I have rich textbook content from Guyton, Ganong, Robbins, Goldman-Cecil, Goodman & Gilman, and Braunwald's. Let me now compile the full integrated notes.Here are your complete Integrated NEET PG Study Notes - Cardiovascular System, compiled from Guyton & Hall, Ganong's Physiology, Robbins Pathology, Goodman & Gilman's Pharmacology, Goldman-Cecil Medicine, and Braunwald's Heart Disease.
CARDIOVASCULAR SYSTEM - Integrated NEET PG Notes
How to Read These Notes
Every section follows the Anatomy → Physiology → Pathology → Pharmacology → Clinical chain. MCQ-high-yield points are marked 🔑. Mnemonics are marked 💡.
MODULE 1: ANATOMY OF THE HEART
Coronary Arteries - The Most Tested Anatomy
| Vessel | Territory Supplied | Clinical Relevance |
|---|
| Left Anterior Descending (LAD) | Anterior LV wall, Anterior 2/3 of IVS, Apex | Occlusion = Anterior STEMI (leads V1-V4) |
| Left Circumflex (LCX) | Lateral & posterior LV wall, LA | Occlusion = Lateral STEMI (leads I, aVL, V5-V6) |
| Right Coronary Artery (RCA) | Right ventricle, Posterior LV (80-90% people), SA node, AV node | Occlusion = Inferior STEMI (leads II, III, aVF) |
🔑 LAD is the "widow maker" - supplies largest territory; its occlusion is the most lethal MI.
🔑 SA node blood supply: From RCA in 60%, LCX in 40%.
🔑 AV node blood supply: From RCA in 80-90%, LCX in 10-20%.
Guyton & Hall Textbook of Medical Physiology - Coronary blood flow in resting adults averages 70 mL/min/100g heart weight (~225 mL/min = 4-5% of total cardiac output).
Key coronary anatomy facts:
- Coronary blood flow occurs mainly in diastole (systole compresses intramyocardial vessels - especially left ventricle)
- Coronary venous return: 75% via coronary sinus into RA; right ventricular blood via anterior cardiac veins directly into RA
- Thebesian veins drain small amount directly into all cardiac chambers
💡 Mnemonic - Coronary dominance: "Right is Right (dominant in 80-90%) - RCA gives posterior descending artery (PDA)"
Conducting System
SA Node (Pacemaker, 60-100/min)
↓ (internodal tracts)
AV Node (delay 0.1 sec - allows ventricular filling)
↓
Bundle of His
↓
Right Bundle Branch + Left Bundle Branch (anterior + posterior fascicles)
↓
Purkinje fibers → Ventricular myocardium
🔑 Intrinsic rates:
- SA node: 60-100/min
- AV node: 40-60/min
- Ventricular (Purkinje): 20-40/min
🔑 Blood supply of conduction system:
- SA node: RCA (60%), LCX (40%)
- AV node: RCA (80-90%), LAD first septal perforator (10-20%)
- Bundle of His: dual supply (RCA + LAD)
Heart Chambers - Key Relations
| Feature | Right Heart | Left Heart |
|---|
| Systolic pressure | 25 mmHg | 120 mmHg |
| Diastolic pressure | 0-8 mmHg | 8-12 mmHg |
| Wall thickness | Thinner (3-5 mm) | Thicker (8-12 mm) |
| Failure signs | JVD, Edema, Hepatomegaly | Pulmonary edema, Orthopnea |
MODULE 2: PHYSIOLOGY - CARDIAC CYCLE
The Complete Cardiac Cycle (at HR 75/min = 0.8 sec)
Ganong's Review of Medical Physiology - Events of the cardiac cycle at HR 75/min
| Phase | Event | Valves | Key Feature |
|---|
| 1 - Atrial Systole | P wave → atrial contraction | MV & TV open | Last 20-30% of ventricular filling (atrial "kick") |
| 2 - Isovolumetric Contraction | QRS → ventricles contract, no flow yet | All 4 valves CLOSED | Highest O2 consumption; pressure ↑ rapidly |
| 3 - Ventricular Ejection | LV pressure > Aortic pressure | Aortic & Pulmonic valves OPEN | Stroke volume ejected; EF = SV/EDV |
| 4 - Isovolumetric Relaxation | T wave → ventricles relax | All 4 valves CLOSED | Pressure falls rapidly |
| 5 - Ventricular Filling (Diastole) | LV pressure < LA pressure | Mitral valve OPENS | Rapid filling (70%), then slow filling, then atrial kick |
🔑 Duration at HR 75: Systole = 0.27 sec | Diastole = 0.53 sec
🔑 At high heart rates, diastole shortens more than systole - compromises coronary filling!
Heart Sounds
| Sound | Cause | Heard Best | Significance |
|---|
| S1 | Closure of MV + TV (beginning of systole) | Apex (mitral area) | Loud in MS; Soft in MR |
| S2 | Closure of AV + PV (end of systole) | Base | Split on inspiration (physiological); Fixed split = ASD |
| S3 | Rapid ventricular filling (early diastole) | Apex, LLD | Pathological in adults > 40 yrs = LV failure; Normal in children |
| S4 | Atrial contraction against stiff ventricle (late diastole) | Apex | Hypertension, AS, LVH - never normal |
🔑 S3 gallop = Heart failure (ventricular overload)
🔑 S4 gallop = Stiff ventricle (diastolic dysfunction, HCM, severe HTN)
🔑 "Tennessee" (S3) vs "Kentucky" (S4) pattern sounds
💡 Mnemonic - Heart sounds: "Many Thanks (S1 = Mitral + Tricuspid closing); Aortic Pulmonic (S2 = Aortic + Pulmonic closing)"
JVP Waveforms
| Wave | Cause | Loss/Exaggeration |
|---|
| a wave | Atrial contraction | Lost in AF; Giant a = TS, Complete heart block |
| c wave | Tricuspid valve closure (bulging into RA) | Often not visible |
| x descent | Atrial relaxation | Prominent in cardiac tamponade |
| v wave | Venous filling against closed TV | Giant v wave = Tricuspid regurgitation |
| y descent | Tricuspid valve opens, blood rushes into RV | Absent y = Cardiac tamponade; Sharp y = Constrictive pericarditis |
🔑 Kussmaul's sign (JVP rises on inspiration) = Constrictive pericarditis, Cardiac tamponade, RV infarct
Cardiac Output & Frank-Starling Law
Cardiac Output (CO) = Heart Rate × Stroke Volume
- Normal CO = 5 L/min
- Cardiac Index = CO/BSA = 2.2-4.2 L/min/m²
Frank-Starling Law: "The heart pumps out what comes in"
- ↑ Preload (venous return) → ↑ EDV → ↑ fiber stretch → ↑ force of contraction → ↑ SV
- This is the basis of why:
- IV fluids improve CO in hypovolemia
- Failing hearts cannot compensate (flat Starling curve)
Determinants of Stroke Volume:
- Preload (EDV - filling pressure)
- Afterload (aortic pressure - resistance to ejection)
- Contractility (inotropy - intrinsic force of contraction)
💡 Mnemonic - Factors ↑ Contractility: "CAT - Catecholamines, Digitalis (↑Ca²⁺), Thyroid hormones"
Blood Pressure Regulation
↓ BP detected by baroreceptors (carotid sinus, aortic arch)
↓
Sympathetic activation
↓
↑ HR + ↑ Contractility + Vasoconstriction
↓
Long-term: RAAS activation (Renin → Angiotensin II → Aldosterone)
↓
Na+ & water retention → ↑ blood volume → ↑ BP
🔑 Renin is secreted by juxtaglomerular cells of kidney in response to: ↓ BP, ↓ Na delivery, sympathetic stimulation
🔑 ACE converts Ang I → Ang II (lungs are main site)
🔑 Aldosterone (adrenal cortex) → ↑ Na reabsorption in collecting duct → ↑ BP
MODULE 3: PATHOLOGY
Atherosclerosis - Mechanism
Endothelial injury (HTN, smoking, diabetes, dyslipidemia)
↓
LDL enters intima → oxidized LDL
↓
Macrophages engulf oxidized LDL → FOAM CELLS
↓
Fatty streak (earliest lesion - reversible)
↓
Fibroblast + SMC migration → Fibrous plaque (atheroma)
↓
Complicated lesion: Calcification, Ulceration, Thrombosis
🔑 Foam cells = Lipid-laden macrophages = Hallmark of early atherosclerosis
🔑 Most common sites: Coronaries, Aorta (especially infrarenal), Carotid bifurcation, Circle of Willis, Popliteal artery
🔑 "Response to injury" hypothesis - Ross (1976/1999)
Myocardial Infarction - The Most Important CVS Topic
Coronary Territory → MI Type
| Artery Occluded | Territory | ECG Leads | MI Type |
|---|
| LAD | Anterior LV, Apex | V1-V4 | Anterior MI |
| LCX | Lateral LV | I, aVL, V5-V6 | Lateral MI |
| RCA | Inferior LV, RV | II, III, aVF | Inferior MI |
| Posterior (PDA from RCA) | Posterior wall | V7-V9 (reciprocal in V1-V2) | Posterior MI |
Timeline of MI Changes (NEET PG favorite!)
| Time | Gross | Microscopy | Cardiac Enzymes |
|---|
| 0-1 hr | None visible | None | Myoglobin ↑ (1st to rise) |
| 1-4 hr | Pallor beginning | Wavy fibers, Early coagulative necrosis | Troponin I & T start rising |
| 4-12 hr | Pallor | Coagulative necrosis begins | Troponin peaks |
| 12-24 hr | Pale, yellow | PMN infiltration begins | CK-MB peaks at 24hr |
| 1-3 days | Yellow-white | Maximum PMN infiltration | CK-MB normalizes by 48-72hr |
| 3-7 days | Yellow-tan (soft) | Macrophage infiltration, Phagocytosis starts | Troponin I normalizes day 7-10 |
| 1-3 weeks | Hyperemic border | Granulation tissue, Neovascularization | Troponin T normalizes week 2 |
| > 6 weeks | White scar | Dense fibrosis, Scar complete | All normal |
🔑 First enzyme to rise: Myoglobin (1-3 hrs)
🔑 Most sensitive & specific: Troponin I & T (rise by 3-6 hrs, peak at 24 hrs, persist 7-10 days Troponin I; 14 days Troponin T)
🔑 CK-MB - Best for re-infarction (normalizes quickly; second rise indicates new MI)
🔑 LDH - Used historically when patient presents late; LDH1 > LDH2 = "flipped LDH" (cardiac)
Zones of MI (Pathology)
Central DEAD zone → Zone of Injury → Zone of Ischemia
(Q wave) (ST elevation) (T wave inversion)
Complications of MI (by time)
| Timing | Complication |
|---|
| 0-24 hrs | Fatal arrhythmias (VF - #1 cause of death in acute MI), Sudden death |
| 1-3 days | Cardiogenic shock (massive MI >40% LV), Pericarditis (early) |
| 3-7 days | Free wall rupture (soft necrotic muscle) → Hemopericardium → Tamponade |
| 5-7 days | Papillary muscle rupture → Acute severe MR → Flash pulmonary edema |
| 7-14 days | IVS (septal) rupture → VSD |
| Weeks-months | LV aneurysm, Dressler's syndrome (autoimmune pericarditis - 2-10 wks) |
🔑 "Dead men tell no tales" at Day 3-5 - highest risk of rupture (maximum softening)
🔑 Dressler's syndrome = fever + pericarditis + elevated ESR 2-10 weeks post-MI
Infective Endocarditis
Duke's Criteria (2 major OR 1 major + 3 minor OR 5 minor = Definite IE)
Major Criteria:
- Blood cultures: typical organism ×2 (S. aureus, Viridans streptococci, HACEK group)
- Echo evidence: vegetation, abscess, new valvular regurgitation
Minor Criteria:
- Predisposing heart condition or IVDU
- Fever >38°C
- Vascular phenomena (emboli, Janeway lesions, splinter hemorrhages)
- Immunological phenomena (Osler nodes, Roth spots, glomerulonephritis, ↑ RF)
- Blood culture positive (not meeting major criterion)
💡 Mnemonic for peripheral signs of IE:
- Janeway lesions = painless, palms/soles (Janeway = J for "Just painless")
- Osler nodes = painful, finger/toe pads (Osler = "Ouch!")
- Roth spots = retinal hemorrhages with pale center
- Splinter hemorrhages = under nails
Organisms in IE by Setting
| Setting | Most Likely Organism |
|---|
| Native valve (normal) | Viridans streptococci (S. viridans) - after dental procedure |
| Native valve (abnormal/RHD) | Viridans streptococci |
| IV drug use | S. aureus (right-sided, tricuspid valve) |
| Prosthetic valve < 2 months | S. epidermidis (CoNS) |
| Prosthetic valve > 2 months | Viridans streptococci |
| Colon cancer | Streptococcus bovis (S. gallolyticus) |
| Nosocomial | S. aureus, CoNS |
Rheumatic Heart Disease
Pathogenesis:
- Group A beta-hemolytic streptococcal pharyngitis (Strep pyogenes)
- Molecular mimicry: Anti-streptococcal M protein antibodies cross-react with cardiac proteins (myosin, laminin)
- Immune injury via antibodies + T cells
- 1-3% of streptococcal pharyngitis cases develop rheumatic fever
Robbins & Kumar Basic Pathology - Aschoff bodies are pathognomonic for rheumatic fever; contain Anitschkow cells (caterpillar cells) - activated macrophages with chromatin condensed into a slender wavy ribbon.
🔑 Aschoff body = Pathognomonic of rheumatic fever = Granuloma-like collection of lymphocytes, plasma cells, Anitschkow cells around fibrinoid necrosis
🔑 Anitschkow cells = "Caterpillar cells" (wavy chromatin)
🔑 VALVES AFFECTED (order of frequency): Mitral > Aortic > Tricuspid > Pulmonic
Jones Criteria for Rheumatic Fever
Major (💡 JONES): Joints (migratory polyarthritis), cOrea (Sydenham's), Nodules (subcutaneous), Erythema marginatum, carditis (pancarditis)
Minor: Fever, ↑ ESR/CRP, Prolonged PR interval, Previous rheumatic fever
Requirement: 2 Major OR 1 Major + 2 Minor PLUS evidence of recent strep infection (↑ASO titer, positive culture/rapid antigen test)
Cardiomyopathies
| Feature | Dilated (DCM) | Hypertrophic (HCM) | Restrictive (RCM) |
|---|
| Gross | Large, dilated, flabby | Heavy, hypertrophied (asymmetric septal) | Normal or slightly enlarged |
| Main defect | Systolic dysfunction ↓EF | Diastolic dysfunction (LVOTO) | Diastolic dysfunction (stiff) |
| Causes | Alcohol, Viral (Coxsackie B), Idiopathic, Peripartum, Doxorubicin | AD mutation (Myosin heavy chain β-MYH7, MYBPC3) | Amyloid, Sarcoid, Hemochromatosis, Löffler's |
| ECG | BBB, ST changes | LVH, Septal Q waves | Low voltage (amyloid) |
| Echo finding | ↓EF, dilated chambers | Asymmetric septal hypertrophy (ASH), SAM of mitral valve, LVOTO gradient | Biatrial enlargement, normal/small ventricles |
| Treatment | ACE-I, BB, MRA, SGLT2i, ICD | Avoid vasodilators/diuretics; Beta-blockers, Verapamil; Septal myectomy/TAVI | Treat underlying cause |
🔑 HCM: Most common cause of sudden cardiac death in young athletes
🔑 SAM = Systolic Anterior Motion of mitral valve → causes dynamic LVOTO in HCM
🔑 HCM murmur increases with Valsalva and standing (↓ preload → ↑ obstruction)
🔑 HCM murmur decreases with squatting and passive leg raise (↑ preload → ↓ obstruction)
MODULE 4: PHARMACOLOGY
Antihypertensive Drugs - Integrated Mechanism Map
RAAS System Sympathetic System Direct Vasodilation
↓ ↓ ↓
ACE Inhibitors Beta-blockers Calcium Channel Blockers
ARBs Alpha-1 blockers Hydralazine (arterioles)
Aliskiren (renin inhibitor) Central: Clonidine Nitrates (veins >> arteries)
Aldosterone antagonists ↓
(Spironolactone, Eplerenone) ↓ HR, ↓ contractility
↓ Renin release
↓
Diuretics (Thiazide, Loop, K-sparing)
↓ Volume → ↓ preload → ↓ BP
Drug Classes - Key Facts
| Class | Example | Mechanism | Key Side Effect | Indication / CI |
|---|
| ACE Inhibitors | Ramipril, Enalapril | Block ACE → ↓ Ang II → ↓ Aldosterone | Dry cough (↑ bradykinin), Angioedema, Hyperkalemia | 1st line HF, Post-MI, CKD with DM; CI: Pregnancy, Bilateral RAS |
| ARBs | Losartan, Valsartan | Block AT1 receptor | Hyperkalemia (no cough) | Same as ACEi; alternative if ACEi cough |
| Beta-blockers | Metoprolol, Carvedilol, Bisoprolol | Block β1 (heart) → ↓ HR, ↓ CO, ↓ Renin | Bradycardia, Bronchospasm (non-selective), Mask hypoglycemia | IHD, HF (with ACEi), Post-MI; CI: Asthma, AV block |
| Calcium Channel Blockers | Amlodipine (DHP), Verapamil (non-DHP) | Block L-type Ca²⁺ channels → Vasodilation / ↓HR | Peripheral edema (DHP), Constipation (Verapamil), Bradycardia (non-DHP) | HTN, Angina; Verapamil + BB = dangerous AV block |
| Thiazide diuretics | Hydrochlorothiazide, Chlorthalidone | Block NCC in DCT → ↓ Na reabsorption | Hypokalemia, Hyponatremia, Hyperuricemia, Hyperglycemia, Hypercalcemia | 1st line HTN (esp. African Americans with CCB) |
| Loop Diuretics | Furosemide, Torsemide | Block NKCC2 in loop of Henle | Hypokalemia, Hyponatremia, Ototoxicity (Furosemide), Hypocalcemia | Acute heart failure, Pulmonary edema, Hypertensive urgency |
| Aldosterone antagonists | Spironolactone, Eplerenone | Block aldosterone receptor → ↑ K, ↑ Mg | Hyperkalemia; Spironolactone: Gynecomastia, Menstrual irregularities | HF (HFrEF), Secondary HTN from hyperaldosteronism; CI: K >5.5 |
| Nitrates | Nitroglycerin, Isosorbide dinitrate | → NO → cGMP → smooth muscle relaxation → Venodilation > arteriodilation | Headache, Postural hypotension, Tolerance (24-hr nitrate-free period) | Angina pectoris, Acute LVF; CI: PDE5 inhibitors (sildenafil) |
| Digoxin | Digoxin | Inhibit Na/K ATPase → ↑ intracellular Ca²⁺ → ↑ Contractility; Vagal tone → ↓ HR | Narrow TI; Toxicity: Yellow-green vision, Arrhythmias; Hypokalemia worsens toxicity | HF with AF; Rate control in AF; CI: WPW, HCM, 2nd/3rd degree AV block |
Drug of Choice - High Yield Summary
| Condition | DOC |
|---|
| HTN + Diabetes with proteinuria | ACE Inhibitor / ARB |
| HTN + Asthma | Amlodipine (CCB) or Thiazide (avoid BB) |
| HTN + Pregnancy | Methyldopa (1st line), Labetalol, Nifedipine |
| HTN + Benign Prostatic Hyperplasia | Alpha-1 blockers (Prazosin, Tamsulosin) |
| HTN + Heart failure | ACE-I + BB + MRA + Diuretic |
| Hypertensive emergency | IV Sodium nitroprusside / IV Labetalol / IV Nicardipine |
| Angina pectoris | Nitrates (short-acting) for acute; BB + Long-acting nitrate for prophylaxis |
| Prinzmetal (vasospastic) angina | Calcium Channel Blockers (NOT Beta-blockers - can worsen) |
| Post-MI cardioprotection | ACE-I + BB + Aspirin + Statin (ABAS) |
| HFrEF (EF <40%) | ACE-I/ARB/ARNI + BB + MRA + SGLT2i + Diuretic (if congested) |
Antiarrhythmic Drugs - Vaughan-Williams Classification
| Class | Mechanism | Examples | Indication |
|---|
| Ia | Na channel block (moderate) + ↑ APD | Quinidine, Procainamide, Disopyramide | AF, VT; Quinidine: Torsades risk (QT prolongation) |
| Ib | Na channel block (fast dissociation) | Lidocaine, Mexiletine, Phenytoin | VT/VF (esp. post-MI), Lidocaine = IV only |
| Ic | Na channel block (slow dissociation) | Flecainide, Propafenone | AF, SVT; CI: Structural heart disease (CAST trial) |
| II | Beta-blockade | Metoprolol, Esmolol, Propranolol | SVT, AF rate control, Post-MI |
| III | K channel block → ↑ APD, ↑ QT | Amiodarone, Sotalol, Ibutilide, Dronedarone | VT, VF, AF; Amiodarone = broadest spectrum |
| IV | Ca channel block | Verapamil, Diltiazem | SVT, AF rate control; CI: WPW, HF with systolic dysfunction |
🔑 Amiodarone = most effective antiarrhythmic but most side effects:
- Pulmonary fibrosis
- Thyroid dysfunction (hypo or hyper - contains iodine)
- Hepatotoxicity
- Peripheral neuropathy
- Corneal microdeposits (bluish-gray skin discoloration with sun)
- Requires monitoring: TFT, LFT, CXR, PFT
🔑 Digoxin toxicity treatment: Stop drug, Correct hypokalemia, Digibind (Fab fragments) for severe toxicity
MODULE 5: CLINICAL MEDICINE (Integrated)
Hypertension
Definition (JNC 8 / ACC/AHA 2017):
- ACC/AHA 2017: ≥ 130/80 mmHg = HTN
- JNC 8: ≥ 140/90 mmHg = Stage 1 HTN
Causes of Secondary HTN (5 H's):
- Hyperaldosteronism (Conn's syndrome) - ↓ K, ↑ aldosterone, ↑ aldosterone:renin ratio
- Hyperthyroidism / Hypothyroidism
- Hyperparathyroidism (rarely)
- Henal artery stenosis (Renovascular HTN) - young woman, bruit
- Pheochromocytoma - triad: Headache, Palpitations, Profuse sweating; 24hr urine catecholamines/VMA/metanephrines
🔑 Most common cause of secondary HTN: Primary hyperaldosteronism (Conn's syndrome) in adults
🔑 Most common cause in children: Renovascular HTN (renal artery stenosis)
🔑 Hypertensive urgency (>180/120, no end-organ damage) vs Emergency (same BP WITH end-organ damage: papilledema, encephalopathy, AKI, MI, aortic dissection)
Heart Failure
HFrEF (Systolic HF, EF <40%) vs HFpEF (Diastolic HF, EF >50%)
| Feature | HFrEF | HFpEF |
|---|
| Defect | ↓ Contractility (systolic) | ↓ Compliance (diastolic) |
| EF | < 40% | ≥ 50% |
| Common causes | IHD, Dilated CM, Myocarditis | Hypertension, HCM, Restrictive CM, Aging |
| BNP | ↑↑ | ↑ (less) |
| Treatment | ACEi/ARB/ARNI + BB + MRA + SGLT2i | Diuretics for congestion; treat cause |
🔑 BNP is released by ventricular myocytes in response to wall stress (volume/pressure overload)
- BNP > 100 pg/mL = HF likely
- BNP < 35 pg/mL = HF unlikely
- NT-proBNP > 125 pg/mL = HF (used more now; longer half-life)
NYHA Classification:
- Class I: No symptoms with normal activity
- Class II: Symptoms with moderate exertion
- Class III: Symptoms with minimal exertion
- Class IV: Symptoms at rest
Signs of Heart Failure:
- Left HF: Dyspnea, Orthopnea (3-pillow), PND, Bilateral basal crepitations, S3 gallop, Displaced apex
- Right HF: JVD, Peripheral pitting edema (legs), Hepatomegaly, Ascites, Pleural effusion (R > L)
Acute Coronary Syndromes
Acute Coronary Syndrome (ACS)
├── Unstable Angina (no troponin rise, no ECG changes)
├── NSTEMI (↑ Troponin, No ST elevation, may have ST depression/T inversion)
└── STEMI (↑ Troponin + ST elevation ≥ 1mm in 2 contiguous limb leads, ≥ 2mm in precordial)
STEMI Management - "TIME IS MUSCLE"
Immediate (First 10 minutes):
- ECG + IV access + O2 (if SpO2 < 94%) + Monitor
- Aspirin 300 mg loading
- P2Y12 inhibitor (Ticagrelor 180 mg or Clopidogrel 300-600 mg)
- IV Morphine (for pain), IV Metoprolol (if no CI)
Reperfusion (within 90 min - Door to Balloon time):
- Primary PCI = preferred (if available within 90 min of first medical contact)
- Thrombolysis (if PCI not available within 120 min) - Streptokinase, tPA (Alteplase)
- CI to thrombolysis: Recent surgery/trauma, Active bleeding, Stroke <3 months, BP >185/110, Aortic dissection
Post-MI medications (ABCDE):
- A - Aspirin (lifelong) + Anti-P2Y12 (12 months DAPT)
- B - Beta-blocker (↓ mortality, ↓ arrhythmia)
- C - Cholesterol (High-intensity Statin - Atorvastatin 80 mg or Rosuvastatin 40 mg)
- D - Diabetes control
- E - ACE inhibitor/ARB (especially if EF reduced, HTN, or DM)
Valvular Heart Diseases
| Valve Lesion | Classic Murmur | Key Feature | Cause |
|---|
| Mitral Stenosis | Rumbling mid-diastolic murmur at apex + Opening snap | Loud S1; Irregularly irregular (AF); "Fish mouth" valve on echo | RHD (#1), Congenital |
| Mitral Regurgitation | Pansystolic murmur at apex radiating to axilla | Soft S1; S3 gallop; Displaced hyperdynamic apex | RHD, MVP, IE, Ruptured papillary muscle |
| Mitral Valve Prolapse | Late systolic murmur + midsystolic click | Click-murmur syndrome; Young females; Associated with Marfan's | Connective tissue disorder |
| Aortic Stenosis | Harsh ejection systolic murmur (RUSB) radiating to carotids | Slow rising pulse; Narrow pulse pressure; Soft A2 | Bicuspid aortic valve (young), Senile calcific (elderly), RHD |
| Aortic Regurgitation | High-pitched early diastolic murmur (LLSB) | Wide pulse pressure; Collapsing pulse (water hammer); Austin Flint murmur | IE, Aortic dissection, RHD, Marfan's, AS |
🔑 Murmur increases with: Valsalva release, Passive leg raise (↑ preload = more blood = louder except HCM)
🔑 AS triad (SAD): Syncope, Angina, Dyspnea (in order of increasing severity; Dyspnea = worst prognosis)
🔑 AR signs: Corrigan's pulse, de Musset's sign, Quincke's sign, Traube's sign, Müller's sign, Duroziez's sign
MODULE 6: QUICK REVISION TABLE - Integrated CVS
| Topic | Anatomy | Physiology | Pathology | Pharmacology | Clinical |
|---|
| MI (Anterior) | LAD occlusion | ↓ CO, ↑ LVEDP | Coagulative necrosis, Troponin ↑ | Aspirin, LMWH, Clopidogrel | V1-V4 ST elevation, PCI |
| MI (Inferior) | RCA occlusion | Risk of AV block | Same as above | Same + Watch Morphine (↓ BP) | II, III, aVF elevation |
| Heart Failure | LV dilatation (dilated) or hypertrophy (HCM) | ↓ EF (HFrEF) or ↓ compliance | Myocyte hypertrophy → fibrosis | ACEi + BB + MRA + SGLT2i | BNP ↑, CXR: Cardiomegaly, Bat-wing opacities |
| HTN | Thickened vessels, LV hypertrophy | ↑ TPR or ↑ CO (Renin) | Hyaline arteriolosclerosis, Fibrinoid necrosis | Thiazide/CCB/ACEi (1st line) | Renal: ↑Creatinine; Eye: AV nicking |
| RHD | Mitral valve fibrosis | MS: ↑ LA pressure | Aschoff bodies, Anitschkow cells | Prophylactic Penicillin G | Mid-diastolic murmur, AF |
| IE | Valve vegetations | Embolic phenomena | Sterile vegetations (earlier), Bacterial vegetations | Penicillin + Gentamicin (IV) | Duke's criteria, Blood cultures ×3 |
| Atherosclerosis | Intimal thickening, Narrowed lumen | ↓ Flow → Ischemia | Foam cells → Fibrous plaque | Statins (↓ LDL, ↑ plaque stability) | Chest pain, Ankle-Brachial Index |
MODULE 7: HIGH-YIELD MNEMONICS & FACTS
💡 "ACTS" - Causes of Wide Fixed Split S2: ASD (most common), Complete RBBB, Total anomalous pulmonary venous connection, Severe PS
💡 "5 T's" of Cyanotic CHD: Tetralogy of Fallot, Transposition of Great Arteries, Total anomalous pulmonary venous connection, Truncus arteriosus, Tricuspid atresia
💡 Endocarditis prophylaxis needed for: Prosthetic valves, Previous IE, Congenital cyanotic HD (unrepaired), Cardiac transplant with valvulopathy - during DENTAL procedures (amoxicillin 2g PO 30-60 min before)
🔑 Pulsus paradoxus (>10 mmHg drop in SBP during inspiration) = Cardiac tamponade, Severe asthma, Constrictive pericarditis
🔑 Beck's Triad (cardiac tamponade) = Hypotension + Muffled heart sounds + JVD
🔑 ECG in Pericarditis = Diffuse saddle-shaped ST elevation (all leads except aVR and V1) + PR depression
🔑 Libman-Sacks endocarditis = Non-bacterial thrombotic vegetations, both surfaces of mitral valve = SLE (lupus)
🔑 Marantic endocarditis = Non-bacterial thrombotic vegetations, associated with malignancy and debilitating illness
🔑 WPW Syndrome ECG: Short PR interval (<0.12 sec) + Delta wave + Wide QRS = Accessory pathway (Bundle of Kent)
- Treatment: Radiofrequency ablation; Avoid Digoxin and Verapamil (can accelerate conduction through accessory pathway → VF)
MODULE 8: PREVIOUS YEAR NEET PG QUESTION THEMES (CVS)
| Theme | Key Fact to Remember |
|---|
| Earliest enzyme in MI | Myoglobin (1-3 hrs) |
| Most sensitive & specific | Troponin I |
| Re-infarction marker | CK-MB |
| Pathognomonic of RHD | Aschoff bodies / Anitschkow cells |
| Sudden death in young athlete | HCM (β-myosin heavy chain mutation) |
| Loud S1 | Mitral stenosis |
| Opening snap | Mitral stenosis (earlier = more severe) |
| Wide fixed split S2 | ASD |
| JVP absent y descent | Cardiac tamponade |
| JVP sharp y descent | Constrictive pericarditis |
| Pulsus paradoxus | Cardiac tamponade |
| Kussmaul's sign | Constrictive pericarditis (NOT tamponade typically) |
| AF + Calcified valve | Mitral stenosis (RHD) |
| Murmur increases with Valsalva | HCM (dynamic LVOTO) |
| Most common cause of MR | MVP (in developed countries) |
| Libman-Sacks | SLE |
| DOC for Prinzmetal angina | CCB (diltiazem/amlodipine) |
| Digoxin toxicity antidote | Digibind (Digoxin-Fab antibody) |
Sources: Guyton & Hall Textbook of Medical Physiology; Ganong's Review of Medical Physiology (26th ed.); Robbins & Kumar Basic Pathology; Goodman & Gilman's The Pharmacological Basis of Therapeutics; Goldman-Cecil Medicine; Braunwald's Heart Disease (15th ed.); Gray's Anatomy for Students