Chapter 20 – Vessels and Circulation

Structure and Function of Blood Vessels

• Three major vessel classes
  • Arteries: carry blood away from heart toward capillaries.
  • Capillaries: microscopic exchange sites between blood & tissues.
  • Veins: return blood from capillary beds back to heart.
• Companion vessels (artery–vein pairs) share pathways but differ in wall thickness, lumen diameter, and pressure profiles (Fig 20.3).

Arteries

• General trends as arteries branch away from heart
  • ↓ Lumen diameter.
  • ↓ Elastic-fiber proportion.
  • ↑ Relative proportion of smooth muscle.
• Elastic (conducting) arteries
  • Largest (diameter ≈ 2.5 cm → 1 cm).
  • Abundant elastic fibers allow stretch & recoil → maintains blood propulsion during ventricular diastole.
  • Examples: aorta, pulmonary trunk, common carotid.
• Muscular (distributing) arteries
  • Medium size (diameter ≈ 1 cm → 0.3 mm).
  • Thick smooth-muscle layer → vigorous vasoconstriction/vasodilation.
  • Distribute flow to specific organs (e.g., brachial, coronary).
• Arterioles
  • Smallest (diameter ≈ 0.3 mm → 10 µm).
  • Large arterioles: 3 tunics; small arterioles: endothelium + 1 smooth-muscle layer.
  • Maintain vasomotor tone (baseline constriction) via brainstem vasomotor center.
  • Primary regulators of systemic blood pressure & flow.

Clinical View – Atherosclerosis

• Progressive plaque (atheroma) formation in elastic & muscular arteries.
• Endothelial injury hypothesis: infection, trauma, hypertension → chronic inflammation → lipid deposition → tunica-intima thickening & lumen narrowing.
• Risk factors: hypercholesterolemia, male sex, smoking, hypertension.
• Consequences often silent until critical stenosis; interventions: angioplasty, coronary bypass.

Clinical View – Aneurysm

• Localized arterial wall dilation → high rupture risk.
• Elastic & muscular arteries lose resilience with age; common sites: aorta, cerebral arteries.

Capillaries

• Dimensions: length ≈ 1 mm; diameter ≈ 8–10 µm → RBCs travel single-file (rouleau).
• Wall: endothelium on basement membrane only → ideal for exchange.
• Types
  • Continuous: tight intercellular clefts; muscles, skin, CNS (blood–brain barrier variant has astrocyte feet & virtually no clefts).
  • Fenestrated: pores (≈ 20–100 nm); rapid fluid transfer (kidney glomeruli, intestines, endocrine glands).
  • Sinusoids: large gaps & discontinuous BM; passage of formed elements (liver, spleen, marrow).
• Capillary beds
  • Fed by metarteriole; drained by post-capillary venule.
  • True capillaries (bulk of bed) gated by pre-capillary sphincters.
  • Vasomotion: cyclical sphincter contraction/relaxation; at any time only ≈ 25 % of beds open.
  • Perfusion metric: mL min⁻¹ g⁻¹.

Veins

• Venules: 8–100 µm; post-capillary venules prime sites of diapedesis.
• Small & medium veins accompany muscular arteries; large veins (e.g., venae cavae) accompany elastic arteries.
• Most contain valves (infoldings of tunica intima) to prevent limb blood pooling.
• Blood reservoir function: ~55–60 % of blood volume resides in systemic veins; sympathetic venoconstriction shifts blood centrally during exertion or blood loss (Fig 20.6).

Pathways of Blood Vessels

• Simple pathway: one artery → capillary → one vein (typical of kidneys).
• Alternative pathways
  • Arterial anastomosis: ≥2 arteries converge (circle of Willis).
  • Venous anastomosis (more common): dorsal hand veins.
  • Arteriovenous anastomosis (shunt): thermoregulation in digits, ears.
  • Portal system: two capillary beds in series; e.g., hepatic portal, hypothalamo-hypophyseal.

Hemodynamics: Cross-Sectional Area & Flow Velocity

• Total cross-sectional area (TCSA) greatest in capillaries because of massive number → velocity minimum → maximizes exchange (Fig 20.9).
• Velocity ∝ \frac{1}{\text{TCSA}}.

Capillary Exchange

• Diffusion
  • Small solutes/O₂ /CO₂ traverse endothelial cells or clefts.
  • Large solutes (proteins) use fenestrations or sinusoid gaps.
• Vesicular transport: pinocytosis & exocytosis for hormones, fatty acids.
• Bulk flow (fluids + solutes) governed by pressure gradients.
  • Filtration: arterial end; driven by blood hydrostatic pressure (HP_b).
  • Reabsorption: venous end; driven by blood colloid osmotic pressure (COP_b).
  • Net filtration pressure: \text{NFP}= (HPb-HP{if})-(COPb-COP{if})
  • Arterial end NFP > 0 (outward); venous end NFP < 0 (inward).
• Lymphatics re-collect ≈ 15 % residual interstitial fluid, returning it to venous circulation.

Local Blood Flow Regulation

• Determinants: tissue vascularity, myogenic response, local chemicals, total flow.
• Angiogenesis: long-term ↑vessel density (training, adipose buildup, tumor growth).
  • Regression occurs when need abates.
• Myogenic response: vessel smooth muscle responds to stretch → keeps flow constant despite systemic BP swings.
• Local short-term regulation: metabolic by-products (CO₂, H⁺, K⁺, adenosine) or injury mediators (histamine, NO) cause vasodilation; endothelins, thromboxane cause constriction.

Blood Pressure, Resistance & Total Flow

• Blood pressure (BP): force exerted by blood on vessel wall.
  • Gradient (ΔP) propels flow; highest in aorta, near zero in right atrium.
• Arterial pressures
  • Systolic (SP): ventricular ejection stretch.
  • Diastolic (DP): elastic recoil.
  • Pulse pressure: PP = SP - DP (reflects arterial compliance).
  • Mean arterial pressure: MAP = DP + \frac{1}{3}PP; < 60 mm Hg → hypoperfusion risk.
• Resistance (R)
  • Factors: viscosity (η), vessel length (L), radius (r).
  • Poiseuille: R \propto \frac{\eta L}{r^4}; thus radius is most potent (doubling r ↑flow 16×).
• Total blood flow (F) equals cardiac output; relation: F \propto \frac{\Delta P}{R}.

Venous Return Mechanisms

• Skeletal muscle pump: contraction compresses deep veins; valves enforce one-way flow.
• Respiratory pump
  • Inspiration: ↓thoracic P, ↑abdominal P → venous blood drawn to thorax.
  • Expiration: reverse gradients push blood into heart.
• Both pumps augmented by exercise; stasis → pooling.

Clinical View – Deep Vein Thrombosis (DVT)

• Calf veins most common; immobility, hypercoagulable states.
• Risk of pulmonary embolism; symptoms: swelling, pain, tachycardia, fever.

Clinical View – Varicose Veins

• Dilated, tortuous superficial veins due to valve failure; factors: heredity, prolonged standing, pregnancy, obesity; in rectum → hemorrhoids.

Clinical View – Circulatory Shock

• Inadequate tissue perfusion; causes: pump failure, low venous return (hemorrhage, dehydration), venous pooling, extreme vasodilation.

Neural Regulation of BP

• Cardiovascular center (medulla)
  • Cardiac center:
  • Cardioacceleratory (sympathetic) ↑HR & contractility.
  • Cardioinhibitory (parasympathetic via CN X) ↓HR.
  • Vasomotor center (sympathetic) → vessel tone via NE; α₁ receptors cause vasoconstriction, β₂ cause vasodilation (skeletal muscle, coronary vessels).
• Baroreceptor reflexes
  • Stretch receptors in carotid sinuses (CN IX) & aortic arch (CN X).
  • ↑BP → ↑stretch → ↑baroreceptor firing → ↓sympathetic, ↑parasympathetic → ↓CO & vasodilation → BP normalization.
  • Reflex responds rapidly but adapts (ineffective long-term).
• Chemoreceptor reflexes
  • Aortic & carotid bodies sense ↑CO₂, ↓pH/O₂ → stimulate vasomotor center → ↑BP to improve gas exchange.
• Higher centers: hypothalamus (temperature, stress), limbic system (emotion) can reset BP set-point.

Hormonal Regulation of BP

• Renin–Angiotensin–Aldosterone System (RAAS)
  • Low BP/low Na⁺ → kidneys release renin → converts angiotensinogen to angiotensin I → ACE forms angiotensin II (powerful vasoconstrictor, stimulates thirst & ADH, triggers aldosterone).
• Aldosterone (adrenal cortex): ↑Na⁺ & water reabsorption → ↑blood volume/BP.
• Antidiuretic hormone (ADH): posterior pituitary; ↑water reabsorption, stimulates thirst; at high [ADH] causes vasoconstriction ("vasopressin").
• Atrial natriuretic peptide (ANP): atrial myocardium; released on stretch; promotes vasodilation & renal Na⁺/water excretion → ↓BP.

Integration

• BP homeostasis involves coordinated adjustments of CO, R, and blood volume: ↑any variable → ↑BP (Fig 20.15, 20.16).

Clinical View – Hypertension & Hypotension

• Hypertension: SP > 140 mm Hg or DP > 90 mm Hg; leads to endothelial damage, atherosclerosis, arteriolosclerosis, heart failure.
• Hypotension: SP < 90 mm Hg or DP < 60 mm Hg; symptoms: dizziness, fainting; orthostatic hypotension = transient BP drop on standing.

Blood Flow During Exercise

• Total flow rises from ≈ 5 L min⁻¹ (rest) to > 17 L min⁻¹ (strenuous).
• Redistribution
  • ↑ flow: skeletal muscle (11×), coronary vessels, skin (thermoregulation).
  • ↓ flow: kidneys, GI tract, spleen.
• Mechanisms: ↑CO, sympathetic venoconstriction mobilizing venous reservoir, local metabolites driving vasodilation in active tissues (Fig 20.17).

Pulmonary Circulation

• Pulmonary arteries/arterioles have low pressure & low resistance (RV SP ≈ 15–25 mm Hg; capillary P ≈ 10 mm Hg) → prevents edema, allows efficient O₂/CO₂ exchange.
• Vessels have less elastic CT, wider lumens, shorter length vs systemic.

Head & Neck – Cerebral Arterial Circle (Circle of Willis)

• Anastomotic ring around sella turcica; formed by posterior cerebral, posterior communicating, internal carotid, anterior cerebral, anterior communicating arteries.
• Equalizes cerebral BP & provides collateral flow if a branch occludes (Fig 20.20b).

Developmental Clinical View – Patent Ductus Arteriosus (PDA)

• Fetal ductus arteriosus fails to close → aortic blood shunts into pulmonary trunk → pulmonary hypertension + mixing of oxygenated/deoxygenated blood.
• Managed with prostaglandin-inhibitors (e.g., indomethacin) or surgical ligation.