Blood Vessels Structure and Function (Part B)

Part 2 Physiology of Circulation

19.6 Flow, Pressure, and Resistance

Definition of Terms

  • Blood Flow:

    • The volume of blood flowing through a vessel, organ, or the entire circulation in a given period (measured in ml/min).

    • Equivalent to Cardiac Output (CO) when considering the entire vascular system.

    • While overall flow is constant at rest (CO=HR×SVCO = HR \times SV), local blood flow can vary significantly based on the metabolic demands of specific tissues (autoregulation).

  • Blood Pressure (BP):

    • The hydrostatic force per unit area exerted on the wall of a blood vessel by the blood it contains.

    • Measured in millimeters of mercury (mm Hg) using systemic arterial BP in the large arteries of the systemic circuit.

    • The Pressure Gradient (ΔP\Delta P) is the difference in BP between two points; this gradient is the driving force for flow. Blood always moves from higher pressure to lower pressure areas.

  • Resistance (Peripheral Resistance):

    • The measure of friction blood encounters as it passes through the vessels.

    • Most friction is encountered in the peripheral (systemic) circulation, far from the heart.

    • Three critical factors determine resistance:

    1. Blood Viscosity: The "internal resistance" to flow related to the thickness of the fluid. Higher hematocrit (e.g., polycythemia) increases viscosity and resistance, while low red blood cell counts (anemia) decrease it.

    2. Total Blood Vessel Length: Resistance is directly proportional to length. As the body grows or gains adipose tissue, total vessel length increases, requiring higher pressure to maintain flow.

    3. Blood Vessel Diameter: The most dynamic and influential factor. Resistance (RR) is inversely proportional to the fourth power of the vessel radius (rr).

Detailed Resistance Dynamics

  • The Radius Power Law:

    • The formula for resistance is documented as:
      R=8ηLπr4R = \frac{8\eta L}{\pi r^4}
      (Where η\eta is viscosity, LL is length, and rr is radius).

    • Because of the fourth-power relationship, small changes in the diameter of arterioles (the primary resistance vessels) lead to massive changes in BP. For example, if a vessel constricts to half its original radius, resistance increases 16-fold (24=162^4 = 16).

  • Laminar vs. Turbulent Flow:

    • Laminar Flow: In normal conditions, fluid close to the walls moves slowly due to friction, while fluid in the center flows fastest.

    • Turbulent Flow: Abrupt changes in diameter or rough surfaces (like fatty atherosclerotic plaques) cause blood to swirl, significantly increasing resistance.

Relationship Between Flow, Pressure, and Resistance

  • The relationship can be expressed with the formula: F=ΔPRF = \frac{\Delta P}{R}

    • Flow (FF) is directly proportional to the pressure gradient. If the heart pumps harder, ΔP\Delta P increases and flow increases.

    • Flow (FF) is inversely proportional to resistance. If vessels constrict (RR increases), flow decreases unless the heart compensates by increasing pressure.

19.7 Systemic Blood Pressure

  • The heart's pumping action creates the pressure, but resistance determines the drop in pressure along the system.

  • Pressure Gradient: In the systemic circuit, pressure is highest in the Aorta (approx. 120 mm Hg) and drops to ~0 mm Hg by the time it reaches the Right Atrium.

Arterial Blood Pressure

  • Reflects two factors: the compliance (elasticity) of the arteries near the heart and the volume of blood forced into them.

  • Systolic Pressure: Peak pressure reached during ventricular contraction (systole) as the aorta stretches.

  • Diastolic Pressure: Lowest arterial pressure reached during ventricular relaxation (diastole) as the aortic valve closes and the elastic walls of the aorta recoil to maintain flow.

  • Pulse Pressure: The surge felt in the artery during systole. PulsePressure=SystolicBP−DiastolicBPPulse Pressure = Systolic BP - Diastolic BP

    • Increased by increased stroke volume or decreased arterial compliance (atherosclerosis).

  • Mean Arterial Pressure (MAP): The average pressure that actually drives blood to the tissues throughout the cardiac cycle. Since diastole lasts longer than systole: MAP=DiastolicBP+13(PulsePressure)MAP = Diastolic BP + \frac{1}{3}(Pulse Pressure)

    • Clinical Note: A MAP of at least 60 mm Hg is typically required to maintain adequate perfusion to vital organs.

Capillary and Venous Pressure

  • Capillary Blood Pressure: Low pressure (35 to 17 mm Hg) is essential because capillaries are fragile and high pressure would burst them; furthermore, most capillaries are very permeable, so low pressure allows for efficient nutrient/gas exchange without excessive fluid loss.

  • Venous Blood Pressure: Venous pressure is too low to promote adequate return to the heart against gravity alone. Three adaptations assist:

    1. Muscular Pump: Skeletal muscle contraction "milks" blood toward the heart; valves prevent backflow.

    2. Respiratory Pump: During inhalation, abdominal pressure increases and thoracic pressure decreases, pulling blood toward the heart.

    3. Sympathetic Venoconstriction: Reduces the volume of blood in the veins (the "blood reservoir"), pushing it toward the heart to increase preload.

19.8 Regulation of Blood Pressure

  • BP regulation requires integrating the heart, blood vessels, and kidneys via the brain.

  • Fundamental relationship: MAP=CO×TPRMAP = CO \times TPR (Total Peripheral Resistance).

Short-Term Regulation: Neural Controls

  • Managed by the Cardiovascular Center in the Medulla Oblongata, consisting of:

    • Cardiac Centers: Cardioacceleratory and cardioinhibitory centers regulate HR and SV.

    • Vasomotor Center: Controls the diameter of blood vessels (primarily arterioles) via sympathetic efferents (vasomotor fibers), maintaining a state of partial constriction known as vasomotor tone.

  • Baroreceptor Reflexes:

    • Stretch receptors in the carotid sinuses (protecting blood flow to the brain) and aortic arch (protecting systemic flow).

    • If BP rises, baroreceptors fire faster → inhibits vasomotor/cardioacceleratory centers → vasodilation and decreased CO → BP drops.

  • Chemoreceptor Reflexes:

    • Detect drops in O<em>2O<em>2 or rises in CO</em>2CO</em>2/H+H^+ in the carotid and aortic bodies. High CO2CO_2 triggers the cardioacceleratory center to increase CO and BP to speed up pulmonary exchange.

Short-Term Regulation: Hormonal Controls

  • Epinephrine and Norepinephrine: From adrenal medulla; increase CO and cause generalized vasoconstriction.

  • Angiotensin II: Part of the RAAS pathway; a potent vasoconstrictor that rapidly increases TPR.

  • Antidiuretic Hormone (ADH/Vasopressin): Causes intense vasoconstriction during extreme BP drops (like hemorrhage) and stimulates water retention by the kidneys.

  • Atrial Natriuretic Peptide (ANP): Produced by the heart atria in response to high stretch (high BP). It antagonizes aldosterone and causes vasodilation, leading to a drop in blood volume and BP.

Long-Term Regulation: Renal Controls

  • Direct Renal Mechanism: High BP causes the kidneys to filter more fluid into the urine, reducing blood volume and BP independently of hormones.

  • Indirect Renal Mechanism (RAAS):

    • Decreased BP triggers the release of Renin from the kidneys.

    • Renin converts Angiotensinogen into Angiotensin I, which is converted to Angiotensin II by ACE (Angiotensin Converting Enzyme).

    • Angiotensin II stimulates Aldosterone secretion (saving Na+Na^+ and water) and ADH release, effectively increasing blood volume and BP over the long term.