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.