PULMO – SECTION 1 (DIAGNOSIS OF RESPIRATORY o Joint symptoms, rash, dry eyes/mouth
DISORDERS) • Malignancy suspicion:
o Respiratory symptoms due to metastasis
284: APPROACH TO THE PATIENT WITH DISEASE OF THE • Drug/radiation history → iatrogenic lung disease
RESPIRATORY SYSTEM Physical Examination
1. Vital Signs
Overview of Respiratory Diseases
• Respiratory rate: Tachypnea or hypopnea
• Three major pathophysiologic categories:
1. Obstructive diseases: Airflow limitation • Pulse oximetry: Hypoxemia at rest or exertion
2. Inspection
▪ Asthma, COPD, bronchiectasis, bronchiolitis
2. Restrictive diseases: Decreased lung expansion • Respiratory distress, accessory muscle use
▪ Interstitial/parenchymal diseases (e.g., IPF) • Chest wall deformities (e.g., kyphoscoliosis)
▪ Chest wall/pleural abnormalities • Inability to speak full sentences → Severe impairment
▪ Neuromuscular disorders 3. Percussion
3. Vascular diseases: • Dullness → Effusion, consolidation
▪ Pulmonary embolism, pulmonary hypertension, • Hyperresonance → Pneumothorax
pulmonary veno-occlusive disease • Assess diaphragm excursion
• Additional overlapping causes: 4. Palpation
o Infectious and neoplastic processes may fall into one or more • Subcutaneous emphysema (barotrauma)
of the above categories. • Tactile fremitus:
• Gas exchange abnormalities classification: o ↑ in consolidation (e.g., pneumonia)
o Hypoxemia (↓ PaO₂), hypercarbia (↑ PaCO₂), or combined o ↓ in pleural effusion or pneumothorax
impairment • Symmetry of chest expansion (ventilation)
5. Auscultation
Clinical Approach • Wheezes:
History Taking o Airway narrowing; polyphonic (asthma), monophonic
1. Key Symptoms (obstruction)
• Dyspnea: • Rhonchi:
o Description helps with etiology: o Secretions in medium-sized airways (bronchitis, COPD)
▪ "Chest tightness" → Asthma
• Stridor:
▪ "Air hunger"/"suffocation" → CHF o Inspiratory, upper airway obstruction (heard over neck)
o Tempo of dyspnea:
▪ Acute: Pneumothorax, PE, pneumonia, edema • Crackles (rales):
o Fluid in alveoli (edema, pneumonia) or interstitial fibrosis (IPF
▪ Chronic progressive: COPD, IPF → Velcro crackles)
▪ Intermittent: Asthma (triggered by allergens, URTI)
o Assess severity: Activity limitation, adaptation • Egophony:
o Exertional dyspnea: Early sign of cardiopulmonary disease o “EEE” → “AH” change in consolidation
• Cough: • Bronchial breath sounds & whispered pectoriloquy:
o Acute productive: Infection (sinusitis, bronchitis, pneumonia) o Suggest consolidation
o Chronic (>8 weeks): 6. Other System Clues
▪ Asthma, COPD, bronchiectasis • Edema:
▪ Nonrespiratory: GERD, postnasal drip o Bilateral → Cor pulmonale
▪ Dry cough → IPF, ILD o Unilateral → DVT (→ PE)
▪ Hemoptysis → urgent evaluation • JVD → Right heart failure
2. Associated Symptoms • Pulsus paradoxus:
• Wheezing: Suggests airway narrowing (asthma) o Suggests severe obstructive disease, impending failure
• Hemoptysis: Infection, malignancy, PE • Skin/Joints:
o Rash, arthritis → Rheumatologic lung disease
• Chest pain:
o From pleura or pulmonary vessels (not parenchyma) • Clubbing: CF, IPF, lung cancer
• Cor pulmonale symptoms: • Cyanosis: >5 g/dL deoxygenated Hb
o Edema, abdominal distention (right heart strain)
3. Social & Environmental History Diagnostic Evaluation
• Smoking history (current, past, secondhand) 1. Pulmonary Function Testing (PFT)
o Pack-years, e-cigarette/vaping use (→ EVALI) • Spirometry:
• Occupational/home exposures: o ↓ FEV₁/FVC <70% → Obstruction
o Asbestos, silica, pet birds, wood smoke o Symmetric ↓ FEV₁ and FVC → May be restrictive →
• Geographic/travel exposures: proceed to lung volumes
o TB, endemic fungi (e.g., Histoplasma) • Flow-volume loop:
4. Systemic Review o Flattened curves → Large airway obstruction
• Fever/chills → Infection • Lung volumes:
• Autoimmune signs: o ↓ TLC <80% predicted → Restriction
, • DLCO (Diffusing capacity):
o ↓ DLCO + restriction → Parenchymal disease
o Normal spirometry + ↓ DLCO → Vascular disease
• Max inspiratory/expiratory pressures:
o For neuromuscular disease
2. Arterial Blood Gas (ABG)
• Determines:
o Hypoxemia (↓ PaO₂)
o Hypercarbia (↑ PaCO₂)
o (A–a) gradient:
▪ ↑ → V/Q mismatch or shunt
3. Imaging
a. Chest Radiography (CXR)
• Initial test: PA + lateral views
• Can detect:
o Consolidation, effusions, masses, opacities, volume loss
• Note: Many airway and vascular diseases may have normal CXR
b. Chest Ultrasound
• Fast diagnosis of:
o Pleural effusions, pneumothorax, consolidation
c. Chest CT
• With or without IV contrast:
o Better defines:
▪ Parenchymal disease
▪ Masses/nodules
▪ Large airways
▪ Pulmonary embolism (CTPA)
▪ Pleural disease
• CT-PET:
o Helps differentiate tumor from scar (metabolic activity)
Further Studies (Case-Specific)
• Bronchoscopy:
o Direct airway visualization
o Bronchoalveolar lavage (BAL)
o Transbronchial biopsy
• Blood tests:
o Inflammatory markers, eosinophils, autoimmune serologies
o Coagulopathy workup for vascular disease
o Genetic testing for heritable lung disease (e.g., CF)
• Sputum studies:
o Gram stain, culture, cytology (for TB, malignancy)
• Echocardiography:
o Evaluate pulmonary hypertension, left/right heart dysfunction
• Surgical lung biopsy:
o For definitive diagnosis in select ILDs or uncertain cases
Summary: Stepwise Diagnostic Approach
1. History & Physical
2. Pulse oximetry ± ABG
3. Chest imaging: US → CXR → CT
4. PFTs
5. Targeted tests:
o Bronchoscopy
o Blood tests
o Sputum
o Echo
o Biopsy
,285: DISTURBANCES OF RESPIRATORY FUNCTION o High airflow velocity → ↓ intraluminal pressure → airway
narrowing.
Overview of Respiratory Function o Causes dynamic airway collapse during forceful exhalation.
• Primary functions: Oxygenation of blood & elimination of CO₂. Flow Limitation
• Gas exchange site: Lung alveoli—blood in capillaries contacts gas • Dynamic airflow limitation: Max flow reached even with increased
across a thin membrane. effort.
o Membrane: Flattened endothelial + epithelial cells. • Spirometry:
• Blood flow: Unidirectional → venous blood loses CO₂, gains O₂. o FEV₁: Volume exhaled in first second → key diagnostic tool.
o Flow falls with lung volume (due to reduced recoil).
• Airflow: Tidal (inflow & outflow alternate).
• Diseases:
• Surface area: ~70 m² within ~7 L thoracic volume. o ↓ Flow: Asthma, chronic bronchitis, emphysema,
• Distribution of gas & blood: Managed through multigenerational tracheomalacia.
branching (airways & vessels). o ↑ Flow: Pulmonary fibrosis (↑ recoil).
• Efficiency: Depends on ventilation–perfusion (V/Q) matching. Inspiration vs. Expiration
• Variability: Due to gravity, anatomy, airway resistance, chest wall • Inspiration: More negative pleural pressure → airway expansion.
compliance. • Expiration: Prone to collapse due to positive pressure.
Requirements for Normal Gas Exchange Work of Breathing
1. Effective tidal ventilation to refresh alveolar gas. In Health
2. Proportional perfusion of each alveolus to its ventilation.
• Minimal at rest (low load, low resistance).
3. Adequate diffusion of O₂ & CO₂ across alveolar-capillary membrane.
4. Adaptability to increased metabolic demand or acid–base • Efficiency: Prefer increased tidal volume over rate at lower levels of
derangements. exertion.
In Disease or Exercise
Components of the Respiratory System • ↑ Work:
• o Due to ↑ ventilation needs or mechanical loads.
1. Lung (including airways) o Conditions: Obstructive disease, pulmonary fibrosis, edema,
resection.
•
2. Neuromuscular system (controls respiratory muscles) • Dynamic Hyperinflation:
o Occurs with airflow obstruction → incomplete exhalation.
• o Operating FRC increases → lung less compliant → ↑ elastic
3. Chest wall (includes muscles, heart, abdomen)
work.
o Seen in severe COPD.
Mechanical Properties of the Respiratory System
Volume-Related (Static) Properties • Clinical sign: Difficulty inhaling (even though the issue is expiratory
flow).
• Lung elasticity:
o Requires positive pressure (transpulmonary) to stay inflated. Ventilatory Control & Adequacy
o Compliance: High at low volumes, low at high volumes. Control System Inputs
• Air trapping: • Chemoreceptors: Respond to:
o Small airways collapse during exhalation → gas trapping. o CO₂ (PaCO₂)
o Exaggerated in obstructive diseases & aging. o O₂ (PaO₂)
• Chest wall: o pH
o Naturally expands with no transmural pressure. • Volitional control: Speech, breath-holding, etc.
o More compliant at high volumes, stiffer at very low volumes
Dead Space Concept
(due to rib cage and diaphragm limits).
• Anatomic Dead Space (VD):
• Functional Residual Capacity (FRC): o Volume in conducting airways (no gas exchange).
o Passive equilibrium point.
o No alveolar ventilation if VT < VD.
o Inward lung recoil = outward chest wall recoil.
o Alveolar pressure = atmospheric; pleural pressure ~ -5 • Functional Dead Space:
cmH₂O. o Alveoli that are ventilated but not perfused (e.g., PE).
Muscular Contribution • Minute Ventilation (V̇E) = VT × RR
• Inspiratory muscles → generate positive pressure. o Dead Space Ventilation (V̇D) = VD × RR
o Alveolar Ventilation (V̇A) = (VT − VD) × RR
• Expiratory muscles → generate negative pressure.
• Vital Capacity (VC): CO₂ Elimination & Alveolar Ventilation
o VC = TLC − RV • CO₂ elimination ∝ alveolar ventilation.
o Reflects mechanical limits, not intrinsic lung function.
• PaCO₂ = CO₂ production / alveolar ventilation
• Maximal pressures vary by lung volume (length-tension + mechanical
advantage). • PaCO₂ ≈ 40 mmHg in normal state.
o ↑ PaCO₂ = hypoventilation.
Flow-Related (Dynamic) Properties o ↓ PaCO₂ = hyperventilation.
Airway Resistance • Ventilatory failure = extreme hypoventilation.
• Frictional resistance is normally low (Raw <2 cmH₂O/L/s).
Alveolar Gas Equation
• Bernoulli Effect:
Formula:
, plaintext o Low V/Q or shunt.
Copy code o Rarely, diffusion limitation.
PAO₂ = FiO₂ × (Pbar - PH₂O) - PaCO₂ / R
• PAO₂: Alveolar O₂ tension. PATHOPHYSIOLOGY
• FiO₂: Inspired O₂ fraction. Common Patterns of Lung Dysfunction
• Pbar: Barometric pressure. Restrictive Lung Disease
• PH₂O: Water vapor pressure (47 mmHg at 37°C). 1. Increased Elastic Recoil (e.g., Idiopathic Pulmonary Fibrosis)
• PaCO₂: Arterial CO₂ tension. • Increased lung recoil lowers:
• R: Respiratory quotient (~0.85). o TLC, FRC, RV, FVC.
Clinical Implication: • Maximal expiratory flows are increased for given lung volumes due to:
• Severe hypoxemia rarely due to hypoventilation alone at sea level. o High recoil.
• More likely at high altitudes due to ↓ barometric pressure. o Outward traction on airways.
GAS EXCHANGE • Airway resistance (Raw): Normal.
Diffusion • Diffusing capacity (DLco): Reduced due to capillary destruction.
• Mechanism: Oxygen diffuses from alveolar gas into capillary blood via • Oxygenation:
the alveolar membrane. o Severely reduced from perfusion of poorly ventilated alveoli.
• Alveolar Membrane: • Flow-volume loop: Smaller and shifted left; flows are relatively higher
o Very large surface area. for volume.
o Minimal thickness. 2. Chest Wall Abnormality (e.g., Moderate Obesity)
o Highly optimized for rapid diffusion. • FRC reduced due to:
• Oxygen Uptake: o Decreased outward chest wall recoil.
o Hemoglobin in red blood cells becomes fully saturated with o Intact lung recoil.
oxygen within the first third of the alveolar capillary transit.
• TLC and RV:
o Therefore, oxygen uptake is perfusion-limited, not o Usually normal unless obesity is massive.
diffusion-limited, under normal conditions.
• Mild hypoxemia:
• CO₂ Diffusion: o Due to airway closure in dependent lung at low FRC.
o CO₂ also rapidly equilibrates across the alveolar membrane.
o Capillary blood gases match alveolar gases in normal lungs. • Raw and DLco:
o Normal unless pulmonary hypertension (e.g., in sleep apnea)
• Diffusion Limitation (rare): lowers DLco.
o High altitudes. 3. Reduced Muscle Strength (e.g., Myasthenia Gravis)
o Elite athletes under maximum exertion.
o Interstitial lung disease where alveolar walls are thickened • FRC: Normal.
but still perfused. • TLC: Decreased.
• RV: Increased.
Ventilation/Perfusion (V/Q) Heterogeneity • FVC and FEV1: Reduced.
• Ideal Gas Exchange: • Raw and DLco: Normal.
o Occurs when ventilation matches perfusion in all alveoli. • Oxygenation: May worsen with severe weakness and atelectasis.
• Causes of V/Q Mismatch:
o Gravity effects on lung mechanics and blood flow. Obstructive Lung Disease
o Anatomical variations in airways and vessels. 1. Decreased Airway Diameter (e.g., Acute Asthma)
• Extreme V/Q Mismatch Examples: • Mechanisms:
1. Ventilation without Perfusion: o Bronchial smooth muscle constriction.
▪ E.g., Pulmonary embolism. o Inflammation and edema.
▪ Results in physiologic dead space (wasted • Flow-volume loop:
ventilation). o Scooped appearance (especially at lower volumes).
2. Perfusion without Ventilation: • Reversibility:
▪ E.g., Alveolar shunt. o β2-agonists (acute).
▪ Venous blood bypasses gas exchange. o Inhaled steroids (chronic).
▪ Leads to arterial hypoxemia refractory to • Lung volumes:
supplemental O₂. o TLC: Normal or high.
▪ Supplemental O₂ doesn't help: o FRC and RV: Elevated due to airway closure.
▪ No O₂ reaches shunted alveoli. • Raw: Increased.
▪ Hemoglobin is already near fully • DLco: Normal or mildly elevated.
saturated in well-ventilated units.
• Oxygenation: Mild hypoxemia responsive to O₂.
• Partial V/Q Mismatch: 2. Decreased Elastic Recoil (e.g., Severe Emphysema)
o More common in disease.
o Low V/Q areas: underventilated but perfused alveoli. • Lung volumes:
o Causes incomplete oxygenation. o TLC and FRC: Elevated.
o Responsive to supplemental O₂. o RV: Severely elevated.
o FVC and FEV1: Markedly reduced.
• Causes of Arterial Hypoxemia:
• Mechanisms:
o Low inspired oxygen (e.g., high altitude).
o Loss of recoil impairs expiratory driving pressure.
o Severe alveolar hypoventilation.
DISORDERS) • Malignancy suspicion:
o Respiratory symptoms due to metastasis
284: APPROACH TO THE PATIENT WITH DISEASE OF THE • Drug/radiation history → iatrogenic lung disease
RESPIRATORY SYSTEM Physical Examination
1. Vital Signs
Overview of Respiratory Diseases
• Respiratory rate: Tachypnea or hypopnea
• Three major pathophysiologic categories:
1. Obstructive diseases: Airflow limitation • Pulse oximetry: Hypoxemia at rest or exertion
2. Inspection
▪ Asthma, COPD, bronchiectasis, bronchiolitis
2. Restrictive diseases: Decreased lung expansion • Respiratory distress, accessory muscle use
▪ Interstitial/parenchymal diseases (e.g., IPF) • Chest wall deformities (e.g., kyphoscoliosis)
▪ Chest wall/pleural abnormalities • Inability to speak full sentences → Severe impairment
▪ Neuromuscular disorders 3. Percussion
3. Vascular diseases: • Dullness → Effusion, consolidation
▪ Pulmonary embolism, pulmonary hypertension, • Hyperresonance → Pneumothorax
pulmonary veno-occlusive disease • Assess diaphragm excursion
• Additional overlapping causes: 4. Palpation
o Infectious and neoplastic processes may fall into one or more • Subcutaneous emphysema (barotrauma)
of the above categories. • Tactile fremitus:
• Gas exchange abnormalities classification: o ↑ in consolidation (e.g., pneumonia)
o Hypoxemia (↓ PaO₂), hypercarbia (↑ PaCO₂), or combined o ↓ in pleural effusion or pneumothorax
impairment • Symmetry of chest expansion (ventilation)
5. Auscultation
Clinical Approach • Wheezes:
History Taking o Airway narrowing; polyphonic (asthma), monophonic
1. Key Symptoms (obstruction)
• Dyspnea: • Rhonchi:
o Description helps with etiology: o Secretions in medium-sized airways (bronchitis, COPD)
▪ "Chest tightness" → Asthma
• Stridor:
▪ "Air hunger"/"suffocation" → CHF o Inspiratory, upper airway obstruction (heard over neck)
o Tempo of dyspnea:
▪ Acute: Pneumothorax, PE, pneumonia, edema • Crackles (rales):
o Fluid in alveoli (edema, pneumonia) or interstitial fibrosis (IPF
▪ Chronic progressive: COPD, IPF → Velcro crackles)
▪ Intermittent: Asthma (triggered by allergens, URTI)
o Assess severity: Activity limitation, adaptation • Egophony:
o Exertional dyspnea: Early sign of cardiopulmonary disease o “EEE” → “AH” change in consolidation
• Cough: • Bronchial breath sounds & whispered pectoriloquy:
o Acute productive: Infection (sinusitis, bronchitis, pneumonia) o Suggest consolidation
o Chronic (>8 weeks): 6. Other System Clues
▪ Asthma, COPD, bronchiectasis • Edema:
▪ Nonrespiratory: GERD, postnasal drip o Bilateral → Cor pulmonale
▪ Dry cough → IPF, ILD o Unilateral → DVT (→ PE)
▪ Hemoptysis → urgent evaluation • JVD → Right heart failure
2. Associated Symptoms • Pulsus paradoxus:
• Wheezing: Suggests airway narrowing (asthma) o Suggests severe obstructive disease, impending failure
• Hemoptysis: Infection, malignancy, PE • Skin/Joints:
o Rash, arthritis → Rheumatologic lung disease
• Chest pain:
o From pleura or pulmonary vessels (not parenchyma) • Clubbing: CF, IPF, lung cancer
• Cor pulmonale symptoms: • Cyanosis: >5 g/dL deoxygenated Hb
o Edema, abdominal distention (right heart strain)
3. Social & Environmental History Diagnostic Evaluation
• Smoking history (current, past, secondhand) 1. Pulmonary Function Testing (PFT)
o Pack-years, e-cigarette/vaping use (→ EVALI) • Spirometry:
• Occupational/home exposures: o ↓ FEV₁/FVC <70% → Obstruction
o Asbestos, silica, pet birds, wood smoke o Symmetric ↓ FEV₁ and FVC → May be restrictive →
• Geographic/travel exposures: proceed to lung volumes
o TB, endemic fungi (e.g., Histoplasma) • Flow-volume loop:
4. Systemic Review o Flattened curves → Large airway obstruction
• Fever/chills → Infection • Lung volumes:
• Autoimmune signs: o ↓ TLC <80% predicted → Restriction
, • DLCO (Diffusing capacity):
o ↓ DLCO + restriction → Parenchymal disease
o Normal spirometry + ↓ DLCO → Vascular disease
• Max inspiratory/expiratory pressures:
o For neuromuscular disease
2. Arterial Blood Gas (ABG)
• Determines:
o Hypoxemia (↓ PaO₂)
o Hypercarbia (↑ PaCO₂)
o (A–a) gradient:
▪ ↑ → V/Q mismatch or shunt
3. Imaging
a. Chest Radiography (CXR)
• Initial test: PA + lateral views
• Can detect:
o Consolidation, effusions, masses, opacities, volume loss
• Note: Many airway and vascular diseases may have normal CXR
b. Chest Ultrasound
• Fast diagnosis of:
o Pleural effusions, pneumothorax, consolidation
c. Chest CT
• With or without IV contrast:
o Better defines:
▪ Parenchymal disease
▪ Masses/nodules
▪ Large airways
▪ Pulmonary embolism (CTPA)
▪ Pleural disease
• CT-PET:
o Helps differentiate tumor from scar (metabolic activity)
Further Studies (Case-Specific)
• Bronchoscopy:
o Direct airway visualization
o Bronchoalveolar lavage (BAL)
o Transbronchial biopsy
• Blood tests:
o Inflammatory markers, eosinophils, autoimmune serologies
o Coagulopathy workup for vascular disease
o Genetic testing for heritable lung disease (e.g., CF)
• Sputum studies:
o Gram stain, culture, cytology (for TB, malignancy)
• Echocardiography:
o Evaluate pulmonary hypertension, left/right heart dysfunction
• Surgical lung biopsy:
o For definitive diagnosis in select ILDs or uncertain cases
Summary: Stepwise Diagnostic Approach
1. History & Physical
2. Pulse oximetry ± ABG
3. Chest imaging: US → CXR → CT
4. PFTs
5. Targeted tests:
o Bronchoscopy
o Blood tests
o Sputum
o Echo
o Biopsy
,285: DISTURBANCES OF RESPIRATORY FUNCTION o High airflow velocity → ↓ intraluminal pressure → airway
narrowing.
Overview of Respiratory Function o Causes dynamic airway collapse during forceful exhalation.
• Primary functions: Oxygenation of blood & elimination of CO₂. Flow Limitation
• Gas exchange site: Lung alveoli—blood in capillaries contacts gas • Dynamic airflow limitation: Max flow reached even with increased
across a thin membrane. effort.
o Membrane: Flattened endothelial + epithelial cells. • Spirometry:
• Blood flow: Unidirectional → venous blood loses CO₂, gains O₂. o FEV₁: Volume exhaled in first second → key diagnostic tool.
o Flow falls with lung volume (due to reduced recoil).
• Airflow: Tidal (inflow & outflow alternate).
• Diseases:
• Surface area: ~70 m² within ~7 L thoracic volume. o ↓ Flow: Asthma, chronic bronchitis, emphysema,
• Distribution of gas & blood: Managed through multigenerational tracheomalacia.
branching (airways & vessels). o ↑ Flow: Pulmonary fibrosis (↑ recoil).
• Efficiency: Depends on ventilation–perfusion (V/Q) matching. Inspiration vs. Expiration
• Variability: Due to gravity, anatomy, airway resistance, chest wall • Inspiration: More negative pleural pressure → airway expansion.
compliance. • Expiration: Prone to collapse due to positive pressure.
Requirements for Normal Gas Exchange Work of Breathing
1. Effective tidal ventilation to refresh alveolar gas. In Health
2. Proportional perfusion of each alveolus to its ventilation.
• Minimal at rest (low load, low resistance).
3. Adequate diffusion of O₂ & CO₂ across alveolar-capillary membrane.
4. Adaptability to increased metabolic demand or acid–base • Efficiency: Prefer increased tidal volume over rate at lower levels of
derangements. exertion.
In Disease or Exercise
Components of the Respiratory System • ↑ Work:
• o Due to ↑ ventilation needs or mechanical loads.
1. Lung (including airways) o Conditions: Obstructive disease, pulmonary fibrosis, edema,
resection.
•
2. Neuromuscular system (controls respiratory muscles) • Dynamic Hyperinflation:
o Occurs with airflow obstruction → incomplete exhalation.
• o Operating FRC increases → lung less compliant → ↑ elastic
3. Chest wall (includes muscles, heart, abdomen)
work.
o Seen in severe COPD.
Mechanical Properties of the Respiratory System
Volume-Related (Static) Properties • Clinical sign: Difficulty inhaling (even though the issue is expiratory
flow).
• Lung elasticity:
o Requires positive pressure (transpulmonary) to stay inflated. Ventilatory Control & Adequacy
o Compliance: High at low volumes, low at high volumes. Control System Inputs
• Air trapping: • Chemoreceptors: Respond to:
o Small airways collapse during exhalation → gas trapping. o CO₂ (PaCO₂)
o Exaggerated in obstructive diseases & aging. o O₂ (PaO₂)
• Chest wall: o pH
o Naturally expands with no transmural pressure. • Volitional control: Speech, breath-holding, etc.
o More compliant at high volumes, stiffer at very low volumes
Dead Space Concept
(due to rib cage and diaphragm limits).
• Anatomic Dead Space (VD):
• Functional Residual Capacity (FRC): o Volume in conducting airways (no gas exchange).
o Passive equilibrium point.
o No alveolar ventilation if VT < VD.
o Inward lung recoil = outward chest wall recoil.
o Alveolar pressure = atmospheric; pleural pressure ~ -5 • Functional Dead Space:
cmH₂O. o Alveoli that are ventilated but not perfused (e.g., PE).
Muscular Contribution • Minute Ventilation (V̇E) = VT × RR
• Inspiratory muscles → generate positive pressure. o Dead Space Ventilation (V̇D) = VD × RR
o Alveolar Ventilation (V̇A) = (VT − VD) × RR
• Expiratory muscles → generate negative pressure.
• Vital Capacity (VC): CO₂ Elimination & Alveolar Ventilation
o VC = TLC − RV • CO₂ elimination ∝ alveolar ventilation.
o Reflects mechanical limits, not intrinsic lung function.
• PaCO₂ = CO₂ production / alveolar ventilation
• Maximal pressures vary by lung volume (length-tension + mechanical
advantage). • PaCO₂ ≈ 40 mmHg in normal state.
o ↑ PaCO₂ = hypoventilation.
Flow-Related (Dynamic) Properties o ↓ PaCO₂ = hyperventilation.
Airway Resistance • Ventilatory failure = extreme hypoventilation.
• Frictional resistance is normally low (Raw <2 cmH₂O/L/s).
Alveolar Gas Equation
• Bernoulli Effect:
Formula:
, plaintext o Low V/Q or shunt.
Copy code o Rarely, diffusion limitation.
PAO₂ = FiO₂ × (Pbar - PH₂O) - PaCO₂ / R
• PAO₂: Alveolar O₂ tension. PATHOPHYSIOLOGY
• FiO₂: Inspired O₂ fraction. Common Patterns of Lung Dysfunction
• Pbar: Barometric pressure. Restrictive Lung Disease
• PH₂O: Water vapor pressure (47 mmHg at 37°C). 1. Increased Elastic Recoil (e.g., Idiopathic Pulmonary Fibrosis)
• PaCO₂: Arterial CO₂ tension. • Increased lung recoil lowers:
• R: Respiratory quotient (~0.85). o TLC, FRC, RV, FVC.
Clinical Implication: • Maximal expiratory flows are increased for given lung volumes due to:
• Severe hypoxemia rarely due to hypoventilation alone at sea level. o High recoil.
• More likely at high altitudes due to ↓ barometric pressure. o Outward traction on airways.
GAS EXCHANGE • Airway resistance (Raw): Normal.
Diffusion • Diffusing capacity (DLco): Reduced due to capillary destruction.
• Mechanism: Oxygen diffuses from alveolar gas into capillary blood via • Oxygenation:
the alveolar membrane. o Severely reduced from perfusion of poorly ventilated alveoli.
• Alveolar Membrane: • Flow-volume loop: Smaller and shifted left; flows are relatively higher
o Very large surface area. for volume.
o Minimal thickness. 2. Chest Wall Abnormality (e.g., Moderate Obesity)
o Highly optimized for rapid diffusion. • FRC reduced due to:
• Oxygen Uptake: o Decreased outward chest wall recoil.
o Hemoglobin in red blood cells becomes fully saturated with o Intact lung recoil.
oxygen within the first third of the alveolar capillary transit.
• TLC and RV:
o Therefore, oxygen uptake is perfusion-limited, not o Usually normal unless obesity is massive.
diffusion-limited, under normal conditions.
• Mild hypoxemia:
• CO₂ Diffusion: o Due to airway closure in dependent lung at low FRC.
o CO₂ also rapidly equilibrates across the alveolar membrane.
o Capillary blood gases match alveolar gases in normal lungs. • Raw and DLco:
o Normal unless pulmonary hypertension (e.g., in sleep apnea)
• Diffusion Limitation (rare): lowers DLco.
o High altitudes. 3. Reduced Muscle Strength (e.g., Myasthenia Gravis)
o Elite athletes under maximum exertion.
o Interstitial lung disease where alveolar walls are thickened • FRC: Normal.
but still perfused. • TLC: Decreased.
• RV: Increased.
Ventilation/Perfusion (V/Q) Heterogeneity • FVC and FEV1: Reduced.
• Ideal Gas Exchange: • Raw and DLco: Normal.
o Occurs when ventilation matches perfusion in all alveoli. • Oxygenation: May worsen with severe weakness and atelectasis.
• Causes of V/Q Mismatch:
o Gravity effects on lung mechanics and blood flow. Obstructive Lung Disease
o Anatomical variations in airways and vessels. 1. Decreased Airway Diameter (e.g., Acute Asthma)
• Extreme V/Q Mismatch Examples: • Mechanisms:
1. Ventilation without Perfusion: o Bronchial smooth muscle constriction.
▪ E.g., Pulmonary embolism. o Inflammation and edema.
▪ Results in physiologic dead space (wasted • Flow-volume loop:
ventilation). o Scooped appearance (especially at lower volumes).
2. Perfusion without Ventilation: • Reversibility:
▪ E.g., Alveolar shunt. o β2-agonists (acute).
▪ Venous blood bypasses gas exchange. o Inhaled steroids (chronic).
▪ Leads to arterial hypoxemia refractory to • Lung volumes:
supplemental O₂. o TLC: Normal or high.
▪ Supplemental O₂ doesn't help: o FRC and RV: Elevated due to airway closure.
▪ No O₂ reaches shunted alveoli. • Raw: Increased.
▪ Hemoglobin is already near fully • DLco: Normal or mildly elevated.
saturated in well-ventilated units.
• Oxygenation: Mild hypoxemia responsive to O₂.
• Partial V/Q Mismatch: 2. Decreased Elastic Recoil (e.g., Severe Emphysema)
o More common in disease.
o Low V/Q areas: underventilated but perfused alveoli. • Lung volumes:
o Causes incomplete oxygenation. o TLC and FRC: Elevated.
o Responsive to supplemental O₂. o RV: Severely elevated.
o FVC and FEV1: Markedly reduced.
• Causes of Arterial Hypoxemia:
• Mechanisms:
o Low inspired oxygen (e.g., high altitude).
o Loss of recoil impairs expiratory driving pressure.
o Severe alveolar hypoventilation.
