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Here is your comprehensive FMGE heart study guide, covering all four subjects: Anatomy, Physiology, Pathology, and Pharmacology.
FMGE Heart - Complete Study Notes
PART 1: ANATOMY OF THE HEART
(Sources: Gray's Anatomy for Students; Color Atlas of Human Anatomy, Vol 2)
1.1 Position and Orientation
- The heart has the shape of a pyramid resting on one side
- Apex - projects forward, downward, and to the LEFT; lies in the 5th left intercostal space, 8-9 cm from midsternal line (formed by inferolateral part of left ventricle)
- Base - faces posteriorly; quadrilateral; lies opposite vertebrae TV to TVIII (standing: TVI to TIX)
- The esophagus lies immediately posterior to the base
1.2 Surfaces
| Surface | Formed by |
|---|---|
| Anterior (sternocostal) | Mostly right ventricle + some RA (right) and LV (left) |
| Diaphragmatic (inferior) | Left ventricle + small portion of RV |
| Left pulmonary | Left ventricle (broad, convex) |
| Right pulmonary | Right atrium (broad, convex) |
| Base (posterior) | Left atrium mostly + small part of RA + proximal great veins |
FMGE High-Yield: The right border on CXR (PA view) = SVC + RA + IVC. The left border = arch of aorta + pulmonary trunk + left auricle + LV.
1.3 Cardiac Borders (X-Ray)
| Border | Structures |
|---|---|
| Right border (PA view) | SVC (upper) + RA (middle) + IVC (lower) |
| Left border (PA view) | Aortic knuckle + Pulmonary trunk + Left auricle + LV |
| Inferior border | RV + LV at apex |
| Right anterior (lateral view) | RV |
| Posterior (lateral view) | LA |
1.4 Chambers
Right Atrium:
- Blood enters via: Superior vena cava (upper posterior), Inferior vena cava (lower posterior), Coronary sinus (lower posterior)
- Interior divided by crista terminalis (muscular ridge) - externally marked by sulcus terminalis
- Posterior to crista = sinus of venae cavae (smooth walls, embryologically from right horn of sinus venosus)
- Anterior to crista = atrium proper with musculi pectinati (pectinate muscles)
- Fossa ovalis = remnant of foramen ovale on interatrial septum; depression with a raised margin called the limbus fossae ovalis
- Blood exits through the right atrioventricular orifice (closed by tricuspid valve)
Right Ventricle:
- Receives blood from RA through tricuspid valve
- Ejects blood into pulmonary trunk through pulmonary valve
- Has trabeculae carneae (muscular ridges), papillary muscles (anterior, posterior, septal), and chordae tendineae
- Moderator band (septomarginal trabecula) - carries right bundle branch, important in conduction
- Wall is thinner than LV (RV:LV wall ratio ~1:3)
Left Atrium:
- Receives 4 pulmonary veins (2 from each lung)
- Smooth walls posteriorly; pectinate muscles only in left auricle
- Forms most of the base of the heart
- Ejects blood through mitral (bicuspid) valve into LV
Left Ventricle:
- Thickest walls (~9-11 mm) - 3x thicker than RV
- Has trabeculae carneae, papillary muscles (anterior and posterior), chordae tendineae
- Ejects blood through aortic valve into the ascending aorta
- Has aortic vestibule = smooth-walled outflow tract
1.5 Cardiac Valves
| Valve | Type | Location | Cusps | Key Point |
|---|---|---|---|---|
| Tricuspid | AV valve | Right AV orifice | 3 (anterior, posterior, septal) | Right side |
| Mitral (bicuspid) | AV valve | Left AV orifice | 2 (anterior, posterior) | Left side |
| Pulmonary | Semilunar | Pulmonary trunk origin | 3 (anterior, left, right) | No chordae |
| Aortic | Semilunar | Aortic orifice | 3 (left, right, posterior/non-coronary) | Sinuses of Valsalva |
FMGE High-Yield: The sinuses of Valsalva (aortic sinuses) - the left and right coronary arteries arise from the left and right aortic sinuses respectively. The posterior/non-coronary cusp has no coronary ostium.
1.6 External Sulci
- Coronary sulcus - encircles the heart, separates atria from ventricles; contains: right coronary artery, small cardiac vein, coronary sinus, circumflex branch of LCA
- Anterior interventricular sulcus - separates ventricles anteriorly; contains: anterior interventricular artery (LAD) + great cardiac vein
- Posterior interventricular sulcus - separates ventricles posteriorly; contains: posterior interventricular artery (PDA) + middle cardiac vein
1.7 Coronary Circulation
Left Coronary Artery (LCA):
- Arises from left aortic sinus
- Divides into: LAD (Left Anterior Descending) and Circumflex artery
- LAD supplies: anterior LV, anterior 2/3 of interventricular septum, apex, anterior papillary muscle
- Circumflex supplies: lateral and posterior LV, posterior papillary muscle
Right Coronary Artery (RCA):
- Arises from right aortic sinus
- Supplies: RA, RV, SA node (55%), AV node (90%), posterior 1/3 of septum (in right-dominant circulation)
- Gives posterior descending artery (PDA) in right-dominant pattern
FMGE High-Yield - Dominance:
- Right-dominant (most common, ~70%) = PDA from RCA
- Left-dominant (~15%) = PDA from circumflex
- Co-dominant (~15%)
FMGE High-Yield - Nodal Blood Supply:
- SA node = RCA (55%), LCA (45%)
- AV node = RCA (90%) - the "AV nodal artery" is a branch of RCA at the crux
1.8 Cardiac Conduction System
| Structure | Location | Feature |
|---|---|---|
| SA node | Junction of SVC and right atrium (crista terminalis) | Pacemaker, 60-100 bpm |
| AV node | Posteroinferior part of interatrial septum (triangle of Koch) | Rate 40-60 bpm; delays impulse |
| Bundle of His | Upper part of interventricular septum | Only conduction pathway between atria and ventricles |
| Right bundle branch | Passes through moderator band to anterior papillary muscle | Reaches RV |
| Left bundle branch | Divides into anterior and posterior fascicles | Reaches LV |
| Purkinje fibers | Subendocardial, end-organs | Rate 20-40 bpm; fastest conduction velocity |
FMGE High-Yield: The triangle of Koch landmarks are: tendon of Todaro (posterior), tricuspid valve annulus (anterolateral), and coronary sinus ostium (inferior). The AV node sits at the apex of this triangle.
1.9 Pericardium
- Fibrous pericardium: tough outer layer; continuous with central tendon of diaphragm; prevents acute overdistension
- Serous pericardium: inner layer; two layers (parietal + visceral/epicardium) with pericardial cavity (15-50 mL fluid)
- Pericardial sinuses:
- Transverse sinus - between great arteries anteriorly and great veins posteriorly (surgically important - surgeon places finger/clamp to stop cardiac output)
- Oblique sinus - behind left atrium between pulmonary veins
Cardiac Tamponade: Rapid fluid accumulation compresses all 4 chambers. Beck's triad: ↓BP + ↑JVP + muffled heart sounds. Kussmaul's sign = JVP rises on inspiration.
PART 2: PHYSIOLOGY OF THE HEART
2.1 Cardiac Action Potentials
Ventricular Myocyte (Fast Response):
| Phase | Ion movement | Change |
|---|---|---|
| Phase 0 | Rapid Na+ influx | Rapid depolarization |
| Phase 1 | K+ efflux (Ito) | Early repolarization |
| Phase 2 | Ca2+ influx = K+ efflux | Plateau (unique to cardiac) |
| Phase 3 | K+ efflux | Rapid repolarization |
| Phase 4 | Na+/K+ ATPase restores | Resting membrane potential (-85 to -90 mV) |
SA/AV Node (Slow Response):
- Phase 0 = slow Ca2+ influx (no fast Na+ channels)
- Phase 4 = spontaneous depolarization (pacemaker potential) via If (funny current) + ICaT
- RMP = -55 to -60 mV (less negative)
FMGE High-Yield: Cardiac muscle has an absolute refractory period that lasts almost as long as the contraction itself - this PREVENTS tetanus (unlike skeletal muscle).
2.2 Cardiac Cycle (Wiggers Diagram)
| Phase | Events |
|---|---|
| Isovolumetric contraction | All valves closed; pressure builds; begins at S1 |
| Rapid ejection | Aortic (pulmonic) valve opens; 70% stroke volume ejected |
| Reduced ejection | Decreasing flow |
| Isovolumetric relaxation | All valves closed; pressure falls; begins at S2 |
| Rapid filling | Mitral (tricuspid) valve opens; 70-75% filling |
| Reduced filling | Passive filling slows |
| Atrial systole (pre-systolic filling) | Atria contract; final 25-30% filling |
Heart Sounds:
- S1 = closure of mitral + tricuspid (AV valves) at start of systole
- S2 = closure of aortic + pulmonic (semilunar valves) at start of diastole
- S3 = early diastole, rapid filling; normal in children, pathological in adults (HF with low EF)
- S4 = late diastole, atrial kick against stiff ventricle; always pathological (LVH, hypertensive heart disease)
2.3 Frank-Starling Law
- Increased preload (venous return, end-diastolic volume) → increased stretch of myocardial fibers → increased force of contraction → increased stroke volume
- Within physiological limits: greater EDV = greater SV
- Mechanism: optimal actin-myosin overlap at sarcomere length of ~2.2 μm
Key definitions:
- Preload = end-diastolic volume (EDV); approximated by end-diastolic pressure
- Afterload = resistance to ejection; approximated by aortic pressure / systemic vascular resistance
- Contractility (inotropy) = intrinsic ability of heart to contract independent of preload/afterload
- Cardiac Output = Heart Rate × Stroke Volume (normal = 5 L/min)
- Ejection Fraction (EF) = SV/EDV × 100%; normal = 55-70%
2.4 Regulation of Heart Rate
| Stimulus | Effect | Receptor |
|---|---|---|
| Sympathetic (NE) | ↑HR, ↑contractility, ↑conduction velocity | β1 receptors |
| Parasympathetic (ACh) | ↓HR, ↓AV conduction | M2 receptors |
| ↑Body temperature | ↑HR | Direct on SA node |
| Hypoxia | Initially ↑HR, then ↓ | Reflex + direct |
| Starling's reflex | ↑HR with ↑venous return | Atrial stretch receptors |
2.5 Pressure Values (FMGE-Memorize)
| Chamber/Vessel | Systolic | Diastolic |
|---|---|---|
| Right atrium | 0-8 mmHg | (mean) |
| Right ventricle | 15-25 | 0-8 |
| Pulmonary artery | 15-25 | 8-15 |
| Pulmonary capillary wedge pressure | ~8-12 mmHg (mean) | |
| Left atrium | 5-12 mmHg | (mean) |
| Left ventricle | 100-140 | 3-12 |
| Aorta | 100-140 | 60-90 |
PART 3: PATHOLOGY OF THE HEART
(Source: Robbins & Kumar Basic Pathology; Goldman-Cecil Medicine)
3.1 Ischemic Heart Disease (IHD)
Risk Factors: Hypertension, hyperlipidemia, smoking, diabetes, family history, obesity, male sex, age.
Pathogenesis: Atherosclerosis → plaque rupture → thrombosis → coronary occlusion → ischemia/infarction.
Spectrum of IHD:
- Stable angina - Fixed plaque, >70% stenosis; pain on exertion, relieved by rest
- Unstable angina - Plaque rupture + non-occlusive thrombus; ACS without troponin rise
- NSTEMI - Partial coronary occlusion; subendocardial infarction; troponin positive; no ST elevation
- STEMI - Complete occlusion; transmural infarction; ST elevation; requires urgent reperfusion
Zones of infarction:
- Zone of necrosis (center)
- Zone of injury (ST elevation on ECG)
- Zone of ischemia (T-wave changes)
Timeline of MI changes (Robbins):
| Time | Gross | Microscopic |
|---|---|---|
| 0-4 hours | None visible | Wavy fibers, edema |
| 4-12 hours | Dark mottling | Coagulative necrosis begins, contraction bands |
| 12-24 hours | Pallor | Neutrophilic infiltration |
| 1-3 days | Pale with yellow center | Neutrophils, nuclear pyknosis |
| 3-7 days | Yellow-tan, softened | Macrophage infiltration begins |
| 1-2 weeks | Yellow-tan with red borders | Granulation tissue, fibroblasts |
| 2-8 weeks | White scar forming | Dense collagen (fibrosis) |
| >2 months | White scar | Complete fibrosis |
Cardiac Biomarkers:
- Troponin I / Troponin T - most specific and sensitive; rises at 3-4 hours, peaks at 24-48 hours, returns to baseline in 7-10 days (high-sensitivity troponin detects at 1-2 hours)
- CK-MB - rises at 4-6 hours, peaks 24 hours, normal at 48-72 hours; useful for re-infarction
- Myoglobin - earliest (1-2 hours), not specific
Complications of MI:
- Arrhythmias - most common cause of death in first 24 hours
- Cardiogenic shock - loss of >40% LV mass
- Papillary muscle rupture - acute MR (2-7 days)
- Free wall rupture - hemopericardium/tamponade (3-7 days)
- Ventricular septal rupture - new harsh systolic murmur (3-7 days)
- LV aneurysm - late complication; persistent ST elevation
- Pericarditis - Dressler syndrome = weeks to months later (autoimmune)
- Mural thrombus → emboli
3.2 Heart Failure
Classification by EF (Goldman-Cecil Medicine):
| Type | EF | Features |
|---|---|---|
| HFrEF (Heart Failure with reduced EF) | ≤40% | Systolic dysfunction; dilated LV |
| HFmrEF (mildly reduced EF) | 41-49% | "Gray zone" |
| HFpEF (Heart Failure with preserved EF) | ≥50% | Diastolic dysfunction; stiff LV |
Staging (ACC/AHA):
- Stage A - Risk factors only; no structural disease; no symptoms
- Stage B - Structural disease (e.g., post-MI, LVH) but no symptoms
- Stage C - Structural disease + current/past symptoms
- Stage D - Refractory HF requiring advanced therapies
NYHA Functional Classification:
- Class I: No symptoms
- Class II: Symptoms with moderate activity
- Class III: Symptoms with minimal activity
- Class IV: Symptoms at rest
Left HF vs Right HF:
| Feature | Left HF | Right HF |
|---|---|---|
| Cause | IHD, HTN, aortic/mitral disease | Left HF, pulmonary HTN, RV infarct |
| Symptoms | Dyspnea, orthopnea, PND, pink frothy sputum | Ankle edema, ascites, RUQ pain |
| Signs | Pulmonary crackles, S3 | JVP raised, hepatomegaly, pitting edema |
3.3 Valvular Heart Disease (FMGE High-Yield)
Aortic Stenosis (AS):
- Most common: calcific/degenerative (elderly) or bicuspid aortic valve (young)
- Murmur: Harsh systolic ejection murmur; radiates to carotids; heard best in aortic area (2nd right ICS)
- Symptoms (SAD triad): Syncope + Angina + Dyspnea
- Signs: slow rising, plateau pulse (pulsus parvus et tardus); narrow pulse pressure; LV heave; absent A2
- FMGE Key: Severe AS = valve area <1 cm², gradient >40 mmHg
Aortic Regurgitation (AR):
- Causes: Rheumatic, infective endocarditis, Marfan syndrome, aortic dissection, syphilitic aortitis
- Murmur: Early diastolic (blowing, decrescendo); heard at left sternal border; Austin Flint murmur (mid-diastolic, apex)
- Pulse: Collapsing/water-hammer pulse; wide pulse pressure
- Signs: Corrigan sign, de Musset sign, Traube sign (pistol shot femoral), Quincke sign (nail pulsations)
Mitral Stenosis (MS):
- Almost always rheumatic in origin
- Murmur: Mid-diastolic with presystolic accentuation; heard best at apex in left lateral position; low-pitched
- Opening snap follows S2 closely in severe MS
- Signs: Malar flush, atrial fibrillation, loud S1, mitral facies
- Complications: AF, pulmonary HTN, right HF, infective endocarditis, systemic emboli
- FMGE Key: Normal valve area = 4-6 cm²; Mild MS >1.5 cm²; Severe MS <1 cm²
Mitral Regurgitation (MR):
- Causes: Rheumatic, MVP, IHD (papillary muscle dysfunction), infective endocarditis
- Murmur: Pansystolic (holosystolic) murmur; at apex; radiates to axilla
- Signs: Displaced, thrusting apex beat; S3 gallop; signs of pulmonary edema
Mitral Valve Prolapse (MVP):
- Most common valvular disease in Western countries
- Mid-systolic click + late systolic murmur
- Associated with Marfan syndrome
3.4 Congenital Heart Disease
Acyanotic (L→R shunts - initially):
| Defect | Features | Murmur |
|---|---|---|
| ASD | Secundum most common; fixed split S2; pulmonary plethora | Ejection systolic in pulmonary area |
| VSD | Most common CHD overall; membranous type most common | Harsh pansystolic, lower left sternal border |
| PDA | Failure of ductus arteriosus to close; bounding pulses; wide pulse pressure | Continuous "machinery" murmur (Gibson murmur) at 2nd left ICS |
Cyanotic (R→L shunts):
| Defect | Features | FMGE Key |
|---|---|---|
| Tetralogy of Fallot (ToF) | VSD + pulmonary stenosis + overriding aorta + RVH | Most common cyanotic CHD; Boot-shaped heart on CXR; squatting relieves cyanosis |
| Transposition of Great Arteries (TGA) | Aorta from RV, pulmonary artery from LV | Egg-on-string/side CXR; incompatible with life without mixing; PDA/ASD/VSD needed |
| Tricuspid Atresia | Absent tricuspid; requires ASD + VSD | |
| Total Anomalous Pulmonary Venous Return (TAPVR) | All pulmonary veins drain into systemic venous system | Snowman (figure-of-8) CXR |
Eisenmenger Syndrome: Reversal of L→R shunt to R→L due to pulmonary hypertension. Cyanosis develops late. Once established, contraindicated for surgical repair.
3.5 Cardiomyopathies
| Type | Pathology | FMGE Key |
|---|---|---|
| Dilated (DCM) | LV/biventricular dilation, systolic dysfunction | Most common (idiopathic, alcohol, viral, post-partum); S3 gallop |
| Hypertrophic (HCM) | LV/septal hypertrophy; diastolic dysfunction; outflow obstruction | AD inheritance; mutations in sarcomere proteins (MYH7, MYBPC3); sudden cardiac death in young athletes |
| Restrictive (RCM) | Stiff ventricle; filling impaired; systolic usually preserved | Amyloidosis, sarcoidosis, hemochromatosis; normal/small heart |
HCM - FMGE High-Yield:
- Outflow obstruction worsened by: vasodilators, dehydration, standing, Valsalva
- Obstruction relieved by: squatting, leg raising, beta-blockers
- Murmur: systolic ejection; increases with Valsalva
3.6 Pericardial Disease
Acute Pericarditis:
- Causes: Viral (most common - Coxsackie B), autoimmune, TB, uremia, post-MI
- Classic symptom: Sharp pleuritic chest pain relieved by sitting forward
- ECG: Diffuse concave-up (saddle-shaped) ST elevation in all leads except aVR and V1; PR depression
- Treatment: NSAIDs + colchicine
Cardiac Tamponade:
- Rapid accumulation of pericardial fluid compresses chambers
- Beck's Triad: Hypotension + Elevated JVP + Muffled heart sounds
- Kussmaul's sign: JVP rises on inspiration (paradoxical - also in constrictive pericarditis)
- Pulsus paradoxus: SBP falls >10 mmHg on inspiration
- Treatment: Pericardiocentesis
Constrictive Pericarditis:
- Causes: TB (especially in developing countries), post-viral, post-radiation
- Kussmaul's sign (positive); pericardial knock (S3-like sound); calcified pericardium on CXR/CT
- Equalization of all diastolic pressures
PART 4: PHARMACOLOGY OF THE HEART
(Source: Goldman-Cecil Medicine; Braunwald's Heart Disease)
4.1 Heart Failure Pharmacology
Drugs Used by Stage (Goldman-Cecil):
| Drug Class | Stage A | Stage B | Stage C (HFrEF) | Stage D |
|---|---|---|---|---|
| ACE Inhibitors / ARBs | ✓ | ✓ | ✓ | ✓ |
| Beta-blockers | - | ✓ | ✓ | ✓ |
| SGLT2 inhibitors | ✓ | ✓ | ✓ | - |
| ARNI (Sacubitril-Valsartan) | - | - | ✓ | ✓ |
| Mineralocorticoid antagonists (Spironolactone) | - | - | ✓ | ✓ |
| Ivabradine | - | - | ✓ | ✓ |
| Digoxin | - | - | ✓ | ✓ |
| Hydralazine + Nitrates | - | - | ✓ | ✓ |
| ICD | - | ✓ | ✓ | (✓) |
| CRT | - | - | ✓ | ✓ |
| LVAD | - | - | - | ✓ |
FMGE Key Facts:
- ARNI (Sacubitril/Valsartan) = neprilysin inhibitor + ARB; preferred over ACEi in Stage C HFrEF
- Carvedilol, Metoprolol succinate, Bisoprolol = beta-blockers with proven mortality benefit in HF
- Spironolactone/Eplerenone = aldosterone antagonists; reduce mortality in HFrEF
- SGLT2i (Dapagliflozin, Empagliflozin) = new evidence for mortality benefit regardless of diabetes status
- Ivabradine = If channel blocker; reduces HR without affecting contractility; use if HR >70 despite beta-blocker
4.2 Antihypertensives (Mechanism and Choice)
| Drug Class | Mechanism | Key Use/Notes |
|---|---|---|
| ACE Inhibitors (-pril) | Block ACE → ↓Angiotensin II → ↓aldosterone, ↓vasoconstriction | 1st line in DM nephropathy, HF, post-MI; SE: dry cough, angioedema |
| ARBs (-sartan) | Block AT1 receptor | Use when ACEi not tolerated (no cough) |
| Beta-blockers | Block β1 (HR, contractility), β2 (bronchoconstriction) | Contraindicated in asthma; 1st line in angina, post-MI, HF |
| Calcium channel blockers (CCBs) | Block L-type Ca2+ channels | Dihydropyridines (amlodipine) = vasodilation; Non-DHP (verapamil, diltiazem) = ↓HR + vasodilation |
| Thiazide diuretics | Inhibit NaCl cotransporter in DCT | 1st line in isolated systolic HTN in elderly; hypokalemia risk |
| Loop diuretics (furosemide) | Inhibit Na-K-2Cl in loop of Henle | Acute pulmonary edema, HF; most potent diuretics |
| Aldosterone antagonists | Block mineralocorticoid receptor | Spironolactone: HF, hyperaldosteronism; Eplerenone: fewer anti-androgen SEs |
| Hydralazine | Direct arteriolar vasodilator | HF in those who cannot tolerate ACEi/ARB; pregnancy-induced HTN |
| Nitrates | Release NO → ↑cGMP → venodilation | Angina; headache SE; tolerance develops |
4.3 Antiarrhythmic Drugs (Vaughan Williams Classification)
| Class | Mechanism | Examples | Used For |
|---|---|---|---|
| Ia | Na+ channel block (moderate); ↑AP duration | Quinidine, Procainamide, Disopyramide | AF, VT |
| Ib | Na+ channel block (fast); ↓AP duration | Lidocaine, Mexiletine | VT, VF (post-MI) |
| Ic | Na+ channel block (strong); no AP duration change | Flecainide, Propafenone | SVT, AF (no structural disease) |
| II | Beta-blockers | Metoprolol, Atenolol, Esmolol | AF rate control, SVT, post-MI |
| III | K+ channel block; ↑AP duration, ↑refractory period | Amiodarone, Sotalol, Ibutilide | AF, VT, VF |
| IV | CCB (non-DHP) | Verapamil, Diltiazem | SVT, AF rate control |
| Unclassified | Adenosine | Adenosine | Drug of choice for acute SVT; causes transient AV block |
| Unclassified | Digoxin | Digoxin | AF rate control; HFrEF |
Amiodarone (FMGE High-Yield):
- Broad-spectrum antiarrhythmic (Class I, II, III, IV properties)
- Most effective antiarrhythmic overall but high toxicity
- Side effects: Pulmonary fibrosis, thyroid dysfunction (hyper/hypo), corneal microdeposits, bluish skin discoloration, hepatotoxicity, peripheral neuropathy
- Prolongs QT interval → risk of Torsades de Pointes
Digoxin:
- Mechanism: Inhibits Na+/K+ ATPase → ↑intracellular Ca2+ → positive inotrope
- Vagomimetic effect on AV node → ↓HR
- Narrow therapeutic index (0.5-2 ng/mL)
- Toxicity: N/V, visual disturbances (xanthopsia = yellow vision), arrhythmias
- Toxicity worsened by: hypokalemia, hypomagnesemia, renal failure
4.4 Drugs in Acute MI
| Drug | Role |
|---|---|
| Aspirin | Immediate (160-325 mg chewed); irreversible COX-1 inhibition |
| P2Y12 inhibitors (Clopidogrel, Ticagrelor) | Dual antiplatelet with aspirin; Ticagrelor preferred in STEMI |
| Heparin/LMWH | Anticoagulation during PCI or thrombolysis |
| Beta-blockers | Reduce O2 demand; prevent arrhythmias; improve survival |
| Nitrates | Relieve chest pain; vasodilation |
| Thrombolytics (Streptokinase, tPA) | If PCI not available within 2 hours; use in STEMI <12 hours |
| ACE Inhibitors | Within 24 hours in STEMI with LV dysfunction; prevent remodeling |
| Statins | High-intensity (Atorvastatin 80 mg) - plaque stabilization |
| Morphine | Pain relief; also mild venodilation |
4.5 Drugs in Angina
| Drug Class | Effect | Notes |
|---|---|---|
| Short-acting nitrates | Venodilation (↓preload) + coronary vasodilation | Sublingual GTN for acute attacks |
| Long-acting nitrates | Prophylaxis | Nitrate tolerance - drug-free interval needed |
| Beta-blockers | ↓HR, ↓contractility → ↓O2 demand | First-line in chronic stable angina |
| CCBs (non-DHP) | ↓HR + vasodilation | Variant (Prinzmetal) angina = CCBs preferred |
| Ranolazine | Inhibits late Na+ current | Add-on; no effect on HR or BP |
| Ivabradine | ↓HR (If channel) | When beta-blockers contraindicated |
FMGE HIGH-YIELD QUICK RECALL
Murmur Summary
| Murmur | Timing | Site | Radiation |
|---|---|---|---|
| Aortic Stenosis | Systolic ejection | 2nd R ICS | Carotids |
| Aortic Regurgitation | Early diastolic | Left sternal border | - |
| Mitral Stenosis | Mid-diastolic | Apex | - |
| Mitral Regurgitation | Pansystolic | Apex | Axilla |
| MVP | Mid-systolic click + late systolic | Apex | - |
| VSD | Pansystolic | Left lower sternal border | - |
| PDA | Continuous machinery | 2nd left ICS | - |
| ASD | Ejection systolic | 2nd left ICS | - |
Congenital Heart Disease CXR
| Condition | CXR Finding |
|---|---|
| ToF | Boot-shaped heart (coeur en sabot) |
| TGA | Egg-on-string / Egg-on-side |
| TAPVR | Snowman sign (figure-of-8) |
| MS | Double right heart border; left atrial enlargement |
| ASD | Pulmonary plethora; RV enlargement |
| PDA | Enlarged LA + LV; pulmonary plethora |
Key Numbers to Memorize
- Normal EF: 55-70%
- HFrEF: EF ≤40%
- Normal mitral valve area: 4-6 cm²
- Severe MS: <1 cm²
- Severe AS: valve area <1 cm², gradient >40 mmHg
- Apex beat: 5th left ICS, 8-9 cm from midsternal line
- SA node innervation: RCA 55%, LCA 45%
- AV node innervation: RCA 90%
Sources: Gray's Anatomy for Students (Gray's); Goldman-Cecil Medicine; Braunwald's Heart Disease (Braunwald); Fuster and Hurst's The Heart, 15th Ed; Robbins & Kumar Basic Pathology
This covers the core heart content tested in FMGE across all four subjects. If you want me to go deeper on any specific topic (e.g., ECG interpretation, congenital heart disease pathophysiology, specific drug mechanisms, arrhythmia management), just ask and I'll pull the relevant textbook sections.
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