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COPD

The document outlines the learning objectives for understanding obstructive and restrictive lung diseases, emphasizing the differentiation between the two based on pathophysiology and clinical features. It covers diagnostic tools such as spirometry and lung volumes, as well as the importance of bronchodilator reversibility testing and plethysmography for accurate diagnosis. Additionally, it highlights the clinical management of conditions like asthma and COPD, focusing on pharmacological targets and treatment strategies.

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Amina Izeria
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0% found this document useful (0 votes)
2 views32 pages

COPD

The document outlines the learning objectives for understanding obstructive and restrictive lung diseases, emphasizing the differentiation between the two based on pathophysiology and clinical features. It covers diagnostic tools such as spirometry and lung volumes, as well as the importance of bronchodilator reversibility testing and plethysmography for accurate diagnosis. Additionally, it highlights the clinical management of conditions like asthma and COPD, focusing on pharmacological targets and treatment strategies.

Uploaded by

Amina Izeria
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

Obstructive and

Restrictive Lung
Diseases

Dr Haouassia Fatima ezzahra


UM6P-FMS
Learning Objectives
By the end of this session, participants will be able to apply clinical knowledge to optimize care for patients with
obstructive and restrictive lung diseases.

Pattern Recognition
1
Differentiate between obstructive and restrictive respiratory
5 Device Optimization
patterns based on pathophysiology.
Optimize inhaler device selection, demonstrate proper technique,
and address adherence barriers.

Data Interpretation
2
Interpret spirometry, lung volumes, and diffusion capacity
(DLCO) results for common disease states. 6 Patient Care
Monitor safety parameters, manage drug interactions, and
provide effective patient counseling.

Clinical Features
3
Recognize distinct clinical manifestations, symptoms, and "red
flags" requiring urgent referral.
Foundational Concepts

Lung Physiology Essentials Mechanics & Volumes

SPIROMETRY VOLUMES

Ventilation Mechanics
This is about how air moves in and out of the lungs
Resistance : How hard it is for air to flow in the airways
Compliance: How easily the lungs can expand
Stiff lungs=low compliance
Elastic Recoil : The tendency of the lungs to retrun to their resting size after
breathing in

Gas Exchange
This explains how oxygen enters the blood and
carbon dioxide leaves

It depends on :

V/Q Matching (Ventilation/Perfusion) and


Diffusion (DL) : movement of O2 and CO2 across
the alveolar-capillary membrane
Surface Tension
This concerns the alveoli

Surfactant reduces surface tension

It prevents alveoli from collapsing at low volumes


(LaPlace's Law).

PHYSIOLOGY | LUNG
VOLUMES
Comparative Overview

Core Concepts: Obstructive vs Restrictive Pathophysiology & Presentation

Obstructive Restrictive
"Hard to get air OUT" "Hard to get air IN"

Primary Mechanism Primary Mechanism

Inflammation leads to increased resistance (↑ Raw). Reduced lung expansion leads to decreased volumes.

Air Trapping: Incomplete expiration causes hyperinflation. Low compliance or extrinsic compression.

PFT Hallmark
PFT Hallmark

FEV1/FVC TLC
FEV1/FVC TLC

Low (<0.70) Normal / High


Normal / High Low (<LLN)

Common Conditions

Common Conditions
Pulmonary Fibrosis (ILD) Obesity (Hypoventilation)

Asthma COPD Bronchiectasis Cystic Fibrosis Neuromuscular Disease


Diagnostic Tools

Pulmonary Function Tests (PFTs) Pharmacist Essentials

LOGIC FLOW
Spirometry Interpretation Framework
The cornerstone of diagnosis. Measures volume and speed of air inhaled and exhaled.

Assess Quality
1
FEV1 FVC Ratio (FEV1/FVC) Is the test acceptable & repeatable?

Lung Volumes
Static measurements via plethysmography ("body box") or gas dilution. Essential for confirming
restriction. Identify Pattern
2
Obstructive vs. Restrictive (FEV1/FVC)

TLC (Total Lung Capacity) RV (Residual Volume)

Diffusion Capacity (DLCO)


Determine Severity
Measures gas transfer efficiency from alveoli to blood using Carbon Monoxide (CO). Differentiates 3
Based on FEV1 % predicted
intrinsic lung disease from other causes.

Provocation Tests
Used when spirometry is normal but asthma is suspected (e.g., Methacholine challenge to induce Assess Reversibility
4
bronchospasm). Response to bronchodilator?
Clinical Practice Guidelines

Spirometry: Indications & Contraindications Test Safety & Selection

Indications Contraindications
"When to perform" "When to avoid"

Diagnostic & Monitoring Absolute

Recent myocardial infarction (within 1


Respiratory symptoms (dyspnea, chronic cough,
wheezing). month) Recent eye surgery (within 1
month) Thoracic/abdominal/cerebral aneurysm
Evaluation:Obstructive lung diseases (Asthma, COPD).
Pneumothorax or Pulmonary embolism
Severety , progression, and preoperative risk. Hemoptysis of unknown origin

Relative
Public Health & Occupational Recent upper respiratory tract infection
Monitoring response to therapy Nausea, vomiting, or facial pain
Dementia, confusion, or acute illness
Occupational/environmental exposure screening

Epidemiological studies & Disability evaluation

© 2026 Clinical Pharmacy Education Page 06


Clinical Practice Guidelines

Clinical Value of Spirometry: GINA & GOLD 2025 Evidence-Based


Medicine

VISUAL CONCEPT
Diagnosis of Asthma (GINA 2025) BDR Visualization
Spirometry is ESSENTIAL for diagnosis
Volume-Time Curve: Pre vs Post Bronchodilator
Documents variable expiratory airflow limitation

Key diagnostic criterion: FEV1/FVC ratio < 0.70

Improvement

Bronchodilator Reversibility Testing (BDR)


Protocol: Baseline spirometry → 400 mcg salbutamol → Repeat after 10–15 min.

GINA 2025 Positive Reversibility Criteria:


Increase in FEV1 ≥ 12% AND ≥ 200 mL from baseline

Clinical Significance
PRE-BD (Blue)
FEV1: 1.80 L
Positive BDR: Supports asthma diagnosis & predicts treatment response POST-BD (Green)
FEV1: 2.25 L (+25%)
Negative BDR: Does NOT exclude asthma (variability over time)
Global Initiative for Chronic Obstructive Lung Disease

GOLD 2025: COPD Diagnosis & Severity Clinical Guidelines

Spirometry: The Gold Standard Bronchodilator Reversibility


Essential for diagnosis. A post-bronchodilator FEV1/FVC < 0.70 Less common than in asthma. Positive reversibility does NOT exclude COPD.
confirms persistent airflow limitation. Symptoms alone are insufficient for Some patients show partial reversibility, but the obstruction remains fixed (Ratio
diagnosis. < 0.70).

FEV1 CRITERIA (Post-Bronchodilator)

Minimal symptoms, patient may not


GOLD 1 Mild FEV1 ≥ 80% predicted realize lung function loss.

Symptoms typically progress (SOB on


GOLD 2 Moderate 50% ≤ FEV1 < 80% exertion). Diagnosis often happens here.
predicted

Significant impact on quality of life. High


GOLD 3 Severe 30% ≤ FEV1 < 50% risk of exacerbations.
predicted

Respiratory failure or heart failure (cor


GOLD 4 Very Severe FEV1 < 30% predicted pulmonale) may be present.
Diagnostic Testing

Bronchodilator Reversibility: Visual Interpretation Post-BD


Assessment

Pre vs. Post Bronchodilator Pre-BD Post-BD Calculation Example

Baseline (Pre) Post-BD


FEV1 = 1.80 L FEV1 = 2.20 L
FVC = 3.00 L FVC = 3.20 L
Ratio = 0.60 (Obs) Ratio = 0.69

Reversibility Calculation

Absolute Change: 2.2 - 1.8 = 0.40 L (400 mL)


% Change: (0.4 / 1.8) × 100 = 22%

Interpretation
Criterion 1: Vol > 200mL

Criterion 2: Increase > 12%


POSITIVE Reversibility
Supports Asthma Diagnosis
Diagnostic Challenges

When Spirometry Shows Restrictive Pattern Next Steps

DIAGNOSTIC WORKFLOW

Suggestive Findings
Normal or high FEV1/FVC ratio (≥ 0.70)

Concurrently reduced FEV1 and FVC


Often reported as "Restrictive pattern" or "Possible restriction" Spirometry Result
FEV1/FVC ≥ 0.70
Reduced FVC

Clinical Context Check


Important Limitation
Symptoms? Exposure?
Spirometry ALONE cannot confirm true restrictive lung Exclude poor effort
disease. Reduced FEV1 & FVC can result from:

True restrictive disease (↓ TLC)


Order Plethysmography
Poor patient effort Measure static lung volumes
Submaximal inspiration (TLC, RV, FRC)

Neuromuscular weakness

TLC < 80% TLC ≥ 80%

Confirmed Restriction Normal Lung Volumes


Gold Standard: Plethysmography Proceed to etiology workup Consider non-pulmonary causes
(DLCO, HRCT) or submaximal effort
Lung Plethysmography is required to measure Total
Lung Capacity (TLC).
Advanced Diagnostics

Lung Plethysmography: Technique & Interpretation Gold Standard for


Volumes

Technique & Key Volume Measurements


Advantages
Body Box Method
Patient sits in a sealed chamber breathing against a closed shutter. Uses Boyle's Law (P1V1
= P2V2) to calculate thoracic gas volume.
TLC RV FRC
Total Lung Capacity Residual Volume Functional Residual
Why Better Than Spirometry? Cap.
Measures ALL lung volumes (including trapped air). More accurate for TLC, FRC, and
RV. Differentiates true restriction from poor effort.
Volume at Remaining after max Volume at
full exhalation resting
inspiration state

OBSTRUCTIVE RESTRICTIVE
PATTERN PATTERN

TLC (Total Capacity)


(Hyperinflation) (True Restriction)
Increased (>120%) Decreased (<80%)
RV (Residual Vol) Decreased
(Air Trapping)
Increased
RV/TLC Ratio Increased Normal or Increased

Clinical Pearl for Pharmacists


If spirometry suggests restriction (low FVC, normal/high ratio), advocate for plethysmography before labeling as restrictive disease. Do not assume restriction without a confirmed TLC
Decision Pathways

Diagnostic Algorithm Spirometry to Plethysmography

Step

Obstructive Pattern Possible Restriction


FEV1/FVC < 0.70 Ratio ≥ 0.70 + ↓ FVC

PERFORM BDR TEST ORDER


PLETHYSMOGRAPHY

Asthma Likely COPD Likely Confirmed Restriction Not Restriction

Result: Positive BDR Result: Negative BDR Result: TLC Reduced Result: Normal TLC
FEV1 ↑ ≥ 12% Minimal or no TLC < 80% predicted TLC ≥ 80% predicted
AND reversibility. Persistent (or < LLN) True volume is normal.
↑ ≥ 200 mL obstruction.
Correlate with exposure (GOLD) Check DLCO, Imaging (ILD, etc.) Consider: Poor effort, weakness
Supports diagnosis (GINA)

Key Takeaway: Spirometry is the gateway, but Bronchodilator Testing differentiates Obstructive diseases, while Plethysmography is required to confirm Restrictive
diseases.
Diagnostic Interpretation

PFT Patterns: Obstructive vs Restrictive Comparative Metrics

OBSTRUCTIVE RESTRICTIVE

FEV1
Decreased Decreased (proportionally to FVC)
Forced Expiratory Volume in 1s

FVC
Normal or Decreased Decreased Significantly
Forced Vital Capacity

FEV1 / FVC Decreased (<0.70)


Normal or Increased
The "Ratio" HALLMARK

TLC Decreased (<LLN)


Normal or Increased (Hyperinflation)
Total Lung Capacity HALLMARK

RV
Increased (Air Trapping) Decreased or Normal
Residual Volume

Interstitial Disease: Decreased


DLCO Emphysema: Decreased
Extrapulmonary: Normal
Diffusion Capacity Asthma: Normal / High
Pattern Recognition

Flow–Volume Loops: Visual Signatures Spirometry Patterns

Obstructive Pattern ASTHMA / COPD Restrictive Pattern FIBROSIS / OBESITY

Visual Cues Visual Cues

Concave Expiratory Limb: "Scooped" appearance due to dynamic airway collapse. Narrow Shape: Resembles a "Witch's Hat" or tall/narrow tower.
Right Shift: Loop shifts right on the volume axis (Decreased TLC & FVC).
Left Shift: Loop shifts left due to air trapping (Increased RV & TLC).

Reduced Peak Flow: PEF is significantly lower than predicted. Preserved Contour: Expiratory descent is steep and straight, not scooped.

vs. Narrow),
Mechanisms & Targets

Obstructive Diseases: Pathophysiology

Bronchoconstriction
Smooth muscle contraction narrows airway lumen.

PHARMACOLOGIC TARGET:

β2-Agonists (SABA/LABA)

Antimuscarinics (SAMA/LAMA)

Airway Inflammation
Mucosal edema, cellular infiltration (Eosinophils/Neutrophils),
remodeling.

PHARMACOLOGIC TARGET:

ICS (Corticosteroids) Leukotriene Modifiers

Biologics (Anti-IgE/IL-5)

Mucus & Structural Damage


Goblet cell hyperplasia (mucus hypersecretion) or alveolar
destruction (Emphysema).

PHARMACOLOGIC TARGET:

PDE4 Inhibitors (Roflumilast)


Clinical Mnemonics

Major Obstructive Conditions (CBABE) Differential Diagnosis

C Cystic Fibrosis
Genetic disorder (CFTR); thick mucus, chronic infection, bronchiectasis.
Shared Pathophysiology

B Bronchiectasis Airflow Limitation


Permanent dilation of bronchi; chronic cough, purulent sputum, recurrent infections.
Primary problem is getting air OUT (expiration). Increased airway
resistance or loss of recoil forces.

A Asthma
Reversible airway inflammation & hyperresponsiveness. Often atopic.

Air Trapping
B Bronchitis (Chronic)
Incomplete emptying leads to increased Residual Volume (RV)
Productive cough ≥3 months/year for 2 years. Mucus hypersecretion (COPD). and potentially Total Lung Capacity (TLC).

E Emphysema
Alveolar wall destruction, loss of elastic recoil, air trapping (COPD).
Diagnostic Hallmark

FEV1/FVC < 0.70


Or Below LLN

© 2026 Clinical Pharmacy Education PATHOLOG | Page 09


Y CLASSIFICATION
Type 2 Inflammation & Targeted
Therapy

Asthma: Pathophysiology & Pharmacology Chronic Management

Type 2 Inflammation
Driven by Th2 cells, ILC2s, cytokines (IL-4,
IL-5, IL-13), and eosinophils. Leads to airway
remodeling and hyperresponsiveness.
KEY TRIGGERS: Exercise NSAIDs (AERD)
Allergens
Viruses

Stepwise Management
Inhaled Corticosteroids (ICS) are the
cornerstone to suppress inflammation.

THERAPEUTIC LADDER:
Mild: ICS-formoterol (MART) or SABA +
ICS
Moderate: ICS/LABA maintenance
Add-ons: LAMA (Tiotropium), LTRA
(Montelukast)
Chronic Obstructive Pulmonary Disease

COPD: Chronic Bronchitis & Emphysema Clinical Phenotypes

Chronic Bronchitis Emphysema


"Blue Bloater" "Pink Puffer"

Pathophysiology Pathophysiology

Hyperlplasia of mucus glands+ goblet cells. Destrcution of alveoli ↓ surface area (↓ DLCO).

Airway Inflammation: Narrowing of bronchioles, fibrosis. Loss of Recoil: Airway collapse on expiration (Air trapping).

Clinical Profile
Clinical Profile
Pathological Diagnosis:
Clinical Diagnosis:
Structural changes; permanent enlargement of airspaces.
Productive cough > 3 months/year for 2 consecutive years.
Dyspnea Barrel Chest Cachexia
Cyanosis Edema (RHF) Rhonchi

Pharmacotherapy Focus

Pharmacotherapy Focus LAMA/LABA ICS (if Eos high) Alpha-1 Augmentation

LAMA/LABA Roflumilast (PDE4i) Mucolytics Macrolides (Azithro) Lung Volume Reduct.


Assessment & Recognition

Obstructive Diseases: Clinical Manifestations Patient Presentation

Symptoms Signs
Patient Reported Clinician Observed

Dyspnea Chronic Cough Prolonged Expiration Hyperresonance


Progressive, exertional breathlessness Dry (Asthma) or Productive (Bronchitis) I:E ratio increases (e.g., 1:3 or 1:4) Due to air trapping (percussion)

Wheezing Chest Tightness Decreased Breath Sounds Barrel Chest


Whistling sound on expiration Often nocturnal or early morning "Quiet lung" in emphysema Increased AP diameter (Late stage)

PROGRESSION TO ACUTE / SEVERE

Exacerbation Cues Red Flags


Signs of Worsening Control Immediate Medical Attention

Increased Rescue Use: SABA needed >2 days/week Silent Chest Cyanosis
Absence of wheeze due to critical airflow Central cyanosis indicating severe hypoxemia.
limitation.
Nocturnal Symptoms: Awakening due to cough/dyspnea

Sputum Changes: Increased volume or purulence (COPD) Confusion Work of Breathing


Altered mental status suggesting hypercapnia. Accessory muscle use, paradoxical breathing.

© 2026 Clinical Pharmacy Education SYMPTOMS |


ASSESSMENT
Mechanisms & Consequences

Restrictive Diseases: Pathophysiology Lung Mechanics

Reduced Compliance ("Stiff Lungs")


Lungs resist expansion due to fibrosis or scarring. Higher pressure
needed for volume change.

CLINICAL CONSEQUENCE:

Rapid Shallow Breathing

Increased Work of Breathing

Interstitial Thickening
Collagen deposition in alveolar walls widens the gap between air
and blood.

DIAGNOSTIC IMPACT:

Reduced DLCO Exertional Desaturation

Extrapulmonary Restriction
Mechanical limitation (Chest Wall/Neuromuscular) compresses
normal lungs.

KEY FEATURES:

Low TLC Normal DLCO (usually)


Clinical Classification

Restrictive Disease Categories Intra vs. Extra-pulmonary

Intrapulmonary
"Parenchymal Disease" "Chest Wall / Neuromuscular"

Mechanism Mechanism

Tissue Damage: Inflammation or scarring of the lung parenchyma (interstitium). Mechanical Limit: Lung tissue is normal, but chest expansion is physically
restricted.

Stiff Lungs: Reduced compliance means lungs resist expansion. Pump Failure: Respiratory muscles cannot generate enough force.

Key Clinical Clue Key Clinical Clue

DIFFUSION CAPACITY DIFFUSION CAPACITY


DLCO is LOW DLCO is NORMAL

Gas exchange surface is damaged. Alveolar-capillary membrane is intact.

Common Conditions Common Conditions

Idiopathic Pulm. Fibrosis Sarcoidosis Pneumonitis Severe Obesity Kyphoscoliosis ALS / Myasthenia

Pleural Effusion
Restrictive Lung Disease

Pulmonary Fibrosis (e.g., IPF) Clinical Management

Clinical Features
Stewardship & Safety
Progressive exertional dyspnea and chronic dry cough.

"Velcro" Crackles Digital Clubbing Hypoxemia


Nintedanib Monitoring
1
Tyrosine kinase inhibitor. Check LFTs monthly x3mo, then
q3mo. Manage diarrhea.

PFT Profile
Classic restrictive pattern with preserved flow rates.
Pirfenidone Monitoring
↓ TLC Normal/↑ FEV1/FVC
↓↓ DLCO 2 Antifibrotic. Photosensitivity (sunscreen mandatory), nausea/GI
upset. Take with food.

Imaging (HRCT)
**UIP Pattern**: Honeycombing, traction bronchiectasis, reticular opacities. Basal and subpleural Drug Interactions
predominance. 3
Pirfenidone (CYP1A2): Smoking induces metabolism (↓ effect).
Ciprofloxacin interaction.

Management Strategy Comprehensive Care


4 Manage GERD (risk factor). Vaccinations (Flu/Pneumo).
Aim to slow decline (not curative). Oxygen, rehab, transplant.
Smoking cessation.
Nintedanib Pirfenidone
Restrictive Disease

Atelectasis: Restrictive Mechanism Acute Restriction

PATHOGENESI
S
Mechanism of Collapse Post-Op Sequence
Reversible collapse of alveoli leading to loss of lung volume. Results in reduced compliance and
intrapulmonary shunting.
Precipitating Event
1
↓ TLC V/Q Mismatch Hypoxemia Surgery, Anesthesia,
Trauma

Common Etiologies
Often multifactorial in hospital settings. Key drivers include hypoventilation due to pain/sedation
and obstruction. Restricted Ventilation
2
Pain leads to shallow breathing (splinting)

Post-operative Mucus Plugging Compression

Prevention & Management


Alveolar Collapse
Focus on lung re-expansion: early mobilization, incentive spirometry, and chest 3
Gas absorption & loss of volume
physiotherapy. Treat the underlying cause.

Pharmacy Role
Optimize analgesia to enable deep breathing (avoid over-sedation). Consider mucolytics (e.g., Pharmacist Intervention
4
N-acetylcysteine) only if mucus plugging is significant. Multimodal analgesia → Deep breathing
Assessment & Recognition

Restrictive Diseases: Clinical Manifestations Patient Presentation

Symptoms Signs
Patient Reported Clinician Observed

Exertional Dyspnea Dry Cough Fine Crackles Digital Clubbing


Breathlessness on activity, rapid progression Non-productive, nagging, persistent "Velcro rales" at lung bases (Inspiratory) Bulbous fingertips (Common in IPF)

Tachypnea Reduced Expansion


Fatigue Chest Pain Rapid, shallow breathing pattern Decreased chest excursion on inspiration
General malaise due to chronic work of Vague discomfort or pleuritic pain
breathing

PROGRESSION & COMPLICATIONS

Functional Impact Complications


Exercise Tolerance Advanced Disease

Exercise Intolerance: Significant limitation due to dyspnea Cor Pulmonale Hypoxemia


Right heart failure due to pulmonary HTN. Chronic resting hypoxemia requiring O2
therapy.
Desaturation: Rapid SpO2 drop on exertion (6MWT)

Infections Acute Exacerbation


Weight Loss: Cachexia in advanced disease stages
Increased susceptibility to pneumonia. Rapid deterioration; high mortality in
IPF.

© 2026 Clinical Pharmacy Education SYMPTOMS | Page 17


Etiology & Risk Assessment

Causes and Risk Factors: Obstructive vs Restrictive Clinical


Comparison

OBSTRUCTIVE RESTRICTIVE

Tobacco Smoke (Main risk for


Silica, Asbestos , Coal dust
Exposures COPD) Biomass fuel exposure Bird proteins (Hypersensitivity Pneumonitis)
Environmental & Occupational Radiation therapy (Chest/Breast CA)
Occupational dusts & chemicals

Autoimmune: RA, Scleroderma,


Atopy / Allergic rhinitis (Asthma)
Host Factors AAT Deficiency (Alpha-1 Antitrypsin) Lupus Neuromuscular: ALS, Guillain-Barré
Genetics & Comorbidities CFTR mutations (Cystic Fibrosis)
Chest wall: Kyphoscoliosis

Amiodarone
Medications Non-selective β-blockers (Propranolol) Methotrexate
Drug-Induced Disease NSAIDs / Aspirin (in AERD patients)
Bleomycin , Nitrofurantoin

Viral triggers (Rhinovirus, Influenza) Post-infectious scarring (TB, Severe Pneumonia)


Infections Childhood respiratory infections Post-COVID-19 fibrosis
Viral & Bacterial Bacterial colonization (Bronchiectasis)
Pleural empyema sequelae

Lifestyle/Other Inhaler Technique Severe Obesity (OHS)


Structural & Behavioral Poor adherence/technique mimics refractory disease Mass loading on chest wall reduces compliance
Decision Pathways

Diagnostic Gold Standards Algorithm & Criteria

Obstructive Pattern Restrictive Pattern


FEV1/FVC < 0.70 TLC < LLN

Asthma COPD ILD (Fibrosis) Extrapulmonary

Diagnostic Criteria Diagnostic Criteria Diagnostic Criteria Diagnostic Criteria

Reversibility: FEV1 increases by Fixed Obstruction: Imaging: HRCT showing UIP pattern Volume Loss: Reduced TLC & FVC.
≥12% AND ≥200 mL Post-bronchodilator FEV1/FVC < (honeycombing).
post-bronchodilator. 0.70.
Physiology: Restrictive PFTs with Normal Parenchyma:Normal DLCO
Variability: Excessive variation in History: Significant exposure reduced DLCO. (corrected for VA).
PEF over time. (tobacco, biomass) + symptoms.
Biopsy only if imaging is atypical.
Methacholine challenge positive if Check MIP/MEP for neuromuscular
spirometry normal. weakness.

GUIDELINE: GINA GUIDELINE: GOLD GUIDELINE: ATS / ERS

Important: Always interpret tests in context of clinical history. Mixed patterns (Obstructive + Restrictive) require careful evaluation of volumes and ABG 6MWT Oximetry
DLCO.
Clinical Triage

Quick Differentiation at a Glance Rapid Assessment

OBSTRUCTIVE RESTRICTIVE

FEV1 / FVC Low (<0.70 or LLN)


Normal or High
Primary Spirometry Ratio HALLMARK

TLC Low (<LLN)


Normal or High (Hyperinflation)
Total Lung Capacity HALLMARK

Low: Intrapulmonary (ILD)


Low: Emphysema
DLCO Normal: Extrapulmonary
Gas Exchange
Normal/High: Asthma

Flow-Volume Loop
Concave / Scooped Expiratory Limb Preserved Shape but Smaller
Visual Shape

Bronchodilator Minimal / No Change


Often Improves (Sig. in Asthma) Reversibility

Pharmacist's Role Key Distinction


Use these patterns to validate diagnosis before optimizing therapy. If a patient on high-dose Obstructive: Can't get air OUT (Flow problem). Restrictive: Can't get air IN (Volume problem).
LABA/LAMA has a restrictive pattern, investigate ILD or refer.
Complex Cases

Mixed Patterns: When It’s Not Either/Or Advanced Interpretation

CLINICAL PROFILE
Common Causes Combined Pulmonary Fibrosis & Emphysema
Coexisting conditions can mask or alter typical patterns. (CPFE)
COPD + Fibrosis (CPFE) Asthma + Obesity ILD + Emphysema

PFT Clues
Look for discordant findings that don't fit a single pattern cleanly.
CPFE
The "Perfect Storm"
Low FEV1/FVC + Low TLC DLCO markedly reduced

Emphysema Fibrosis

Diagnostic Approach
PFTs alone are insufficient. Integrate High-Resolution CT (HRCT) imaging, lung
volumes (plethysmography), DLCO, and detailed clinical history.

Therapeutic Implications
Nuanced pharmacotherapy required. Supplemental oxygen is often needed earlier. Pulmonary
rehab referral is critical.
Pathophysiology & Mechanisms

V/Q Mismatch Fundamentals Ventilation / Perfusion

Low V/Q (Shunt-like)


Poor Ventilation, Good Perfusion.

Caused by :Fluid or collapsed, or airway


obstructed.
Common examples :COPD (secretions),
Pneumonia, Atelectasis.

Result: Hypoxemia that typically responds to O .


2

High V/Q (Dead Space)


Good Ventilation, Poor Perfusion.

Mechanism: Blockage of blood flow to alveoli.


Pulmonary Embolism (PE),
Emphysema (capillary destruction).

Ventilation; increased work of breathing.

Clinical Pearl: Hypoxemia from V/Q mismatch generally corrects with


supplemental oxygen, whereas a true "Shunt" (V/Q = 0) is refractory to O2.
Comparison of ventilation (V) and perfusion (Q) abnormalities in lung disease states.
Diffusing Capacity of the lung (DLCO)

DLCO measures the ability of the lungs to tranfer gas from alveoli to the pulmonary capillary blood
It reflects the efficiency of the alveolar-capillary membrane and pulmonary capillary blood volume
Measurement Method:
o Single breath technique ( most commonly used)
o Patient inhales a gas mixture containing a small of CO
o Breath hold for 10 seconds
o Exhaled gas is analyzed to calcuate CO uptake
Normal Values
o Expressed as % of predicted value
o Normal : >80 % predicted
o Mild decrease : 60-79 %
o Moderate decrease : 40-59%
o Severe decrease : <40 %
Clinical Importance :
o Assessment of parenchymal and vascular lung diseases
o Evaluation of dyspnea
o Monitoring disease progression
o Preoperative risk assessment
Conclusion

Summary and Key Clinical Pearls

Takeaways

Optimize Delivery
Obstructive Match device to patient ability. Assess technique at
every visit.
Problem: Getting air out (Airflow Limitation). Check the Ratio (FEV1/FVC)
A
If < 0.70 (or LLN) → Obstructive.
Targeted Therapy
Asthma (Inflammation) Apply guidelines (GINA/GOLD). Step up/down based on
Check Total Capacity (TLC) control & exacerbations.
COPD (Bronchitis/Emphysema) B
If Low → Restrictive.
*(If High → Hyperinflation)* Holistic Care
Smoking cessation, vaccinations, and managing
Restrictive comorbidities.
C Check Diffusion (DLCO)
Problem: Getting air in (Volume Limitation). Low: Emphysema or Fibrosis (Parenchymal
disease).
Intrinsic (Fibrosis, ILD) Normal: Asthma or Chest Wall/Obesity.
"The best drug is useless if the patient cannot use the device
Extrinsic (Obesity, Chest
correctly."
Wall)

Questions?

REVIEW |
APPLICATION
Thank you for your attention
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