderness
 Ascites
 Epigastric distress
 Peripheral edema
 Weight gain
 Acute exacerbations of chronic bronchitis
 Acute respiratory failure

126
Tuberculosis

Pathophysiology


Mycobacterium
tuberculosis
Tubercle bacillus
127
Tuberculosis
Etiology
 Assoc. w/








Poverty
Malnutrition
Overcrowding
Substandard housing
Inadequate health care
Elderly
HIV
Prison
128
Tuberculosis



5-10% become
active
Only contagious
when active
Primarily affect
lungs but…




Kidneys
Liver
Brain
Bone
129
Tuberculosis
Pathophysiology
 Mode of transmission



Air-borne
 alveoli
Multiplies in alveoli
130
Tuberculosis

Immune response phase
Macrophages attack TB
 TB has waxy cell wall that protects it from
macrophages
 Immune system surrounds the infected
macrophages
 Forms a Lesion
 Called a Tubercle

131
Clinical manifestations of
Tuberculosis
(active phase)
 NOC sweats
 Low grade fever
 Weight loss
 Chronic productive cough



Rust colored sputum
Thick
Hemoptysis
132
Natural history of tuberculosis in a
newly infected (adult) contact (infection is
not necessarily disease)
NO INFECTION
CONTACT
Defenses
NO DISEASE (90%)
INFECTION
EARLY DISEASE (5%)
Cell-mediated
immunity
DISEASE
LATE DISEASE
(5%)
133
TB PATHOPHYSIOLOGY
systemic infection
 primary infection/disease
 progressive primary disease
 miliary disease
 meningitis
 chronic TB (re-activation)

134
Inhalation of Infected
Droplet Nuclei
non-specific bronchopneumonia
1) skin test sensitization
2) resistance to exogenous reinfection
3) lympho-hematogenous spread
complete resolution
(rare)
progression
massive necrosis
(rare)
healing with granuloma formation
stable
breakdown with development of
(re-activation)TB DISEASE
135
TB: PRIMARY Infection



95% of cases begin
with pulmonary focus
usually a SINGLE
focus
hypersensitivity
develops 2 to 6
weeks


until then, focus may
grow larger
hypersensitivity brings
caseation
136
PRIMARY Infection:
Lympho-hematogenous spread




8-14 weeks after onset of
TB
usually occult
Mantoux positive during this
phase
body wide seeding occurs
during this phase


bone, kidney, meninges etc.
3% of children with nl CXR’s
develop calcifications in lung
apices (SIMON FOCI)
137
138
PRIMARY TB:
endo-bronchial consequences
lymph nodes draining primary infection
site become involved
 lymph node capsule becomes adherent
to bronchial wall

infection can progress to ulceration into the
bronchial wall
 bronchial compression occurs with more
than one node at same level
 with healing, bronchial constriction/stenosis
can occur

139
INFECTION TO ENDO-BRONCHIAL DISEASE
TO STENOSIS
140
HEALED PRIMARY INFECTION
SIMON FOCI
CALCIFIED nodes
and peripheral lesion
(Ghon complex)
other VISCERAL sites
141
USUAL PROGRESSION
OF PRIMARY INFECTION
infection
lympho-hematogenous
spread
healed PRIMARY
infection
142
PROGRESSIVE PRIMARY
TB(DISEASE)
occasional (3.7%) local progression, despite
hypersensitivity (more common in younger pt)
 can be cavitary
 can have endo-bronchial spread
 similar in appearance to adult type,
“reactivation” disease
 2/3 of cases progress to death in the
untreated

143
PROGRESSIVE PRIMARY DISEASE
lymph node involvement
cavitation
pleural effusion
144
Progressive Primary Disease
145
ENDOBRONCHIAL SPREAD
WITH SUBSEQUENT
BRONCHOPNEUMONIA
146
MILIARY Disease
Generalized Hematogenous
Tuberculosis

generalized dissemination through
bloodstream
caseous focus ruptures into blood vessel
 growth of tubercle within the blood vessel
 may be acute, occult or chronic

uniformly fatal if not treated
 rare
 usually occurs in the first 4 months after
primary infection

147
CHRONIC PULMONARY TB
(re-activation/adult type)

occurs only after primary infection
0.5-10 % incidence (7% by Lincoln)
 usually not less than 1 year of age
 most cases occur when primary infection
aquired after 7 years of age

minute areas of bronchopneumonia
 tissue hypersensitivity (Type IV
hypersensitivity reaction - cavity
formation
 few symptoms early on in disease

148
Pulmonary embolism
149
Epidemiology & Pathophysiology-1
Thrombi commonly form in deep veins in
the calf
 propagate into the proximal veins,
including & above the popliteal veins
 from which they are more likely to
embolize

150
Epidemiology & Pathophysiology-2
About 79% of patients with PE have
evidence of DVT in their legs
 PE occurs in up to 50% of patients with
proximal DVT
 Dual pulmonary circulation ( pulmonary &
bronchial arteries ), pulmonary infarction :
not usually present

151
152
Epidemiology & Pathophysiology-3
APE, anatomical obstruction is the most
important cause of compromised
physiology
 release of vasoactive & bronchoactive
agents (serotonin from platelets )---deleterious ventilation–perfusion matching

153
Epidemiology & Pathophysiology-4
As RV afterload increases, tension in RV
wall rises
 dilatation, dysfunction, & ischemia of RV
 Death results from RV failure.

154
155
Virchow's classic triad of risk
Hypercoagulability
 Stasis
 Venous injury

156
McCance & Heuther 32.17
NURSING 621
Adult Respiratory Pathophysiology
W. Rose
Pulmonary hypertension
158
Predisposing factors
Defective fibrinolytic systems
 Presence of lupus-like anticoagulant
 Deficiency of protein C, protein S, and
antithrombin III
 Malignancy
 Atrial septal defects
 Indwelling venous catheters

159
Pulmonary Hypertension
Etiology/Contributing factors

Primary:

•
•
•
•
•
Rare
Female > Male
Age 20-40 years
hereditary tendency
usually die within 5 years of diagnosis
Secondary:

•
Existing cardiac or pulmonary disease
•
•
Mitral valve disease
COPD
160
Pulmonary Hypertension
Pathophysiology

Pulmonary arteries narrow

•
Vasoconstriction
Increased Pulmonary BP

•
(>30 mmHg)
How do you measure pulmonary BP?

•
Only can be measured during right side heart
catheterization
161
Pulmonary Hypertension

Pathophysiology
If increase in BP 
 Right ventricle has to work harder
 Right ventricle hypertrophy

• enlargement and dilation 


Right ventricle fails
Precursor to Cor Pulmonale
162
Pulmonary Hypertension in COPD
Chronic hypoxia
Pulmonary vasoconstriction
Muscularization
Pulmonary hypertension
Intimal
hyperplasia
Fibrosis
Cor pulmonale
Obliteration
Edema
Death
Source: GOLD 2007
163
McCance & Heuther 32.18
NURSING 621
Adult Respiratory Pathophysiology
W. Rose
Selected etiologic conditions giving
rise to pulmonary hypertension










1. Pulmonary Arterial hypertension
2. Pulmonary Venous hypertension
3. Pulmonary hypertension associated with disorders of the
respiratory system and/or hypoxaemia
4. Pulmonary hypertension due to chronic thrombotic and/or
embolic disease
4.1. Thromboembolic obstruction of proximal pulmonary
arteries.
4.2. Obstruction of distal pulmonary arteries
a). Pulmonary embolism (thrombus, tumour, ova and/or
parasites, foreign material)
b). In-situ thrombosis
c). Sickle cell disease
5.Pulmonary hypertension due to disorders directly affecting the
pulmonary vasculature.
165
“honeymoon period”
The existence of a “honeymoon period”
during which time pulmonary hypertension
is present but the subject exhibits few
symptoms, if any. It is during this time that
compensatory hypertrophy of the right
ventricle occurs in an effort to maintain
cardiac output in the presence of increased
pulmonary vascular resistance (PVR).
166
The pathophysiological
events in the progression of
pulmonary hypertension
during this period have not
been well defined.
167
Pulmonary Hypertension
Clinical manifestations of

Pulmonary hypertension without right
sided heart failure

•
•
•
•
(Not clinically evident until late in progression)
Dyspnea and fatigue that worsens over time
Cyanosis and Tachypnea
Crackles and decrease breath sounds
168
Pulmonary Hypertension

Clinical manifestations of…

Right sided heart failure
•
•
•
•
•
•
Peripheral edema
Ascites
Distended neck veins
Liver engorgement
Crackles
Heart murmur
169
Pulmonary Hypertension
Diagnostic exams/procedures

ABG’s:

•
PaO2
•
•
•
Decreased
Hypoxemia
PaCO2
•
•
Decreased
Hypercapnia
170
Pulmonary Hypertension

Diagnostic exams

ECG
• Shows right ventricular hypertrophy

Cardiac catheterization
• Right sided heart catheterization only way to
measure pulmonary pressure
X-ray
 Pulmonary function test

171
Pulmonary Hypertension
Treatment

Oxygen therapy
Vasodilators (in some people)
Anticoagulants –



•


Warfarin (Coumadin)
Diuretic to decrease blood volume
Heart/lung transplant
•
Really there is no cure – death within 2-3 years of
diagnosis unless transplant
172
Pulmonary Hypertension

A 66-year-old client takes a potassiumdepleting diuretic. Foods that will help to
keep the client’s potassium level within
normal limits include
•
•
•
•
•
•
Bananas
Oranges
Cantaloupe
fish
Spinach
whole-grain cereals
173
Restrictive lung disease:
idiopathic pulmonary fibrosis
174
Background
The lung volumes are reduced either because of:
1.
Alteration in lung parenchyma.
2.
Diseases of the pleura, chest wall or neuromuscular
apparatus.
Physiologically restrictive lung diseases are defined
by reduced total lung capacity, vital capacity and
functional residual capacity, but with preserved air
flow.
175
Restrictive lung diseases may be divided into the
following groups:

Intrinsic lung diseases (diseases of the lung
parenchyma)

Extrinsic disorders (extra-parenchymal
diseases)
176
Intrinsic Lung Diseases
These diseases cause either:
 Inflammation and/or scarring of lung
tissue (interstitial lung disease)
or
 Fill the air spaces with exudate and
debris (pneumonitis).

These diseases are classified further
according to the etiological factor.
177
Extrinsic Lung Diseases
The chest wall, pleura and respiratory muscles
are the components of respiratory pump.
Disorders of these structures will cause lung
restriction and impair ventilatory function.
These are grouped as:
 Non-muscular diseases of the chest wall.
 Neuromuscular disorders.
178
Pathophysiology
Intrinsic lung diseases:
 Diffuse parenchymal disorders cause reduction in all
lung volumes.
 This is produced by excessive elastic recoil of the
lungs.
 Expiratory flows are reduced in proportion to lung
volumes.
 Arterial hypoxemia is caused by ventilation/perfusion
mismatch.
 Impaired diffusion of oxygen will cause exerciseinduced desaturation.
 Hyperventilation at rest secondary to reflex
179
stimulation.
Extrinsic Disorders
Diseases of the pleura, thoracic cage, decrease
compliance of respiratory system.
 There is reduction in lung volumes.
 Secondarily, atelectasis occurs leading to V/Q
mismatch  hypoxemia.
 The thoracic cage and neuromuscular
structures are a part of respiratory system.
 Any disease of these structures will cause
restrictive disease and ventilatory dysfunction.

180
Diffuse Interstitial Pulmonary
Fibrosis

Synonyms: idiopathic pulmonary fibrosis, interstitial
pneumonia, cryptogenic fibrosing alveolitis.
Pathology:





Thickening of interstitium.
Initially, infiltration with lymphocytes and plasma cells.
Later fibroblasts lay down thick collagen bundles.
These changes occur irregularly within the lung.
Eventually alveolar architecture is destroyed –
honeycomb lung
181
Etiology
Unknown, may be immunological reaction.
Clinical Features
 Uncommon disease, affects adults in late
middle age.
 Progressive exertional dyspnea, later at rest.
 Non-productive cough.
 Physical examination shows finger clubbing,
fine inspiratory crackles throughout both lungs.
 Patient may develop respiratory failure
terminally.
 The disease progresses insidiously, median
survival 4-6 years.
182
183
184