Anatomy and Physiology of the Vascular System

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The vascular system is a closed network of arteries, arterioles, capillaries, venules, and veins that delivers oxygen and nutrients, removes metabolic waste, transports hormones, and maintains blood pressure and tissue perfusion. Its performance depends on vessel wall structure (especially smooth muscle and elastin), endothelial signalling, and coordinated neural–hormonal control of vascular tone and blood volume.

🏗️ 1) Vascular Anatomy: The “Tree” from Heart to Tissue and Back

• Arteries → carry blood away from the heart under high pressure.
• Arterioles → the main resistance vessels; regulate flow into each organ.
• Capillaries → the main exchange vessels; nutrients/gases/waste cross here.
• Venules → collect blood from capillary beds; important in inflammation.
• Veins → low-pressure capacitance vessels that return blood to the heart.

💡 Clinical frame: arteries determine pressure, arterioles determine distribution, capillaries determine exchange, and veins determine volume reserve.

🧱 2) Vessel Wall Structure (Shared Blueprint)

• Tunica intima:
  • Endothelium + basement membrane.
  • Key role in thrombosis control, inflammation, and vasomotor tone.
• Tunica media:
  • Vascular smooth muscle + elastin/collagen.
  • Controls vasoconstriction/vasodilation (thus resistance and BP).
• Tunica adventitia:
  • Connective tissue; contains vasa vasorum (for large vessels) and nerves.

🟥 3) Arteries: Types and Functional Specialisation

🟧 Elastic (Conducting) Arteries

• Examples: aorta, pulmonary artery, common carotids.
• High elastin content → “Windkessel” effect:
  • Stretch in systole stores energy.
  • Recoil in diastole maintains forward flow and diastolic pressure.

🟨 Muscular (Distributing) Arteries

• Examples: femoral, radial, coronary arteries.
• More smooth muscle → regulate regional distribution of blood flow.

🟥 Arterioles (Resistance Vessels)

• Small lumen + thick smooth muscle.
• Primary determinant of systemic vascular resistance (SVR) and therefore arterial BP.
• Highly responsive to:
  • Sympathetic tone (α1 constriction)
  • Local metabolites (adenosine, CO₂, H⁺, K⁺, lactate)
  • Endothelial factors (NO, endothelin)

🟦 4) Capillaries and Microcirculation (Where Exchange Happens)

Capillaries are single-layer endothelial tubes designed for diffusion and bulk flow. Exchange occurs across the endothelial barrier and its glycocalyx, driven by concentration gradients and pressure gradients.

🔬 Capillary Types

• Continuous (tight junctions, low permeability): skeletal muscle, skin, lung, CNS (BBB is specialised).
• Fenestrated (pores increase permeability): kidney, endocrine glands, small intestine.
• Sinusoidal/Discontinuous (very permeable): liver, spleen, bone marrow.

🚪 Precapillary Sphincters and Flow Distribution

• Local smooth muscle at capillary entrances.
• Direct flow to areas with high metabolic demand (e.g., working muscle).

💧 Starling Forces (Fluid Movement)

Fluid movement across capillaries reflects a balance between hydrostatic pressure pushing fluid out and oncotic pressure pulling fluid in. When outward forces exceed inward forces, net filtration occurs → interstitial fluid; lymphatics return excess fluid to circulation.

• Increased capillary hydrostatic pressure (e.g., heart failure, venous obstruction) → oedema.
• Reduced plasma oncotic pressure (e.g., low albumin from liver disease, nephrotic syndrome) → oedema.
• Increased capillary permeability (e.g., inflammation, sepsis) → protein-rich oedema.
• Lymphatic obstruction (e.g., malignancy, filariasis) → lymphoedema.

🟪 5) Venous System (Capacitance and Return)

• Veins contain most of the blood volume at rest (capacitance reservoir).
• Thin walls, larger lumen, lower smooth muscle than arteries.
• Valves (especially in legs) prevent backflow.

⬆️ Venous Return: How Blood Gets Back to the Heart

• Skeletal muscle pump + valves (walking compresses deep veins).
• Respiratory pump: inspiration lowers intrathoracic pressure → draws venous blood to thorax.
• Sympathetic venoconstriction increases stressed volume → boosts venous return and preload.

📌 Clinical link: venodilation (e.g., nitrates) reduces venous return (preload) → helpful in angina and pulmonary oedema.

🧠 6) Control of Vascular Tone (Who Sets the Diameter?)

🧬 Endothelium (A “Hidden Endocrine Organ”)

• Nitric oxide (NO) → vasodilation (↑ cGMP), inhibits platelet aggregation.
• Prostacyclin (PGI₂) → vasodilation + anti-platelet effect.
• Endothelin-1 → potent vasoconstrictor.
• ACE/Angiotensin signalling interacts with endothelial tone and remodelling.

🧠 Neural Control

• Sympathetic:
  • α1 receptors → vasoconstriction (skin, gut, kidney).
  • β2 receptors → vasodilation (skeletal muscle, mainly via adrenaline).
• Parasympathetic: minimal direct effect on most systemic vessels (exceptions in specific beds).

🧪 Hormonal Control

• RAAS: angiotensin II constricts; aldosterone retains salt/water.
• ADH (vasopressin): vasoconstriction at higher concentrations + water retention.
• ANP/BNP: vasodilation + natriuresis.

❤️ 7) Haemodynamics: The Core Relationships

Key equations explain many bedside phenomena:

• Blood pressure: MAP ≈ CO × SVR
• Flow: Q = ΔP / R
• Resistance: (Poiseuille) R ∝ 1 / r⁴ → tiny radius change massively alters resistance.
• Shear stress stimulates NO release → adaptive vasodilation.

🩺 Pulse Pressure and Arterial Stiffness

• Pulse pressure rises with arterial stiffness (e.g., ageing, atherosclerosis).
• Loss of elastic recoil → higher systolic and lower diastolic pressures.

🧫 8) Lymphatics (Often Forgotten, Always Important)

• Return excess interstitial fluid and proteins to circulation.
• Central for immune surveillance (lymph nodes).
• Failure → lymphoedema (classically non-pitting later on, skin thickening).

⚠️ 9) Clinical Correlations (High-Yield)

• Atherosclerosis: endothelial dysfunction + lipid deposition → plaque; can reduce flow or rupture → thrombosis.
• Shock states:
  • Hypovolaemic: low preload → low CO.
  • Cardiogenic: pump failure → low CO, high filling pressures.
  • Distributive (sepsis): low SVR from vasodilation + leak.
• Hypertension: chronic arteriolar constriction/remodelling increases SVR; damages end organs via shear and microvascular injury.
• Venous disease: valve failure → venous hypertension → oedema, varicosities, ulcers (gaiter area).
• DVT/PE: venous stasis + endothelial injury + hypercoagulability (Virchow’s triad).

📊 Quick Revision Table

📝 Summary

Vascular physiology is the integration of structure (intima–media–adventitia), tone control (endothelium, autonomics, hormones), and haemodynamics (pressure–flow–resistance). Arterioles are the main resistance regulators, capillaries are the main exchange sites, and veins are the main volume reservoirs. Most clinical vascular problems can be framed as failures of tone (shock), wall integrity (atherosclerosis/aneurysm), or fluid balance (oedema).