Pulmonology
1. What this chapter covers, and how NEET PG actually tests it
Stems give spirometry, a chest radiograph description, a blood gas, or an acute breathless patient needing an immediate decision.
The organising principle is that one ratio splits the subject in half.
| Pattern | Ratio of forced expiratory volume to forced vital capacity | Vital capacity | Diseases |
|---|---|---|---|
| Obstructive | Reduced, below 0.7 | Normal or reduced | Asthma, chronic obstructive disease, bronchiectasis |
| Restrictive | Normal or increased | Reduced | Interstitial disease, chest wall and neuromuscular disease |
The two groups share almost no diseases, so establishing the pattern removes most of the differential immediately.
Diffusing capacity then separates the diseases within each group, because it measures the alveolar-capillary interface rather than airflow.
| Diffusing capacity | Interpretation |
|---|---|
| Low with obstruction | Emphysema, where alveolar walls are destroyed |
| Normal with obstruction | Asthma or chronic bronchitis, where alveoli are intact |
| Low with restriction | Interstitial lung disease |
| Normal with restriction | Chest wall or neuromuscular cause, since the lung itself is normal |
2. Asthma and chronic obstructive pulmonary disease
| Feature | Asthma | Chronic obstructive disease |
|---|---|---|
| Onset | Often childhood | After years of smoking |
| Variability | Marked, diurnal and seasonal | Little day-to-day change |
| Reversibility | Significant with a bronchodilator | Incomplete at best |
| Diffusing capacity | Normal | Reduced in emphysema |
| Atopy | Common | Not characteristic |
Reversibility is demonstrated by a rise in forced expiratory volume of both a proportional and an absolute amount after a bronchodilator, and both thresholds must be met.
2.1 Acute severe asthma
Severity is assessed by peak flow, respiratory rate, heart rate and the ability to complete sentences.
Life-threatening features are a silent chest, cyanosis, bradycardia, exhaustion, confusion and a very low peak flow.
A normal or rising carbon dioxide tension in acute asthma is an ominous sign, not a reassuring one. A patient with severe airflow obstruction should be hyperventilating and hypocapnic, so a normal value means the respiratory muscles are failing.
That single interpretation is the most examined point in the chapter, because the number looks normal and the patient is close to arrest.
Treatment is oxygen, repeated inhaled bronchodilators, systemic corticosteroid and ipratropium, with magnesium for severe cases not responding.
Corticosteroid takes hours to act, which is why it is given early rather than reserved for failure of the bronchodilator.
Antibiotics are not given routinely in acute asthma, since most exacerbations are viral, and the presence of sputum alone does not indicate bacterial infection.
Sedation is contraindicated outside a setting prepared to intubate, because it removes the respiratory drive that is keeping the patient alive.
The commonest error in chronic asthma is escalating drug therapy without checking inhaler technique and adherence, both of which account for far more apparent treatment failure than genuine refractoriness.
A patient using a metered dose inhaler incorrectly deposits most of the drug in the oropharynx, so the prescription looks adequate on paper while almost nothing reaches the airway.
Peak flow diaries and reliever use are more informative than symptom recall, because patients systematically underestimate how limited they have become when the decline has been gradual.
2.2 Chronic obstructive disease
Management is staged by symptoms and exacerbation frequency, with inhaled long-acting bronchodilators as the foundation and inhaled corticosteroid reserved for those with frequent exacerbations or eosinophilia.
Smoking cessation and long-term oxygen therapy in chronic hypoxaemia are the only two interventions that prolong survival, which is the point most often examined.
Long-term oxygen must be used for a substantial part of each day to confer that benefit, since intermittent use does not reverse the pulmonary vasoconstriction that drives cor pulmonale.
3. Pneumonia
Severity assessment guides the site of care, using confusion, urea, respiratory rate, blood pressure and age above sixty-five.
| Setting | Typical organisms |
|---|---|
| Community-acquired | Streptococcus pneumoniae, then Mycoplasma and other atypicals |
| Hospital-acquired | Gram-negative organisms, Staphylococcus aureus |
| Aspiration | Anaerobes and oral flora, right lower lobe in an upright patient |
| Immunocompromised | Pneumocystis, fungi, mycobacteria |
Atypical organisms lack a cell wall or are intracellular, so they do not respond to beta-lactams and require a macrolide or tetracycline.
Legionella characteristically produces hyponatraemia and diarrhoea alongside pneumonia, and it is diagnosed by urinary antigen.
Aspiration goes to the right lower lobe in an upright patient and to the posterior segment of the right upper lobe in a supine one, because the right main bronchus is wider and more vertical.
Empyema is suspected when a patient with pneumonia fails to defervesce, and it is confirmed by pleural fluid that is frankly purulent, has a low pH or grows organisms.
An empyema must be drained rather than merely treated with antibiotics, because antibiotics penetrate an established collection poorly and the loculated fluid becomes progressively organised.
The pH of pleural fluid is therefore measured in every parapneumonic effusion, since a low value identifies a collection that will not resolve on antibiotics alone.
Lung abscess produces a cavity with an air-fluid level and copious foul sputum, and it is usually managed with prolonged antibiotics rather than drainage because it drains through the bronchus.
4. Pleural disease
Light criteria separate an exudate from a transudate, and any one of the three being met makes the fluid an exudate.
| Criterion | Exudate if |
|---|---|
| Ratio of pleural to serum protein | Above 0.5 |
| Ratio of pleural to serum lactate dehydrogenase | Above 0.6 |
| Pleural lactate dehydrogenase | Above two thirds of the upper limit of the serum reference range |
The criteria are deliberately biased toward calling fluid an exudate, because missing an exudate means missing infection or malignancy, while over-calling one leads only to further investigation.
Tuberculous effusion is lymphocytic with a raised adenosine deaminase, and organisms are rarely seen because the fluid is a hypersensitivity reaction.
Tension pneumothorax is a clinical diagnosis and must not wait for a radiograph. Immediate needle decompression precedes imaging, because the delay involved in confirming it is what kills the patient.
A simple pneumothorax is managed by observation, aspiration or drainage depending on size and symptoms, and a secondary pneumothorax in diseased lungs is treated more aggressively than a primary one.
5. Interstitial lung disease
The pattern of zonal involvement narrows the cause substantially.
| Upper zone | Lower zone |
|---|---|
| Silicosis and coal worker pneumoconiosis | Asbestosis |
| Hypersensitivity pneumonitis | Idiopathic pulmonary fibrosis |
| Ankylosing spondylitis | Connective tissue disease |
| Sarcoidosis | Drug-induced fibrosis |
Idiopathic pulmonary fibrosis shows basal and subpleural reticulation with honeycombing, and its prognosis is poor with antifibrotic drugs slowing rather than halting decline.
Corticosteroids are actively harmful in idiopathic pulmonary fibrosis, which distinguishes it sharply from the inflammatory interstitial diseases where they are the mainstay.
Establishing whether an interstitial process is inflammatory or fibrotic therefore determines whether steroids will help or harm, and it cannot be inferred from breathlessness alone.
Fine end-inspiratory crackles with clubbing and a restrictive pattern in an older patient is the characteristic combination.
Hypersensitivity pneumonitis improves on removing the antigen, which is why the occupational and hobby history is the most productive part of the assessment.
Sarcoidosis causes bilateral hilar lymphadenopathy with a raised angiotensin-converting enzyme and hypercalcaemia, and most cases resolve without treatment.
6. Lung cancer and the solitary nodule
The first division is between small cell and non-small cell carcinoma, because it determines whether surgery is even considered.
| Type | Location and behaviour |
|---|---|
| Small cell | Central, metastasises early, almost never surgical, chemosensitive |
| Squamous cell | Central, cavitates, associated with parathyroid hormone-related peptide |
| Adenocarcinoma | Peripheral, commonest in non-smokers, targetable mutations |
| Large cell | Peripheral, poorly differentiated |
Small cell carcinoma is treated as a systemic disease from the outset, because micrometastases are present in almost every patient at diagnosis, so chemotherapy rather than resection is the primary treatment even in apparently limited disease.
The paraneoplastic syndromes follow the cell type: small cell produces inappropriate antidiuresis, ectopic corticotropin and Lambert-Eaton syndrome, while squamous cell produces hypercalcaemia through parathyroid hormone-related peptide.
Pancoast tumours at the apex produce shoulder pain, a Horner syndrome and wasting of the small hand muscles by invading the sympathetic chain and lower brachial plexus.
A solitary pulmonary nodule is assessed by size, margin, growth rate and the patient's risk profile.
Smooth margins, small size, dense central or laminated calcification and stability over two years all favour a benign lesion, while spiculated margins and growth favour malignancy.
Comparison with an old radiograph is the single most valuable investigation, because two years of stability effectively excludes malignancy without any further test.
7. Airway and sleep disorders
Bronchiectasis is permanent bronchial dilatation from repeated infection and impaired clearance, presenting with copious sputum and recurrent infection.
Post-tuberculous damage is the commonest cause in India, which differs from Western series where cystic fibrosis and immunodeficiency dominate.
High-resolution computed tomography is the diagnostic test, showing dilated airways larger than the accompanying artery, the signet ring appearance.
Obstructive sleep apnoea presents with snoring, witnessed apnoeas and daytime somnolence, and it is confirmed by sleep study.
It is an under-recognised secondary cause of hypertension, and it also contributes to atrial fibrillation, pulmonary hypertension and perioperative risk.
Continuous positive airway pressure is the treatment, and it works by splinting the pharynx open rather than by delivering oxygen.
7.1 Haemoptysis
The causes divide into airway, parenchymal and vascular, and in India tuberculosis and bronchiectasis dominate the list.
Massive haemoptysis is managed by positioning the patient with the bleeding side down, which protects the healthy lung from soiling, and by bronchial artery embolisation.
Patients with massive haemoptysis die of asphyxiation rather than exsanguination, which is why airway protection takes priority over volume replacement.
8. Pulmonary embolism
Clinical probability is scored first, and the score determines whether the next step is a D-dimer or immediate imaging.
D-dimer is useful only to exclude and only in low probability, because it is raised in infection, malignancy, pregnancy, surgery and old age, so a positive result in a high-probability patient adds nothing.
Computed tomographic pulmonary angiography is the standard confirmatory test, with a ventilation-perfusion scan used where contrast or radiation must be avoided.
Massive embolism with haemodynamic compromise is treated with thrombolysis, while stable embolism is anticoagulated.
Right ventricular strain on echocardiography identifies an intermediate-risk group requiring closer monitoring even when the blood pressure is preserved.
Anticoagulation is started on clinical suspicion while imaging is arranged, unless bleeding risk forbids it, because the delay between suspicion and confirmation is when patients die.
Most emboli arise from deep veins of the leg and pelvis, so the absence of leg signs does not argue against the diagnosis, since the clot has by definition already left.
8.1 Pulmonary hypertension
Pulmonary hypertension is classified by mechanism rather than by severity, and the group determines the treatment entirely.
| Group | Mechanism |
|---|---|
| Pulmonary arterial | Disease of the small pulmonary arteries themselves |
| Left heart disease | Backward transmission of raised left atrial pressure |
| Lung disease and hypoxia | Hypoxic vasoconstriction and vascular destruction |
| Chronic thromboembolic | Organised clot obstructing the pulmonary arteries |
Pulmonary vasodilators benefit the first and fourth groups but can be harmful in the second, because dilating the pulmonary bed pushes more blood into a left heart that already cannot accept it.
That distinction is the reason right heart catheterisation is required before treatment, since echocardiography estimates the pressure but cannot reliably identify the mechanism.
9. Respiratory failure
| Type | Oxygen | Carbon dioxide | Mechanism |
|---|---|---|---|
| Type 1 | Low | Normal or low | Ventilation-perfusion mismatch, shunt, diffusion defect |
| Type 2 | Low | High | Alveolar hypoventilation |
Type 2 failure means the patient is not moving enough air, whatever the cause, so the treatment addresses ventilation rather than oxygen alone.
Non-invasive ventilation is the treatment of choice in an exacerbation of chronic obstructive disease with respiratory acidosis, and it reduces both intubation and mortality.
Oxygen is targeted to a lower saturation range in patients at risk of carbon dioxide retention, because excessive oxygen worsens hypercapnia mainly by increasing dead space through reversal of hypoxic vasoconstriction.
Acute respiratory distress syndrome is defined by acute onset, bilateral opacities, a low ratio of arterial oxygen to inspired fraction, and an origin not fully explained by cardiac failure.
Low tidal volume ventilation is the intervention that reduces mortality in this syndrome, and it works by limiting the stretch injury that larger volumes inflict on already inflamed lung.
Prone positioning improves survival in severe cases by recruiting dependent lung and distributing ventilation more evenly.
10. Worked examples
Example 1. A patient in acute severe asthma has a carbon dioxide tension of 40 mmHg. What does this indicate?
Impending respiratory arrest. Severe obstruction should drive hyperventilation and hypocapnia, so a normal value means the respiratory muscles are tiring and ventilation is failing.
Example 2. Spirometry shows a reduced ratio with a low diffusing capacity. What is the likely diagnosis?
Emphysema. Obstruction with impaired diffusion indicates destruction of the alveolar walls, whereas asthma obstructs airflow while leaving the alveolar surface intact.
Example 3. A hypotensive patient with absent breath sounds on one side and tracheal deviation is sent for a chest radiograph. What is wrong?
Tension pneumothorax is a clinical diagnosis requiring immediate needle decompression. Waiting for imaging is the delay that causes death.
Summary
One ratio splits the subject: obstructive and restrictive patterns share almost no diseases.
Diffusing capacity then separates diseases within each pattern by testing the alveolar surface.
Low diffusion with obstruction means emphysema; normal diffusion with obstruction means asthma.
Normal diffusion with restriction means a chest wall or neuromuscular cause rather than lung disease.
Reversibility requires both a proportional and an absolute rise in expiratory volume.
Life-threatening asthma shows a silent chest, cyanosis, bradycardia, exhaustion and a very low peak flow.
A normal carbon dioxide in acute severe asthma means exhaustion and impending arrest.
Corticosteroid is given early in asthma because it takes hours to act.
Smoking cessation and long-term oxygen are the only interventions prolonging survival in chronic obstructive disease.
Oxygen must be used for most of the day to reverse hypoxic pulmonary vasoconstriction.
Atypical organisms lack a cell wall or are intracellular and need a macrolide or tetracycline.
Legionella gives hyponatraemia and diarrhoea and is diagnosed by urinary antigen.
Aspiration reaches the right lower lobe upright and the posterior right upper lobe supine.
Any one Light criterion makes fluid an exudate, and the criteria are biased toward that call deliberately.
Tuberculous effusion is lymphocytic with raised adenosine deaminase and few organisms.
Tension pneumothorax is decompressed before imaging.
Upper zone fibrosis suggests silicosis, hypersensitivity pneumonitis or sarcoidosis; lower zone suggests asbestosis or idiopathic fibrosis.
Hypersensitivity pneumonitis improves on antigen removal, so the exposure history matters most.
D-dimer excludes embolism only in low probability, because it rises in many other conditions.
Massive embolism with haemodynamic compromise is thrombolysed; stable embolism is anticoagulated.
Type 1 failure is a problem of oxygenation; type 2 is a problem of ventilation.
Non-invasive ventilation reduces intubation and mortality in exacerbations with respiratory acidosis.
Oxygen targets are lower in carbon dioxide retainers, chiefly because of increased dead space.
Low tidal volume ventilation reduces mortality in acute respiratory distress syndrome.
Prone positioning improves survival in severe cases by recruiting dependent lung.
Permissive hypercapnia is accepted as the price of low tidal volumes, because the acidosis is better tolerated than the barotrauma that larger volumes cause.
Positive end-expiratory pressure keeps alveoli open through expiration, preventing the repeated collapse and reopening that itself injures lung tissue.
The syndrome is a description rather than a diagnosis, so the underlying cause, most often sepsis, aspiration or pancreatitis, must be identified and treated in parallel.
Small cell carcinoma is systemic from the outset, so chemotherapy rather than surgery is primary.
Squamous cell cavitates and secretes parathyroid hormone-related peptide; small cell causes antidiuresis and Lambert-Eaton.
A Pancoast tumour gives shoulder pain, Horner syndrome and small hand muscle wasting.
Two years of radiographic stability effectively excludes malignancy in a solitary nodule.
Post-tuberculous damage is the commonest cause of bronchiectasis in India.
Sleep apnoea is an under-recognised secondary cause of hypertension, treated by splinting the pharynx open.
In massive haemoptysis, position the bleeding side down, because patients die of asphyxiation rather than blood loss.
Start anticoagulation for suspected embolism while imaging is arranged, since the interval between suspicion and confirmation is when patients die.
Absent leg signs do not argue against embolism, because the clot has by definition already left the leg.
Pulmonary vasodilators help arterial and thromboembolic pulmonary hypertension but harm the group caused by left heart disease.
Permissive hypercapnia is accepted in the distress syndrome, because acidosis is better tolerated than barotrauma.
