---

🫀 CARDIOVASCULAR SYSTEM - EXAM CRUSH GUIDE

Pathology + Medicine Combined | Pattern-Based Memory Aids + Flowcharts

---

🗺️ THE BIG PICTURE MAP (Start Here)

RISK FACTORS
(HTN, DM, Smoking, Hyperlipidemia, Family Hx)
        ↓
   ATHEROSCLEROSIS
   (Endothelial Injury → Foam Cells → Plaque)
        ↓
  ┌─────────┬──────────┬─────────┐
  ↓         ↓          ↓         ↓
 IHD    STROKE     PAD      ANEURYSM
(angina,MI)  (TIA,CVA)  (claudication) (aorta)
  ↓
MYOCARDIAL INFARCTION
  ↓
HEART FAILURE / ARRHYTHMIAS / SUDDEN DEATH

---

⚡ MODULE 1 — ATHEROSCLEROSIS

Pathophysiology Flowchart (Robbins Basic Pathology)

ENDOTHELIAL INJURY (HTN, oxidized LDL, smoking, toxins)
         ↓
  Increased permeability → LDL enters intima
         ↓
  Monocytes migrate in → become MACROPHAGES
         ↓
  Macrophages engulf oxidized LDL → FOAM CELLS
         ↓
  Fatty streak (earliest visible lesion — reversible)
         ↓
  SMC migration from media → Intima
  SMC proliferation + ECM synthesis
         ↓
  FIBROUS PLAQUE (lipid core + fibrous cap)
         ↓
  Calcification, Necrosis, Inflammation
         ↓
  COMPLICATED PLAQUE
  ├── Stable: gradual stenosis → Stable angina
  └── Unstable: PLAQUE RUPTURE → Thrombosis → ACS/MI

Fatty streak → Oxidized LDL eaten → Atheroma forms → Macrophages become foam cells

• Plaque rupture (NOT stenosis) = most common cause of MI
• Fibrous cap is thin at shoulder regions = rupture-prone
• Stable plaque = thick cap, calcified, less lipid
• Vulnerable plaque = thin cap, large lipid core, lots of macrophages

---

❤️ MODULE 2 — CARDIAC HYPERTROPHY → HEART FAILURE

Pathophysiology Flowchart (Robbins Cotran & Kumar)

---

🔄 MODULE 3 — HEART FAILURE VICIOUS CYCLE

Compensatory Response Flowchart (Katzung Pharmacology)

The Vicious Spiral (MUST KNOW)

↓ Cardiac Output
    ↙              ↘
↓ Baroreceptor     ↓ Renal blood flow
  firing
    ↓                   ↓
↑ SNS discharge     ↑ Renin → ↑ Ang II → ↑ Aldosterone
    ↓                   ↓
↑ HR, contractility  ↑ Na+/H₂O retention
    ↓                   ↓
       ↑ PRELOAD + ↑ AFTERLOAD
              ↓
    MORE ↓ Cardiac Output  ← VICIOUS CYCLE
              ↓
    Remodeling (fibrosis, hypertrophy → dysfunction)

Renin-Angiotensin-Aldosterone-System causes vasoconstriction + fluid retention → worsens HF. Drugs that block RAAS (ACEi, ARB, MRA) break the cycle.

Left vs Right Heart Failure - "BACK UP" Pattern

---

💥 MODULE 4 — MYOCARDIAL INFARCTION

Time-Based Pathology (The Classic Exam Sequence)

MI Complications - "DRESSLER + PUMP"

---

🌡️ MODULE 5 — SYSTOLIC vs DIASTOLIC HF

---

💊 MODULE 6 — DRUG TARGETS IN HF (Med School Killer Topic)

The Targets Map

         NEUROHUMORAL AXIS
              ↓
    ┌─────────┴──────────┐
    SNS                 RAAS
  β1-receptor        ACE/AT1 receptor
     ↓                    ↓
  β-BLOCKERS           ACEi / ARBs
(carvedilol,           (enalapril,
 metoprolol)           sacubitril/valsartan)
                         ↓
                    Aldosterone
                         ↓
                  MRA (spironolactone,
                       eplerenone)

  FLUID OVERLOAD → DIURETICS (furosemide, HCTZ)
  GLUCOSE pathway → SGLT2i (dapagliflozin) ← NEW 1st line
  
  INOTROPES (acute only): Dobutamine (β1), Milrinone (PDE3i)
  VASODILATORS: Nitrates (↓ preload), Hydralazine (↓ afterload)
  DIGOXIN: ↑ contractility (Na/K-ATPase inhibitor) — narrow TI

ACEi/ARB (or sacubitril-valsartan) | Beta-blocker | MRA (mineralocorticoid antagonist) | Big add: SGLT2 inhibitor

---

🚦 MODULE 7 — ANGINA PATTERNS QUICK COMPARE

---

🧠 MODULE 8 — VALVULAR DISEASE CHEAT SHEET

Stenosis vs Regurgitation Sound Pattern

Pulmonary/Aortic Stenosis = Systolic murmur Mitral/Tricuspid Stenosis = Diastolic murmur Regurgitation = OPPOSITE valve timing

---

🔬 MODULE 9 — HIGH-YIELD PATHOLOGY BUZZWORDS

---

📋 MODULE 10 — ONE-LINE MEMORY AIDS COLLECTION

Stenosis (aortic/mitral) | Arrhythmias | Dilated CMP | Left IHD | Ischaemia | Valve disease | Endocarditis | Septal defects

Carditis | Arthritis (migratory) | Sydenham's Chorea | Subcutaneous nodules | Erythema marginatum Minor: Fever, ↑ ESR/CRP, Prolonged PR interval Mnemonic = "CASES + FP"

Aspirin + Anticoagulant | Beta-blocker | Clopidogrel/P2Y12 inhibitor | Dual antiplatelet | Early PCI (door-to-balloon <90 min)

Delay (weeks later) | Dull chest pain | Diffuse ST elevation (pericarditis) | Diagnose with Echo | Drug = NSAIDs / Colchicine

---

🏁 EXAM PATTERN RECOGNITION GUIDE

"What Does the Exam Give You?" Pattern Matching

---

---

🫀 CARDIOVASCULAR PATHOPHYSIOLOGY — EXAM CRUSH MASTER GUIDE

IHD · CCF · Rheumatic Fever · Atheroma · Arteriosclerosis + More

---

═══════════════════════════════════

PART 1 — ARTERIOSCLEROSIS & ATHEROMA

═══════════════════════════════════

🔷 1A. ARTERIOSCLEROSIS — 3 Types (The Forgotten Comparison)

         ARTERIOSCLEROSIS
      (Hardening of arteries)
              │
    ┌─────────┼─────────────┐
    ▼         ▼             ▼
ATHEROSCLEROSIS  ARTERIOLOSCLEROSIS  MONCKEBERG'S
(Large/medium     (Small arteries      MEDIAL
 arteries)         & arterioles)      CALCIFICATION
    │                  │                   │
Lipid plaque      2 sub-types:        Calcium deposits
in INTIMA        ① Hyaline (benign    in MEDIA of
                    HTN, DM)           medium arteries
                 ② Hyperplastic       NO atheroma
                    (malignant HTN)    NO lumen change
                    "Onion-skin"       CLINICALLY SILENT
                                       (incidental X-ray)

---

🔷 1B. ATHEROMA (Atherosclerosis) — Complete Pathophysiology Flowchart

RISK FACTORS
┌─────────────────────────────────────────────┐
│ HTN · Smoking · DM · Hyperlipidemia         │
│ Obesity · Age · Male sex · Family Hx        │
└─────────────────────────────────────────────┘
                    ↓
         ENDOTHELIAL INJURY / DYSFUNCTION
         (Mechanical stress, oxidized LDL, toxins)
                    ↓
    ┌───────────────────────────────┐
    │  ↑ Permeability of intima     │
    │  LDL enters & oxidizes        │
    │  Monocytes adhere & migrate   │
    └───────────────────────────────┘
                    ↓
         FATTY STREAK (EARLIEST LESION)
         Macrophages engulf oxidized LDL
              → FOAM CELLS form
         T lymphocytes accumulate
                    ↓
         FIBROUS PLAQUE
         SMC migrate media → intima
         SMC proliferate + secrete ECM
         Lipid core + Fibrous cap forms
                    ↓
        COMPLICATED PLAQUE (ADVANCED)
   ┌────────────────────────────────────┐
   │ Calcification  Ulceration          │
   │ Haemorrhage    Thrombosis          │
   └────────────────────────────────────┘
        ↙                         ↘
STABLE PLAQUE              VULNERABLE PLAQUE
(Thick fibrous cap,         (Thin cap, large
 heavy calcification,        lipid core, many
 gradual stenosis)           macrophages)
        ↓                         ↓
   STABLE ANGINA            PLAQUE RUPTURE
                                  ↓
                          ACUTE THROMBOSIS
                                  ↓
                  ┌───────────────┬─────────────┐
                  ↓               ↓             ↓
              STEMI / MI      UNSTABLE      SUDDEN
                               ANGINA       DEATH

Atheroma Memory Aids:

Fat (dyslipidaemia) · Family history · Fags (smoking) · Fat (obesity) · Forty+ (age)

Fatty streak → Oxidised LDL phagocytosed → Accumulate in macrophages → Macrophages = FOAM cells

Lumen
─────────────────────────────
        FIBROUS CAP
   (Smooth muscle + collagen)
─────────────────────────────
       LIPID CORE
   (Cholesterol + necrotic
    debris + foam cells)
─────────────────────────────
   SHOULDER REGION ← Rupture-prone!
   (Macrophages, T cells, thin cap)
─────────────────────────────
        Media

---

═══════════════════════════════════

PART 2 — ISCHEMIC HEART DISEASE (IHD)

═══════════════════════════════════

🔴 2A. IHD Master Flowchart

CORONARY ATHEROSCLEROSIS (90% of IHD)
          ↓
   ┌──────┴───────┐
   ↓              ↓
STABLE         UNSTABLE/RUPTURE
(Fixed stenosis  (Plaque rupture
 >70% lumen)      + thrombus)
   ↓              ↓
STABLE         ACUTE CORONARY
ANGINA         SYNDROMES (ACS)
               ┌──────┬──────┐
               ↓      ↓      ↓
           UNSTABLE  NSTEMI  STEMI
           ANGINA

🔴 2B. Oxygen Supply vs Demand — The Core Concept

MYOCARDIAL ISCHAEMIA occurs when:

 DEMAND > SUPPLY

DEMAND ↑ by:            SUPPLY ↓ by:
• ↑ Heart rate          • Stenotic artery (atheroma)
• ↑ Contractility       • Coronary spasm (Prinzmetal)
• ↑ Wall tension        • Thrombosis
• ↑ BP (afterload)      • Anaemia (↓ O₂ carrying)
• Hypertrophy           • Tachycardia (↓ diastolic
                          filling time)

🔴 2C. Angina Types — Side-by-Side Pattern

         STABLE          UNSTABLE        PRINZMETAL
         ANGINA          ANGINA          (VARIANT)
─────────────────────────────────────────────────────
CAUSE    Fixed plaque    Plaque rupture  Vasospasm
         (>70%)          + partial       (no fixed
                         thrombus        plaque needed)

TRIGGER  Exertion        Rest OR less    REST, often
                         exertion        nocturnal
                         than before

ECG      ST ↓ (during    ST ↓ / T-wave   ST ↑
         episode)        inversion       (transient!)

TROPONIN Negative        Often +ve       Usually –ve
         
RELIEF   Rest/GTN        Partial GTN     Ca-channel
                                         blockers

TREATMENT BB + Nitrates  DAPT + Heparin  Diltiazem/
          + CCB          + PCI           Verapamil

🔴 2D. MYOCARDIAL INFARCTION — Sequence of Events

The Time-Based Pathology Table (Exam Favourite)

TIME          GROSS                HISTOLOGY            KEY EXAM POINT
─────────────────────────────────────────────────────────────────────
0–4 hrs       NORMAL               Wavy/elongated        No change on
                                   fibres (EM)           H&E! (trick Q)
                                   No H&E change

4–12 hrs      Pale / dark          Coagulative           Earliest
              mottling             necrosis begins,      VISIBLE change
                                   pyknosis, loss        on H&E
                                   of striations

12–24 hrs     Pale / mottled       Neutrophil            Neutrophils
                                   infiltration          arrive
                                   (peak day 2–3)

1–3 days      YELLOW               Dense neutrophils,    Peak necrosis
              soft centre          nuclear debris        period

3–7 days      YELLOW, SOFT         Macrophages           ⚠ HIGHEST
              (most danger!)       phagocytose           RUPTURE RISK
                                   debris

1–3 wks       Red-grey rim         Granulation tissue    Angiogenesis
                                   (vascular +           begins
                                   fibroblasts)

>6 wks        White fibrous        Dense collagen        SCAR complete
              scar                 scar, no cells        Non-contractile

N-ormal · N-eutrophils · M-acrophages · G-ranulation · S-car

MI Complications Flowchart

ACUTE MI
│
├─ 0–24h:  ARRHYTHMIAS (VF = #1 early death)
│           ↑ K+ leaks from necrotic cells → VF
│
├─ 1–3d:   CARDIOGENIC SHOCK
│           Loss >40% LV myocardium
│           ↓CO → ↓BP → ↓organ perfusion
│
├─ 3–7d:   MECHANICAL COMPLICATIONS (softening phase)
│   ├──── FREE WALL RUPTURE → Haemopericardium → TAMPONADE
│   │      (sudden death; Beck's triad: ↓BP, ↑JVP, muffled sounds)
│   ├──── PAPILLARY MUSCLE RUPTURE → Acute MR
│   │      (sudden pulmonary oedema, holosystolic murmur → axilla)
│   └──── SEPTAL RUPTURE (VSD)
│          (harsh holosystolic murmur, step-up in RV O₂)
│
├─ Days–Weeks: MURAL THROMBUS
│           Adherent to endocardium of infarcted zone
│           Risk of systemic emboli (stroke, mesenteric ischaemia)
│
├─ 2–10wks: DRESSLER SYNDROME
│           Autoimmune pericarditis post-MI
│           Fever + pleuritic chest pain + friction rub
│           Treatment: NSAIDs / Colchicine
│
└─ Months:  VENTRICULAR ANEURYSM
            Persistent ST elevation on ECG
            Paradoxical systolic bulge
            Risk of thrombus + refractory HF

---

═══════════════════════════════════

PART 3 — CONGESTIVE CARDIAC FAILURE (CCF)

═══════════════════════════════════

💙 3A. CCF Master Pathophysiology Flowchart

UNDERLYING CAUSE
┌─────────────────────────────────────────────────────┐
│ IHD · HTN · Valvular disease · Cardiomyopathy       │
│ Congenital · Myocarditis · Arrhythmia               │
└─────────────────────────────────────────────────────┘
                     ↓
          ↓ MYOCARDIAL CONTRACTILITY
          or ↑ WORKLOAD (pressure/volume)
                     ↓
             ↓ CARDIAC OUTPUT
                     ↓
         ┌───────────┴──────────┐
         ▼                      ▼
  ↓ Baroreceptor           ↓ Renal Perfusion
  firing (carotid)              ↓
         ↓                 ↑ Renin → Ang II
  ↑ Sympathetic            ↑ Aldosterone
  discharge                     ↓
  ↑ HR, contractility,     Na+/H₂O retention
  vasoconstriction              ↓
         ↓                 ↑ Circulating volume
         └─────────┬────────┘
                   ↓
          ↑ PRELOAD + ↑ AFTERLOAD
                   ↓
         CARDIAC HYPERTROPHY/DILATION
                   ↓
         FURTHER ↓ CARDIAC OUTPUT
                   ↓
              VICIOUS CYCLE → DEATH

💙 3B. LEFT vs RIGHT Heart Failure Flowchart

LEFT HEART FAILURE              RIGHT HEART FAILURE
(Most common: IHD, HTN)         (Most common CAUSE = Left HF!)
         ↓                                ↓
LV cannot pump forward          RV cannot pump forward
         ↓                                ↓
Blood backs up into             Blood backs up into
PULMONARY CIRCULATION           SYSTEMIC VENOUS circulation
         ↓                                ↓
Pulmonary venous HTN            ↑ Systemic venous pressure
         ↓                                ↓
Pulmonary oedema                Peripheral oedema
                                Hepatomegaly / ascites
SYMPTOMS:                       SYMPTOMS:
• Dyspnoea on exertion          • Pitting oedema (legs)
• Orthopnoea (2+ pillows)       • JVP elevation
• Paroxysmal nocturnal          • Hepatomegaly (tender)
  dyspnoea (PND)                • Ascites
• Pink frothy sputum            • Anorexia / nausea
• Fine crackles (lungs)         • Engorged neck veins

PATHOLOGY:                      PATHOLOGY:
• Heavy wet lungs               • Nutmeg liver
• Heart failure cells           • Congestive
  (haemosiderin-laden             splenomegaly
  macrophages)                  • Peripheral oedema
• Pulmonary oedema

Lasix (furosemide) · Morphine · Nitrates · Oxygen · Posture (sit upright)

💙 3C. Systolic vs Diastolic HF (HFrEF vs HFpEF)

              HFrEF                    HFpEF
           (Systolic)               (Diastolic)
─────────────────────────────────────────────────
EF         < 40%                    ≥ 50%

PROBLEM    Can't SQUEEZE            Can't RELAX
           (↓ contractility)        (↑ stiffness)

CAUSE      MI, Dilated CMP,         HTN, HCM,
           Myocarditis,             Old age, DM,
           Alcohol, Viral           Amyloid

WALL       Thin + Dilated           Thick + Stiff
           (Eccentric hypertrophy)  (Concentric hypertrophy)

Rx TARGET  Reduce remodelling:      Rate control,
           ACEi + BB + MRA +        Diuretics
           SGLT2i                   (treat cause)

INOTROPES? YES (in acute)           NO (may worsen)

---

═══════════════════════════════════

PART 4 — RHEUMATIC FEVER & RHD

═══════════════════════════════════

🟡 4A. Pathogenesis Flowchart (Molecular Mimicry)

Group A Streptococcus (GAS)
pharyngitis
         ↓
  2–3 week latent period
  (Antibody production time)
         ↓
Antibodies to Streptococcal M protein
CROSS-REACT with cardiac antigens
         ↓
  ┌──────────────────────────────┐
  │  Molecular Mimicry           │
  │  (Strep M protein ≈ cardiac  │
  │   sarcolemmal proteins)      │
  └──────────────────────────────┘
         ↓
T cell + Antibody-mediated
IMMUNE ATTACK on heart
         ↓
PANCARDITIS = Pericarditis
           + Myocarditis
           + Endocarditis
         ↓
ASCHOFF BODIES in myocardium
(pathognomonic!)
         ↓
With repeated attacks:
CHRONIC RHEUMATIC HEART DISEASE

🟡 4B. Acute Rheumatic Fever — JONES CRITERIA

JONES CRITERIA (Diagnosis requires 2 MAJOR or 1 MAJOR + 2 MINOR)
+ Evidence of preceding GAS infection

MAJOR CRITERIA              MINOR CRITERIA
("CASE C")                  ("FFFPPP")
─────────────────────────────────────────────────────
C arditis                   F ever
A rthritis (migratory,      F↑ ESR / CRP
  large joints — "flitting") P rolonged PR interval
S ydenham's Chorea           (1st degree AV block)
  ("St Vitus' dance")
E rythema Marginatum
  (skin — macular, central
   clearing, like a map)
S ubcutaneous Nodules
  (over bony prominences)

PLUS: Evidence of GAS infection
• ↑ ASO titre · Throat culture · Recent scarlet fever

Carditis · Arthritis · Sydenham's chorea · Erythema marginatum · Subcutaneous nodules + Fever · Prolonged PR

🟡 4C. Pathology — Morphological Features

ACUTE RHD                    CHRONIC RHD
─────────────────────────────────────────────────
ASCHOFF BODIES               VALVE SCARRING
• Myocardial foci of         • Fibrous thickening
  T-lymphocytes +             of leaflets
  plasma cells +             • Commissural fusion
  ANITSCHKOW cells           • Chordae thickening
  ("caterpillar cells")        and fusion
                             
VERRUCAE                     FISH-MOUTH / BUTTON-
• Small 1–2mm vegetations     HOLE STENOSIS
  on valve line of closure   (mitral valve — classic)
  (ALONG closure line,
  unlike IE which is on      NEOVASCULARISATION
  leaflet surface)            of valve leaflets

MACCALLUM PLAQUE             VALVES AFFECTED:
• Left atrial subendo-       Mitral > Mitral+Aortic
  cardial thickening          > Tricuspid (rare)

🟡 4D. RHD → Mitral Stenosis Chain

Repeated RF episodes
         ↓
Mitral valve leaflet fusion + thickening
         ↓
MITRAL STENOSIS (RHD = virtually ONLY cause)
         ↓
"Fish mouth" / "button hole" valve orifice
         ↓
↑ LA pressure → LA ENLARGEMENT
         ↓
   ┌─────┴──────┐
   ↓            ↓
ATRIAL        PULMONARY
FIBRILLATION  HYPERTENSION
(risk of LA     ↓
 thrombus +  Right heart
 embolism)   failure (cor pulmonale)

Opening Snap (OS) after S2
     +
Mid-diastolic rumbling murmur (at apex)
     +
Loud S1 (due to valve snapping shut)
= MITRAL STENOSIS (rheumatic)

---

═══════════════════════════════════

PART 5 — CARDIOMYOPATHIES (Bonus High-Yield)

═══════════════════════════════════

🟣 The 3 Types — Pattern Table

         DILATED (DCM)    HYPERTROPHIC (HCM)   RESTRICTIVE (RCM)
──────────────────────────────────────────────────────────────────
PATHOLOGY  Dilation +        Asymmetric septal    Stiff myocardium
           systolic dysfun.  hypertrophy          Diastolic dysfun.

CAUSE      Idiopathic (40%)  GENETIC (AD)         Amyloid, sarcoid,
           Alcohol, viral    MYH7 / MYBPC3        haemochromatosis
           myocarditis,      mutation             eosinophilia
           peripartum

SHAPE      Dilated,          Thick                Normal size /
           thin walls        asymmetric           slightly enlarged
                             septum               stiff wall

OUTFLOW    Normal            OBSTRUCTION          Normal
           (until late)      (HOCM — LVOTO)

MURMUR     S3 gallop         Systolic ejection    ↑ JVP, ↓ pulse
                             murmur               pressure

KEY Rx     ACEi + BB +       BB / Verapamil       Treat cause
           Diuretics         Avoid inotropes!     Diuretics (careful)
           SGLT2i            ICD if at risk

EXAM CLUE  Young patient     Young athlete        Congo red +
           + AF + dilated    + syncope +          birefringence
           LV on echo        septal hypertrophy   = AMYLOID

"Young athlete drops dead OR syncopes on exertion + systolic murmur that INCREASES with Valsalva/standing, DECREASES with squatting/leg raise"

---

═══════════════════════════════════

PART 6 — ENDOCARDITIS COMPARISON

═══════════════════════════════════

🔶 Endocarditis Types — Quick Pattern

          INFECTIVE (IE)      RHEUMATIC     LIBMAN-SACKS    MARANTIC
                                (RHD)          (SLE)        (Terminal)
──────────────────────────────────────────────────────────────────────
VEGETAT.  LARGE, irregular,    Small (1–2mm)  Small, sterile, Small, sterile
SIZE      friable              along closure  on BOTH sides  multiple
                               line           of leaflet

LOCATION  Atrial surface of    Closure line   Both surfaces  Any valve
          AV valves;           of mitral      of mitral
          ventricular          valve          valve
          surface of
          semilunar

ORGANISM  Strep viridans       NONE           NONE           NONE
          (dental); Staph      (immune)       (immune)       (debilitating
          aureus (IV drug);                                   illness)
          Strep bovis
          (colon cancer link!)

KEY EXAM  Roth spots,          Aschoff        SLE patient,   Cancer/
FEATURES  Osler nodes,         bodies,        antiphospholipid cachexia
          Janeway lesions,     caterpillar    syndrome       patient
          splinter haemorrhages cells, mitral
                               stenosis

Fever · Roth spots (retina) · Osler nodes (painful, fingers) · Murmur · Janeway lesions (painless palms) · Anaemia · Nail (splinter haemorrhages) · Emboli (septic)

---

═══════════════════════════════════

PART 7 — TREATMENT FLOWCHARTS

═══════════════════════════════════

💊 STEMI Management — "TIME = MUSCLE"

STEMI Diagnosed (ST elevation + symptoms)
         ↓
   IMMEDIATE (within 10 minutes):
   Aspirin 300mg + P2Y12 inhibitor (ticagrelor/clopidogrel)
   + Anticoagulation (heparin/fondaparinux)
   + O₂ only if SpO₂ <94%
   + GTN if no hypotension
         ↓
   REPERFUSION STRATEGY:
   ┌─────────────────────────────┐
   │  PCI available?             │
   │  YES → Primary PCI          │
   │        (door-to-balloon     │
   │         <90 mins)           │
   │  NO → Thrombolysis          │
   │        (within 12h onset)   │
   │        Streptokinase/       │
   │        Alteplase            │
   └─────────────────────────────┘
         ↓
   SECONDARY PREVENTION:
   DAPT (12 months)
   Beta-blocker (reduce remodelling)
   ACEi/ARB (reduce remodelling, ↓ mortality)
   Statin (stabilise plaque, ↓ LDL)
   +/– Eplerenone (if EF <40%)

💊 CCF/HFrEF Treatment — The "A-BOMB" Rule

ALL HFrEF PATIENTS (EF <40%) get:

A — ACEi (or ARB, or sacubitril/valsartan)
    ↓ Afterload, ↓ remodelling, ↓ mortality

B — Beta-Blocker (carvedilol, bisoprolol, metoprolol)
    ↓ HR, ↓ remodelling, ↓ sudden death
    
M — MRA (spironolactone or eplerenone)
    ↓ Aldosterone effects, ↓ fibrosis
    
+SGLT2 inhibitor (dapagliflozin / empagliflozin)
    New 1st line — reduces HF hospitalisation

+ DIURETICS for symptoms (furosemide for oedema)

For refractory/advanced HF:
+ Ivabradine (if HR >70 in sinus rhythm)
+ Hydralazine + Isosorbide dinitrate (if ACEi intolerant)
+ ICD (if EF <35% despite 3 months Rx)
+ CRT (if LBBB + EF <35%)

---

═══════════════════════════════════

PART 8 — ONE-PAGE BUZZ-WORD MAP

═══════════════════════════════════

---

═══════════════════════════════════

PART 9 — EXAM PATTERN RECOGNITION

═══════════════════════════════════

QUESTION GIVES YOU:               THINK:
──────────────────────────────────────────────────────────
Young + sore throat + 3 wks later  RHEUMATIC FEVER
fever, migratory arthritis,         (Jones criteria!)
carditis

↑ ASO titre + 1st degree AV block  RF minor criteria
+ fever

Mid-diastolic rumble + opening snap MITRAL STENOSIS
+ AF + history of RF                (RHD)

Acute MI + day 5 + sudden           PAPILLARY MUSCLE
holosystolic murmur + pulmonary     RUPTURE → acute MR
oedema

Acute MI + day 5 + harsh            VENTRICULAR SEPTAL
holosystolic murmur + right heart   RUPTURE (VSD)
strain + step-up in RV O₂

Acute MI + sudden drop in BP +      FREE WALL RUPTURE
JVP rising + muffled sounds         → TAMPONADE

Persistent ST elevation 3 months    VENTRICULAR
post-MI + paradoxical wall motion   ANEURYSM

Young athlete + syncope +           HCM (HOCM)
↑ murmur with Valsalva

Fever + new murmur + IV drug user   INFECTIVE
or recent dental work               ENDOCARDITIS
+ Osler nodes + Roth spots

SLE patient + valve vegetations     LIBMAN-SACKS
on both sides                       ENDOCARDITIS

Elderly + calcific aortic stenosis  NORMAL WEAR
(crescendo-decrescendo murmur       (NOT rheumatic)
radiating to neck)

Marfan / Syphilis patient +         AORTIC
early diastolic murmur              REGURGITATION

---