Cardiology
1. What this chapter covers, and how NEET PG actually tests it
Cardiology stems give a murmur with a manoeuvre, an electrocardiogram, or an acute presentation, and ask for the lesion, the next investigation or the immediate management.
The organising principle is that every lesion loads the ventricle with either pressure or volume.
| Load | Compensation | Examples | Failure mode |
|---|---|---|---|
| Pressure | Concentric hypertrophy, thick wall, small cavity | Aortic stenosis, hypertension | Cannot fill; diastolic failure |
| Volume | Eccentric hypertrophy, dilated cavity | Mitral and aortic regurgitation | Cannot empty; systolic failure |
Pressure overload is tolerated for decades and then decompensates abruptly; volume overload is tolerated with a slow silent decline. That difference explains why aortic stenosis presents with sudden symptoms while chronic regurgitation is often found late and already irreversible.
2. Reading a murmur
Timing places the lesion, and the manoeuvre confirms it.
| Manoeuvre | Effect | Murmurs that increase |
|---|---|---|
| Valsalva strain | Reduces preload | Hypertrophic cardiomyopathy, mitral valve prolapse |
| Standing from squatting | Reduces preload | Hypertrophic cardiomyopathy, mitral valve prolapse |
| Squatting | Increases preload and afterload | Almost all others |
| Handgrip | Increases afterload | Mitral regurgitation, aortic regurgitation, ventricular septal defect |
Two murmurs behave in the opposite direction from everything else, and the exam relies on it. Hypertrophic cardiomyopathy and mitral valve prolapse both get louder when the ventricle is emptier, because a smaller cavity worsens outflow obstruction in the first and allows more leaflet prolapse in the second.
Handgrip raises afterload, which increases regurgitant flow backwards and decreases forward flow through a stenosis, so it separates aortic stenosis from mitral regurgitation at the bedside.
2.1 The heart sounds
The second sound splits normally on inspiration, because increased venous return delays pulmonary valve closure, and the pattern of abnormal splitting names the lesion.
| Splitting | Meaning |
|---|---|
| Wide and fixed | Atrial septal defect |
| Wide but varying with respiration | Right bundle branch block, pulmonary stenosis |
| Reversed, widening on expiration | Left bundle branch block, severe aortic stenosis |
| Single | Pulmonary hypertension, single functional valve |
Fixed splitting in an atrial septal defect occurs because the defect equalises atrial filling between the two sides, so the respiratory variation that normally alters right-sided return is abolished.
Reversed splitting means left-sided closure has been delayed past the right, which requires either electrical delay from left bundle branch block or mechanical delay from severe outflow obstruction.
A third heart sound reflects rapid early filling into a dilated ventricle and is normal in the young but indicates volume overload or failure in older patients.
A fourth heart sound reflects atrial contraction against a stiff ventricle, so it cannot occur in atrial fibrillation, and it accompanies pressure overload rather than volume overload.
2.2 The jugular venous pulse
The waveform is a direct window on right atrial events, and three abnormalities are examined repeatedly.
| Finding | Meaning |
|---|---|
| Absent a wave | Atrial fibrillation, since there is no coordinated atrial contraction |
| Cannon a waves | Atrium contracting against a closed tricuspid valve, as in complete heart block |
| Giant v waves | Tricuspid regurgitation, with the ventricle emptying into the atrium |
Raised pressure with a normal waveform suggests volume overload, while raised pressure with a steep descent suggests constriction.
3. Valvular disease
| Lesion | Murmur | Load | Key point |
|---|---|---|---|
| Mitral stenosis | Mid-diastolic rumble with opening snap | Pressure on left atrium | Rheumatic in almost all Indian cases |
| Mitral regurgitation | Pansystolic, radiating to axilla | Volume on left ventricle | Ejection fraction overestimates function |
| Aortic stenosis | Ejection systolic, radiating to carotids | Pressure on left ventricle | Triad of angina, syncope, dyspnoea |
| Aortic regurgitation | Early diastolic, wide pulse pressure | Volume on left ventricle | Collapsing pulse, many eponymous signs |
Rheumatic heart disease remains the dominant cause of valve disease in India, and mitral stenosis is its commonest single lesion, affecting women more often than men.
A shorter interval between the second heart sound and the opening snap indicates more severe mitral stenosis, because a higher left atrial pressure opens the valve earlier.
In aortic stenosis the symptom determines the prognosis. Angina implies survival of about five years untreated, syncope about three and heart failure about two, and the appearance of any of the three is an indication for valve replacement.
In mitral regurgitation the ventricle ejects into a low-pressure atrium, so ejection fraction looks deceptively good, and a value below sixty per cent already indicates significant dysfunction.
Balloon valvotomy is preferred in mitral stenosis when the valve is pliable and non-calcified without significant regurgitation, which is often the case in the young Indian patient.
4. Ischaemic heart disease
4.1 Classification and electrocardiography
Acute coronary syndrome divides by electrocardiogram and troponin into ST elevation infarction, non-ST elevation infarction and unstable angina.
| Leads | Territory | Artery |
|---|---|---|
| II, III, aVF | Inferior | Right coronary in most people |
| V1 to V4 | Anteroseptal | Left anterior descending |
| I, aVL, V5, V6 | Lateral | Left circumflex |
| Tall R and ST depression in V1 to V3 | Posterior | Right coronary or circumflex |
An inferior infarct with hypotension demands right-sided leads, because right ventricular infarction changes management completely: these patients are preload dependent, so nitrates and diuretics cause profound hypotension and fluids are given instead.
4.2 Management
Primary percutaneous intervention is preferred if it can be delivered within ninety minutes of first medical contact at a capable centre, or within one hundred and twenty minutes if transfer is required.
Fibrinolysis is given when that window cannot be met, with a target from arrival to needle of thirty minutes.
Antiplatelet therapy, anticoagulation, high-intensity statin, beta blocker and an angiotensin-converting enzyme inhibitor form the standard package, with the last two started once the patient is stable.
Troponin is the marker of choice, rising within a few hours and remaining elevated for up to two weeks, which makes it useless for detecting reinfarction in that window.
Creatine kinase MB is retained precisely because it falls back to normal within two to three days, so a second rise identifies reinfarction that troponin would miss.
Non-ST elevation syndromes are risk stratified rather than taken immediately to the catheter laboratory, with early invasive management for those at high risk and medical stabilisation for the rest.
The distinction that matters is that ST elevation reflects complete occlusion needing immediate reperfusion, while non-ST elevation reflects partial occlusion where immediate lysis is harmful rather than helpful.
4.3 Complications by timing
| Timing | Complication |
|---|---|
| First hours | Ventricular fibrillation, the commonest cause of early death |
| 3 to 5 days | Papillary muscle rupture, ventricular septal rupture |
| 3 to 7 days | Free wall rupture with tamponade |
| 2 to 10 weeks | Dressler syndrome, an autoimmune pericarditis |
The mechanical complications cluster at three to seven days because that is when the infarcted myocardium is maximally softened by macrophage infiltration before fibrosis has developed.
5. Heart failure
Failure is classified by ejection fraction, and the distinction drives treatment.
Reduced ejection fraction reflects a ventricle that cannot empty, typically after infarction or in dilated cardiomyopathy.
Preserved ejection fraction reflects a stiff ventricle that cannot fill, typically after long-standing hypertension, and it is commoner in older women.
Four drug classes together form the foundation of treatment in reduced ejection fraction, and their benefit is additive.
| Class | Example |
|---|---|
| Angiotensin receptor-neprilysin inhibitor or angiotensin-converting enzyme inhibitor | Sacubitril-valsartan, enalapril |
| Beta blocker | Bisoprolol, carvedilol, metoprolol succinate |
| Mineralocorticoid receptor antagonist | Spironolactone, eplerenone |
| Sodium-glucose cotransporter 2 inhibitor | Dapagliflozin, empagliflozin |
Diuretics relieve congestion and improve symptoms but do not prolong life, which is the distinction the exam tests.
Sodium-glucose cotransporter 2 inhibitors are now the one class with clear benefit in preserved ejection fraction as well, where most other agents have failed to show mortality benefit.
6. Arrhythmias
Atrial fibrillation is identified by an irregularly irregular rhythm with absent P waves, and management has three components: rate control, rhythm control where appropriate, and anticoagulation.
Anticoagulation is decided by stroke risk score, not by whether the rhythm has been restored, because restoring sinus rhythm does not remove the risk.
Direct oral anticoagulants are preferred over warfarin except in two situations: a mechanical prosthetic valve, and moderate to severe mitral stenosis, where warfarin remains mandatory.
Supraventricular tachycardia is narrow and regular and responds to vagal manoeuvres then adenosine, while ventricular tachycardia is broad and demands cardioversion if the patient is unstable.
A broad complex tachycardia in a patient with previous infarction is ventricular tachycardia until proven otherwise, and treating it as supraventricular is dangerous.
Complete heart block shows atrioventricular dissociation with a slow escape rhythm and requires pacing.
Second-degree block divides into a progressively lengthening interval before a dropped beat, which is usually benign and nodal, and a sudden dropped beat without warning, which is infranodal and progresses to complete block.
That distinction determines management entirely, since the first is observed while the second is paced.
Torsades de pointes arises on a prolonged QT interval and is treated with magnesium regardless of the serum magnesium level.
7. Hypertension
Diagnosis rests on repeated measurement, and Indian practice generally uses a threshold of 140 over 90, while some guidelines set stage one hypertension at 130 over 80.
Secondary causes are sought when hypertension is severe, resistant, of very early or very late onset, or accompanied by suggestive features.
| Clue | Cause |
|---|---|
| Hypokalaemia without diuretics | Primary hyperaldosteronism |
| Episodic headache, palpitation, sweating | Phaeochromocytoma |
| Radiofemoral delay | Coarctation of the aorta |
| Abdominal bruit, rise in creatinine after an inhibitor | Renal artery stenosis |
| Snoring and daytime somnolence | Obstructive sleep apnoea |
Angiotensin-converting enzyme inhibitors are first choice where there is diabetes with proteinuria or heart failure, calcium channel blockers in older patients, and thiazides in most others, with combinations used early rather than maximising a single agent.
Hypertensive emergency means raised pressure with acute organ damage, and the reduction must be gradual, since an abrupt fall causes cerebral hypoperfusion in a brain autoregulating at a higher pressure.
Hypertensive urgency, meaning a very high reading without organ damage, is managed with oral agents over days and does not require admission, and treating it as an emergency causes more harm than the pressure itself.
Aortic dissection is the exception that requires rapid rather than gradual lowering, because propagation of the dissection depends on the rate of rise of pressure as well as its height, so a beta blocker is given first to reduce that rate before any vasodilator.
Giving a vasodilator first in dissection causes reflex tachycardia, which raises the shearing force and can extend the tear, and this sequencing question is examined directly.
8. Other conditions
Acute rheumatic fever is diagnosed by the revised Jones criteria, and India is classed as a high-risk population, which lowers the threshold so that monoarthritis and polyarthralgia can count.
Infective endocarditis is diagnosed by the modified Duke criteria combining blood cultures and echocardiographic evidence with predisposition, fever, vascular and immunological phenomena.
Hypertrophic cardiomyopathy causes asymmetric septal hypertrophy with systolic anterior motion of the mitral valve, and it is the leading cause of sudden death in young athletes.
Acute pericarditis gives widespread concave ST elevation with PR segment depression, which distinguishes it from the localised convex elevation of infarction.
Cardiac tamponade produces hypotension, raised jugular pressure and muffled sounds, with pulsus paradoxus and electrical alternans.
Kussmaul sign, a rise in jugular pressure on inspiration, occurs in constrictive pericarditis but not in tamponade, and that contrast is examined repeatedly.
In tetralogy of Fallot, squatting raises systemic vascular resistance and therefore reduces right-to-left shunting, which is why children adopt the posture instinctively.
Eisenmenger syndrome is the reversal of a left-to-right shunt once pulmonary pressures exceed systemic, and once established it makes surgical closure contraindicated.
8.1 Congenital lesions sorted by cyanosis
| Acyanotic, left to right | Cyanotic, right to left |
|---|---|
| Atrial septal defect | Tetralogy of Fallot |
| Ventricular septal defect | Transposition of the great arteries |
| Patent ductus arteriosus | Tricuspid atresia |
| Coarctation of the aorta | Total anomalous pulmonary venous return |
Cyanosis appears when deoxygenated blood reaches the systemic circulation, which requires either a right-to-left shunt or complete mixing.
Tetralogy comprises pulmonary stenosis, a ventricular septal defect, an overriding aorta and right ventricular hypertrophy, and the degree of pulmonary stenosis determines how cyanosed the child is.
Differential cyanosis, with pink hands and blue feet, indicates a patent ductus with reversed shunting, because the duct enters the aorta beyond the vessels supplying the head and right arm.
Transposition is incompatible with life unless a mixing point exists, which is why prostaglandin is given to keep the duct open until surgery.
A ventricular septal defect produces a louder murmur when it is smaller, since a large defect allows free flow and generates little turbulence, and this inverse relationship between murmur intensity and defect size is regularly examined.
9. Worked examples
Example 1. A systolic murmur becomes louder on standing and softer on squatting. What is the lesion?
Hypertrophic cardiomyopathy, or mitral valve prolapse. Both worsen when preload falls, because a smaller ventricular cavity increases outflow obstruction or allows more leaflet prolapse. Nearly all other murmurs behave the opposite way.
Example 2. A patient with an inferior infarct becomes hypotensive after sublingual nitrate. What was missed?
Right ventricular infarction, which should have been sought with right-sided chest leads. These patients depend on preload, so nitrates and diuretics are avoided and fluid loading is the treatment.
Example 3. A patient with atrial fibrillation and moderate mitral stenosis asks for a direct oral anticoagulant. What is the answer?
Warfarin is required. Direct agents are contraindicated in moderate to severe mitral stenosis and in mechanical prosthetic valves, which are the two exceptions to their otherwise general preference.
Summary
Ask whether the lesion loads the ventricle with pressure or with volume; the compensation, murmur and failure mode follow.
Pressure overload gives concentric hypertrophy and diastolic failure; volume overload gives dilatation and systolic failure.
Hypertrophic cardiomyopathy and mitral valve prolapse are the two murmurs that increase when preload falls.
Handgrip raises afterload, increasing regurgitant murmurs and reducing those of stenosis.
Rheumatic disease dominates Indian valve pathology, and mitral stenosis is its commonest lesion.
A shorter second sound to opening snap interval means more severe mitral stenosis.
In aortic stenosis, angina implies five years, syncope three and heart failure two, and any symptom mandates replacement.
In mitral regurgitation an ejection fraction below sixty per cent already indicates significant dysfunction.
Inferior leads are II, III and aVF; anteroseptal is V1 to V4; lateral is I, aVL, V5 and V6.
Inferior infarct with hypotension means right ventricular involvement, so give fluids and avoid nitrates.
Primary intervention within ninety minutes is preferred, with fibrinolysis if the window cannot be met.
Mechanical complications cluster at three to seven days when the infarct is maximally soft.
Four classes form the foundation of reduced ejection fraction therapy, and diuretics are not among them.
Sodium-glucose cotransporter 2 inhibitors are the class with clear benefit in preserved ejection fraction.
Anticoagulation in atrial fibrillation follows stroke risk, not restoration of rhythm.
Direct oral anticoagulants are contraindicated in mechanical valves and moderate to severe mitral stenosis.
A broad complex tachycardia after previous infarction is ventricular until proven otherwise.
Torsades is treated with magnesium regardless of the serum level.
Hypokalaemia without diuretics suggests hyperaldosteronism; radiofemoral delay suggests coarctation.
Blood pressure in a hypertensive emergency is lowered gradually, because the brain is autoregulating at a higher pressure.
India is a high-risk population under the revised Jones criteria, which lowers the diagnostic threshold.
Pericarditis gives widespread concave ST elevation with PR depression.
Kussmaul sign occurs in constriction, not tamponade; pulsus paradoxus occurs in tamponade.
Squatting in tetralogy raises systemic resistance and reduces right-to-left shunting.
Fixed splitting of the second sound means an atrial septal defect; reversed splitting means left bundle branch block or severe aortic stenosis.
A fourth heart sound cannot occur in atrial fibrillation, because it requires atrial contraction.
Cannon a waves indicate atrial contraction against a closed tricuspid valve, as in complete heart block.
Differential cyanosis with pink hands and blue feet indicates a reversed patent ductus.
A smaller ventricular septal defect makes a louder murmur, because a large one generates little turbulence.
Troponin stays raised for two weeks, so creatine kinase MB is used to detect reinfarction within that window.
Hypertensive urgency is treated orally over days; aortic dissection is the exception needing rapid lowering, with a beta blocker before any vasodilator.
