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Disturbances of Respiratory Function

Chapter 296 | Part 7: Disorders of the Respiratory System

KEY CLINICAL POINTS

  • Respiratory system functions include oxygenation of blood and CO2 elimination via gas exchange in alveoli.
  • Ventilation-perfusion (V/Q) matching is critical for efficient gas exchange; mismatches cause hypoxemia/hypercapnia.
  • Spirometry and flow-volume loops assess lung volumes, airflow obstruction, and dynamic hyperinflation.
  • Pulmonary fibrosis increases lung recoil pressure, while emphysema reduces it, altering maximal expiratory flows.
  • Arterial blood gas analysis (ABG) and alveolar-arterial O2 gradient (A-aDO2) help diagnose hypoxemia causes.

1. DEFINITION & OVERVIEW

The respiratory system oxygenates blood and eliminates CO2 via gas exchange in alveoli. This requires tidal ventilation, perfusion matching, and diffusion across the alveolar-capillary membrane. Abnormalities disrupt these processes, leading to hypoxemia, hypercapnia, or respiratory failure.

Table: Pulmonary Function Abnormalities in Common Respiratory Conditions

Parameter Idiopathic Pulmonary Fibrosis Obesity Myasthenia Gravis Asthma Emphysema
TLC (%) 60% 95% 75% 100% 130%
FRC (%) 60% 65% 100% 102% 220%
RV (%) 60% 100% 120% 120% 310%
FVC (%) 60% 92% 60% 90% 60%
FEV1 (%) 75% 92% 60% 75% 38%
Raw (cmH2O/L/s) 1.0 1.0 1.0 2.5 1.5
DLCO (%) 60% 95% 80% 120% 40%

1.1 Respiratory Mechanics

Lung compliance and chest wall mechanics interact to determine functional residual capacity (FRC). Ventilation-perfusion (V/Q) matching ensures optimal gas exchange. Dynamic hyperinflation in obstructive diseases increases work of breathing.

1.2 Gas Exchange

Oxygen diffuses from alveoli to capillaries via a thin membrane. CO2 diffuses in the opposite direction. Alveolar gas equation (Pao2 = Fio2*(Patm - PH2O) - Paco2/R) quantifies gas exchange efficiency.

2. EPIDEMIOLOGY

Respiratory diseases are leading causes of morbidity/mortality globally. Chronic obstructive pulmonary disease (COPD) and asthma affect ~650 million people worldwide. Pulmonary fibrosis and interstitial lung diseases have incidence rates of 1-2/100,000. Obesity-related hypoventilation affects ~1-2% of obese individuals.

2.1 Risk Factors

Smoking, air pollution, occupational exposures, genetic predisposition (e.g., alpha-1 antitrypsin deficiency), and comorbidities (e.g., diabetes, heart failure) increase risk. Obesity and sedentary lifestyle contribute to ventilatory restriction.

3. ETIOLOGY & PATHOPHYSIOLOGY

Pathophysiology involves ventilation-perfusion mismatch, airway narrowing, parenchymal destruction, or chest wall abnormalities. Key mechanisms include dynamic hyperinflation, alveolar collapse, and impaired diffusion due to thickened membranes.

3.1 Ventilation-Perfusion Mismatch

Shunt (unventilated perfused lung) and dead space (perfused unventilated lung) disrupt gas exchange. Alveolar hypoventilation causes elevated A-aDO2. Pulmonary embolism creates perfusion-only regions.

3.2 Airflow Obstruction

Bronchoconstriction (asthma), airway wall thickening (COPD), or alveolar destruction (emphysema) increase airway resistance. Dynamic hyperinflation in obstructive diseases raises intrinsic PEEP.

4. CLINICAL FEATURES

Symptoms include dyspnea, hypoxemia, hypercapnia, and fatigue. Signs may show crackles (interstitial lung disease), wheezing (asthma), or cyanosis. Complications include respiratory failure, pulmonary hypertension, and right heart strain.

4.1 Hypoxemia Patterns

Severe hypoxemia (PaO2 < 55 mmHg) occurs with pulmonary shunt or diffusion impairment. Altitude exacerbates hypoxemia in patients with baseline V/Q mismatch.

5. DIFFERENTIAL DIAGNOSIS

Distinguish between obstructive (asthma, COPD) and restrictive (pulmonary fibrosis, obesity hypoventilation) patterns. Consider cardiac causes (congestive heart failure) and mixed patterns (interstitial lung disease with airway disease).

5.1 Key Differentiators

Obstructive: FEV1/FVC < 70%, reversible airflow obstruction. Restrictive: TLC reduction, normal FEV1/FVC. Diffusion impairment: reduced DLCO with normal spirometry.

6. INVESTIGATIONS & DIAGNOSIS

Arterial blood gas analysis, chest imaging (CXR/CT), spirometry, and flow-volume loops assess function. Alveolar-arterial O2 gradient (A-aDO2) helps identify shunt or diffusion defects.

6.1 Spirometry

Measure FVC, FEV1, and FEV1/FVC ratio. Flow-volume loops show patterns of obstruction (scooping), restriction (flat), or mixed abnormalities. Bronchodilator response tests for reversible obstruction.

6.2 Imaging

Chest X-ray detects consolidation, effusion, or mass lesions. CT identifies interstitial lung disease, nodules, or vascular abnormalities. Pulmonary angiography confirms embolism.

7. MANAGEMENT & TREATMENT

Optimize oxygen delivery, manage acute exacerbations, and address underlying causes. Pharmacologic therapies include bronchodilators, corticosteroids, and immunomodulators. Non-pharmacologic approaches include pulmonary rehabilitation and oxygen therapy.

7.1 Acute Exacerbations

Administer supplemental oxygen (target SpO2 88-92%), bronchodilators (beta-agonists, anticholinergics), and corticosteroids. Mechanical ventilation may be required for severe respiratory failure.

7.2 Chronic Management

Long-acting bronchodilators (LABAs, LAMAs), inhaled corticosteroids, and biologics for asthma/COPD. Oxygen therapy for chronic hypoxemia (SpO2 < 88%). Pulmonary rehabilitation improves exercise tolerance.

8. PROGNOSIS & COMPLICATIONS

Prognosis varies by disease: COPD has 5-year survival ~5-10%, while interstitial lung disease may progress to respiratory failure. Complications include pulmonary hypertension, right ventricular failure, and ventilatory muscle fatigue.

8.1 Complications

Progressive hypoxemia leads to pulmonary vasoconstriction and cor pulmonale. Chronic hypercapnia causes respiratory acidosis and ventilatory muscle atrophy.

9. SPECIAL CONSIDERATIONS

Pregnancy: Obstructive lung disease worsens due to diaphragmatic elevation. Pediatrics: Asthma is common, with variable response to bronchodilators. Elderly: Increased risk of atelectasis and ventilatory muscle weakness.

9.1 Pregnancy

Monitor for worsening dyspnea and hypoxemia. Avoid NSAIDs in third trimester. Consider delivery if severe respiratory compromise occurs.

10. KEY POINTS & CLINICAL PEARLS

  1. Alveolar gas equation (Pao2 = Fio2*(Patm - PH2O) - Paco2/R) quantifies gas exchange. 2. Flow-volume loops distinguish obstructive (scooping) vs restrictive (flat) patterns. 3. Dynamic hyperinflation in COPD increases work of breathing. 4. DLCO reduction indicates parenchymal disease. 5. Oxygen therapy must be titrated to avoid CO2 retention in chronic hypercapnia.