Internal medicine: cardiovascular and respiratory diseases

In short

Cardiovascular and respiratory diseases together form the largest block of general medicine: they cause roughly two-fifths of all deaths in India, with ischaemic heart disease and chronic obstructive pulmonary disease the two single biggest contributors. The chapter covers coronary artery disease, hypertension, heart failure, valvular and rheumatic heart disease, arrhythmias, pericardial disease, and on the respiratory side asthma, COPD, pneumonia, tuberculosis-related lung damage, pleural disease, pulmonary embolism, bronchiectasis and interstitial lung disease. In MBBS it carries the heaviest weight in Medicine paper I, long cases and viva, and it dominates NEET-PG/INI-CET and the licentiate-style questions. Clinically it is the core of casualty and ICU work, of NPCDCS screening in primary care, and of every DM Cardiology or DM Pulmonary entrance interview.

Explained

Ischaemic heart disease and acute coronary syndromes

• Pathology: atherosclerotic plaque in a coronary artery; stable angina from fixed stenosis (usually >70%), acute coronary syndrome (ACS) from plaque rupture with superimposed thrombus.
• Risk factors: non-modifiable (age, male sex, family history, South Asian ethnicity — Indians develop CAD about a decade earlier and with less obesity); modifiable (smoking/tobacco chewing, hypertension, diabetes, dyslipidaemia with high triglycerides and low HDL — the "Asian Indian phenotype", central obesity, inactivity, stress).
• ACS spectrum: (1) unstable angina — ischaemic pain at rest/crescendo, no troponin rise; (2) NSTEMI — troponin rise, no persistent ST elevation; (3) STEMI — ST elevation ≥1 mm in two contiguous leads (≥2 mm in V2–V3 for men ≥40 y) or new LBBB, from complete occlusion.
• Presentation: retrosternal pressure/heaviness >20 min, radiating to left arm/jaw, with sweating, nausea, dyspnoea. Silent or atypical MI in diabetics, elderly and women — epigastric pain, isolated breathlessness or syncope.
• Investigations: ECG within 10 minutes of arrival and serially; high-sensitivity troponin I/T at 0 and 1–3 h (rise-and-fall pattern); CK-MB only if troponin unavailable; echocardiography for regional wall motion and complications; coronary angiography.
• STEMI treatment: immediate MONA-plus — oxygen only if SpO₂ <90%, sublingual nitrate, morphine for pain, dual antiplatelet (aspirin 325 mg chewed + clopidogrel/ticagrelor loading), anticoagulation, high-dose statin.
  • Primary PCI is the preferred reperfusion if achievable within 120 min of first medical contact (door-to-balloon ≤90 min).
  • Otherwise thrombolysis within 30 min of arrival (door-to-needle) if presentation is within 12 h — streptokinase, reteplase or tenecteplase; tenecteplase is a single weight-based bolus and is the practical choice in Indian district hospitals. Follow with transfer for angiography (pharmaco-invasive strategy — the STEMI-India/Tamil Nadu hub-and-spoke model).
  • Absolute contraindications to thrombolysis: any prior intracranial haemorrhage, known cerebral AVM or malignant intracranial tumour, ischaemic stroke within 3 months, suspected aortic dissection, active bleeding, significant closed head trauma within 3 months.
• Secondary prevention (lifelong): aspirin, statin, beta-blocker, ACE inhibitor/ARB (especially with LV dysfunction, diabetes or hypertension), P2Y12 inhibitor for 12 months, plus smoking cessation, cardiac rehabilitation and glycaemic/BP control.
• Complications: arrhythmias (VF in first hours — commonest cause of pre-hospital death), heart failure and cardiogenic shock, mitral regurgitation from papillary muscle rupture, ventricular septal rupture, free-wall rupture with tamponade, LV aneurysm, mural thrombus, Dressler syndrome (late pericarditis).

Hypertension

• Definition (adult, office BP): ≥140/90 mmHg on two occasions — the threshold used by Indian guidelines (ICMR/Indian Hypertension Guidelines, India Hypertension Control Initiative). The 2017 ACC/AHA cut-off of ≥130/80 is lower; state which you are using in an exam answer.
• Staging (Indian/ESH style): Stage 1 140–159/90–99; Stage 2 ≥160/100; isolated systolic hypertension systolic ≥140 with diastolic <90 (common in the elderly); hypertensive urgency very high BP without organ damage; hypertensive emergency high BP *with* acute target-organ damage (encephalopathy, pulmonary oedema, ACS, dissection, eclampsia, acute kidney injury).
• Types: primary/essential (~90–95%); secondary — renal parenchymal disease (commonest secondary cause), renal artery stenosis, primary hyperaldosteronism, phaeochromocytoma, Cushing syndrome, thyroid disease, obstructive sleep apnoea, coarctation, drugs (NSAIDs, steroids, oral contraceptives, erythropoietin). Suspect secondary cause if age <30 or >55 at onset, resistant hypertension, hypokalaemia, abdominal bruit or paroxysmal symptoms.
• Target-organ damage: LV hypertrophy and heart failure, CAD, stroke and vascular dementia, hypertensive retinopathy (Keith–Wagener grades I–IV), chronic kidney disease with albuminuria, peripheral arterial disease.
• Workup: urine routine and albumin-creatinine ratio, serum creatinine/eGFR, electrolytes, fasting glucose/HbA1c, lipids, ECG, fundus examination; echo and renal imaging as indicated.
• Management: salt restriction (<5 g salt/day), DASH-style diet, weight loss, exercise, alcohol and tobacco cessation. Drugs: ACE inhibitor or ARB, calcium channel blocker (amlodipine), thiazide-like diuretic; beta-blockers when there is CAD, heart failure or arrhythmia. Single-pill combinations are the standard first step in most adults; the IHCI protocol uses amlodipine then adds telmisartan then a thiazide.
• Special situations: ACEi/ARB contraindicated in pregnancy (use labetalol, methyldopa, nifedipine); ACEi/ARB preferred with diabetic kidney disease; avoid ACEi+ARB combination.

Heart failure, valvular and rheumatic heart disease

• Heart failure (HF): inability of the heart to meet metabolic demand at normal filling pressures. Classified by ejection fraction — HFrEF (EF ≤40%), HFmrEF (41–49%), HFpEF (≥50%); and by side — left (dyspnoea, orthopnoea, PND, basal crackles), right (raised JVP, tender hepatomegaly, ascites, pedal oedema).
• Causes in India: ischaemic heart disease, hypertension, rheumatic valvular disease, dilated cardiomyopathy (including peripartum and alcoholic), endomyocardial fibrosis in the south, anaemia and thyrotoxicosis as high-output causes.
• NYHA functional class I–IV grades symptoms; Framingham criteria are used for clinical diagnosis; BNP/NT-proBNP is the rule-out test and echocardiography the confirmatory test.
• HFrEF therapy — the four pillars: ACEi/ARB or ARNI (sacubitril-valsartan), beta-blocker (carvedilol, metoprolol succinate, bisoprolol), mineralocorticoid receptor antagonist (spironolactone), SGLT2 inhibitor (dapagliflozin/empagliflozin). Loop diuretics relieve congestion but do not alter mortality; digoxin for symptoms and rate control; ivabradine if heart rate stays high in sinus rhythm; device therapy (ICD, CRT) in selected patients.
• Acute pulmonary oedema: sit up, oxygen, IV furosemide, nitrates, non-invasive ventilation (CPAP/BiPAP); inotropes or vasopressors only in shock.
• Rheumatic heart disease (RHD): sequel of group A streptococcal pharyngitis; still a major Indian burden. Revised Jones criteria (2015, with the high-risk-population modification India uses) — major: carditis (clinical or subclinical on echo), polyarthritis *or* monoarthritis/polyarthralgia in high-risk settings, chorea, erythema marginatum, subcutaneous nodules; minor: fever, raised ESR/CRP, prolonged PR interval, monoarthralgia. Diagnosis needs 2 major or 1 major + 2 minor with evidence of preceding streptococcal infection.
• Secondary prophylaxis: benzathine penicillin G 1.2 million units IM every 3 weeks (0.6 MU if <27 kg) — 5 years or until age 21 for RF without carditis, 10 years or until 21 with carditis, and lifelong (or until 40) with significant valve disease.
• Valve lesions — key signs: mitral stenosis (loud S1, opening snap, mid-diastolic rumble, malar flush, AF, haemoptysis); mitral regurgitation (apical pansystolic murmur to axilla, soft S1); aortic stenosis (ejection systolic murmur to carotids, slow-rising pulse, narrow pulse pressure, syncope on exertion); aortic regurgitation (early diastolic murmur, wide pulse pressure, collapsing pulse, Corrigan/De Musset/Quincke signs).
• Infective endocarditis: modified Duke criteria (2 major, or 1 major + 3 minor, or 5 minor). Three sets of blood cultures before antibiotics; echo for vegetations. Viridans streptococci in subacute native-valve disease, *Staphylococcus aureus* in acute and IV-drug-related disease.

Arrhythmias and pericardial disease

• Atrial fibrillation: irregularly irregular pulse, absent P waves, pulse deficit (apex rate > radial rate). Rate control (beta-blocker, diltiazem, digoxin), rhythm control (cardioversion, amiodarone, ablation), and stroke prevention by CHA₂DS₂-VASc score — anticoagulate men ≥2 and women ≥3; DOACs preferred except in moderate-severe mitral stenosis or a mechanical valve, where warfarin with INR monitoring is mandatory. HAS-BLED estimates bleeding risk.
• Other tachyarrhythmias: paroxysmal SVT (vagal manoeuvres, IV adenosine), ventricular tachycardia (haemodynamically unstable → synchronised cardioversion; stable → amiodarone), ventricular fibrillation and pulseless VT (immediate unsynchronised defibrillation and CPR).
• Bradyarrhythmias: sinus node dysfunction, AV blocks — first degree (PR >200 ms), second degree Mobitz I (progressive PR lengthening) and Mobitz II (sudden dropped beat, high risk), third degree (complete AV dissociation); atropine then pacing for symptomatic high-grade block.
• Pericarditis: sharp pleuritic chest pain relieved by sitting forward, pericardial rub, widespread saddle-shaped ST elevation with PR depression; NSAIDs plus colchicine. In India, tuberculous pericarditis is a leading cause of large effusion and of constrictive pericarditis.
• Cardiac tamponade: Beck triad (hypotension, raised JVP, muffled heart sounds) with pulsus paradoxus and electrical alternans — treat by urgent pericardiocentesis.

Obstructive airway disease: asthma and COPD

• Asthma: chronic airway inflammation with variable, reversible expiratory airflow limitation and hyper-responsiveness. Episodic wheeze, cough (often nocturnal), chest tightness; triggers include allergens, cold air, exercise, NSAIDs, beta-blockers, smoke and occupational dust.
  • Diagnosis: spirometry showing FEV1/FVC below the lower limit of normal with reversibility — FEV1 rise ≥12% *and* ≥200 mL after bronchodilator; peak-flow diurnal variability >10%; methacholine challenge or FeNO where available.
  • Management (GINA-aligned): inhaled corticosteroid-containing treatment for everyone — as-needed low-dose ICS-formoterol at Steps 1–2, regular ICS-LABA at Steps 3–4, add-on LAMA/biologics at Step 5. SABA-only treatment is no longer recommended. Inhaler technique, spacer use, trigger avoidance and a written action plan matter as much as the drug.
  • Acute severe asthma: oxygen to SpO₂ 93–95%, repeated nebulised salbutamol + ipratropium, systemic steroids, magnesium sulphate in severe cases. Life-threatening signs: silent chest, exhaustion, bradycardia, confusion, SpO₂ <92%, and a *normal or rising* PaCO₂ (a normal PaCO₂ in a tiring asthmatic is an emergency, not reassurance).
• COPD: persistent respiratory symptoms with incompletely reversible airflow limitation — post-bronchodilator FEV1/FVC <0.70. Chronic bronchitis (cough with sputum ≥3 months for 2 consecutive years) and emphysema (alveolar destruction) overlap. Indian risk factors: smoking and bidi use, plus biomass/chulha smoke in women (a major non-smoker COPD cause), occupational dust and post-tubercular lung damage.
  • GOLD spirometric grades by post-bronchodilator FEV1 % predicted: GOLD 1 ≥80%, GOLD 2 50–79%, GOLD 3 30–49%, GOLD 4 <30%. Symptom/exacerbation groups A, B and E (GOLD merged old C and D into E for the high-exacerbation group) using mMRC or CAT score.
  • Treatment: smoking/biomass cessation (the only intervention that slows decline), inhaled LAMA ± LABA, ICS added if eosinophils are high or exacerbations continue, pulmonary rehabilitation, influenza and pneumococcal vaccination, and long-term oxygen therapy if PaO₂ ≤55 mmHg (or ≤59 mmHg with cor pulmonale/polycythaemia) for ≥15 h/day — the only therapy besides cessation with a survival benefit.
  • Acute exacerbation: controlled oxygen targeting SpO₂ 88–92%, nebulised bronchodilators, systemic steroids for about 5 days, antibiotics if sputum is purulent, and NIV (BiPAP) for hypercapnic acidosis (pH <7.35 with PaCO₂ high) — NIV reduces intubation and mortality.
  • Cor pulmonale: right ventricular failure from chronic lung disease via pulmonary hypertension — raised JVP, loud P2, pedal oedema, hepatomegaly.

Infective, vascular and parenchymal lung disease

• Pneumonia: classified as community-acquired (CAP), hospital-acquired/ventilator-associated, and aspiration. Typical CAP — *Streptococcus pneumoniae*, *Haemophilus influenzae*, *Klebsiella* (upper-lobe "bulging fissure", in alcoholics/diabetics); atypical — *Mycoplasma*, *Chlamydophila*, *Legionella*. Consolidation signs: bronchial breathing, increased vocal resonance, crackles, dull percussion.
  • Severity: CURB-65 (Confusion, Urea >7 mmol/L, Respiratory rate ≥30, BP <90 systolic or ≤60 diastolic, age ≥65) — 0–1 outpatient, 2 ward admission, ≥3 consider ICU. PSI is the alternative.
  • Empirical therapy: amoxicillin or amoxicillin-clavulanate ± macrolide for outpatients; ceftriaxone + macrolide (or respiratory fluoroquinolone) in hospital; de-escalate on culture. Always consider pulmonary tuberculosis in any Indian patient with cough >2 weeks — send sputum for NAAT/CBNAAT under NTEP; TB itself is covered in the infectious disease note.
• Pleural effusion: stony dull percussion, absent breath sounds and vocal resonance, trachea pushed away when large. Light's criteria separate exudate from transudate. In India tuberculous effusion is the commonest exudate (lymphocytic, high ADA, raised pleural fluid ADA/protein); others — malignancy, parapneumonic/empyema, pancreatitis. Transudates: heart failure, cirrhosis, nephrotic syndrome. Pneumothorax gives hyper-resonance with absent sounds; tension pneumothorax needs immediate needle decompression before any X-ray.
• Pulmonary embolism: sudden dyspnoea, pleuritic pain, haemoptysis, tachycardia, hypoxia with a clear chest. Risk by Wells score; D-dimer rules out low-probability cases; CT pulmonary angiography confirms. ECG may show sinus tachycardia, S1Q3T3, right bundle branch block. Treat with anticoagulation (LMWH/DOAC); thrombolysis if haemodynamically unstable (massive PE).
• Bronchiectasis: permanent bronchial dilatation with copious purulent sputum, clubbing, coarse crackles; post-tubercular bronchiectasis is the commonest Indian cause; HRCT (signet-ring sign, tram-track) is diagnostic; management is airway clearance, physiotherapy, antibiotics for exacerbations.
• Interstitial lung disease: restrictive pattern (FEV1/FVC normal or high, FVC and TLC reduced, DLCO low) with dry cough, exertional dyspnoea, fine end-inspiratory Velcro crackles and clubbing. Causes — idiopathic pulmonary fibrosis, connective tissue disease, hypersensitivity pneumonitis, sarcoidosis, drugs (amiodarone, methotrexate, bleomycin), and occupational pneumoconioses (silicosis in Rajasthan/Gujarat stone and quartz work, coal worker's pneumoconiosis, asbestosis, byssinosis). Occupational lung disease now sits under the Occupational Safety, Health and Working Conditions Code, 2020, in force from 21 November 2025, which replaced the Factories Act, 1948 — notifiable occupational diseases and employer duties flow from it.
• Obstructive sleep apnoea: snoring, witnessed apnoeas, daytime somnolence, obesity; Epworth score and polysomnography (AHI ≥5 with symptoms); treated with weight loss and CPAP.

National programmes and the Indian context

• NPCDCS, now folded into the National Programme for Prevention and Control of Non-Communicable Diseases (NP-NCD), runs population-based screening for hypertension and diabetes from age 30 at Ayushman Arogya Mandirs (health and wellness centres).
• India Hypertension Control Initiative (IHCI) — ICMR/WHO/MoHFW: simple drug protocol, free drugs, team care and BP registers; a model answer for "how would you improve hypertension control in a district".
• STEMI care networks (Tamil Nadu STEMI programme, Kerala, Telangana hub-and-spoke) use a pharmaco-invasive pathway; Ayushman Bharat PM-JAY funds angioplasty and valve surgery packages for eligible families.
• National Tobacco Control Programme and COTPA, 2003 regulate tobacco; the National Clean Air Programme addresses ambient PM, and PMUY (Ujjwala) LPG access targets household biomass smoke — relevant to both COPD and ischaemic heart disease.
• Essential cardiac and respiratory drugs (aspirin, enalapril, amlodipine, furosemide, atorvastatin, salbutamol, budesonide, ipratropium) are in the National List of Essential Medicines, with ceiling prices set by NPPA under the DPCO.

Key points

• ACS triad of diagnosis - chest pain history, ECG within 10 minutes, serial high-sensitivity troponin.
• STEMI - ST elevation in two contiguous leads or new LBBB; reperfusion is time-critical, primary PCI within 120 min of first contact else thrombolysis within 30 min of arrival.
• NSTEMI vs unstable angina - identical presentation; troponin elevation is the only separator.
• Secondary prevention after MI - aspirin + P2Y12 inhibitor, statin, beta-blocker, ACEi/ARB, plus tobacco cessation and rehabilitation.
• Hypertension - ≥140/90 by Indian guidelines; most patients need two drugs, ideally as a single-pill combination.
• Hypertensive emergency - high BP *with* acute target-organ damage; lower mean arterial pressure by about 25% in the first hour, never abruptly.
• HFrEF four pillars - ARNI/ACEi, beta-blocker, MRA, SGLT2 inhibitor; diuretics treat symptoms only.
• NYHA class grades symptoms, ejection fraction grades pump function - they do not correlate tightly.
• Rheumatic fever - revised Jones criteria 2015; benzathine penicillin every 3 weeks is secondary prophylaxis, duration set by carditis and valve damage.
• Atrial fibrillation - irregularly irregular pulse with pulse deficit; anticoagulate by CHA₂DS₂-VASc, warfarin (not a DOAC) with mitral stenosis or a mechanical valve.
• Cardiac tamponade - Beck triad plus pulsus paradoxus; pericardiocentesis, not diuretics.
• Asthma - reversible obstruction, FEV1 improves ≥12% and ≥200 mL after bronchodilator; every patient gets ICS-containing therapy, never SABA alone.
• COPD - post-bronchodilator FEV1/FVC <0.70; GOLD grades by FEV1 % predicted; only cessation and long-term oxygen alter survival.
• Biomass smoke is a major cause of COPD in Indian women who have never smoked.
• COPD exacerbation with hypercapnic acidosis - BiPAP early, target SpO₂ 88-92%, avoid high-flow oxygen.
• CURB-65 decides where a pneumonia patient is treated; 2 means admit, ≥3 consider ICU.
• Light's criteria separate exudate from transudate; tuberculous effusion is the commonest exudate in India.
• Pulmonary embolism - hypoxia and tachycardia with a clear chest; CTPA confirms, thrombolysis only if unstable.

Formulas and examples

Example 1 — MAP and hypertensive emergency target. A 52-year-old man presents with BP 230/130 mmHg, headache and papilloedema.

• MAP = 130 + (230 − 130)/3 = 130 + 33.3 = 163.3 mmHg.
• A 25% reduction in the first hour: 163.3 × 0.75 = 122.5 mmHg MAP, i.e. roughly 175/95 mmHg — the target for hour 1 with IV labetalol or nitroglycerine.
• Pulse pressure = 230 − 130 = 100 mmHg. Dropping MAP to a "normal" 93 mmHg immediately risks watershed cerebral, renal and coronary hypoperfusion.

Example 2 — Ejection fraction and heart failure class. Echo gives EDV 180 mL, ESV 117 mL, heart rate 88/min.

• Stroke volume = 180 − 117 = 63 mL. EF = 63/180 × 100 = 35% → HFrEF.
• Cardiac output = 88 × 63 = 5,544 mL/min = 5.54 L/min. With BSA 1.6 m², cardiac index = 5.54/1.6 = 3.46 L/min/m² (normal 2.5–4.0) — output is maintained by tachycardia despite a poor EF.
• Management: all four pillars of HFrEF therapy; EF ≤35% with symptoms also raises the question of an ICD.

Example 3 — Spirometry interpretation. A 58-year-old bidi smoker: FEV1 1.40 L (predicted 2.80 L), FVC 2.60 L; after salbutamol FEV1 1.52 L.

• FEV1/FVC = 1.40/2.60 = 0.538 → obstruction (<0.70).
• Reversibility = (1.52 − 1.40)/1.40 × 100 = 8.6%, absolute gain 120 mL — fails both the ≥12% and ≥200 mL thresholds → not significantly reversible.
• FEV1 % predicted = 1.40/2.80 × 100 = 50% → GOLD 2 (50–79%), at the lower boundary. Diagnosis: COPD, GOLD 2; group assigned by CAT/mMRC score and exacerbation history.

Example 4 — CURB-65 in pneumonia. A 70-year-old woman: confused, urea 9.2 mmol/L, respiratory rate 34/min, BP 88/56 mmHg.

• Confusion 1 + Urea >7 → 1 + RR ≥30 → 1 + SBP <90 → 1 + age ≥65 → 1 = score 5.
• Score ≥3 → severe CAP: admit to ICU, IV ceftriaxone plus a macrolide, blood and sputum cultures, fluids and oxygen; 30-day mortality at this score is high (roughly 40% in the original derivation).

Example 5 — Light's criteria. Pleural fluid protein 4.2 g/dL, serum protein 7.0 g/dL; pleural LDH 320 IU/L, serum LDH 400 IU/L (upper normal 250 IU/L).

• Protein ratio = 4.2/7.0 = 0.60 (>0.5 → exudate). LDH ratio = 320/400 = 0.80 (>0.6 → exudate). Pleural LDH vs ⅔ × 250 = 166.7 → 320 > 166.7 → exudate.
• All three satisfied → exudative effusion. In an Indian adult with fever, weight loss and a lymphocyte-predominant fluid, work up for tuberculous pleural effusion (ADA, CBNAAT, pleural biopsy).

Where it is used

• Casualty, ICU and CCU practice: chest-pain triage, thrombolysis decisions, NIV for COPD and pulmonary oedema, ACLS — the daily work of junior residents in AIIMS, PGIMER, CMC and district hospitals.
• Primary care and NP-NCD screening: medical officers at Ayushman Arogya Mandirs screening BP and diabetes from age 30, running IHCI registers and referring suspected RHD and COPD.
• Cardiology and pulmonology ecosystems: cath labs and valve programmes at Narayana Health, Apollo, Fortis, Medanta, SCTIMST and AIIMS; sleep labs, PFT labs and pulmonary rehabilitation units.
• Industry and clinical research roles: medical advisers and medical science liaisons with Cipla, Sun Pharma, Dr Reddy's, Lupin, Glenmark and Torrent (inhalers, antiplatelets, statins, SGLT2 inhibitors); clinical trial monitors under CDSCO/New Drugs and Clinical Trials Rules, 2019.
• Insurance, public health and policy: PM-JAY package adjudication, medical underwriting, disability and fitness certification, pneumoconiosis assessment under the OSH Code, 2020.
• Teaching and competitive progression: these diseases supply most of the long and short cases in MBBS and MD practicals and dominate NEET-PG/INI-CET and DM entrance interviews.

Interview questions

• Q: How do you distinguish NSTEMI from unstable angina? A: Both present with ischaemic rest pain and no persistent ST elevation; a rise and fall of cardiac troponin indicates myocardial necrosis and defines NSTEMI, whereas unstable angina has normal troponin.
• Q: A STEMI patient reaches a district hospital 90 minutes after symptom onset, with the nearest cath lab 4 hours away. What do you do? A: Thrombolyse immediately — tenecteplase bolus within 30 minutes of arrival after checking contraindications — then transfer for angiography within 3–24 hours (pharmaco-invasive strategy), because PCI cannot be achieved within 120 minutes.
• Q: Why is the oxygen target lower in a COPD exacerbation than in asthma? A: In chronic hypercapnic COPD, high-flow oxygen worsens CO₂ retention through loss of hypoxic ventilatory drive and increased V/Q mismatch, so SpO₂ is targeted at 88–92% rather than 93–95%.
• Q: An asthmatic in severe distress has a normal PaCO₂. Is that reassuring? A: No — it is alarming. A tiring patient who can no longer hyperventilate shows a normalising or rising PaCO₂, which signals impending respiratory failure and the need for ICU care.
• Q: Which four drug classes reduce mortality in HFrEF? A: ARNI or ACEi/ARB, an evidence-based beta-blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor; loop diuretics relieve congestion but do not improve survival.
• Q: Why would you choose warfarin over a DOAC in atrial fibrillation? A: In moderate-to-severe mitral stenosis or a mechanical prosthetic valve — common in Indian rheumatic heart disease — DOACs are not effective or are harmful, so warfarin with INR monitoring is required.
• Q: How long does secondary prophylaxis for rheumatic fever continue? A: Five years or until age 21 without carditis, ten years or until 21 with carditis and no residual valve disease, and lifelong (often stated as until age 40 or longer) with persistent valvular disease — whichever is longer.
• Q: What are the absolute contraindications to thrombolysis in STEMI? A: Previous intracranial haemorrhage, known cerebral vascular malformation or malignant intracranial tumour, ischaemic stroke within 3 months, suspected aortic dissection, active bleeding or bleeding diathesis, and significant closed head or facial trauma within 3 months.
• Q: How do you differentiate cardiac from respiratory dyspnoea at the bedside? A: Orthopnoea with paroxysmal nocturnal dyspnoea, raised JVP, displaced apex, S3 and basal crackles with a raised BNP suggest cardiac causes; wheeze, prolonged expiration, hyperinflation and a reversible or obstructive spirometry pattern with normal BNP suggest airway disease.
• Q: Why do Indians develop coronary disease earlier than Western populations? A: The Asian Indian phenotype — central obesity with insulin resistance, high triglycerides, low HDL, raised lipoprotein(a) and small dense LDL, with high tobacco use — produces premature, often multi-vessel and diffuse disease at lower BMI.
• Q: Pleural fluid protein ratio is 0.45 and LDH ratio 0.75. Transudate or exudate? A: Exudate — Light's criteria are satisfied if any one criterion is met, so the raised LDH ratio alone classifies it as exudative.
• Q: What is pulsus paradoxus and where is it found? A: An inspiratory fall in systolic blood pressure of more than 10 mmHg; it occurs in cardiac tamponade, severe acute asthma, constrictive pericarditis and tension pneumothorax.

Common mistakes

• Treating a hypertensive emergency by normalising blood pressure immediately instead of lowering MAP by about 25% in the first hour.
• Writing "ST elevation in one lead" as STEMI — two contiguous leads (or new LBBB) are required.
• Diagnosing COPD on the pre-bronchodilator ratio, or omitting the absolute 200 mL criterion when assessing reversibility.
• Giving high-flow oxygen in a COPD exacerbation, and delaying BiPAP until the patient is exhausted.
• Prescribing a DOAC in rheumatic mitral stenosis or a mechanical valve, where warfarin is mandatory.
• Forgetting blood cultures before starting antibiotics in suspected infective endocarditis, which makes it culture-negative.
• Missing tuberculosis — any Indian patient with cough beyond two weeks, a lymphocytic exudative effusion or an upper-lobe shadow needs NAAT/CBNAAT under NTEP.
• Confusing NYHA class with ejection fraction, or treating a tamponade or large effusion with diuretics instead of drainage.

Related topics

Electrocardiography (ECG): recording and interpretation · Arterial blood gas analysis · X-ray imaging basics · Clinical history taking and physical examination · Infectious and tropical diseases in India · Internal medicine: gastrointestinal, renal and endocrine diseases