Heart failure Coronary Artery Disease Valvular Heart Disease Arrhythmias
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I now have excellent, detailed content from authoritative textbooks across all 4 topics. Let me synthesize comprehensive clinical notes.Here are your detailed clinical notes at medical student level, sourced from Textbook of Family Medicine 9e, Tintinalli's Emergency Medicine, Braunwald's Heart Disease, and Goldman-Cecil Medicine.
1. HEART FAILURE (HF)
Definition & Overview
Heart failure is a clinical syndrome resulting from the inability of the heart to meet the metabolic requirements of the body at normal filling pressures. It affects over 5 million Americans, with more than 650,000 new cases diagnosed annually and a mortality of ~50% within 5 years.
Key distinction: The term "heart failure" is preferred over "congestive heart failure" because pulmonary congestion may be absent.
Classification
By Ejection Fraction
| Type | EF | Mechanism |
|---|---|---|
| HFrEF (reduced EF) | <40-45% | Impaired LV contraction (systolic dysfunction) |
| HFmrEF (mildly reduced) | 41-49% | Intermediate |
| HFpEF (preserved EF) | ≥50% | Impaired LV relaxation/filling (diastolic dysfunction) |
ACC/AHA Staging (complements NYHA)
| Stage | Description | ~US Population |
|---|---|---|
| A | At risk, no symptoms, no LV dysfunction | >60 million |
| B | LV dysfunction, asymptomatic (= NYHA I) | ~10 million |
| C | LV dysfunction + symptoms on exertion (= NYHA II-III) | ~5 million |
| D | Symptoms at rest (= NYHA IV) | ~200,000 |
NYHA Functional Classes
- Class I: No symptoms with ordinary activity
- Class II: Slight limitation, comfortable at rest
- Class III: Marked limitation, comfortable only at rest
- Class IV: Symptoms at rest, any activity causes discomfort
Pathophysiology
The central concept is LV remodeling - stretching and dilation of the LV with progressive reduction in function, triggered by injuries including CAD, MI, hypertension, valvular disease, diabetes, anemia, and alcoholism.
Neurohormonal activation drives the process:
- RAAS activation: Angiotensin II promotes cardiomyocyte apoptosis, hypertrophy, and ventricular fibrosis; also stimulates aldosterone, which augments these effects and promotes adverse remodeling. Aldosterone "escapes" ACE inhibitor suppression, requiring selective aldosterone blockade.
- Sympathetic nervous system (SNS): Catecholamines cause myocardial toxicity via β-adrenoceptor-mediated calcium overload and suppress adrenergic receptors.
- Endothelin-1: From dysfunctional endothelium, causes vasoconstriction.
- Inflammatory cytokines: Further exacerbate endothelial dysfunction.
- Cellular level: MMPs increase leading to cardiac fibrosis; altered calcium fluxes and β-receptor down-regulation occur; metabolism shifts to glycolysis from fatty acid oxidation.
Etiology / Common Causes
- Ischemic heart disease (CAD, MI) - most common
- Hypertension (systemic)
- Valvular heart disease
- Dilated cardiomyopathy (idiopathic, alcoholic, viral, peripartum, drug-induced)
- Diabetes mellitus
- Tachycardia-induced cardiomyopathy
- Takotsubo (stress) cardiomyopathy
- High-output states: anemia, thyrotoxicosis, AV malformations, beriberi
Clinical Presentation
Symptoms:
- Dyspnea on exertion (most sensitive)
- Orthopnea (dyspnea lying flat)
- Paroxysmal nocturnal dyspnea (PND)
- Peripheral edema
- Fatigue, exercise intolerance
- Reduced urine output
Signs:
- S3 gallop (most specific for systolic HF)
- Elevated JVP
- Crackles (rales) at lung bases
- Peripheral pitting edema
- Displaced apex beat (volume-loaded ventricle)
- Hepatomegaly / hepatojugular reflux
Evaluation
- ECG: Look for ischemia, LVH, arrhythmias, bundle branch block
- Chest X-ray: Cardiomegaly, pulmonary vascular congestion, Kerley B lines, pleural effusions
- Echocardiogram: Cornerstone - assesses EF, wall motion, valves, filling pressures
- BNP / NT-proBNP: Elevated in HF; useful for diagnosis and monitoring
- Labs: CBC, BMP (electrolytes, creatinine), LFTs, thyroid function, iron studies, fasting glucose, urinalysis
- Coronary angiography: In significant LV dysfunction with suspicion of CAD
- Endomyocardial biopsy: In new-onset HF (<2 weeks) with hemodynamic compromise or failure to respond to therapy
Pharmacologic Treatment
HFrEF (Guideline-Directed Medical Therapy - "4 Pillars")
| Drug Class | Examples | Mechanism / Benefit |
|---|---|---|
| ACE inhibitors | Enalapril, lisinopril, ramipril | Block RAAS; reduce mortality 15-20%, reduce HF hospitalizations 30-35% |
| ARBs (if ACE-I intolerant) | Losartan, valsartan, candesartan | Substitute for ACE-I |
| Beta-blockers | Carvedilol, metoprolol succinate, bisoprolol | Block SNS; reduce mortality; must titrate to max tolerated dose |
| Aldosterone antagonists | Spironolactone, eplerenone | Block aldosterone escape; used in Class III-IV or post-MI |
| SGLT2 inhibitors | Dapagliflozin, empagliflozin | Reduce HF hospitalization and CV death (newer pillar) |
| ARNI | Sacubitril/valsartan (Entresto) | Neprilysin inhibitor + ARB; superior to ACE-I alone |
| Diuretics | Furosemide, torsemide | Symptom relief for fluid overload; no mortality benefit |
| Digoxin | Digoxin | Reduces symptoms and hospitalizations; no mortality benefit; narrow TI |
| Ivabradine | Ivabradine | For HR >70 in sinus rhythm on max beta-blocker |
Start beta-blocker and ACE-I at low dose and titrate up. Do not start diuretic and ACE-I simultaneously (risk of hypotension and AKI).
HFpEF
- Aggressive BP control
- Diuretics for volume overload
- Beta-blockers or non-DHP CCBs (diltiazem/verapamil)
- Treat underlying causes (HTN, CAD, AF)
Device Therapy
- ICD: Indicated when EF <35% with NYHA II-III (primary prevention) or after sustained VT/VF (secondary prevention)
- CRT (biventricular pacing): For wide QRS (>120-150 ms), EF <35%, NYHA III-IV - improves symptoms and reduces hospitalizations
- LVAD / Heart transplant: End-stage (INTERMACS 1-3) as bridge to transplant or destination therapy
2. CORONARY ARTERY DISEASE (CAD)
Definition
CAD refers to atherosclerotic narrowing of the coronary arteries, leading to a spectrum of disease from stable angina to acute coronary syndromes (ACS). It is the leading cause of death globally.
Risk Factors
| Modifiable | Non-Modifiable |
|---|---|
| Hypertension | Age (men >45, women >55) |
| Hypercholesterolemia | Male sex / postmenopausal female |
| Diabetes mellitus | Family history (1st degree relative with CAD <55M/<65F) |
| Tobacco use | Genetic factors (~40% of CAD risk) |
| Obesity (truncal) | |
| Sedentary lifestyle | |
| Cocaine use | |
| HIV / HAART |
When all modifiable risk factors are optimal, lifetime CAD risk at age 45 is <5%. With 2+ major risk factors, it rises to 50% in men and 31% in women. Modifiable risk factors account for >90% of population-attributable MI risk globally.
Pathobiology / Pathophysiology
- Atherosclerosis: Lipid-laden plaques accumulate in the intima of coronary vessels over years
- Plaque vulnerability: "Vulnerable plaques" have a thin fibrous cap, large lipid core, and rich inflammatory infiltrate
- Plaque rupture: The usual initiating event for acute MI - exposes circulating blood to thrombogenic plaque material
- Thrombus formation: Platelet aggregation and coagulation cascade → partial or complete coronary occlusion
- Superficial erosion: Up to 1/3 of MIs occur due to fibrous cap erosion rather than rupture
- Supply-demand mismatch: Stable plaques cause angina when demand exceeds supply across a fixed stenosis
Clinical Spectrum
Stable Angina (Chronic Coronary Syndrome)
- Predictable chest pain/pressure with exertion, relieved by rest or nitrates within minutes
- Typically substernal pressure, may radiate to left arm, jaw, back
- Triggered by exercise, emotion, cold, large meals
Acute Coronary Syndromes (ACS)
| Type | ECG | Troponin | Mechanism |
|---|---|---|---|
| Unstable Angina (UA) | No ST elevation | Negative | Plaque disruption, partial occlusion |
| NSTEMI | No ST elevation | Positive | Partial occlusion + myocardial necrosis |
| STEMI | ST elevation | Positive | Complete occlusion → transmural infarct |
UA and NSTEMI differ only in the presence of elevated troponin (necrosis).
Symptoms and Signs of ACS
Associated with higher likelihood of ACS:
- Radiation to right arm or shoulder (LR 2.31)
- Radiation to both arms or shoulders (LR 2.58)
- Pain associated with exertion (LR 2.81)
- Associated diaphoresis (LR 1.50)
- Pressure/squeezing sensation (LR 1.52)
Lower likelihood:
- Sharp, pleuritic, or positional pain
- Pain reproduced by palpation
Classic ischemic symptoms are not universal in either men or women. Non-classic presentations (fatigue, dyspnea, jaw/back pain) are common in diabetics, elderly, and women.
Diagnosis
- ECG: First test - ST changes, T-wave inversions, new LBBB, Q waves
- High-sensitivity troponin (hsTnI/hsTnT): Gold standard for myocardial necrosis; 0/1-hour algorithm for rapid rule-in/rule-out
- CXR: Pulmonary edema, cardiac size
- Echocardiogram: Wall motion abnormalities; assess function
- Stress testing (stable CAD): Exercise ECG, stress echo, nuclear perfusion
- Coronary CT angiography (CCTA): Non-invasive anatomic assessment
- Invasive coronary angiography: Gold standard for anatomy + guides revascularization
Management
Stable Angina - Medical Therapy
- Nitrates: Short-acting (SL NTG for acute) + long-acting (isosorbide)
- Beta-blockers: First-line anti-anginal; reduce HR, contractility, oxygen demand
- Calcium channel blockers: Alternative or add-on (especially if beta-blocker not tolerated)
- Ranolazine: Late sodium channel blocker; add-on for refractory angina
- Risk factor modification: Statins (plaque stabilization + LDL lowering), aspirin, BP control, smoking cessation
ACS - Acute Management
Anti-ischemic:
- Supplemental O2 (if SaO2 <90%), IV/SL nitrates, IV beta-blockers (if no contraindications)
Antiplatelet:
- Aspirin 325 mg loading dose (then 81 mg daily)
- P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) - dual antiplatelet therapy (DAPT)
- GPIIb/IIIa inhibitors (tirofiban, eptifibatide) in high-risk NSTEMI
Anticoagulation:
- Heparin (UFH or LMWH/enoxaparin) during ACS
Revascularization:
- STEMI: Primary PCI within 90 minutes of first medical contact is preferred; fibrinolysis if PCI unavailable within 120 min
- NSTEMI/UA: Early invasive strategy (PCI within 24-48 h) in high-risk patients; conservative strategy in low-risk
- CABG: For left main disease, multi-vessel disease with reduced EF, diabetics with multi-vessel disease
Secondary prevention (post-ACS/chronic CAD):
- Aspirin lifelong
- DAPT (at least 12 months post-ACS)
- High-intensity statin (atorvastatin 40-80 mg, rosuvastatin 20-40 mg)
- Beta-blocker (especially post-MI with reduced EF)
- ACE inhibitor/ARB (post-MI with EF <40%, HTN, or DM)
- Aldosterone antagonist (post-MI EF <40% + diabetes or HF)
3. VALVULAR HEART DISEASE (VHD)
Overview
VHD encompasses stenosis (obstruction to forward flow) and regurgitation (backward flow) of any of the 4 cardiac valves. The most clinically significant are the aortic and mitral valves.
A. AORTIC STENOSIS (AS)
Causes
- Calcific/degenerative: Most common in patients >70 years; shares risk factors with atherosclerosis
- Congenital bicuspid aortic valve: Most common in younger patients (age 40-60); 1/3 become stenotic
- Rheumatic: Uncommon in developed countries; cusp fusion after streptococcal infection
Severity (by valve area)
| Degree | Valve Area |
|---|---|
| Normal | 3.0-4.0 cm² |
| Mild AS | >1.5 cm² |
| Moderate AS | 1.0-1.5 cm² |
| Severe AS | ≤1.0 cm² |
Symptoms typically do not appear until valve area is <1/4 of normal. Valve area narrows ~0.12 cm²/year.
Classic Triad of Symptoms (and prognosis)
| Symptom | Mean Survival Without Surgery |
|---|---|
| Angina | ~5 years |
| Syncope | ~3 years |
| Heart Failure (dyspnea) | ~1-2 years |
Sudden cardiac death risk is ~5% in symptomatic severe AS patients.
Physical Exam
- Slow-rising, delayed carotid pulse (pulsus parvus et tardus)
- Harsh crescendo-decrescendo systolic ejection murmur at right 2nd intercostal space, radiating to carotids
- Soft S2 (as aortic component fades)
- S4 gallop (stiff, hypertrophied LV)
- Sustained apex beat
Management
- Asymptomatic: Serial echocardiography monitoring (every 3-5 years mild, 1-2 years moderate, annually severe)
- Symptomatic severe AS: Aortic valve replacement (AVR) - surgical (SAVR) or transcatheter (TAVR)
- TAVR: For high-surgical-risk or inoperable patients; PARTNER trial demonstrated 50.7% vs 30.7% 1-year mortality (conservative vs TAVR)
- Statin therapy: Not shown to slow AS progression
- Contraindication: Exercise stress testing in symptomatic severe AS
B. AORTIC REGURGITATION (AR)
Causes
- Valve infection (endocarditis)
- Aortic root dilation (HTN, Marfan syndrome, dissection)
- Trauma
- Congenital bicuspid valve
- Prosthetic valve dysfunction
Pathophysiology
AR causes volume overload of the LV. The LV dilates chronically to accommodate the increased volume. In chronic AR, the LV dilates slowly and patients may remain asymptomatic for years. In acute AR, sudden volume overload is poorly tolerated - the LV cannot acutely dilate, causing rapid rise in LVEDP and acute pulmonary edema.
Signs
Chronic AR (many eponymous signs of wide pulse pressure):
- Diastolic blowing murmur at left sternal border (heard in expiration, patient leaning forward)
- Wide pulse pressure (e.g., 160/40)
- Corrigan's (water-hammer) pulse - bounding carotid pulse
- De Musset's sign - head bobbing
- Quincke's sign - pulsatile nail capillary flushing
- Austin Flint murmur - low-pitched diastolic rumble at apex (severe AR)
Acute AR:
- Short diastolic murmur, soft S1, tachycardia
- Signs of pulmonary edema
Management
- Periodic echocardiography in asymptomatic severe AR
- Vasodilators (nifedipine, ACE-I) in severe AR with symptoms or LV dysfunction to reduce afterload
- Aortic valve replacement: For symptomatic patients or when LV function deteriorates (EF <55% or ESD >55 mm)
C. MITRAL STENOSIS (MS)
Causes
- Rheumatic heart disease - by far the most common cause worldwide
- (Rare) Congenital, carcinoid, calcified annulus, myxoma
Severity
- Normal mitral valve area: 4-6 cm²
- Severe MS: valve area <1 cm²
- Clinically significant: ≤1.5 cm² with NYHA III-IV symptoms or pulmonary HTN (PASP >50 mmHg at rest)
Pathophysiology
MS impedes LV filling → elevated left atrial pressure → pulmonary venous hypertension → pulmonary HTN → right heart failure. Left atrial enlargement predisposes to AF and thrombus formation with embolic stroke.
Symptoms
- Progressive dyspnea and fatigue (most common)
- Orthopnea, PND (advanced disease)
- Right HF symptoms: edema, hepatomegaly, RUQ pain (when RV fails)
- Palpitations (from AF)
- Thromboembolic stroke
Auscultation
- Loud S1 (accentuated)
- Opening snap (OS): High-pitched, early diastole; heard between LSB and apex; shorter A2-OS interval = more severe MS
- Low-pitched diastolic rumble at apex: Heard best with bell in left lateral decubitus position
- Loud P2 + RVH signs (in severe pulmonary HTN)
ECG/Imaging
- ECG: Bifid P wave in lead II (P mitrale), biphasic P in V1, AF in advanced disease
- Echo: Diastolic doming of anterior mitral leaflet (hockey-stick deformity), assess valve score (leaflet mobility, thickening, calcification, subvalvular apparatus)
- TEE: Needed pre-valvuloplasty to rule out left atrial thrombus
Treatment
- Rate control: Beta-blockers or verapamil (increase diastolic filling time)
- AF management: Rate control + anticoagulation (warfarin) to prevent stroke
- Mitral balloon valvuloplasty (percutaneous): Preferred for suitable anatomy (valve score <8, no LA thrombus, minimal MR)
- Surgical commissurotomy or MVR: For unsuitable anatomy or significant MR
- Endocarditis prophylaxis: For all rheumatic valvular disease
D. MITRAL REGURGITATION (MR)
Causes
- Primary (organic): MVP (mitral valve prolapse), rheumatic, endocarditis, chordal rupture, congenital
- Secondary (functional): LV dilation or ischemia causing annular dilation (most common cause in developed countries)
Key Exam Finding
- Holosystolic murmur at apex radiating to axilla
- Soft S1, S3 gallop
- Laterally displaced apex
Management
- Asymptomatic severe primary MR: Surgery when EF <60% or ESD >40 mm
- Secondary MR: Treat underlying cause (revascularization, HF therapy)
- Mitral valve repair preferred over replacement when feasible
E. MITRAL VALVE PROLAPSE (MVP)
- Most common valvular abnormality (~2-3% of population)
- Myxomatous degeneration of mitral leaflets
- Mid-systolic click + late systolic murmur at apex
- Generally benign; rarely causes severe MR
- Not independently associated with stroke in young patients
4. ARRHYTHMIAS
Classification by Origin (Vaughan Williams)
Atrial Rhythms
- Sinus rhythm, sinus bradycardia/tachycardia, sinus pause/arrest
- Premature atrial contractions (PACs)
- Atrial tachycardia (ectopic, multifocal)
- Atrial fibrillation (AF)
- Atrial flutter
Junctional Rhythms
- Premature junctional beats, junctional rhythm
- AV nodal reentrant tachycardia (AVNRT) - most common paroxysmal SVT
- AV conduction blocks (1st, 2nd type I Wenckebach, 2nd type II Mobitz, 3rd degree/complete)
Ventricular Rhythms
- Premature ventricular contractions (PVCs)
- Accelerated idioventricular rhythm (AIVR)
- Ventricular tachycardia (VT) - monomorphic or polymorphic
- Ventricular fibrillation (VF)
Special Rhythms
- Pre-excitation (WPW syndrome)
- AV reciprocating tachycardia (AVRT)
- Long QT syndrome
- Paced rhythms
ATRIAL FIBRILLATION (AF)
Overview
AF is the most common sustained arrhythmia; prevalence increases dramatically with age. Characterized by chaotic atrial electrical activity with irregular ventricular response.
Classification
| Type | Duration |
|---|---|
| Paroxysmal | Terminates spontaneously <7 days |
| Persistent | >7 days, requires cardioversion |
| Long-standing persistent | >12 months |
| Permanent | Rhythm control no longer pursued |
Complications
- Thromboembolic stroke: Most feared; left atrial appendage thrombus formation due to blood stasis
- Tachycardia-induced cardiomyopathy: Unrecognized AF with rapid ventricular response → LV dysfunction
Principles of Management
1. Rate Control (ventricular rate <110 bpm at rest, lenient strategy):
- Beta-blockers (metoprolol, atenolol)
- Non-DHP CCBs (diltiazem, verapamil)
- Digoxin (adjunct, especially with HF)
2. Rhythm Control (restore/maintain sinus rhythm):
- Pharmacologic cardioversion: Flecainide, propafenone (no structural heart disease); amiodarone, dofetilide (structural heart disease)
- Electrical cardioversion (DCCV): TEE first if AF >48 hours (exclude LAA thrombus)
- Catheter ablation (pulmonary vein isolation): For symptomatic, drug-refractory AF
3. Stroke Prevention (Anticoagulation):
- CHA₂DS₂-VASc score guides anticoagulation decisions
- DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) preferred over warfarin (except valvular AF)
- Left atrial appendage occlusion (WATCHMAN): For patients with high bleeding risk on anticoagulation
VENTRICULAR TACHYCARDIA (VT)
Definition
VT = ≥3 consecutive ventricular beats at rate >100 bpm with wide QRS
| Type | Feature |
|---|---|
| Non-sustained VT | <30 seconds, terminates spontaneously |
| Sustained VT | ≥30 seconds or causes hemodynamic compromise |
| Monomorphic VT | Same QRS morphology - usually from scar (post-MI, cardiomyopathy) |
| Polymorphic VT | Varying QRS - often due to ischemia or long QT |
| Torsades de Pointes | Polymorphic VT with long QT; twisting around baseline |
Management
- Hemodynamically unstable VT: Immediate synchronized DC cardioversion
- Hemodynamically stable VT: IV amiodarone, lidocaine, or procainamide
- Torsades de Pointes: IV magnesium sulfate; remove offending drug; correct electrolytes
- Recurrent VT/VF: ICD implantation (secondary prevention)
- ICD primary prevention: EF <35%, NYHA II-III (MADIT-II, SCD-HeFT criteria)
AV CONDUCTION BLOCKS
| Block | ECG Finding | Progression |
|---|---|---|
| 1st degree | PR >200 ms, all P waves conduct | Benign |
| 2nd degree Type I (Wenckebach) | Progressive PR prolongation → dropped beat | Usually benign (AV nodal) |
| 2nd degree Type II (Mobitz II) | Constant PR, sudden non-conducted P wave | Risk of complete block; pacemaker usually needed |
| 3rd degree (Complete) | P waves and QRS dissociated; escape rhythm | Pacemaker required |
ANTIARRHYTHMIC DRUGS (Vaughan Williams Classification)
| Class | Mechanism | Examples | Key Notes |
|---|---|---|---|
| Ia | Na⁺ channel block (intermediate) + K⁺ | Quinidine, procainamide, disopyramide | Prolongs QT; lupus (procainamide); avoid with LV dysfunction |
| Ib | Na⁺ channel block (fast off) | Lidocaine, mexiletine | VT in acute MI; do not affect atrial tissue |
| Ic | Na⁺ channel block (slow off) | Flecainide, propafenone | Contraindicated post-MI / structural heart disease (CAST trial) |
| II | Beta-blockade | Metoprolol, atenolol, carvedilol | Rate control AF, VT, SVT |
| III | K⁺ channel block (prolong repolarization) | Amiodarone, sotalol, dofetilide | Amiodarone: many toxicities (pulmonary, thyroid, hepatic, corneal deposits); most broad-spectrum |
| IV | Ca²⁺ channel block | Diltiazem, verapamil | Rate control AF/flutter, AVNRT |
| Other | - | Adenosine | Drug of choice for acute AVNRT termination |
| Other | - | Digoxin | Rate control; narrow therapeutic window |
The CAST trial demonstrated that Class Ic drugs (encainide, flecainide) increased mortality in post-MI patients despite suppressing PVCs - reinforcing that antiarrhythmic drugs carry proarrhythmic risk.
ICD Indications Summary
| Indication | Criteria |
|---|---|
| Secondary prevention | Survived VT/VF arrest, or syncope with inducible VT + structural heart disease |
| Primary prevention - EF-based | EF ≤35%, NYHA II-III, on optimal medical therapy >3 months, life expectancy >1 year |
| Primary prevention - post-MI | EF ≤30%, >40 days post-MI (MADIT-II) |
Sources: Textbook of Family Medicine 9e, Tintinalli's Emergency Medicine, Braunwald's Heart Disease 2 Vol Set (Cardiovascular Medicine), Goldman-Cecil Medicine (International Edition)
---Here is a summary of what each section covers:
What's in these notes:
1. Heart Failure - Covers HFrEF vs HFpEF vs HFmrEF, ACC/AHA staging (A-D) and NYHA classes, RAAS/SNS neurohormonal pathophysiology, LV remodeling, full work-up, the 4 pharmacologic pillars (ACE-I/ARB, beta-blocker, aldosterone antagonist, SGLT2i), plus device therapy (ICD, CRT, LVAD).
2. Coronary Artery Disease - Risk factors and population-attributable risk, plaque rupture/erosion mechanism, the full ACS spectrum (stable angina → UA → NSTEMI → STEMI), symptom likelihood ratios, STEMI/NSTEMI diagnostic and management pathways, revascularization strategies (PCI vs CABG), and secondary prevention drug regimens.
3. Valvular Heart Disease - Detailed clinical notes on all 5 key valvular conditions: Aortic Stenosis (classic triad, TAVR vs SAVR), Aortic Regurgitation (acute vs chronic, wide pulse pressure signs), Mitral Stenosis (rheumatic disease, valvuloplasty criteria), Mitral Regurgitation (primary vs secondary), and Mitral Valve Prolapse.
4. Arrhythmias - Full rhythm classification, AF management (rate control/rhythm control/anticoagulation/CHA₂DS₂-VASc), VT types and acute management, AV block grading, Vaughan Williams drug classification with the critical CAST trial lesson on Class Ic drugs, and ICD indications (primary and secondary prevention).
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