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AN5.1-8 | General features of the cardiovascular system — Part 2

Fetal Circulation and Changes at Birth (AN5.4)

Fetal Circulation — Key Features:

Figure: Fetal Circulation and Changes at Birth (AN5.4)

Fetal blood is oxygenated in the placenta (not lungs). The lungs are non-functional. Three special structures bypass:

Structure	Location	Function	Closes at birth
Umbilical vein	Umbilicus → liver → IVC	Carries oxygenated blood from placenta	Ligamentum teres hepatis
Ductus venosus	Umbilical vein → IVC	Bypasses liver sinusoids	Ligamentum venosum
Foramen ovale	Interatrial septum	RA → LA: bypasses pulmonary circulation	Fossa ovalis (functional closure at birth; anatomical by 1 year)
Ductus arteriosus	Pulmonary trunk → aorta	Bypasses pulmonary circulation from right side	Ligamentum arteriosum (by 1–3 months)
Umbilical arteries	Fetal iliac arteries → placenta	Carry deoxygenated blood TO placenta	Medial umbilical ligaments

Fetal blood oxygenation: The most oxygenated blood (from umbilical vein) flows through ductus venosus → IVC → RA → preferentially through foramen ovale (Eustachian valve directs it) → LA → LV → brain and coronary arteries (most oxygenated blood goes to most vital organs).

Changes at birth:
1. Lungs expand → pulmonary vascular resistance drops dramatically → pulmonary blood flow increases
2. Foramen ovale closes — left atrial pressure rises above right atrial (due to increased pulmonary venous return) → pushes the septum primum against the septum secundum
3. Ductus arteriosus closes — rising pO₂ + falling prostaglandins (with cord clamping) → smooth muscle contraction → functional closure within 24–48 hours; anatomical closure by 3 months
4. Umbilical vessels close — cord clamping → vessels contract

Congenital defects from failed closure:
- PDA (patent ductus arteriosus): left-to-right shunt → pulmonary hypertension; continuous machinery murmur
- ASD (atrial septal defect): patent foramen ovale — often asymptomatic; risk of paradoxical embolism
- Indomethacin closes PDA (inhibits prostaglandin synthesis); prostaglandin E1 keeps it open (used in duct-dependent congenital heart lesions)

Lymphatic System, Venous Drainage, End Arteries, and Collaterals (AN5.5–5.8)

Lymphatic System (AN5.5):

Figure: Lymphatic System, Venous Drainage, End Arteries, and Collaterals (AN5.5–5.8)

Lymph capillaries → collecting vessels → lymph nodes → lymph trunks → ducts

• Right lymphatic duct: drains right thorax, right arm, right head/neck → right venous angle
• Thoracic duct: drains everything else → left venous angle
• Functions: return interstitial fluid to blood; transport dietary fats (chylomicrons); immune surveillance (lymph nodes filter lymph)
• India: lymphatic filariasis (Wuchereria bancrofti) — most common cause of secondary lymphoedema in India; adult worms block lymphatics → elephantiasis (limbs, scrotum)

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Venous Drainage — Principles (AN5.6):

• Deep veins: accompany arteries; named similarly; have valves in limbs; drain muscle compartments



Figure: Venous Drainage — Principles (AN5.6):

• Superficial veins: lie in superficial fascia; independently named (cephalic, basilic, great saphenous, small saphenous); drain into deep veins via perforators
• Perforating veins: connect superficial to deep; valves normally allow one-way flow (superficial → deep)
• Varicose veins: valve failure in perforators → retrograde flow → superficial vein dilation
• Great saphenous vein: longest vein in body; medial aspect of leg → femoral vein at saphenofemoral junction (4 cm below inguinal ligament) — used for coronary artery bypass grafts (CABG)

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End Arteries (AN5.7):

An end artery is an artery that is the sole supply to a part with no significant anastomosis. Occlusion → infarction.

Figure: End Arteries (AN5.7):

True end arteries:
- Central artery of the retina → retinal infarction = permanent blindness
- Labyrinthine artery → cochlear/vestibular infarction
- Renal interlobular arteries (beyond arcuate) → renal infarcts

Functional end arteries (some anastomosis exists but insufficient to prevent infarction):
- Coronary arteries (in acute occlusion, collaterals insufficient acutely) → MI
- Cerebral arteries (in acute stroke, limited collaterals via Circle of Willis) → stroke
- Splenic artery branches (at splenic hilum)

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Collateral Circulation (AN5.8):

Collateral vessels are pre-existing smaller vessels that enlarge when the main artery is slowly occluded, providing an alternative supply.

Figure: Collateral Circulation (AN5.8):

• Develop best when occlusion is slow and progressive (allows time for arteriogenesis)
• Poor development with acute occlusion → infarction even if arteries are not true end arteries
• Examples:
• Coronary collaterals: develop with chronic stable angina — can partially compensate for gradual coronary stenosis
• Profunda femoris collaterals: sustain limb in chronic femoral artery occlusion (Leriche syndrome)
• Coarctation of aorta: intercostal arteries enlarge as collaterals → rib notching
• Carotid occlusion: Circle of Willis provides collateral routes to the brain