Cardiovascular Physiology – Vascular Hemodynamics & Blood Pressure (Ch 19, p 714–719)

Venous Structure & Function

• Venous valves
  • Prevent retrograde blood flow; maintain unidirectional movement toward the heart.
  • Formed by folds of the tunica intima resembling semilunar flaps.
  • Especially numerous in the limbs where gravity opposes return.
• Blood distribution in systemic circuit
  • Veins = low-pressure, high-capacity “blood reservoirs.”
  • Contain a markedly larger proportion of blood volume than arteries at any given time.

Vascular Anastomoses (“Coming Together”)

• Arterial anastomoses
  • Merge branches supplying the same region → create collateral channels.
  • Protect tissues: if one branch occludes, alternate route sustains perfusion.
  • Common around joints (movement can kink vessels), abdominal viscera, heart, brain (e.g., cerebral arterial circle).
  • Poor/absent in retina, kidneys, spleen → ischemia here ⇒ rapid cell death.
• Arteriovenous anastomoses
  • Exemplified by metarteriole-thoroughfare shunts bypassing capillary beds.
• Venous anastomoses
  • More numerous & freely interconnecting than arterial ones.
  • Surface example: dorsal hand veins visible through skin.
  • Vessel occlusion rarely fatal; alternate drainage abundant.

Big-Picture Circulatory Dynamics

• Heart = pump; arteries = pressure reservoirs/conduits; arterioles = resistance vessels controlling distribution; capillaries = exchange sites; veins = reservoirs & conduits back to heart.
• Blood must continually circulate to sustain life; regulation of pressure & flow is analogous to climbing a mountain—challenging conceptually but rewarding once understood.

Key Hemodynamic Definitions

• Blood flow (F)
  • Volume of blood moving through a vessel, organ, or entire circulation per unit time (mL/min).
  • For whole system at rest, F = CO (cardiac output) ≈ constant, but organ-specific flow varies with metabolic demand.
• Blood pressure (BP)
  • Force per unit area exerted on vessel wall by blood (mm Hg).
  • Unless stated, refers to systemic arterial pressure in large arteries near the heart.
  • Drives blood from high → low pressure regions.
• Resistance (Total Peripheral Resistance, TPR)
  • Opposition to flow from friction within systemic vessels.
  • Sources:
  • Blood viscosity
  • Total vessel length
  • Vessel diameter (most dynamic/important)

Sources of Resistance—Detailed

• Viscosity (η)
  • “Thickness / stickiness.”
  • ↑ η (e.g., polycythemia) ⇒ ↑ TPR ; ↓ η (e.g., anemia) ⇒ ↓ TPR.
  • Generally constant short-term.
• Total blood vessel length (L)
  • Longer path ⇒ more cumulative friction.
  • Growth from infancy to adulthood ↑ L, therefore ↑ BP.
• Radius/diameter (r, d)
  • Friction concentrated at wall; smaller radius → larger % of blood in contact.
  • Mathematical rule: R \propto \frac{1}{r^4}
  • Doubling radius ⇒ \frac{1}{16} original resistance.
  • Tripling radius ⇒ \frac{1}{81} original, etc.
  • Small arterioles (dynamic r) = major TPR regulators.
• Turbulence
  • Caused by abrupt diameter change, rough surfaces (e.g., atherosclerotic plaques).
  • Converts laminar → turbulent flow → dramatically ↑ TPR.

Flow–Pressure–Resistance Relationship

• Core equation: F = \frac{\Delta P}{TPR}
  • (\Delta P) = pressure gradient between two points.
• Locally, diameter (→ TPR) is most effective variable to alter flow because systemic BP may remain unchanged.

Systemic Blood Pressure Profile

• Highest at aorta (~120 mm Hg systolic).
• Steepest drop across arterioles (greatest resistance site).
• Approaches 0 mm Hg at right atrium.
• Arterial pressures
  • Systolic (SBP) ≈ 120 mm Hg (ventricular ejection peak).
  • Diastolic (DBP) ≈ 70–80 mm Hg (elastic recoil during relaxation).
  • Pulse pressure (PP) = SBP – DBP (felt as arterial “pulse”).
  • Mean arterial pressure (MAP) = DBP + \frac{PP}{3}
  • Example: 120/80 ⇒ MAP = 80 + \frac{40}{3} = 93 \text{ mm Hg}.
  • Atherosclerosis stiffens arteries → chronically ↑ PP.
• Capillary pressure
  • Entry ~35 mm Hg → exit ~17 mm Hg.
  • Low pressure prevents rupture & limits filtrate loss.
• Venous pressure
  • Non-pulsatile; gradient ~15 mm Hg from venules to venae cavae.
  • Very low due to energy dissipation by TPR.

Clinical Assessment: Pulses & BP

• Pulse points / pressure points (Fig 19.8): radial (most common), carotid, temporal, brachial, femoral, popliteal, posterior tibial, dorsalis pedis, etc.
  • Compression of these points can control distal hemorrhage.
• Auscultatory BP measurement (sphygmomanometer)
  1. Cuff above elbow; inflate > SBP to occlude flow.
  2. Release pressure slowly while auscultating brachial artery.
  3. First Korotkoff sound = SBP; disappearance of sound = DBP.

Venous Return Mechanisms

• Muscular pump (Fig 19.9)
  • Skeletal muscle contractions squeeze deep veins → unidirectional “milking.”
• Respiratory pump
  • Inspiration ↑ abdominal pressure & ↓ thoracic pressure → venous blood moves superiorly.
• Sympathetic venoconstriction
  • α-adrenergic activation contracts venous smooth muscle, reducing capacitance & propelling blood toward heart.
• These mechanisms ↑ venous return ⇒ ↑ EDV ⇒ ↑ SV (Frank-Starling) ⇒ ↑ CO.

Blood Pressure Regulation—Key Variables (Fig 19.10)

• MAP determinants
  • MAP = CO \times TPR
  • CO = Heart rate × Stroke volume.
  • TPR governed mainly by arteriolar diameter.
  • Blood volume modulates SV; kidneys provide long-term control.
• Increasing any of the following can acutely raise MAP:
  • HR (via SA node influence)
  • SV (via contractility & venous return)
  • Blood viscosity, vessel length, arteriolar constriction

Short-Term Neural Regulation

• Cardiovascular center (medulla)
  • Integrates cardiac (cardioacceleratory & cardioinhibitory) and vasomotor center outputs.
  • Sympathetic vasomotor fibers (T1–L2) maintain vasomotor tone (baseline arteriolar constriction).
• Baroreceptor reflexes
  • Stretch receptors in carotid sinuses, aortic arch, large neck/thorax arteries.
  • ↑ BP → ↑ baroreceptor firing → medullary inhibition of sympathetic & activation of parasympathetic pathways:
  • Vasodilation (↓ TPR)
  • ↓ HR & contractility (↓ CO)
  • Net ↓ MAP toward set-point.
  • ↓ BP has opposite effect: enhanced sympathetic drive → vasoconstriction & ↑ CO.
• Chemoreceptor/higher-center influences (briefly noted)
  • CO₂, H⁺, O₂ levels, hypothalamus, cortical input can reset or override reflexes (e.g., exercise, fight-or-flight).

Quick Numerical Explorations (from “Apply” boxes)

• Vasoconstriction to one-third diameter
  • Radius → (\frac{1}{3}); Resistance R{new} = \left(\frac{1}{3}\right)^{-4} = 81 \times R{old}
  • Flow ↓ to \frac{1}{81} (assuming constant (\Delta P)).
• Comparing tubes
  • Short, wide straw analogy: lowest resistance = highest flow; long, narrow straw = highest resistance.

Ethical / Clinical / Real-World Connections

• Occupational hazards: prolonged standing (hairdressers, cashiers) → venous pooling, edema, fainting.
• Polycythemia in athletes or high-altitude dwellers boosts O₂ capacity but raises viscosity & BP.
• Early detection of atherosclerosis crucial; plaque-induced turbulence ↑ afterload & risk of clotting.
• Vital signs (temperature, respiratory rate, pulse, BP) provide rapid snapshot of cardiovascular & systemic health.

High-Yield Equations & Constants

• F = \frac{\Delta P}{TPR}
• R \propto \frac{\eta L}{r^4}
• MAP = DBP + \frac{PP}{3}
• \Delta P = CO \times TPR
• Normal adult reference values
  • SBP ≈ 120 mm Hg; DBP ≈ 80 mm Hg; PP ≈ 40 mm Hg; MAP ≈ 93 mm Hg.
  • Capillary entry ≈ 35 mm Hg; venous gradient ≈ 15 mm Hg.

Summary & Integration

• Venous valves and low-pressure adaptations safeguard venous return despite gravity.
• Anastomoses provide critical redundancy; more extensive in venous than arterial networks.
• Moment-to-moment perfusion depends on dynamic arteriolar radius; long-term BP hinges on blood volume.
• Neural reflex arcs (baroreceptor-center-effector) furnish rapid correction; kidney-mediated mechanisms (not detailed here) establish chronic set-points.
• Understanding the interplay among CO, TPR, and blood volume is fundamental for diagnosing hypertension, shock, and other circulatory disorders.