Findings and investigation In bronchial asthama Chronic bronchitis Emphysema And their reasons for each why elevated

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Findings & Investigations in Bronchial Asthma, Chronic Bronchitis, and Emphysema

I. BRONCHIAL ASTHMA

Clinical Findings

Finding	Reason
Episodic wheeze, dyspnea, chest tightness	Bronchoconstriction from IgE-mast cell mediated release of leukotrienes, acetylcholine, histamine
Nocturnal/early-morning predominance	Circadian dip in cortisol + increased vagal tone at night
Prolonged expiration	Air trapping due to bronchospasm - airways narrow further on expiration
Hyperinflated lungs (during attack)	Air trapping from mucus plugs and bronchoconstriction - inhaled air cannot escape fully
Cyanosis (severe/status asthmaticus)	Severe V/Q mismatch from extensive bronchospasm

Investigations & Why They Are Abnormal

Spirometry / Pulmonary Function Tests

Parameter	Change	Reason
FEV₁	Decreased	Obstruction - narrowed airways resist forced expiratory flow
FVC	Decreased or normal	Air trapping reduces effective expiratory volume
FEV₁/FVC ratio	Decreased (<0.7)	Obstructive pattern - FEV₁ falls proportionally more than FVC
FEV₁ reversibility	>12% and >200 mL after bronchodilator	Hallmark of asthma - bronchospasm is reversible (unlike COPD)
PEFR (Peak Expiratory Flow Rate)	Decreased; diurnal variation >20%	Airway caliber varies with time - diagnostic of asthma
TLC / RV	Increased (during attack)	Air trapping behind mucus plugs and closed airways
DLCO	Normal	Alveolar structure intact; no parenchymal destruction

Blood

Finding	Reason
Eosinophilia	Atopic asthma driven by IL-5 (from Th2 cells) which activates eosinophils
Elevated total serum IgE	Allergen sensitization triggers B cells (via IL-4/IL-13) to produce IgE
Arterial blood gas (ABG) during attack: Respiratory alkalosis (early), then hypoxia	Early: hyperventilation blows off CO₂ → ↓ PaCO₂. Late/severe: respiratory fatigue → CO₂ retention → hypercapnia

Sputum

Finding	Reason
Eosinophils	IL-5 driven eosinophilic airway inflammation
Charcot-Leyden crystals	Composed of galectin-10 from eosinophils - strong inducers of inflammation and mucus
Curschmann spirals	Mucus plugs extruded from subepithelial mucous gland ducts or bronchioles

Chest X-ray (CXR)

Finding	Reason
Normal between attacks	Structural parenchyma is preserved
Hyperinflation during attack	Air trapping from bronchoconstriction and mucus plugging
Flattened diaphragm	Lungs overinflated, pushing diaphragm downward

Skin Prick Test / RAST

Positive to specific allergens in atopic asthma - confirms IgE-mediated sensitization

II. CHRONIC BRONCHITIS

Definition: Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years, in the absence of other cause.

Clinical Findings

Finding	Reason
Chronic productive cough ("blue bloater")	Hypersecretion from hypertrophied mucous glands + goblet cell hyperplasia
Cyanosis	Hypoventilation → CO₂ retention + hypoxia → V/Q mismatch; patient does not compensate with increased respiratory drive
Obesity	Common comorbidity further reducing ventilation, especially during sleep
Right heart failure (cor pulmonale)	Chronic hypoxia causes vasoconstriction → pulmonary hypertension → RV hypertrophy/failure
Peripheral edema	Right heart failure → elevated venous pressure
Recurrent chest infections	Excess mucus is an ideal medium for bacterial/viral growth

Investigations

Spirometry

Parameter	Change	Reason
FEV₁	Decreased	Small airway obstruction from mucus plugging + bronchiolar wall fibrosis
FVC	Reduced	Air trapping from airway obstruction
FEV₁/FVC ratio	Decreased (<0.7)	Obstructive pattern
FEV₁ reversibility	Partial/absent	Airway inflammation and fibrosis are fixed components, unlike pure asthma
TLC / RV / FRC	Increased	Air trapping from chronic obstruction
DLCO	Variable - often reduced in combined COPD	Emphysematous changes destroy alveolar surface area for diffusion

ABG

Finding	Reason
Hypoxemia (↓ PaO₂)	V/Q mismatch from mucus plugging and airway obstruction
Hypercapnia (↑ PaCO₂)	Hypoventilation - patients do not increase respiratory drive adequately; CO₂ is retained ("CO₂ retainers")
Respiratory acidosis	Chronic CO₂ retention lowers pH
↑ Bicarbonate (metabolic compensation)	Kidney retains HCO₃ to compensate for chronic respiratory acidosis

Blood

Finding	Reason
Polycythemia (↑ Hb, ↑ RBC, ↑ PCV)	Chronic hypoxia stimulates renal EPO production → increased red cell mass
Elevated WBC	Recurrent bacterial infections of airways
Elevated PCV	Secondary polycythemia from chronic hypoxia

Sputum

Finding	Reason
Mucopurulent / purulent sputum	Bacterial infection (H. influenzae, S. pneumoniae, M. catarrhalis common) superimposed on excess mucus
Macrophages, neutrophils (no eosinophils)	Innate immune response to smoke and bacterial pathogens; eosinophils are NOT a feature (unlike asthma)

CXR

Finding	Reason
"Dirty chest" - increased bronchovascular markings	Thickened bronchial walls + peribronchial inflammation increase radiodensity
Cardiomegaly (right-sided)	Cor pulmonale from pulmonary hypertension
Tramline / ring shadows	Thickened bronchial walls seen end-on and tangentially

ECG / Echo

Finding	Reason
P pulmonale (tall peaked P in II)	Right atrial enlargement from pulmonary hypertension
Right ventricular hypertrophy (RVH)	Pressure overload of RV from chronic pulmonary hypertension

III. EMPHYSEMA

Definition: Irreversible enlargement of airspaces distal to the terminal bronchiole with destruction of alveolar walls, without significant fibrosis.

Clinical Findings

Finding	Reason
"Pink puffer"	Compensatory hyperventilation maintains near-normal O₂ at the cost of significant respiratory effort
Barrel chest	Chronic air trapping → lungs held at high lung volume → AP diameter increases
Pursed-lip breathing	Creates back-pressure (auto-PEEP) to prevent dynamic airway collapse during expiration
Use of accessory muscles	Flattened diaphragm is mechanically disadvantaged; intercostals and neck muscles recruited
Weight loss, cachexia	Increased work of breathing; systemic inflammation
Hyper-resonance on percussion	Hyperinflated, air-filled lungs with loss of solid alveolar tissue
Reduced breath sounds	Loss of lung parenchyma reduces turbulence; airflow decreased

Investigations

Spirometry (most important)

Parameter	Change	Reason
FEV₁	Markedly decreased	Loss of elastic recoil → airway collapse on expiration even without mechanical obstruction; radial traction on airways is lost
FVC	Decreased	Air trapping; slow, reduced expiratory flow
FEV₁/FVC ratio	Decreased (<0.7)	Obstructive pattern
TLC	Markedly increased	Destruction of alveolar walls removes elastic recoil → lungs hyperinflate at rest
RV (Residual Volume)	Markedly increased	Airways collapse early in expiration (before full expiration) - air is trapped
FRC (Functional Residual Capacity)	Increased	Equilibrium point shifts toward higher lung volume due to reduced recoil
DLCO (diffusing capacity for CO)	Markedly reduced - KEY feature	Destruction of alveolar walls = loss of alveolar-capillary surface area for gas exchange; this distinguishes emphysema from other obstructive diseases
FEV₁ reversibility	Minimal	Obstruction is from structural loss of elastic recoil, not reversible bronchospasm

ABG

Finding	Reason
PaO₂	Normal or slightly low (until late stage)
PaCO₂	Normal or low (until late stage)
Late disease: Hypoxemia + Hypercapnia	Respiratory muscle fatigue, V/Q mismatch becomes uncorrectable

CXR / CT Chest

Finding	Reason
Hyperinflated lungs	Increased TLC from loss of elastic recoil
Flat diaphragm	Lungs push diaphragm inferiorly; flattening on PA film (below level of anterior 6th rib)
Increased AP diameter ("barrel chest" on lateral film)	Air trapping and hyperinflation
Hyperlucent lung fields	Fewer alveolar walls = less radiodense tissue; more air per unit volume
Reduced vascular markings peripherally	Loss of alveolar capillaries from parenchymal destruction
Bullae	Coalescence of destroyed airspaces into large air-filled cysts
CT: centrilobular or panlobular low-density areas	Gold standard for imaging diagnosis; shows exact distribution (upper lobes = smoking; lower lobes = α1-AT deficiency)

Blood

Finding	Reason
Polycythemia (late stage)	Late hypoxemia stimulates EPO
α1-antitrypsin level (if panacinar, young patient, non-smoker)	α1-AT deficiency removes the main inhibitor of neutrophil elastase → unchecked proteolytic destruction of alveoli

Quick Summary Table

Parameter	Asthma	Chronic Bronchitis	Emphysema
FEV₁/FVC	↓ (reversible)	↓	↓
DLCO	Normal	Variable	Markedly ↓
TLC	↑ (attack)	↑	Markedly ↑
Sputum eosinophils	✓✓	✗	✗
IgE	↑ (atopic)	Normal	Normal
PaCO₂	↓ (early), ↑ (late)	↑ (chronic)	Normal/↓ (early), ↑ (late)
Polycythemia	Rare	✓✓	Late
CXR	Normal / hyperinflation	Dirty chest, ↑ markings	Hyperlucent, flat diaphragm
Key sputum	Curschmann, Charcot-Leyden, eosinophils	Mucopurulent, neutrophils	Not specific

Sources: Robbins, Cotran & Kumar - Pathologic Basis of Disease (Robbins & Kumar Basic Pathology); Murray & Nadel's Textbook of Respiratory Medicine

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