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📚 PHASE 1 — FOUNDATION REFRESHER | WEEK 1

Heart Structure & Vessels

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🫀 DAY 1 — Gross Anatomy of the Heart: Chambers, Valves, Great Vessels, Pericardium

The Heart as a Pump

• Right heart → pumps deoxygenated blood → pulmonary circulation (low pressure)
• Left heart → pumps oxygenated blood → systemic circulation (high pressure)

🧠 Exam tip: "The heart is a two-pump circuit in series. ALL blood from RV must pass through pulmonary circulation before entering LV." - Sabiston

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4 Chambers - Key Facts

🧠 Exam tip: LV wall is 4-5x thicker than RV wall because systemic vascular resistance is much higher than pulmonary vascular resistance.

Why is the LV thicker?

• LV generates pressure ~5-7x greater than RV
• The RV is crescent-shaped and moves like a "bellows" - the septum acts as a splint
• LV contraction also assists RV function (ventricular interdependence)

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Great Vessels

🧠 Remember: Pulmonary artery is the ONLY artery that carries deoxygenated blood. Pulmonary veins are the ONLY veins that carry oxygenated blood.

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The 4 Valves

A) Atrioventricular (AV) Valves — between atria and ventricles

• Mitral valve (bicuspid) - Left side - 2 leaflets
• Tricuspid valve - Right side - 3 leaflets

B) Semilunar Valves — between ventricles and great arteries

• Aortic valve - LV → Aorta - 3 cusps
• Pulmonary valve - RV → Pulmonary artery - 3 cusps

🧠 Memory trick: "Try Before Pumping Aorta" = Tricuspid → Bicuspid (mitral) → Pulmonary → Aortic (left to right, top to bottom)

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Pericardium

• Two-layer sac surrounding the heart
• Outer layer: Fibrous pericardium (tough, protects, anchors heart to mediastinum)
• Inner layer: Serous pericardium
  • Parietal layer (lines fibrous pericardium)
  • Visceral layer = Epicardium (directly on heart surface)
• Pericardial cavity: Between parietal and visceral layers; contains ~15-50 mL of serous fluid (lubricant)

🧠 Clinical link (Exam): Excess fluid in pericardial cavity = Pericardial effusion → can compress heart → Cardiac tamponade. Treatment = pericardiocentesis.

Sketch to Draw - Day 1:

        ┌─────────────────────────────────┐
        │  PULMONARY ARTERY   AORTA       │
        │         ↑               ↑       │
        │  ┌────────┐     ┌────────────┐  │
        │  │   RV   │     │    LV      │  │
        │  │        │  ←  │  (thick    │  │
        │  └────────┘     │   wall)    │  │
        │  Pulm. valve     └────────────┘  │
        │  Tricuspid ↕    ← Mitral ↕       │
        │  ┌────────┐     ┌────────────┐  │
        │  │   RA   │     │    LA      │  │
        │  │(SVC+   │     │(Pulm veins)│  │
        │  │ IVC)   │     │            │  │
        │  └────────┘     └────────────┘  │
        └─────────────────────────────────┘

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⚡ DAY 2 — Coronary Arteries & Cardiac Conduction System

A. Coronary Arteries

Why? During systole, subendocardial vessels experience retrograde flow and compression. The coronary ostia are also partially covered by aortic valve leaflets during systole.

Two Main Coronary Arteries (arise from aortic root just above aortic valve):

🧠 Exam tip (ECG link): LAD occlusion → Anterior MI → ST elevation in V1-V4. RCA occlusion → Inferior MI → ST elevation in II, III, aVF. LCx occlusion → Lateral MI → ST elevation in I, aVL, V5-V6.

🧠 "The LAD is the widow maker" - supplies the largest territory of LV.

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B. Cardiac Conduction System

"The specialized excitatory and conductive fibers of the heart contract feebly because they contain few contractile fibrils; instead, they exhibit automatic rhythmical electrical discharge — providing an excitatory system that controls the rhythmical beating of the heart."

The Pathway (learn this in order):

SA Node → AV Node → Bundle of His → Left + Right Bundle Branches → Purkinje Fibres

Why the AV node delay matters:

• Allows atria to contract before ventricles
• Ensures atrial "kick" fills ventricle before it contracts
• This is seen on ECG as the PR interval (0.12-0.20 sec)

🧠 Conduction velocities to memorize:

• Purkinje fibres = 4 m/sec (fastest)
• Ventricular muscle = 0.3-0.5 m/sec
• AV node = 0.05 m/sec (slowest - causes the delay)

Hierarchy of Pacemakers (backup system):

Lower the pacemaker, slower the rate - this is called an escape rhythm

Clinical Link:

• SA node dysfunction → Sick Sinus Syndrome
• AV node block → Heart block (1st, 2nd, 3rd degree)
• Bundle branch dysfunction → Bundle Branch Block (BBB) on ECG

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Flowchart to Draw - Day 2:

SA Node (60-100 bpm) → [through atrial muscle → P wave on ECG]
         ↓
AV Node (delay: 0.05 m/sec) → [PR interval]
         ↓
Bundle of His
         ↓
Left Bundle Branch    Right Bundle Branch
         ↓                     ↓
Purkinje Fibres (4 m/sec) → [QRS complex on ECG — ventricular activation]
         ↓
Ventricular muscle contraction

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💓 DAY 3 — Cardiac Cycle & Physiology

What is the Cardiac Cycle?

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Two Main Phases:

1. SYSTOLE (Ventricular Contraction) - ~0.3 sec

2. DIASTOLE (Ventricular Relaxation) - ~0.5 sec

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Heart Sounds

🧠 Exam tip: "S3 = heart failure. S4 = stiff heart (hypertension, LVH)."

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Key Values to Memorize:

🧠 EF < 40% = Reduced EF heart failure (HFrEF)

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Wiggers Diagram - Key to Understanding:

1. Aortic pressure
2. LV pressure
3. LA pressure
4. LV volume
5. ECG
6. Heart sounds

• LV pressure > LA pressure → Mitral valve CLOSES (S1) → start of isovolumetric contraction
• LV pressure > Aortic pressure → Aortic valve OPENS → ejection begins
• LV pressure < Aortic pressure → Aortic valve CLOSES (S2) → start of isovolumetric relaxation
• LV pressure < LA pressure → Mitral valve OPENS → rapid filling begins

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📊 DAY 4 — Hemodynamics: Preload, Afterload, Contractility, Frank-Starling Law

Cardiac Output (CO)

• Normal CO = 4-6 L/min (at rest)
• Cardiac Index (CI) = CO / Body Surface Area (BSA) → normal = 2.5-4.0 L/min/m²

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The 3 Determinants of Stroke Volume:

1. PRELOAD

• Definition: The volume/pressure in the ventricle at the END of diastole (= EDV)
• Represents the stretch on myocardial fibers before contraction begins
• Measured clinically by: Central Venous Pressure (CVP) for RV; Pulmonary Capillary Wedge Pressure (PCWP) for LV

• Increased venous return (IV fluids, lying down, exercise)
• Slow heart rate (more time to fill)
• Increased blood volume

• Diuretics (furosemide, spironolactone)
• Vasodilators (nitroglycerin - venodilator)
• Blood loss, dehydration

🧠 Drug link: Diuretics and nitrates reduce preload → used in heart failure to reduce pulmonary congestion.

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2. AFTERLOAD

• Definition: The resistance the ventricle must overcome to eject blood (= wall tension during systole)
• For LV: determined mainly by Systemic Vascular Resistance (SVR) and aortic pressure
• For RV: determined by Pulmonary Vascular Resistance (PVR)

• Hypertension (↑ SVR)
• Aortic stenosis
• Vasoconstriction

• ACE inhibitors (ACEi) - e.g., enalapril, lisinopril
• Vasodilators (hydralazine, amlodipine)
• Sodium nitroprusside

🧠 Drug link: ACE inhibitors reduce afterload (and preload) → cornerstone treatment for heart failure and hypertension.

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3. CONTRACTILITY (Inotropy)

• Definition: The intrinsic ability of the myocardium to contract at a given preload and afterload
• Independent of preload and afterload
• Increased by: Catecholamines (adrenaline, noradrenaline), digoxin, dobutamine, Ca²⁺
• Decreased by: Beta-blockers, heart failure, myocardial ischemia, acidosis

🧠 Exam tip: Positive inotropes = increase contractility = increase SV = increase CO. Examples: digoxin, dobutamine, dopamine.

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Frank-Starling Law

"The more the heart is filled during diastole, the greater the force of contraction during systole — up to a physiological limit."

    Stroke
    Volume
      ↑         ___________  ← Normal (plateau = physiological limit)
      |       /
      |      /
      |     /
      |    /
      |___/
      +------------------------→ Preload (EDV / filling pressure)

Flowchart:

↑ Preload (EDV) → ↑ Fibre stretch → ↑ Actin-myosin overlap → ↑ Force of contraction
→ ↑ Stroke Volume → ↑ Cardiac Output

Preload ──→ Stroke Volume ──→ Cardiac Output
Afterload ─↓
Contractility ─↑
Heart Rate ─────────────────→ Cardiac Output

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🩸 DAY 5 — Blood Vessel Structure, Vascular Smooth Muscle, Arterial/Venous System

Classification of Blood Vessels

Heart → Arteries → Arterioles → Capillaries → Venules → Veins → Heart
         (high P)   (resistance   (exchange)   (collect)  (low P,
                     vessels)                             capacitance)

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A. Arterial Wall Structure — 3 Layers

🧠 Exam tip: In atherosclerosis, lipid deposition starts in the intima (as foam cells/fatty streaks). In hypertension, the media undergoes hypertrophy.

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B. Comparison: Arteries vs. Veins

🧠 Veins are capacitance vessels - they hold ~65% of total blood volume. Venodilators (nitroglycerin) shift blood to veins → reduce preload.

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C. Vascular Smooth Muscle - How Vessels Are Controlled

🧠 Drug link: ACE inhibitors block Angiotensin II → vasodilation + reduced Na retention → lower BP and afterload.

Diagram to Draw - Day 5:

ARTERY CROSS-SECTION:

         ←──── Tunica Adventitia (collagen, vasa vasorum)
         ←──── Tunica Media (smooth muscle + elastic fibres)
         ←──── Internal elastic lamina
         ←──── Tunica Intima (endothelium)
         ←──── Lumen (blood flow)

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📝 DAY 6 — WEEKLY REVISION SELF-QUIZ

1. Draw the 4-chamber heart with all valves and great vessels labeled.
2. Write the conduction pathway from SA node to Purkinje fibres with speeds.
3. Draw the Wiggers diagram labeling pressure curves, valve events, and ECG.
4. Write the formula for CO and name the 3 determinants of SV.
5. Explain Frank-Starling law in 3 sentences.
6. Name the 3 layers of an artery and their key components.

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📖 Sources: Guyton & Hall Textbook of Medical Physiology (Chapters 9 & 10), Barash's Clinical Anesthesia 9e (Chapter 12: Cardiac Anatomy and Physiology), Sabiston's Textbook of Surgery (Cardiac Physiology section)