Summary: Respiratory System

Table of Contents
1. Spirometry
2. Pulmonary Capacities
3. Pulmonary Tuberculosis (TB)
4. Investigations for TB
5. Tuberculosis and HIV
6. Drug-Resistant TB
7. Obstructive Sleep Apnea Syndrome (OSAS)
8. Pneumonia
9. Pleural Effusion
10. Asthma
11. Pulmonary Embolism (PE)
12. PE Management
13. Imaging and Procedures in Pulmonology
14. Air Embolism
15. Fat Embolism
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Spirometry

• Residual volume (RV) is not measured by spirometry; best estimated by body plethysmography.
• Patterns on flow-volume curves:
  • Normal pattern - typical expiratory curve.
  • Obstructive pattern - prolonged expiration, reduced FEV1, mild FVC reduction, low FEV1/FVC; diffusion capacity usually normal (may be reduced in emphysema).
  • Restrictive pattern - reduced TLC and VC, modest FEV1 fall, marked FVC reduction, normal/increased FEV1/FVC; diffusion capacity decreased.
  • Variable extrathoracic obstruction - flattened inspiratory curve only.
  • Variable intrathoracic obstruction - flattened expiratory curve only.
  • Fixed large airway obstruction - flattened curves in both inspiration and expiration.
• How to read spirometry:
  • Lower Y-axis = inspiration; upper Y-axis = expiration.
  • Obstructive disease: expiration prolonged, curve may shift right (↑RV).
  • Restrictive disease: recording is smaller and shifts left (↓TLC, ↓RV).
• Diffusion capacity (DLco) assesses gas transfer across alveolar membrane.

Pulmonary Capacities

• Total Lung Capacity (TLC) = IRV + TV + ERV + RV ≈ 6 L.
• Inspiratory Capacity (IC) = TV + IRV ≈ 3.8 L.
• Vital Capacity (VC) = IRV + TV + ERV ≈ 4.5-4.8 L.
• Functional Residual Capacity (FRC) = ERV + RV ≈ 2.2 L.

Pulmonary Tuberculosis (TB)

• Transmission: Primarily by respiratory droplets; ingestion, vertical spread, and direct contact are other routes.
• Primary TB: Often asymptomatic; initial lung lesion = Ghon focus; hilar node enlargement = Ghon complex; calcified healed form = Ranke complex. Failure to contain infection → primary progressive TB with caseous pneumonia, bronchopneumonia, or miliary spread.
• Latent TB infection: No active disease or transmission; ~6% risk of progression to active TB without preventive treatment.
• Clinical features: Chronic cough, fatigue, weight loss, fever (evening rise), night sweats, pleuritic chest pain, and later hemoptysis; disseminated TB can follow vascular invasion.
• Miliary TB: Hematogenous spread producing millet-seed granulomas; may show choroidal tubercles; chest X-ray may show miliary pattern but can be normal early or in HIV.
• Organs rarely affected: Cornea, vagina, pancreas, myocardium.
• Risk factors: Adolescence/elderly, HIV, silicosis, lymphoma/leukemia, hemophilia, chronic renal failure/hemodialysis, type 1 diabetes, malnutrition, old healed TB lesions, immunocompromised states.

Investigations for TB

• Microscopy for AFB needs ≥10 bacilli/mL sputum.
• Culture/Detection: BACTEC (growth 5-8 days), SEPTICHECK (biphasic), Mycobacteria Growth Indicator Tube (fluorescence).
• Nucleic acid/PCR: AMPLICOR (~7 hours), Xpert MTB/RIF (≈98% sensitivity; WHO recommended initial test for MDR and HIV-associated TB).
• T-cell IFN-γ release assays: measure IFN-γ release to MTB antigens; ex-vivo tests include T-SPOT.TB (T-cell count) and QuantiFERON-TB Gold (IFN-γ concentration).
• Mantoux (Tuberculin) test: 0.1 mL PPD intradermal; read 48-72 h. Interpretation: 0-4 mm negative; 5-9 mm positive in specific high-risk cases; ≥10 mm positive. Mantoux is prognostic, not diagnostic.

Tuberculosis and HIV

• HIV increases rapid progression, extrapulmonary disease, lymphadenopathy, and mycobacteremia; fewer smear-positive cases and Mantoux false negatives; CXR may be normal.
• Granulomas often absent; TBM more common.
• Xpert MTB/RIF is the preferred initial diagnostic test in HIV patients.
• Treatment combines HAART and ATT; start ATT before ART to reduce Immune Reconstitution Inflammatory Syndrome (IRIS). Replace rifampicin with rifabutin when needed with certain ART drugs.

Drug-Resistant TB

• Resistance arises from point mutations and from inadequate therapy or poor adherence (monotherapy risk).
• Primary resistance = in untreated patients; acquired resistance = develops during inadequate treatment.
• Associated gene mutations: rpoB (rifampicin), pncA (pyrazinamide), InhA (isoniazid).

Obstructive Sleep Apnea Syndrome (OSAS)

• Definition: Repeated pharyngeal collapse during sleep causing apneas ≥10 s, oxygen desaturation ≥3% or cortical arousal.
• Prevalence ~1-4% in middle-aged men; lower in women.
• OSAS raises daytime blood pressure by ~5-10 mmHg and may increase heart attack and stroke risk.
• Treatment criteria: Epworth Sleepiness Score >11, persistent sleepiness while driving/working, or >15 apneas/hypopneas per hour. Some patients with 5-15 events/h also improve subjectively.
• Complications: Pulmonary hypertension, cor pulmonale, type II respiratory failure, systemic hypertension, MI, stroke, arrhythmias.
• Polysomnography monitors oxygen saturation, nasal/oral airflow, ECG, EMG (chin/leg), EEG, EOG.
• Severity by AHI: Mild 5-14, Moderate 15-29, Severe ≥30 events/hour.
• Treatment: smoking cessation, ≥10% weight loss, CPAP (5-20 mmHg), with benefits to breathing, sleepiness, BP, cognition, mood; other measures as indicated.

Pneumonia

• Lower respiratory infections often result from aspiration from the oropharynx.
• Types: Community-acquired (CAP) and Ventilator-associated (VAP); healthcare-associated/nosocomial pneumonia occurs >48 h after admission.
• Common pathogens: Non-MDR - Streptococcus pneumoniae; MDR - Pseudomonas aeruginosa. HAP organisms include MRSA, S. pneumoniae, Klebsiella.
• CAP features: Consolidation with air bronchograms on CXR; radiological resolution ~6 weeks.
• Essentials of diagnosis: Fever or hypothermia, tachypnea, cough, dyspnea, chest discomfort, bronchial breath sounds/crackles, parenchymal opacity on CXR. Pneumonia outside hospital or within 48 h of admission.
• CURB-65 for admission: Confusion; Uremia; RR >30/min; BP ≤90/60 mmHg; Age ≥65 years.
• Treatment guidance: no recent antibiotics/comorbidity → macrolide; with comorbidity/recent antibiotics → levofloxacin or beta-lactam.
• HIV-associated pneumonia: Caused by Pneumocystis jirovecii; interstitial pattern; diagnosis by BAL Giemsa; treat and prophylax with trimethoprim-sulfamethoxazole.
• Alcoholic with red currant jelly sputum suggests Klebsiella; treatment IV cefotaxime + IV amikacin.
• Psittacosis (bird-handler's pneumonia) by Chlamydia psittaci treated with azithromycin for 10-14 days after fever subsides.
• Legionella: lower lobe involvement, relative bradycardia, may cause SIADH; treat with macrolides (erythromycin ± rifampicin).
• Mycoplasma: atypical pneumonia in youth; treat with erythromycin; penicillin ineffective.
• Anaerobic aspiration: common organisms Bacteroides fragilis, Peptostreptococci; pH <2.4 causes="" chemical="" injury/necrotising="" pneumonia;="" treat="" with="" penicillin="" +="" metronidazole="" or="">
• VAP assessment uses clinical pulmonary infection score (fever, leukocytosis, oxygenation, X-ray, tracheal aspirate); max score 12. Severe inflammation markers: CRP, procalcitonin.
• Sputum for culture adequate if >25 neutrophils and <10 squamous="" epithelial="">
• Normal pleural fluid volume: 5-15 mL.

Pleural Effusion

• Types: Transudative (hydrostatic/oncotic imbalance) and Exudative (inflammation ↑pleural permeability).
• Symptoms: dyspnea (large effusion), cough, respirophasic chest pain, bulging intercostal spaces; percussion stony dullness and diminished breath sounds.
• Pleural tap usually USG guided.
• Causes: Malignancy (lung, breast, mesothelioma, lymphoma), left-sided causes (pancreatitis, pericarditis, oesophageal rupture, subdiaphragmatic abscess, thoracic duct above D5), right-sided causes (amoebic liver abscess, Meig's syndrome, thoracic duct below D5), bilateral (pulmonary infarction, hypoalbuminaemia, malignancy).

Asthma

• Nature: Reversible airway narrowing; type I hypersensitivity; chronic cases may produce fixed obstruction.
• Diagnosis: episodic symptoms, nocturnal worsening; bronchodilator response = ≥12% rise in FEV1 after salbutamol.
• Investigations: spirometry (reduced FEV1), PEFR variability, ↑eosinophils in extrinsic asthma, ↑IgE, CXR shows hyperinflation with flattened diaphragms.
• Triggers: occupational exposures, exercise-induced bronchoconstriction, cardiac causes (cardiac asthma), drug-induced (COX-1 inhibitors → LOX pathway ↑).
• Treatment:
  • Acute exacerbation: salbutamol nebulization (oxygen-driven).
  • Recurrent attacks: inhaled corticosteroid + LABA.
  • Chronic severe: biologics (e.g., omalizumab) as indicated.
  • Brittle asthma: subcutaneous adrenaline for severe unpredictable attacks.
  • Prophylaxis: leukotriene modifiers and mast cell stabilizers.
• Status asthmaticus: monosyllabic speech, accessory muscle use, rhonchi, pulsus paradoxus, rising PaCO2 (>45 mmHg) indicates Type II respiratory failure. Treatment includes oxygen-driven salbutamol nebulization, parenteral terbutaline if needed, IV hydrocortisone, and possibly IV magnesium sulfate; avoid anxiolytics and cautious use of mucolytics.
• Brittle asthma types: persistent wide variability requiring oral steroids/continuous beta-2 agonist infusion or sudden unpredictable falls in function; best treated with subcutaneous epinephrine in severe attacks.

Pulmonary Embolism (PE)

• Risk factors: venous stasis (immobility), hyperviscosity, increased venous pressure (pregnancy), orthopaedic/pelvic surgery, OCP/HRT, hyperhomocysteinemia, antiphospholipid antibodies, Factor V Leiden, deficiencies of protein C/S or antithrombin III.
• Classification: Massive PE (5-10%), Submassive (20-25%) with RV dysfunction, Low risk (70-75%).
• Clinical features: unexplained breathlessness, tachypnea (most reliable), massive PE → syncope, hypotension, cyanosis; DVT signs in legs; upper limb DVT after central lines.
• Clinical prediction rule items: DVT signs (3.0), alternative diagnosis less likely (1.5), HR >100 (1.5), recent immobilization/surgery (1.0), prior PE/DVT (1.0), hemoptysis (1.0), cancer (1.0). Score >4 → likely PE; <4 →="">
• D-dimer useful to rule out PE when clinical score <4 (sensitivity="" ~95%;="" false="" positives="" in="" mi,="" pneumonia,="">
• ECG: common sinus tachycardia; specific SI Q3 T3 pattern; RV strain T-wave inversions V1-V4.
• Venous ultrasound for DVT: loss of compressibility; MR venography if inconclusive.
• Radiologic signs: Hampton hump (wedge opacity), Westermark sign (oligemia), Palla sign (enlarged right descending pulmonary artery). CTPA is preferred diagnostic test; lung scan and perfusion/ventilation mismatch also used. Pulmonary angiography is gold standard. Echocardiography assesses RV strain; McConnell sign suggests RV dysfunction.
• ABG often shows respiratory alkalosis.

PE Management

• Massive PE with hypotension: volume repletion (500 mL NS), inotropes (dopamine/dobutamine), fibrinolysis (tPA 100 mg over 2 h within 14 days), catheter-directed pharmacomechanical therapy, or surgical embolectomy.
• Submassive PE: anticoagulation (heparin/LMWH) with transition to warfarin or novel oral anticoagulants; anti-Xa agents like rivaroxaban used.
• Anticoagulation duration:
  • Provoked DVT (surgery/trauma/estrogen/catheter): 3 months.
  • Proximal leg DVT provoked: 3-6 months.
  • Unprovoked DVT: lifelong.
  • Therapeutic INR: first 6 months 2-3; subsequent 6 months 1.5-2.
• IVC filter indications: contraindication to anticoagulation (active bleeding) or recurrent thrombosis despite adequate anticoagulation.

Imaging and Procedures in Pulmonology

• HRCT is preferred for parenchymal lung disease (bronchiectasis, interstitial lung disease) and initial imaging in hemoptysis; follow with bronchoscopy as needed.
• Pulmonary angiography for lung sequestration.
• CXR sufficient for pleural effusion or pneumothorax; chest US best for loculated effusion.
• CT angiography superior for pulmonary embolism compared with V/Q scan.
• Bronchoalveolar lavage (BAL) during bronchoscopy indicated for suspected malignancy, pneumonia in immunosuppressed patients, suspected TB with negative sputum, and certain interstitial lung diseases.

Air Embolism

• Causes: seated neurosurgery (venous sinus injury), internal jugular vein injury, central line insertion, decompression sickness.
• Features: respiratory distress, syncope, hypotension, mill wheel murmur, sudden fall in end-tidal O2; TEE can detect air in right heart.
• Management: initial left lateral decubitus then Trendelenburg positioning; definitive treatment is air aspiration via cardiac catheterization.

Fat Embolism

• Occurs after long-bone fractures; fat globules trigger inflammatory response affecting lungs and brain.
• Major diagnostic criteria: respiratory insufficiency, cerebral effects, petechial rash.
• Minor criteria include tachycardia >110 bpm, fever >38.5°C, retinal/petechial changes, renal dysfunction, jaundice, acute anemia, thrombocytopenia, raised ESR, fat in blood/urine/sputum.
• Treatment is supportive: high-flow oxygen and intermittent positive pressure ventilation as needed.