Chronic obstructive pulmonary disease (COPD) is defined as a lung condition characterized by airflow limitation that is not fully reversible. The document discusses COPD, including its types (chronic bronchitis and emphysema), pathology, evaluation, diagnosis, and physiotherapy management. Physiotherapy management focuses on removing secretions, improving breathing patterns, increasing exercise tolerance, and preventing dyspnea through techniques like breathing exercises, postural drainage, inspiratory muscle training, and ergonomic advice.

1. CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE
Dr. Abhijit DiwateDr. Abhijit Diwate
Associate ProfessorAssociate Professor
DVVPF College of Physiotherapy,DVVPF College of Physiotherapy,
Ahmednagar 414111Ahmednagar 414111

2. ObjectivesObjectives
• DefinitionDefinition
• Types of COPDTypes of COPD
• PathologyPathology
• Evaluation & diagnosisEvaluation & diagnosis
• Physiotherapy managementPhysiotherapy management

3. INTRODUCTIONINTRODUCTION
There are two forms of RespiratoryThere are two forms of Respiratory
DiseaseDisease
• Obstructive diseasesObstructive diseases
• Restrictive diseasesRestrictive diseases
DEFINITIONDEFINITION
COPD has been defined by the Global InitiativeCOPD has been defined by the Global Initiative
for Chronic Obstructive Lung Disease (GOLD)for Chronic Obstructive Lung Disease (GOLD)
as a disease state characterized by airflowas a disease state characterized by airflow
limitation that is not fully reversible.limitation that is not fully reversible.

4. TYPES OF COPDTYPES OF COPD
It is a condition of the lung characterized byIt is a condition of the lung characterized by
permanent dilatation of the air spaces distal topermanent dilatation of the air spaces distal to
the terminal bronchioles with destruction of thethe terminal bronchioles with destruction of the
walls of these airways.walls of these airways.
• Chronic BronchitisChronic Bronchitis
It is a disease characterized by daily cough withIt is a disease characterized by daily cough with
sputum for at least 3 months of the year for atsputum for at least 3 months of the year for at
least 2 consecutive years and airwayleast 2 consecutive years and airway
obstruction which is irreversible.obstruction which is irreversible.
•EmphysemaEmphysema

6. EPIDEMIOLOGYEPIDEMIOLOGY
Worldwide COPD is the 6Worldwide COPD is the 6thth
most commonmost common cause ofcause of
deathdeath
RISK FACTORS:RISK FACTORS:
Cigarette SmokingCigarette Smoking
Airway ResponsivenessAirway Responsiveness
Respiratory InfectionsRespiratory Infections
Occupational ExposuresOccupational Exposures
Air PollutionAir Pollution
Passive or Second Hand Smoking ExposurePassive or Second Hand Smoking Exposure
Alpha1 Anti-trypsin deficiencyAlpha1 Anti-trypsin deficiency

7. PATHOLOGYPATHOLOGY
• PATHOLOGYPATHOLOGY OF CH.BRONCHITISOF CH.BRONCHITIS
Irritative substance enters the respiratory tractIrritative substance enters the respiratory tract
Over activity of the mucus secreting gland and the gobletOver activity of the mucus secreting gland and the goblet
cellscells
Increase in the secretion of mucusIncrease in the secretion of mucus
Mucus coats the walls of the airways and blocks themMucus coats the walls of the airways and blocks them
Goblet cells increase in size and also block the airwaysGoblet cells increase in size and also block the airways
Airways become narrow and show inflammatory changesAirways become narrow and show inflammatory changes
Ciliary action is also inhibitedCiliary action is also inhibited

9. – PATHOLOGY OF EMPHYSEMAPATHOLOGY OF EMPHYSEMA
Smoking causes clustering of alveolarSmoking causes clustering of alveolar
macrophages and release proteolytic enzymes.macrophages and release proteolytic enzymes.
Leukocytes present also release an enzyme.Leukocytes present also release an enzyme.
These 2 enzymes destroy the lung tissue.These 2 enzymes destroy the lung tissue.
To stop the action of these enzymes Alpha1To stop the action of these enzymes Alpha1
antitrypsin is required.antitrypsin is required.
But the oxidants released by smoke inactivateBut the oxidants released by smoke inactivate
alpha1 antitrypsin and the tissue damagealpha1 antitrypsin and the tissue damage
continues.continues.

10. Subsequently theSubsequently the
walls of airwayswalls of airways
become weak andbecome weak and
collapse on expiration.collapse on expiration.
The intra-alveolarThe intra-alveolar
pressure increasespressure increases
leading to break ofleading to break of
alveolar septa andalveolar septa and
bullae formation.bullae formation.
The capillaries aroundThe capillaries around
the alveoli are alsothe alveoli are also
stretched.stretched.

11. TYPES OF EMPHYSEMATYPES OF EMPHYSEMA
• CENTRILOBULAR/CENTRILOBULAR/
CENTRIACINARCENTRIACINAR
 Affects the bronchioles &Affects the bronchioles &
alveoli remain normalalveoli remain normal
 Upper zones are affectedUpper zones are affected
 DisturbedDisturbed
ventilation/perfusionventilation/perfusion
relationshiprelationship
• PANLOBULAR/PANLOBULAR/
PANACINARPANACINAR
 Affects both bronchiolesAffects both bronchioles
& alveoli& alveoli
 Lower zones are affectedLower zones are affected
 Less effect on theLess effect on the
ventilation/perfusionventilation/perfusion
relationshiprelationship

12. CLINICAL PRESENTATIONCLINICAL PRESENTATION
• EMPHYSEMAEMPHYSEMA
 Pink puffersPink puffers
 General thinnessGeneral thinness
 Anxious expressionsAnxious expressions
 Severe breathlessnessSevere breathlessness
 Little or no sputumLittle or no sputum
productionproduction
 Less or no coughLess or no cough
• CH. BRONCHITISCH. BRONCHITIS
 Blue bloatersBlue bloaters
 ObesityObesity
 No such expressionsNo such expressions
 Mild dysponeaMild dysponea
 Copious sputum whichCopious sputum which
may be infectedmay be infected
 Cough present for manyCough present for many
yearsyears

13. Central cyanosis &Central cyanosis &
development of cordevelopment of cor
pulmonale in laterpulmonale in later
stagesstages
No peripheralNo peripheral
oedemaoedema
Increase in total lungIncrease in total lung
capacitycapacity
Normal PaONormal PaO22 &PaCO&PaCO22
Central cyanosis withCentral cyanosis with
cor pulmonale seen incor pulmonale seen in
early stagesearly stages
Peripheral oedemaPeripheral oedema
Increase in residualIncrease in residual
volumevolume
Low PaOLow PaO22 & PaCO& PaCO22

14. COR PULMONALECOR PULMONALE
VENTILATION/PERFUSION ABNORMALITYVENTILATION/PERFUSION ABNORMALITY
HYPOXIAHYPOXIA
HYPOXIC PULMONARY VASOCONSTRICTONHYPOXIC PULMONARY VASOCONSTRICTON
PULMONARY HYPERTENSIONPULMONARY HYPERTENSION

15. PULM. HYPERTENSIONPULM. HYPERTENSION
RIGHT HEART FAILURERIGHT HEART FAILURE
+ RENAL HYPOXIA++ RENAL HYPOXIA+
POLYCYTHAEMIAPOLYCYTHAEMIA
INCREASE IN SYSTEMIC BLOOD PRESSUREINCREASE IN SYSTEMIC BLOOD PRESSURE
LEFT VENTRICULAR FAILURELEFT VENTRICULAR FAILURE

16. POSITIVE FINDINGSPOSITIVE FINDINGS
Barrel shape chest is seen.Barrel shape chest is seen.
Chest movements are diminishedChest movements are diminished
Mediastinum is centrally placedMediastinum is centrally placed
Tactile vocal fremitus is diminishedTactile vocal fremitus is diminished
On percussion there is resonant noteOn percussion there is resonant note
Breath sounds are diminished and expiration isBreath sounds are diminished and expiration is
prolongedprolonged
On auscultation we get wheezeOn auscultation we get wheeze

17. EVALUATION OF PATIENTEVALUATION OF PATIENT
• INVESTIGATIONSINVESTIGATIONS
SputumSputum
SpirometrySpirometry
Blood gasBlood gas
investigationinvestigation

18. X ray findingsX ray findings
• Hyper translucency ofHyper translucency of
lung fieldslung fields
• Low flat diaphragmLow flat diaphragm
• Tubular heartTubular heart
• Hyperlucent bullaeHyperlucent bullae
• Increase intercoastalIncrease intercoastal
spacesspaces

19. COMPLICATIONSCOMPLICATIONS
Type II respiratory failureType II respiratory failure
PneumothoraxPneumothorax
Cor pulmonaleCor pulmonale
Peripheral oedemaPeripheral oedema

20. ICIDHICIDH22
• STRUCTURAL IMPAIMENTSSTRUCTURAL IMPAIMENTS
Increased mucus secretionIncreased mucus secretion
Abnormal and permanent enlargement ofAbnormal and permanent enlargement of
airwaysairways
Thickening of the walls of airwaysThickening of the walls of airways
Reduced elastic recoiling of the lungReduced elastic recoiling of the lung
Damage to the lung tissueDamage to the lung tissue
Bullae formation are seenBullae formation are seen
Weakness of accessory musclesWeakness of accessory muscles
Elevation of shoulderElevation of shoulder
Barrel shaped chestBarrel shaped chest

21. • FUNCTIONAL IMPAIRMENTSFUNCTIONAL IMPAIRMENTS
BreathlessnessBreathlessness
Cough with expectorationCough with expectoration
Easy fatigabilityEasy fatigability
Use of accessory musclesUse of accessory muscles
Inability to do vigorous activitiesInability to do vigorous activities

22. GOALSGOALS
• SHORT-TERM GOALSSHORT-TERM GOALS
 Education of patientEducation of patient
 To relieve any bronchospasm & facilitate the removal ofTo relieve any bronchospasm & facilitate the removal of
secretions.secretions.
 To improve breathing pattern ,breathing control &controlTo improve breathing pattern ,breathing control &control
of dyspnoea.of dyspnoea.
 Maximize aerobic capacity & efficiency of OMaximize aerobic capacity & efficiency of O22 transport.transport.
 To teach local relaxation ,improve posture & help allayTo teach local relaxation ,improve posture & help allay
fear and anxiety.fear and anxiety.
 Optimize physical endurance & Exercise capacity.Optimize physical endurance & Exercise capacity.
 Optimize respiratory muscle strength & endurance.Optimize respiratory muscle strength & endurance.

23. • LONG-TERM GOALLONG-TERM GOAL
Reduction & cessation of smokingReduction & cessation of smoking
Continue with breathing exercise &Continue with breathing exercise &
relaxation techniques.relaxation techniques.
Increase aerobic capacity by doingIncrease aerobic capacity by doing
regular exerciseregular exercise
Avoid any kind of allergy & vigorous work.Avoid any kind of allergy & vigorous work.
Design a healthy lifestyle & continueDesign a healthy lifestyle & continue
rehabilitation program.rehabilitation program.
Self management in activities of dailySelf management in activities of daily
living.living.

24. MANAGEMENTMANAGEMENT
• MEDICAL MANAGEMENTMEDICAL MANAGEMENT
BRONCHODILATORSBRONCHODILATORS
CORTICOSTEROIDSCORTICOSTEROIDS
ANTIBIOTIC THERAPYANTIBIOTIC THERAPY
OO22 THERAPYTHERAPY
• SURGICAL MANAGEMENTSURGICAL MANAGEMENT
LUNG VOLUME REDUCTION SURGERYLUNG VOLUME REDUCTION SURGERY
BULLECTOMYBULLECTOMY
LUNG TRANSPLANTATIONLUNG TRANSPLANTATION

25. PHYSIOTHERAPYPHYSIOTHERAPY
MANAGEMENTMANAGEMENT
Removal of secretionRemoval of secretion
1.The active cycle of1.The active cycle of
breathing techniquebreathing technique
a) thoracic expansiona) thoracic expansion
exercisesexercises
b) forced expiratoryb) forced expiratory
techniquetechnique
2. Postural drainage2. Postural drainage
3. Humidification3. Humidification

26. Improving breathing patternImproving breathing pattern
Increasing and maintaining exercise toleranceIncreasing and maintaining exercise tolerance
Inspiratory muscle trainingInspiratory muscle training
1.inspiraory resistance training1.inspiraory resistance training
2. Diaphragmatic training using weights2. Diaphragmatic training using weights
Preventing & relieving episodesPreventing & relieving episodes
of dyspnoeaof dyspnoea
Ergonomic adviceErgonomic advice

27. SummarySummary
• DefinitionDefinition
• Types of COPDTypes of COPD
• PathologyPathology
• Evaluation & diagnosisEvaluation & diagnosis
• Physiotherapy management.Physiotherapy management.

28. QUESTIONSQUESTIONS
1.1. DEFINE COPD AND EXPLAIN THEDEFINE COPD AND EXPLAIN THE
TYPES OF COPD.TYPES OF COPD.
2.2. WRITE THE PHYSIOTHERAPYWRITE THE PHYSIOTHERAPY
MANEGMENT IN COPD.MANEGMENT IN COPD.

29. THANK YOUTHANK YOU