NEET SS Cardiology (DM) Syllabus

Cardiology (DM) syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Cardiology (DM) in NEET SS, not a summary of it.

1. 1

   Coronary Artery Disease and Acute Coronary Syndromes

   5 topics

   • Pathophysiology of Atherosclerosis and Plaque Rupture
     • Endothelial dysfunction and lipid deposition
     • Vulnerable plaque and thrombus formation
     • Risk factors and primary prevention
   • Stable Ischemic Heart Disease
     • Anti-anginal pharmacotherapy
     • Functional and anatomical ischemia testing
     • Indications for revascularization
   • ST-Elevation Myocardial Infarction (STEMI)
     • Reperfusion strategy and primary PCI
     • Fibrinolysis and pharmacoinvasive approach
     • Mechanical complications of MI
   • Non-ST-Elevation ACS (NSTE-ACS)
     • Risk stratification (GRACE, TIMI scores)
     • Antiplatelet and anticoagulant regimens
     • Timing of invasive strategy
   • Chronic Coronary Syndromes and Secondary Prevention
     • Statin and lipid-lowering targets
     • Antiplatelet duration after stenting
2. 2

   Heart Failure and Cardiomyopathies

   4 topics

   • HFrEF Pathophysiology and Guideline-Directed Therapy
     • Neurohormonal activation (RAAS, sympathetic)
     • Four-pillar therapy (ARNI, beta-blocker, MRA, SGLT2i)
     • Device therapy (CRT, ICD) indications
   • HFpEF and HFmrEF
     • Diastolic dysfunction assessment
     • Diagnostic algorithms (H2FPEF, HFA-PEFF)
   • Dilated, Hypertrophic and Restrictive Cardiomyopathies
     • Genetic basis and family screening
     • HOCM management and septal reduction
     • Infiltrative disease (amyloid, sarcoid)
   • Advanced Heart Failure and Cardiac Transplantation
     • Mechanical circulatory support (LVAD, IABP, ECMO)
     • Inotrope use and palliative considerations
3. 3

   Arrhythmias and Electrophysiology

   4 topics

   • Supraventricular Tachycardias
     • AVNRT, AVRT and accessory pathways
     • Atrial flutter and focal atrial tachycardia
   • Atrial Fibrillation
     • Rate vs rhythm control
     • Stroke risk and anticoagulation (CHA2DS2-VASc)
     • Catheter ablation strategies
   • Ventricular Arrhythmias and Sudden Cardiac Death
     • Channelopathies (LQTS, Brugada, CPVT)
     • ICD indications and risk stratification
   • Bradyarrhythmias and Cardiac Pacing
     • AV block classification
     • Pacemaker modes and conduction system pacing
4. 4

   Valvular, Congenital and Structural Heart Disease

   4 topics

   • Aortic and Mitral Valve Disease
     • Severity grading by echocardiography
     • TAVR and transcatheter mitral interventions
     • Rheumatic heart disease and BMV
   • Adult Congenital Heart Disease
     • Left-to-right shunts (ASD, VSD, PDA)
     • Eisenmenger physiology
   • Infective Endocarditis
     • Modified Duke criteria
     • Antibiotic and surgical timing
   • Pericardial Diseases
     • Acute pericarditis and tamponade
     • Constrictive pericarditis
5. 5

   Pulmonary Hypertension, Hypertension and Vascular Cardiology

   4 topics

   • Systemic Hypertension
     • Secondary hypertension workup
     • Resistant hypertension and target organ damage
   • Pulmonary Hypertension
     • WHO classification groups
     • PAH-specific vasodilator therapy
   • Aortic Diseases
     • Aortic dissection and aneurysm
     • Marfan and connective tissue disorders
   • Venous Thromboembolism and Pulmonary Embolism
     • Risk stratification and thrombolysis

Cardiology (DM) flashcards for NEET SS

24 of 50 cards from the Cardiology (DM) deck — real questions with worked answers.

1. What is the central event that converts a stable atherosclerotic plaque into an acute coronary syndrome?

   Plaque rupture (or erosion) exposing the thrombogenic lipid core/subendothelial collagen to blood, triggering platelet adhesion and thrombus formation. Rupture-prone (vulnerable) plaques have a large lipid core, thin fibrous cap (<65 microns), and dense macrophage/inflammatory infiltration.

2. Which features distinguish a 'vulnerable' (rupture-prone) plaque from a 'stable' plaque?

   Vulnerable: thin fibrous cap, large necrotic lipid core, macrophage infiltration, high MMP activity, positive (outward) remodeling, neovascularization. Stable: thick fibrous cap, small lipid core, abundant smooth muscle/collagen, often causing luminal stenosis and stable angina.

3. What is the classic definition and presentation of stable ischemic heart disease (chronic stable angina)?

   Reproducible chest discomfort precipitated by exertion or emotion, lasting a few minutes, relieved within ~5 min by rest or sublingual nitroglycerin. Caused by a fixed coronary stenosis (usually >70%) producing demand-supply mismatch without acute thrombosis.

4. What is the first-line anti-anginal and the cornerstone prognostic therapy in stable ischemic heart disease?

   Symptom relief: beta-blockers (first-line anti-anginal), plus nitrates and calcium channel blockers. Prognosis/secondary prevention: high-intensity statin and antiplatelet (aspirin). Revascularization reserved for refractory symptoms or high-risk anatomy (e.g., left main, 3-vessel disease).

5. Define STEMI electrocardiographically and state the reperfusion time targets.

   New ST-elevation at the J-point in >=2 contiguous leads: >=1 mm in limb leads, and in V2-V3 >=2 mm (men >=40y), >=2.5 mm (men <40y), or >=1.5 mm (women); or new LBBB with symptoms. Targets: primary PCI within 90 min of first medical contact (120 min if transfer); fibrinolysis within 30 min (door-to-needle) if PCI unavailable.

6. Match the STEMI territory to the culprit coronary artery: anterior, inferior, lateral, posterior, and right ventricular infarcts.

   Anterior (V1-V4) = LAD; Inferior (II, III, aVF) = RCA (or LCx); Lateral (I, aVL, V5-V6) = LCx; Posterior (tall R/ST depression V1-V2, ST elevation in V7-V9) = RCA/LCx; Right ventricular (ST elevation in V4R) = proximal RCA.

7. Why are nitrates relatively contraindicated in inferior/right ventricular STEMI?

   RV infarction is preload-dependent; nitrates reduce venous return (preload) and can precipitate severe hypotension. Management is fluid loading and avoiding nitrates/diuretics. Also avoid nitrates within 24-48h of phosphodiesterase-5 inhibitor use.

8. How is NSTE-ACS distinguished from STEMI and from unstable angina?

   NSTE-ACS lacks persistent ST-elevation; ECG may show ST-depression, T-inversion, or be normal. NSTEMI = ischemic symptoms WITH elevated troponin (myonecrosis). Unstable angina = ischemic symptoms WITHOUT troponin rise. STEMI = persistent ST-elevation from total occlusion.

9. What score guides risk stratification and timing of invasive strategy in NSTE-ACS?

   GRACE score (and TIMI score). High GRACE (>140) or refractory ischemia/hemodynamic instability warrants early invasive angiography (<24h, or immediate <2h if very high risk). Components reflect ischemia, troponin, age, hemodynamics, and renal function.

10. List the components of guideline-directed secondary prevention in chronic coronary syndrome.

    Antiplatelet (aspirin, often with P2Y12 inhibitor for a defined period), high-intensity statin (+/- ezetimibe/PCSK9 inhibitor to LDL goal <55 mg/dL), ACEi/ARB (especially with LVD/HTN/DM), beta-blocker post-MI, SGLT2 inhibitor in diabetics, lifestyle (smoking cessation, diet, exercise), and BP/glycemic control.

11. Define HFrEF and outline the four foundational pillars of guideline-directed medical therapy.

    HFrEF = HF with LVEF <=40%. Four pillars: (1) ARNI (or ACEi/ARB), (2) beta-blocker (carvedilol, bisoprolol, metoprolol succinate), (3) MRA (spironolactone/eplerenone), (4) SGLT2 inhibitor (dapagliflozin/empagliflozin). All four reduce mortality and should be initiated and uptitrated early.

12. Describe the neurohormonal compensatory mechanisms that drive progression of HFrEF.

    Reduced cardiac output activates the sympathetic nervous system (catecholamines) and RAAS (angiotensin II, aldosterone), causing vasoconstriction, sodium/water retention, and increased preload/afterload. Chronically these promote adverse remodeling, fibrosis, and apoptosis - the rationale for blocking these pathways.

13. What are the criteria for HFpEF and HFmrEF, and which therapy has proven mortality/hospitalization benefit?

    HFmrEF: LVEF 41-49%; HFpEF: LVEF >=50% with evidence of elevated filling pressures/diastolic dysfunction and elevated natriuretic peptides. SGLT2 inhibitors (empagliflozin, dapagliflozin) reduce HF hospitalization across this spectrum; otherwise treat comorbidities (HTN, AF, obesity) and congestion.

14. Contrast the hemodynamics and key echocardiographic features of dilated vs hypertrophic vs restrictive cardiomyopathy.

    Dilated: dilated LV, systolic dysfunction (low EF), eccentric remodeling. Hypertrophic: asymmetric septal hypertrophy, normal/small cavity, diastolic dysfunction +/- LVOT obstruction with SAM. Restrictive: normal-sized non-dilated ventricles, severe diastolic dysfunction, biatrial enlargement, preserved EF early.

15. In hypertrophic obstructive cardiomyopathy (HOCM), how do interventions change the murmur intensity?

    The dynamic LVOT murmur INCREASES with reduced preload/afterload (Valsalva strain, standing, amyl nitrite) and DECREASES with increased preload/afterload (squatting, handgrip, passive leg raise). This is opposite to most murmurs and to aortic stenosis.

16. What is the single most important prognostic intervention for HCM patients at high risk of sudden cardiac death?

    Implantable cardioverter-defibrillator (ICD) for primary prevention. Major risk markers: prior cardiac arrest/sustained VT, family history of SCD, unexplained syncope, massive LV wall thickness (>=30 mm), LV apical aneurysm, extensive LGE on CMR, and abnormal BP response to exercise.

17. Name common causes of restrictive cardiomyopathy and the classic catheterization finding.

    Causes: amyloidosis, sarcoidosis, hemochromatosis, endomyocardial fibrosis, Loeffler endocarditis, radiation. Cath shows elevated, equalized diastolic pressures with a 'dip-and-plateau' (square-root sign). Constrictive pericarditis is the key differential (discordant ventricular pressures with respiration favor constriction).

18. Define advanced (stage D) heart failure and list contraindications to cardiac transplantation.

    Advanced HF: persistent NYHA III-IV symptoms despite optimized GDMT, recurrent hospitalizations, intolerance to therapy, end-organ dysfunction (INTERMACS profiles). Transplant contraindications: fixed severe pulmonary hypertension (PVR >5-6 Wood units unresponsive), active infection/malignancy, irreversible end-organ damage, ongoing substance abuse, advanced age with comorbidities.

19. Differentiate the mechanism of AVNRT, AVRT, and atrial tachycardia among supraventricular tachycardias.

    AVNRT: reentry within dual AV nodal pathways (most common SVT). AVRT: reentry using an accessory pathway (e.g., WPW) - orthodromic (narrow QRS) or antidromic (wide). Atrial tachycardia: an ectopic atrial focus independent of the AV node. Vagal maneuvers/adenosine terminate node-dependent SVTs (AVNRT, AVRT).

20. In Wolff-Parkinson-White with atrial fibrillation, which drugs are dangerous and why?

    AV nodal blockers (adenosine, verapamil, diltiazem, digoxin, beta-blockers) are contraindicated - they block the node and promote rapid conduction down the accessory pathway, risking ventricular fibrillation. Use procainamide/ibutilide or synchronized cardioversion; definitive therapy is accessory pathway ablation.

21. State the CHA2DS2-VASc components and how the score guides anticoagulation in atrial fibrillation.

    CHF (1), Hypertension (1), Age >=75 (2), Diabetes (1), prior Stroke/TIA/thromboembolism (2), Vascular disease (1), Age 65-74 (1), Sex category female (1). Oral anticoagulation (preferably a DOAC) recommended for men >=2 and women >=3; consider for men =1. DOACs preferred over warfarin except in mechanical valves/moderate-severe mitral stenosis.

22. Contrast the rate-control vs rhythm-control strategies in atrial fibrillation.

    Rate control: beta-blockers, non-dihydropyridine CCBs, or digoxin to keep ventricular rate controlled. Rhythm control: antiarrhythmics (e.g., amiodarone, flecainide, dronedarone) or catheter ablation. Early rhythm control (EAST-AFNET 4) and ablation benefit symptomatic and HFrEF patients; anticoagulation decisions are independent of strategy.

23. What are the primary-prevention ICD indications for ventricular arrhythmia / sudden cardiac death?

    LVEF <=35% with NYHA II-III (ischemic or non-ischemic cardiomyopathy) on >=3 months optimal GDMT, or LVEF <=30% post-MI NYHA I, with expected survival >1 year. Wait >=40 days post-MI and >=90 days post-revascularization before reassessing EF.

24. Describe the management of polymorphic VT/torsades de pointes and its relation to QT.

    Torsades is polymorphic VT in the setting of long QT. Treat with IV magnesium sulfate, correct hypokalemia/hypomagnesemia, stop QT-prolonging drugs, and overdrive pacing or isoproterenol to increase heart rate (shorten QT). Defibrillate if hemodynamically unstable. Acquired causes: drugs, electrolyte abnormalities; congenital long-QT syndromes use beta-blockers/ICD.

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