Post on 27-Dec-2015
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Lecture Outline1- Spirometry: Volume/Time & Flow/Volume Curves
2- Use of Spirometry in Obstructive & Restrictive Lung Diseases
3- Spirometry Live Demonstration
4- Aetiology & Pathological Features of Chronic Bronchitis
5- Aetiology & Pathological Features of Emphysema
6- Effect of Obstructive Lung Disease on Lung Volumes & Capacities
7- Aetiology & Pathological Features of Restrictive Lung Disease
8- Respiratory Function Tests- Diagnostic Significance
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Spirometry- Vol/Time
Vol
um
e (L
)
0
1
2
3
4
5
6
Time (s)0 1 2 3 4
FE
V1
Normally,FEV1/FVC ratio= 0.8
or FEV1 = 80% FVC
For
ced
Vit
al C
apac
ity
FV
C
From fully inspired statepatient expels all air in theirlungs as forcefully as possible
25%
75%
Slope of the initial line
gives the flow rateFEF25% -75%
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Forced Expiratory Flow (FEF 25% – 75% )
Measure of expiratory flow rate (V/t) over middle half of the
FVC curve
More conveniently done on Flow-Vol spirometry … Directly read off from the curve
SIG = Early airflow obstruction
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Vol-Time Spirometry in Obstructive Lung DiseaseV
olu
me
(L)
0
1
2
3
4
5
6
Time (s)0 1 2 3 4
Obstructive Lung DiseaseTotal Volume (TLC and
FVC) may be normalbut FEV1 is reduced
And FEV1/FVC ratio <0.8(<50% here)
For
ced
Vit
al C
apac
ity
FE
V1
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Vol-Time Spirometry in Restrictive Lung DiseaseV
olu
me
(L)
0
1
2
3
4
5
6
Time (s)0 1 2 3 4
Restrictive Lung Disease: Total Volume reduced and
FVC reduced, FEV1 reducedBut FEV1/FVC ratio =
NORMAL!
FE
V1
For
ced
Vit
al C
apac
ity
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Spirometry: Flow/Volume Loop
Flo
w (
L s
-1)
Expired Lung Volume (L)0
2
4
6
2
4
6
Exp
irat
ion
Insp
irat
ion
1 2 3 4 5
FEF75
FEF 25
Vital Capacity
1 s mark
Measurement of flow rates; contemporary technique
● 1 sec
●
PEF
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Flow/Volume Loops inObstructive Lung Disease
Flo
w (
L s
-1)
Lung Volume (L)
0
2
4
6
2
4
6
Exp
irat
ion
Insp
irat
ion
1 2 3 4 5
FEF50
FIF50
●
● 1 sec
PEF
Scooped out appearance
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Flo
w (
L s
-1)
Lung Volume (L)
0
2
4
6
2
4
6
Exp
irat
ion
Insp
irat
ion 1 2 3 4 5
FEF50
FIF50
● 1 sec
●
PEF
Flow/Volume Loops inRestrictive Lung Disease
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Chronic Bronchitis
Clinical definition: “A cough productive of sputum on most days for three months of the
year, for at least two consecutive years”- WHO- CD10
• Airways show Hypersecretion of mucus with mucus gland Hyperplasia = an increase in airflow
resistance in the large airways
• The airway obstruction is due to Luminal Narrowing and Mucus Plugging
Could be part of underlying disease process; eg asthma, cystic fibrosis,Dyskinetic cilia syndrome…etc – Not 1ry diagnosis
Chronic Obstructive Lung Diseases (COPDs)
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Chronic Bronchitis
Metaplasia:Ciliated Columnar Ep cells Replaced by SquamousEp cells
Hypertrophy of submucosal glands & Hyperpalsiaof goblet cells
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Chronic BronchitisChronic Bronchitis leads to:
1. Alveolar Hypoventilation 2. Hypoxaemia (low arterial PO2) 3. Hypercapnia (↑blood CO2) 4. Respiratory Failure may occur
• Individuals are typically cyanosed but may not have Dyspnoea (Respiratory distress)
• In some cases chronic bronchitis may lead to Hypoxic Pulmonary Vasoconstriction, and Secondary Pulmonary Hypertension
• This may lead to right sided heart failure
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Emphysema• Permanent enlargement (dilation) of any part respiratory
acinus (distal to the bronchi)
• Destruction of alveolar walls (without scarring)
• Loss of elastic recoil in the lungs as the respiratory tissue is destroyed
• Thus: area for gas exchange is reduced
• There are two patterns: 1. CENTRIACINAR 2. PANACINAR
Acinus = Terminal duct + alveoli
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Emphysema
• Proposed to be caused by unregulated activity of extracellular proteases secreted from inflammatory cells
• This is a response to chronic exposure to cigarette smoke or other inhaled irritants
• Linked to an imbalance of protease and the protease inhibitor 1-antitrypsin
• Proteases (particularly Elastase) cause the breakdown of alveolar walls and collapse of small airways
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Aetiology of Emphysema
Antielastaseactivity
1 AntitrypsinDeficiency
(genetic)
Smoking
ElastaseElastic Damage
Emphysema
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Emphysema
• The classic presentation = barrel-chested and dyspnoeic
• Patients have prolonged expiration and may sit forward in a hunched position attempting to squeeze the air out of the lungs
• The loss of elastic recoil and structural support leads to:
1. Trapping of air in lungs 2. Over inflated lungs 3. Decreased rate of airflow on expiration
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Emphysema• Reduced oxygen uptake despite increased
ventilation
• blood oxygenation may be maintained by rapid respiration, but subjects breathless on the slightest exertion and become hypoxic
• Patients are known as ‘PINK PUFFERS’
• Cyanosis, hypercapnia and cor pulmonale (enlargement of the right ventricle) occur late in the disease after progressive decline in lung
function
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• Emphysema progresses slowly and worsens over time.
• Increased effort in breathing leads to progressive breathlessness
• Some do not progress (Pink Puffers)
• In some cases the disease progresses leading to chronic hypoxia and hypercapnia (Blue
Bloaters)
Emphysema
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Effects of Obstructive Disease on Lung Volumes
• TLC is elevated (why?)• Residual Volume is elevated• Expiratory Capacity is elevated• So FRC is elevated (What about IRV & IC?)
Elevations are due to air trapped in lungs following expiration
• Vital capacity may be reduced• FEV1 is reduced
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Effects of Obstructive Disease on Lung Volumes• Airflow is reduced due to airway obstruction.
• VC and FEV1 are reduced but FEV1 is > FVC
Therefore FEV1/FVC ratio is much lower than the normal 70% - 80% of FVC (as low as 25%)
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Restrictive Lung Diseases
• Restrictive lung diseases are caused by a reduction in total lung capacity• Features include:
1. Increased Lung Density (Stiff Lung).
3. Reduced Compliance (V/P)
4. Breathlessness (Dyspnoea) 5. Greater Effort to Inflate Lungs 6. Abnormality of Alveolar Walls which renders them rigid
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Restrictive Lung Diseases
• Characterised by damage to the alveolar walls and capillaries
• An increase in interstitial fluid or fibrosis produce a stiff lung
• Damage to the alveolar epithelium and vasculature produce abnormalities in the ventilation/ perfusion ratio (normally 5/6 ~ 0.8)
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Restrictive Lung Disease• ACUTE - Adult Respiratory Distress Syndrome (ARDS) Trauma or acute illness Inflammation of lung paranchyma- pulmonary edema- eg
Pneumonia• CHRONIC - Pneumoconiosis- occupational lung disease- Asbestosis
silicosis, byssinosis (cotton dust) - Idiopathic Pulmonary Fibrosis (IPF)-unknown
cause - Sarcoidosis- immune system disorder-
small inflammatory nodules (granulomas)- leading to fibrosis
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Chronic Restrictive Lung Diseases
• Develop over months/years and leads to a slowly decreasing respiratory efficiency
• With chronic interstitial fibrosis leading to ‘honeycomb’ lung
• There is an infiltration of macrophages and microcyst formation.
• Clinically patients exhibit dyspnoea, cough and in advanced cases hypoxemia and cyanosis, eventually respiratory failure
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Proposed Mechanism for Fibrosis
T Lymphocyte
BLymphocyte
ActivatedMacrophage
Unknown Antigen
Immune complexes
cytokines
Oxidants & Proteases
Injury to type I pneumocytes (epithelial cells)
Fibrogenic cytokines
Fibrogenic cytokines
Fibroblasts
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Effects of Restrictive Disease on Lung Volumes
• Reduced FVC• Reduced FEV1
• Relatively Normal FEV1/FVC ratio• Relatively Normal PEFR
• TLC is reduced (Why?)• Inspiratory capacity is reduced.• Residual Volume is normal
Reflect loss of compliance
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Respiratory Function Tests – Diagnostic Significance
• Peak Expiratory Flow Rate - Reduced with obstructive lung disease.• FEV1- * Reduced with obstructive disease * Reduced with pulmonary fibrosis (restrictive)
• Forced Vital Capacity (FVC) - * Reduced in COPD
* Reduced with a corresponding decrease in total lung volume in fibrosis or oedema
* Reduced with muscle weakness
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Respiratory Function Tests – Diagnostic Significance
Forced Expiratory Ratio: FEV1/FVC -
* Low in obstructive lung disease
* Normal or high in restrictive defects