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Biology of Disease
CH0576
Respiratory Disorders I
Dr Suad Awad
[email protected]
Room A305 Ellison’s- Ext 3816
1
Lecture Objectives
* Identify lung volumes & capacities
* Explain effect of relevant pressures in pulmonary
ventilation
* Discuss causes and consequence of Pneumothorax
* Explain the aetiology of obstructive lung disease
* Discuss causes and pathological features of Asthma
* Explain the basis of pulmonary compliance
* Discribe pathological features of
Respiratory Distress Syndrome
2
Lecture Outline
* Spirometry: Lung Volumes & Capacities
* Pneumothorax
* Resistance to Airflow
* Chronic Obstructive Lung Diseases:
Asthma
* Pulmonary Compliance:
Respiratory Distress Syndrome
3
Lung Volumes & Capacities
Classic Spirometer
Spirometry: Measure
air
entering or leaving
lung
Change in Lung
Volume
4
Fig 26-1A- Boron
Lung Volumes & Capacities
Inspiration: Upward deflection,
Expiration: Downward deflection
TV= Tidal volume
IRV= Inspiratory Reserve
Volume
Max volume inhaled at end
of quiet inspiration
ERV= Expiratory Reserve
Volume
Max volume expired at end
of quiet expiration
RV= Residual Volume
Air remaining in lung
after max exp effort
Fig 26-1B- Boron
RV= Can not be measured
5
by a Spirometer
Lung Volumes & Capacities
TLC= Total Lung Capacity
Sum of all 4 volumes
FRC= Functional Residual
capacity
Sum of ERV + RV
Air remaining after
quiet expiration
IC= Inspiratory Capacity
Sum of IRV + TV
max inspired volume
after a quiet expiration
VC= Vital Capacity
Sum of IRV + TV + ERV
max inspired achievable
tidal volume
Fig 26-1B- Boron
Any capacity that includes
the RV can not be measured6
by a Spirometer
Lung Volumes & Capacities
FEV1
Forced Expiratory Volume in
One Second
~ 80% VC in Healthy Young
Adults
Affected in Pulmonary
Disorders with increased
Airway resistance
Eg Asthma
Fig 26-1B- Boron
7
Lung Volumes & Capacities
Volumes & Capacities
Typical Ranges
(L)
IRV (Inspiratory Reserve Volume)
TV (Tidal Volume)
1.9- 2.5
0.4- 0.5
ERV (Expiratory Reserve Volume)
RV (Residual Volume)
TLC (Total Lung Capacity)
1.1- 1.5
1.5- 1.9
4.9- 6.4
IC (Inspiratory Capacity)
2.3- 3.0
FRC (Functional Residual Capacity)
VC (Vital Capacity)
2.6- 3.4
3.4- 4.5
8
Spirometry: FEV1/VC ratio
• FEV1 This is the forced expiratory volume in one
second. It reflects airway narrowing and is
relatively independent of effort
• FVC = the forced vital capacity
Normally FEV1 = 70%-80% of the FVC
FEV1 and FVC used to differentiate between
Obstructive and Restrictive patterns of lung disease
9
Peak Flow Metre
• Peak Expiratory Flow Rate (PEFR) is defined
as the highest air flow (Vol/time) achieved at the
mouth during a forced expiration
• It is a measure of the existence and severity of
airflow obstruction
• The PEFR obtained by a patient is compared to
that of a normative standard (use height, age,
gender). It is calculated as % of the expected
PEFR.
10
Peak Flow Meter
Measured by modern Spirometry: Next Lecture
11
FRC
Functional Residual Capacity
Volume of air remaining in the lungs at the end of a quiet
expiration
Determined by the lung and chest wall
elastic recoils
12
Factors affecting Ispiratory & Expiratory
Reserve Volumes
* Current Volume
The greater the current volume, the less are the
reserve volumes
* Lung Compliance
A measure of how easy to inflate the lungs
* Muscle Strength
* Comfort
* Posture
Problems with innervation - muscle weakness
Pain (injury) limit desire or ability to make insp efforts
Recumbent position = IRV falls- Difficult for diaphragm to
move abdominal contents
* Flexibility of Skeleton
Arthritis, Kyphoscoliosis = Reduce IRV
13
Important Pressures in Pulmonary
Ventilation
* Atmospheric Pressure - Barometric pressure
* Intra-alveolar Pressure - Pressure within the
alveoli
Fluctuates during breathing cycle: -ve inspiration, +ve expiration
* Intrapleural Pressure - Pressure inside the
thoracic cavity
Less than Barometric P (-ve)
14
Pneumothorax
• Occurs when the Intrapleural Pressure
equilibrates with atmospheric P.
As a result lungs collapse - inherent elastic recoil
• Traumatic Pneumothorax - caused by
the chest wall being punctured
• Spontaneous Pneumothorax 1. Due to a hole in the wall of the lung
2. Congenital defect in connective tissue in
alveolar wall
15
Pneumothorax
Traumatic
COLLAPSED
LUNG
Spontaneous
16
Pneumothorax
17
Factors Influencing Airflow Through
the Lung
Airflow (F) depends on:
1. Pressure Gradient PDifference between atmospheric pressure
and intra-alveolar pressure.
2. Resistance of Airways (R)Determined by the radii of the airways
F is inversely related to R
F = P/R
18
Resistance to Airflow
F = P/R
• Main determinant of resistance to airflow (R)
is the RADIUS of the conducting airways
• In the healthy lung the radius is relatively large
and so R is low
• The airways normally offer such a low resistance
that only small pressure gradients are needed for
adequate airflow into the lung
19
Adjustment of Airway Size
• Normally modest changes in airway size, to meet
the body’s needs, are achieved through the
AUTONOMIC nervous system
• In quiet respiration Parasympathetic
stimulation promotes bronchiolar smooth muscle
contraction causing Bronchoconstriction
Maintains muscle tone in airways
• Sympathetic stimulation brings about
Bronchodilation by bronchiolar smooth
muscle, Decreasing airway resistance during
exercise, fight or flight situations
20
Pulmonary Diseases Associated
with Narrowing of the Airways
• Increased Resistance is an extremely
important impediment to airflow when airways
become narrowed due to disease:
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
• COPD is a group of lung diseases including Chronic Bronchitis, Asthma and Emphysema
• COPD is characterised by Increased Airway
Resistance
21
Chronic Obstructive Pulmonary Disease
* Sufferers have to work harder to breathe
• F = P/R
When resistance is increased, a larger pressure
gradient is needed to maintain a normal airflow.
e.g. If resistance is doubled by narrowing of airway
lumens, P must be doubled through increased
respiratory muscle workload
• Expiration is more difficult to accomplish than
inspiration giving rise to the characteristic
‘WHEEZE’ as air is forced out of narrow airway
22
Chronic Obstructive Lung Diseases (COPDs)
Aetiology:
• Group of diseases in which there is a chronic
limitation to airflow
• Flow is reduced for one of two reasons:
1. Narrowing of the Airways causing increased
resistance - Asthma, Chronic Bronchitis
2. Loss of Elastic Recoil - Reduction
in the outflow pressure - Emphysema
23
Asthma
• Asthma is the Greek word for ‘Breathless’ or
‘to breathe opened mouthed’
• It is caused by Chronic Inflammatory Responses
in the airways
• This leads to REVERSIBLE airway obstruction.
• It is characterised by breathlessness and
wheezing
caused by generalised narrowing of
intrapulmonary airways
24
Causes of Asthma
Asthma is a heterogeneous disease triggered by
a variety of inciting agents (Genetic + Environ)
• Extrinsic Factors
Caused by Type I hypersensitivity reactions on
exposure to extrinsic allergen (pollen, perfume,
dust mite, others?)
• Intrinsic Factors
Non-immune trigger mechanism e.g.
hormonal, stress, exercise
25
Asthma
There are three main features of asthma:
Remember: (F = P/R)
1. Muscle Spasm – Bronchospasm (Narrowing of
airway lumen- increased airway R)
2. Mucus Plugging- (air trapping in distal
bronchioles- increased RV, and relevant volume &
capacities; eg? )
3. Mucosal Oedema- (Narrowing of lumen- increased
R- increased pressure- increased work for
respiratory muscles)
26
Pathological Features of Asthma
* Mucosal Oedema
- Inflammatory cell infiltration (Eosinophils 5%-50%)
- Basement membrane thickening
- Goblet cell and submucosal gland hyperplasia
- Hypertrophy and hyperplasia of the smooth muscle
in the bronchial wall
These events lead to - Airway Obstruction
Bronchial Muscle Constriction
Airway Congestion
27
Early
phase
response in
asthma
Dust mite, pollen
Other??
SM spasm followed
By inflammation
Lamina propria
Histamine induces
SM contraction
Through H1 Rs
28
Late phase
response in
asthma
Eosinophill
Infiltration,
(MBP, ECP)
Loss of Epithelial
Cells
Increased mucus
secretion
Edema
SM
Hypersensitivity
(histamine),
Infiltration of
Basophils &
Neutrophils
29
Pathological Features of Asthma
30
Bronchioles in Asthma
31
Features of Asthma in Status
Asthmatics
• Lungs are Overdistended - Due to trapped air
• May be small areas of Atelectasis
• The most striking feature is the blocking of
bronchi and bronchioles with thick mucus plugs
• The mucus plugs contain
- Whorls of shed epithelium
- Eosinophils
- Charcot - Leyden Crystals
32
Charcot Leyden Crystals
Crystallised
Lysophospolipase
Enzyme produced
By Eosinophils
Up to 50 m
length
Normally colourless
Stains reddish by
trichrome
Indicative of a disease involving eosinophilic inflammation
& proliferation
33
Asthma - Clinical Course
• Severe Dyspnoea with wheezing
• Hyperinflation of lungs, with air trapped distal
to the bronchi which are constricted and full
of mucus (which volumes & capacities are affected?)
• This leads to Hypercapnia, acidosis and hypoxia
• Asthma tends to be severely debilitating rather
than lethal
34
COMPLIANCE
• A factor influencing the pressure gradient P in
the lung is the ELASTIC behaviour of the lung
• This affects alveolar and lung volume,
and therefore the pressure gradient needed to inflate lung
• COMPLIANCE refers to how much effort is
required to stretch or distend the lungs
• Specifically Compliance is a measure of the
change in lung volume due to a given
change in transmural pressure
(The Force That Stretches the Lung)
C = V/ P
35
COMPLIANCE
• A HIGHLY compliant lung stretches further for
a given increase in pressure than does a LESS
compliant lung (eg inflating a very flexible Vs stiff balloon)
• A LESS compliant lung will require MORE
Effort (P) to produce a given degree of inflation
• A POORLY compliant lung is referred to as a
‘STIFF LUNG’
• Compliance is reduced in pulmonary diseases
e.g. FIBROSIS of the lung
36
Factors Affecting Pulmonary Compliance
Pulmonary compliance depends on various factors:
1. Highly Elastic Connective Tissue
2. Alveolar Surface Tension:- due to a
thin liquid film lining each alveolus.
It resists any force that increases
surface area (thus OPPOSES expansion)
3. Pulmonary Surfactant:- Surface Active Agent - detergent !
produced by TYPE II alveolar cells, decreases surface
37
tension (70 dynes/cm Vs 25 dynes/cm)
Pulmonary Compliance
38
Effect of Pulmonary Surfactant
• It REDUCES the surface tension and
contributes to lung stability
• It acts by interspersing water molecules
lining the alveolus, which reduces surface tension
Benefits of Reducing Surface Tension:
a) Increases pulmonary compliance - thus reducing
the effort needed to inflate the lungs
b) It stabilises the alveoli so they do not collapse at
end of expiration
39
Newborn Respiratory Distress Syndrome
• Surfactant produced by 34th wk gestation
* Premature infants- Deficiency in lung surfactant
leads to Newborn Respiratory Distress Syndrome
• Very strenuous inspiratory efforts are required to
overcome the high surface tension in the alveoli
The lungs are Poorly Compliant
• It may require transmural pressure gradients of
20-30 mm Hg (normally 4-6 mm Hg) to overcome
the tendency of the lungs to collapse
40
NEWBORN RDS
• The problem is compounded as the newborn’s
muscles are still very weak
• Deficiency in surfactant leads to alveolar
instability and severe respiratory failure
• Life threatening condition
• Newborn RDS can be treated by:
a) Artificially increasing atmospheric pressure
b) Treating with exogenous surfactant
41
Useful Textbooks
Rhoades & Bell, 3rd ed. Medical Physiology:
Principles of Clinical Medicine. LWW
Boron & Boulpeap, 2nd ed. Medical Physiology:
Saunders
42