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π« Cardiovascular System - Complete Notes
TOPIC 1 β Cardiovascular Tests & Procedures
(Merck Manual, Section 7, Ch. 75)
β‘ Electrocardiography (ECG)
- Records electrical activity of the heart - P wave (atrial depolarization), QRS (ventricular depolarization), T wave (ventricular repolarization)
- Uses: Arrhythmias, MI, hypertrophy, conduction defects, pericarditis
- 12-lead ECG - standard; captures 12 views of the heart
| ECG Finding | Think of... |
|---|
| ST elevation | STEMI / pericarditis |
| ST depression | NSTEMI / ischemia |
| Wide QRS | Bundle branch block |
| PR prolongation | 1st degree AV block |
| Delta wave | WPW syndrome |
π Echocardiography
- Ultrasound of the heart - shows structure + function in real time
- Transthoracic echo (TTE) - standard bedside probe
- Transesophageal echo (TEE) - probe goes into esophagus, better image quality (used for valves, clots, aorta)
- What it tells you: EF (ejection fraction), wall motion, valve function, pericardial effusion, septal defects
π Normal EF = 55-70%. EF < 40% = heart failure with reduced EF (HFrEF)
π¬ Cardiac Catheterization
- A catheter is inserted (usually via femoral or radial artery) and guided to the heart/coronaries
- Left heart cath - coronary angiography; identifies blockages
- Right heart cath (Swan-Ganz) - measures pulmonary pressures, cardiac output
- Indications: Chest pain, pre-CABG, valve disease workup, suspected cardiomyopathy
π Stress Testing
- Heart is stressed (exercise treadmill or pharmacologic with dobutamine/adenosine)
- ECG monitored during stress to look for ischemia
- Positive test: ST depression β₯1mm during exercise
- Nuclear stress test adds imaging (thallium/technetium) - better sensitivity
π Percutaneous Coronary Intervention (PCI)
- Balloon angioplasty + stent placed in blocked coronary artery
- Done via cardiac cath - first-line treatment for STEMI ("primary PCI")
πͺ Coronary Artery Bypass Grafting (CABG)
- Surgical bypass using saphenous vein or internal mammary artery
- For: multi-vessel disease, left main disease, failed PCI, diabetics with multi-vessel disease
β’οΈ Radionuclide Imaging
- Radioactive tracer (Tc-99m sestamibi or thallium-201) injected IV
- Shows perfusion of myocardium at rest and stress
- Cold spots on stress = ischemia; Fixed cold spots = old infarct (scar)
π Tilt Table Testing
- Patient strapped to table; tilted upright 60-80Β°
- Monitors BP and HR over 20-45 minutes
- Used for: Unexplained recurrent syncope - to reproduce vasovagal episodes
TOPIC 2 β Arteriosclerosis
(Merck Manual, Section 7, Ch. 77)
"Arteriosclerosis = hardening of the arteries" - umbrella term
Types at a Glance:
| Type | Vessels Affected | Key Feature |
|---|
| Atherosclerosis | Large/medium arteries | Plaque (lipid + fibrous cap) |
| Arteriolosclerosis | Arterioles | Hyaline or hyperplastic thickening |
| MΓΆnckeberg's sclerosis | Medium muscular arteries | Calcification in media; lumen NOT affected |
| Fibromuscular hyperplasia | Medium arteries | Intimal SMC proliferation |
Atherosclerosis (Most Important)
Core idea: Endothelial injury β lipid accumulation β plaque formation
Step-by-step pathogenesis:
- Endothelial injury (from HTN, smoking, DM, dyslipidemia)
- LDL enters intima β oxidized LDL
- Monocytes recruited β become macrophages β engulf ox-LDL β become foam cells
- Foam cells accumulate β fatty streak (earliest lesion - reversible)
- Smooth muscle cells migrate from media to intima
- Fibrous cap forms over lipid core β atheromatous plaque
- Plaque rupture β thrombus β MI / stroke
Vascular response to injury (A) and atheromatous plaque anatomy (B) - Robbins Pathology
Risk factors (modifiable): Hypertension, smoking, hypercholesterolemia, DM, obesity
Risk factors (non-modifiable): Age, male sex, family history
Complications of plaque:
- Stable angina - plaque narrows lumen, ischemia on exertion
- ACS (unstable angina / NSTEMI / STEMI) - plaque rupture + clot
- Stroke - carotid plaque
- Aneurysm - weakened media from ischemia
Non-Atheromatous Arteriosclerosis
MΓΆnckeberg's (Medial Calcification):
- Calcification of the media of muscular arteries (no lumen narrowing)
- Common in >50 years; diabetics
- Seen on X-ray as "pipe-stem" arteries or on mammography as "railroad track" calcification
- Clinically silent usually
MΓΆnckeberg sclerosis - note calcium deposits, lumen is unaffected - Robbins Pathology
TOPIC 3 β Endocarditis, Pericardial & Myocardial Diseases
(Merck Manual, Section 7, Ch. 82 & Ch. 86)
π¦ Infective Endocarditis (IE)
- Infection of heart valves / endocardium
- Most common organisms:
- Sub-acute IE - Streptococcus viridans (dental procedures)
- Acute IE - Staphylococcus aureus (IV drug users, prosthetic valves)
- HACEK organisms - gram-negative culture-negative causes
Clinical features (OSLER'S criteria - Duke Criteria):
- Fever
- New murmur (regurgitation)
- Osler's nodes (painful, fingers/toes)
- Janeway lesions (painless, palms/soles)
- Roth spots (retina hemorrhages)
- Splinter hemorrhages (under nails)
- Splenomegaly
- Embolic events (stroke, renal infarcts)
Diagnosis: Blood cultures (Γ3) + Echocardiography (TEE preferred)
Treatment: IV antibiotics 4-6 weeks; surgery if valve destruction / refractory
π« Non-Infective Endocarditis
| Type | Key Feature | Associated With |
|---|
| Libman-Sacks | Sterile vegetations on BOTH sides of mitral valve | SLE |
| Marantic (NBTE) | Small thrombus on valve leaflets | Malignancy, prolonged illness |
| Rheumatic | Mitral stenosis (late); Aschoff bodies | Group A Strep pharyngitis |
β€οΈβπ₯ Myocarditis
- Inflammation of the myocardium
- Causes: Viral (Coxsackievirus B most common), bacterial, autoimmune (SLE, sarcoid), drugs (doxorubicin)
- Features: Chest pain, fever, dyspnea, arrhythmias, heart failure
- ECG: Diffuse ST changes, tachycardia, PVCs
- Diagnosis: Echo (wall motion abnormalities), cardiac MRI (gold standard), biopsy (Dallas criteria)
- Risk: Can progress to dilated cardiomyopathy
ECG - Myocarditis / Perimyocarditis:
Note widespread ST elevation across multiple leads - characteristic of perimyocarditis
π« Pericardial Diseases
Pericarditis (Acute):
- Inflammation of the pericardial sac
- Causes: Viral (most common - Coxsackie, Echo), bacterial (TB), post-MI (Dressler's), uremia, autoimmune
- Symptoms: Sharp pleuritic chest pain - worse lying flat, better leaning forward
- ECG classic 4 stages:
- Stage 1: Diffuse ST elevation (saddle-shaped / concave) + PR depression
- Stage 2: ST returns to baseline
- Stage 3: T-wave inversion
- Stage 4: Normalization
- Treatment: NSAIDs + colchicine (first line); steroids only if refractory
π Key differentiator: Pericarditis ST elevation is diffuse (all leads) + concave (saddle-shaped); STEMI is localized + convex
Pericardial Effusion:
- Fluid accumulates in pericardial sac (normally <50 mL)
- Slowly accumulating: can tolerate up to 2L (pericardium stretches)
- Rapidly accumulating: even 200-300 mL can cause tamponade
Cardiac Tamponade:
- Fluid compresses heart β impairs filling β obstructive shock
- Beck's Triad: Hypotension + muffled heart sounds + JVD (distended neck veins)
- ECG: Electrical alternans (QRS alternating in size with each beat)
- Treatment: Pericardiocentesis (emergency drainage)
Constrictive Pericarditis:
- Fibrous scarring of pericardium β rigid shell around heart
- Causes: TB (most common globally), radiation, prior cardiac surgery
- Features: JVD, Kussmaul's sign (JVD increases with inspiration), ascites, edema
- Treatment: Pericardiectomy (surgical stripping)
TOPIC 4 β Cardiomyopathy
(Merck Manual, Section 7, Ch. 79)
3 main types - remember them by what goes wrong structurally:
Dilated = big floppy heart | Hypertrophic = thick walled | Restrictive = stiff but normal size
1. Dilated Congestive Cardiomyopathy (DCM)
- Most common (90% of cardiomyopathies)
- Ventricles dilate + thin walls β systolic dysfunction (EF drops)
- Heart can't squeeze properly
Causes (think "ABC's"):
- Alcohol (most common toxin)
- Babies (peripartum cardiomyopathy)
- Coxsackievirus (post-myocarditis)
- Drug (doxorubicin, cocaine)
- E = genetic (titin mutations, autosomal dominant) - up to 50%
Features: Dilated all 4 chambers, S3 gallop, pulmonary edema, MR/TR from annular dilation, AF
Treatment: ACE inhibitors, beta-blockers, diuretics, ICD if EF <35%, heart transplant
2. Hypertrophic Cardiomyopathy (HCM)
- Massive asymmetric septal hypertrophy β outflow tract obstruction (LVOTO)
- Diastolic dysfunction (can't relax) - not systolic
- Genetic: autosomal dominant mutations in sarcomere proteins (beta-myosin heavy chain most common)
Features:
- Young athlete with syncope on exertion or sudden cardiac death
- Harsh systolic murmur at lower left sternal border
- Murmur increases with Valsalva/standing; decreases with squatting (opposite of most murmurs)
ECG: LVH, deep narrow Q waves (pseudo-infarct pattern in lateral leads), giant T-wave inversion
Treatment: Beta-blockers or verapamil (slow heart, improve filling); avoid nitrates/digoxin; ICD for high-risk; septal myomectomy or alcohol septal ablation for obstruction
3. Restrictive Cardiomyopathy
- Least common
- Myocardium becomes stiff + non-compliant β diastolic dysfunction
- Ventricles normal size, but can't fill properly β elevated filling pressures
Causes:
- Amyloidosis (apple-green birefringence on Congo red stain)
- Sarcoidosis
- Hemochromatosis
- Radiation fibrosis
- Hypereosinophilic syndrome (LΓΆffler's)
Features: Signs of both right and left heart failure, elevated JVP, Kussmaul's sign
ECG: Low voltage despite thick walls (amyloid), conduction defects
Key comparison table:
| Feature | Dilated | Hypertrophic | Restrictive |
|---|
| Dysfunction | Systolic | Diastolic | Diastolic |
| Wall thickness | Thin | Thick (especially septum) | Normal/mildly thick |
| Chamber size | Dilated | Normal/reduced LV cavity | Normal |
| EF | Reduced | Normal or increased | Normal |
| Key cause | Alcohol, viral | Genetic (AD) | Amyloid, sarcoid |
TOPIC 5 β Shock, Diseases of the Aorta & Branches
(Merck Manual, Section 7, Ch. 74, 81; Section 6, Ch. 71, 72)
π΅ Syncope
- Transient loss of consciousness due to cerebral hypoperfusion - self-limiting, full recovery
- Types:
- Vasovagal (neurocardiogenic) - most common; triggered by pain/emotion/standing; vagal tone surges β bradycardia + vasodilation
- Orthostatic hypotension - BP drops on standing; elderly, dehydration, medications
- Cardiac syncope - arrhythmias (VT, SSS, AV block), structural (AS, HCM) - most dangerous
- Carotid sinus hypersensitivity - tight collar, head turning β carotid sinusμμ β profound bradycardia
β οΈ Sudden syncope during exertion = cardiac cause until proven otherwise
Workup: ECG, Holter monitor, echo, tilt table test, carotid sinus massage
β‘ Shock
Shock = inadequate tissue perfusion β cellular hypoxia β organ failure
| Type | Mechanism | CO | SVR | CVP | Example |
|---|
| Hypovolemic | Volume loss | β | β | β | Hemorrhage, dehydration |
| Cardiogenic | Pump failure | β | β | β | MI, severe HF, tamponade |
| Distributive (Septic) | Vasodilation | β (early) | β | β | Sepsis, anaphylaxis, neurogenic |
Clinical features of all shock: Hypotension, tachycardia, altered consciousness, cold/clammy skin (except distributive - warm)
Management principles:
- Hypovolemic: IV fluids, blood transfusion (hemorrhage)
- Cardiogenic: Inotropes (dobutamine), vasopressors (norepinephrine), mechanical support (IABP), revascularization
- Septic: Fluids + antibiotics within 1 hour + vasopressors (norepinephrine first-line)
π« Aortic Aneurysm
- Abdominal Aortic Aneurysm (AAA): Dilation >3 cm; most common below the renal arteries
- Risk: Old males, smokers, HTN, atherosclerosis
- Screening: Ultrasound in males >65 who ever smoked
- Repair when >5.5 cm or rapid growth (>1 cm/year) or symptomatic
- Thoracic Aortic Aneurysm (TAA): Associated with Marfan's, bicuspid aortic valve, syphilis
π₯ Aortic Dissection
- Tear in the intima β blood enters media β creates false lumen
- Severe tearing/ripping chest pain radiating to the back - maximal at onset
- Pulse deficit (different BP in both arms)
- Aortic regurgitation murmur (if ascending involved)
- Marfan's syndrome - classic predisposition
Stanford Classification:
| Type | Location | Treatment |
|---|
| Type A | Ascending aorta (+ arch) | Emergency surgery |
| Type B | Descending aorta only | Medical (BP control - beta-blockers); TEVAR if complications |
First-line imaging = CT angiography; give IV beta-blockers to reduce aortic wall stress
π΄ Aortitis
- Inflammation of the aorta
- Causes: Takayasu's arteritis, giant cell arteritis, syphilis (tertiary), ankylosing spondylitis
π Takayasu's Arteritis (Aortic Arch Syndrome)
- Granulomatous vasculitis of large vessels - aorta and main branches
- Affects young women (<40 yrs), more common in Asia
- "Pulseless disease" - absent radial pulses
Phases:
- Inflammatory phase: Fever, fatigue, elevated ESR/CRP
- Fibrotic/occlusive phase: Absent pulses, BP difference between arms, bruits, limb claudication, hypertension (renal artery involvement)
Diagnosis: MR angiography; ESR/CRP elevated
Treatment: Corticosteroids (first-line); methotrexate, tocilizumab for refractory; revascularization
π©Έ Abdominal Aortic Branch Occlusion
- Renal artery stenosis: Hypertension (renovascular), elevated creatinine, bruit over flank
- Celiac/SMA occlusion: Gut ischemia - "intestinal angina" (postprandial pain + weight loss)
- Iliac/femoral occlusion: Leriche syndrome = claudication + erectile dysfunction + absent femoral pulses
TOPIC 6 β Peripheral Arterial Disorders
(Merck Manual, Section 7, Ch. 87)
𦡠Peripheral Arterial Disease (PAD)
- Atherosclerosis of arteries to the limbs (mostly lower limbs)
- Symptoms:
- Intermittent claudication = reproducible calf pain on walking, relieved by rest
- Rest pain = severe disease; pain in foot at rest, worse at night, relieved by dangling leg
- Critical limb ischemia = tissue loss (ulcers, gangrene)
Signs: Cool, pale limb; absent pulses; slow capillary refill; non-healing ulcers (at pressure points / toes)
Diagnosis:
- ABI (Ankle-Brachial Index) - key diagnostic test
- Normal: >0.9
- Mild PAD: 0.7-0.9
- Moderate: 0.4-0.7
- Severe: <0.4
ABI = ankle systolic BP Γ· arm systolic BP - values <0.9 indicate PAD
Treatment:
- Lifestyle: Quit smoking (most important), exercise
- Medications: Antiplatelet (aspirin/clopidogrel), statins, cilostazol (for claudication)
- Revascularization: Angioplasty/stent or bypass surgery
βοΈ Raynaud's Syndrome
- Episodic vasospasm of digital vessels triggered by cold or stress
- Color changes: White (ischemia) β Blue (cyanosis) β Red (reactive hyperemia)
- Primary (Raynaud's disease): Young women, no underlying disease, benign
- Secondary (Raynaud's phenomenon): Associated with connective tissue disease (scleroderma most common), SLE, drugs (beta-blockers)
Treatment: Avoid cold; calcium channel blockers (nifedipine); sympathectomy if severe
π₯ Thromboangiitis Obliterans (Buerger's Disease)
- Segmental inflammatory thrombosis of small/medium arteries AND veins
- Classic patient: Young male, heavy smoker
- Affects extremities: digits, hands, feet β ulcers, gangrene
- No atherosclerosis - but strongly linked to tobacco
- Treatment: Absolute smoking cessation (only effective treatment); prostaglandins; amputation if needed
π Acrocyanosis
- Persistent, painless, bluish discoloration of hands/feet
- Benign vasospasm of cutaneous arterioles
- Worsens with cold, improves with warmth
- No tissue ischemia; no ulcers
- Distinguished from Raynaud by: persistent (not episodic) and painless
π΄ Erythromelalgia
- Opposite of Raynaud - burning, red, hot extremities
- Triggered by warmth; relieved by cold water immersion
- Associated with polycythemia vera, myeloproliferative disorders
- Treatment: Aspirin (especially in polycythemia), avoid heat
π©Έ Fibromuscular Dysplasia (FMD)
- Non-inflammatory, non-atherosclerotic disease of medium arteries
- Causes beaded appearance of renal arteries (renovascular HTN) and carotid arteries (stroke/TIA in young women)
- "String of beads" on angiography
- Treatment: Percutaneous transluminal angioplasty
π΅ Peripheral Arterial Aneurysms
- Popliteal artery - most common peripheral aneurysm
- Risk: thrombosis, embolism β limb ischemia
- Treatment: Surgical when >2 cm or symptomatic
TOPIC 7 β Peripheral Venous & Lymphatic Disorders
(Merck Manual, Section 7, Ch. 88)
π©Έ Deep Venous Thrombosis (DVT)
- Clot in deep veins (usually lower limb - femoral, popliteal, calf)
- Virchow's Triad (risk factors):
- Stasis - immobility, long flights, pregnancy
- Hypercoagulability - oral contraceptives, cancer, thrombophilia (Factor V Leiden)
- Endothelial injury - surgery, trauma
Symptoms: Unilateral leg swelling, pain, warmth, redness
Clinical rule: Use Wells Score to pre-test probability
Diagnosis:
- D-dimer - sensitive but not specific; if negative β rules out DVT
- Compression ultrasound - gold standard; non-compressibility of vein = DVT
Left: DVT present - vein doesn't compress. Right (COMP): Normal vein collapses with probe pressure
Complication: Pulmonary Embolism (PE) - clot travels to pulmonary circulation β chest pain, dyspnea, hypoxia, tachycardia; can be fatal
Treatment:
- Anticoagulation: DOACs (rivaroxaban, apixaban) first line; LMWH in cancer; warfarin
- Duration: 3-6 months provoked; β₯12 months or lifelong if unprovoked/recurrent
- IVC filter if anticoagulation contraindicated
π΄ Superficial Venous Thrombosis (SVT)
- Clot in superficial veins - visible, tender, cord-like vein
- Usually in varicose veins or after IV cannulation
- Less dangerous than DVT; can extend to DVT (especially if near saphenofemoral junction)
- Treatment: NSAIDs, compression stockings; fondaparinux if high risk of extension
π Varicose Veins
- Tortuous, dilated superficial veins - due to incompetent venous valves
- More common in women, pregnancy, prolonged standing
- Symptoms: Aching, heaviness, visible bulging veins, ankle swelling
- Complications: Skin changes (lipodermatosclerosis), venous ulcers (medial ankle)
- Treatment: Compression stockings; sclerotherapy; laser ablation; vein stripping
𦡠Chronic Venous Insufficiency & Post-Phlebitic Syndrome
- Long-term venous hypertension β valve damage (often after DVT)
- Features: Edema, skin pigmentation (hemosiderin), lipodermatosclerosis, venous ulcers (shallow, over medial malleolus, irregular border)
π Venous ulcer vs Arterial ulcer:
- Venous: Medial ankle, shallow, irregular, painless, surrounding skin changes
- Arterial: Toes/pressure points, deep, punched out, very painful, absent pulses
π§ Lymphedema
- Impaired lymphatic drainage β protein-rich fluid accumulates β non-pitting edema
- Primary: Congenital (Milroy's disease) or idiopathic
- Secondary: Most common - after lymph node dissection (breast cancer surgery), radiation, or filariasis (parasitic - Wuchereria bancrofti - worldwide)
- Features: Pitting β non-pitting edema; skin becomes thickened (peau d'orange); "Stemmer's sign" - can't pinch skin at base of second toe
- Complications: Recurrent cellulitis, lymphangiosarcoma (Stewart-Treves)
- Treatment: Complex decongestive physiotherapy (CDT), compression garments, pneumatic compression; no cure
π΅ Idiopathic Telangiectasia
- Dilated superficial capillaries/venules ("spider veins")
- Cosmetic; may be hereditary (HHT - Hereditary Hemorrhagic Telangiectasia / Osler-Weber-Rendu)
- HHT: Epistaxis + GI bleeding + pulmonary AVM
- Treatment of spider veins: Sclerotherapy or laser
π Arteriovenous Fistula (AVF)
- Abnormal connection between artery and vein (bypassing capillaries)
- Congenital or acquired (trauma, surgery - e.g., dialysis access)
- Features: Machine-like continuous murmur over site; distal ischemia; high-output heart failure (if large)
- Treatment: Surgical ligation or embolization; dialysis AVF is deliberately created and maintained
Quick Revision Summary
| Topic | Killer Fact |
|---|
| ECG | ST elevation + PR depression = pericarditis |
| Atherosclerosis | Foam cells β fatty streak β plaque β rupture β MI |
| IE | Osler's nodes (painful) vs Janeway lesions (painless) |
| Tamponade | Beck's triad + electrical alternans on ECG |
| DCM | Big floppy heart; alcohol/viral; systolic dysfunction |
| HCM | Murmur increases with Valsalva; young athlete SCD |
| Restrictive | Low voltage ECG + signs of HF = think amyloid |
| Takayasu | Young Asian woman + pulseless disease |
| Aortic dissection | Tearing chest-to-back pain; Type A = surgery |
| PAD | ABI <0.9 = PAD; ABI <0.4 = critical ischemia |
| Buerger's | Young smoker + digital gangrene; STOP SMOKING |
| DVT | Non-compressible vein on USG; treat with DOACs |
| Lymphedema | Non-pitting; secondary to breast cancer surgery most common |
*All content referenced from Merck Manual 20th Edition (2018) - Section 7, supplemented by Robbins Pathology and Braunwald's Heart Disease.*All 7 topics done! Here's what's included in your notes:
What you got:
- Topic 1 (CV Tests) - ECG interpretation table, Echo types, Cath types, Stress test, PCI vs CABG, Radionuclide imaging, Tilt table
- Topic 2 (Arteriosclerosis) - All 4 types in a comparison table, full atherosclerosis pathogenesis step-by-step, plaque structure diagram + histology image from Robbins
- Topic 3 (Endocarditis/Pericarditis/Myocarditis) - IE organisms + Duke criteria features, non-infective types, Myocarditis with a real perimyocarditis ECG, Pericarditis ECG stages, Tamponade triad, Constrictive pericarditis
- Topic 4 (Cardiomyopathy) - All 3 types with the heart diagram showing structural differences, full comparison table, HCM murmur trick (Valsalva)
- Topic 5 (Shock/Aorta) - Syncope types, Shock table (CO/SVR/CVP for each type), Aortic dissection Stanford A vs B, Takayasu phases, Leriche syndrome
- Topic 6 (Peripheral Arterial) - PAD with ABI chart and diagram, Raynaud color changes, Buerger's key points, Acrocyanosis vs Erythromelalgia, FMD
- Topic 7 (Venous/Lymphatic) - DVT with Virchow's triad + real ultrasound image, PE complication, SVT, Varicose veins, Venous vs Arterial ulcer comparison, Lymphedema, AVF