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Laminar Flow and Velocity Profile

Laminar flow occurs when blood moves smoothly through vessels. The fluid flows in parallel layers without mixing. Central blood layers stay in the middle. Outer blood layers remain near the walls. This stream movement contrasts directly with turbulent flow.

Laminar movement creates a distinct parabolic velocity pattern. Fluid touching vessel walls moves slowest due to adherence. Inner fluid layers slip past outer layers progressively. Central blood layers travel at maximum speed. This creates a bullet-shaped parabolic velocity profile.

• Blood flows smoothly in parallel streamlines.
• Each fluid layer maintains wall distance.
• Central blood remains in the center.
• Laminar flow opposes disorderly turbulent flow.
• Center velocity exceeds outer edge velocity.
• Stationary fluids develop parabolic interfaces moving.
• Wall-touching molecules adhere and move slowly.
• Adjacent molecular layers slip past each other.
• Concentric layers flow progressively faster inward.
• Center fluids move most rapidly overall.

Turbulent Flow Mechanics

Turbulence develops when blood flow becomes highly disorderly. High velocities and physical obstructions disrupt streamline patterns. Sharp vessel turns and rough surfaces also trigger turbulence. Disrupted fluid forms crosswise patterns called eddy currents.

Eddy currents act like whirlpools in fast rivers. These currents greatly increase resistance within the vessel. Increased resistance results from severe internal fluid friction. Reynolds' number predicts the likelihood of turbulent flow. Higher numbers indicate a greater tendency for turbulence.

• Excessive flow rates cause turbulent flow.
• Obstructions and turns trigger fluid turbulence.
• Rough vessel surfaces disrupt streamline flow.
• Blood flows crosswise and forms eddy currents.
• Eddy currents mimic river whirlpools.
• Eddies add tremendous friction to blood.
• Turbulent blood experiences much higher resistance.
• Tendency increases with higher flow velocity.
• Tendency increases with larger vessel diameter.
• Higher blood density increases turbulence tendency.
• Higher blood viscosity decreases turbulence tendency.
• Reynolds' number measures overall turbulence tendency.
• Normal blood viscosity equals one-thirtieth poise.
• Normal blood density slightly exceeds value one.
• Values above 200 cause branch turbulence.
• Branch turbulence dies along smooth vessels.
• Values above 2000 cause straight-vessel turbulence.
• Large arteries normally reach values 200-400.
• Arterial branching points frequently exhibit turbulence.
• Proximal aorta reaches several thousand Reynolds.
• Proximal pulmonary artery reaches high Reynolds.
• Rapid ventricular ejection creates aortic turbulence.
• High velocity promotes proximal artery turbulence.
• Pulsatile flow promotes proximal artery turbulence.
• Sudden diameter changes promote local turbulence.
• Large vessel diameters promote local turbulence.
• Small vessels rarely exhibit turbulent flow.

Blood Pressure Measurement Units

Blood pressure represents force exerted against vascular walls. Millenniums of physiological study utilize mercury manometers. Poiseuille introduced mercury reference standards in 1846. Pressures push mercury columns against force of gravity.

Centimeters of water provide another pressure unit. Water columns measure lighter pressure dynamics accurately. Mercury density exceeds water density by 13.6 times. Conversion factors relate both measurement units precisely.

• Pressure measures force against vessel walls.
• Millimeters mercury serves as standard unit.
• Poiseuille invented mercury manometer in 1846.
• Fifty mmHg elevates mercury column 50mm.
• One hundred mmHg elevates mercury 100mm.
• Pressure sometimes uses centimeters of water.
• Ten cmH2O elevates water column 10cm.
• Mercury specific gravity equals 13.6 times.
• One mmHg equals 1.36 cmH2O pressure.

Vascular Resistance Concepts

Vascular resistance impedes blood flow through vessels. Direct physical measurement of resistance is impossible. Calculations require pressure difference and flow rate. One peripheral resistance unit equals baseline parameters.

Physical sciences express resistance using CGS units. Dynamic seconds per centimeter to the fifth power represents physical drag. Systemic vascular resistance equals total peripheral resistance. Pulmonary circuits maintain significantly lower total resistance.

• Resistance impedes blood flow in vessels.
• Resistance cannot be measured directly.
• Calculations use flow and pressure differences.
• One PRU equals 1mmHg per 1ml/sec.
• CGS unit equals dyne sec/cm5.
• CGS formula converts standard resistance units.
• Cardiac output equals systemic blood flow.
• Adult flow averages 100 milliliters per second.
• Systemic pressure gradient averages 100 mmHg.
• Normal total peripheral resistance equals 1 PRU.
• Severe vasoconstriction elevates resistance to 4 PRU.
• Great vasodilation lowers resistance to 0.2 PRU.
• Mean pulmonary arterial pressure averages 16 mmHg.
• Mean left atrial pressure averages 2 mmHg.
• Net pulmonary pressure difference equals 14 mmHg.
• Total pulmonary resistance equals 0.14 PRU.
• Pulmonary resistance equals one-seventh systemic resistance.

Conductance and Fourth Power Law

Conductance measures blood flow for a given pressure difference. Units express volume flow per pressure unit. Conductance functions as exact reciprocal of resistance. Minor diameter increases produce massive conductance gains.

Poiseuille's law explains diameter effects via concentric rings. Streamlined layers move faster toward vessel centers. Large vessels possess fast-moving central streams. Small vessels lack central rapidly flowing streams.

• Conductance measures flow for pressure differences.
• Units express volume flow per pressure.
• Conductance equals exact reciprocal of resistance.
• Diameter changes alter conductance tremendously.
• Fourfold diameter increase yields 256-fold flow.
• Conductance increases proportional to diameter fourth-power.
• Concentric blood rings flow at different velocities.
• Endothelium-touching blood barely flows at all.
• Progressive inward rings flow at higher speeds.
• Small vessels lack rapidly flowing central streams.
• Integrating ring velocities derives Poiseuille's law.
• Flow directly correlates to radius fourth power.
• Vessel radius dominates blood flow determination.

Arteriolar Resistance Control

Arterioles supply two-thirds of total systemic resistance. Internal arteriolar diameters range from 4 to 25 micrometers. Strong muscular walls allow massive diameter shifts. Vascular walls change internal diameters up to fourfold.

The fourth power law empowers precise flow regulation. Small diameter adjustments control major tissue delivery. Nervous and chemical signals modulate arteriolar tone. Tissues alter localized blood flow over 100-fold.

• Arterioles provide two-thirds total systemic resistance.
• Internal diameters span 4 to 25 micrometers.
• Muscular walls permit fourfold diameter changes.
• Fourfold enlargement increases local flow 256-fold.
• Small diameter shifts vastly alter tissue flow.
• Nervous signals control local arteriolar diameter.
• Chemical signals control local arteriolar diameter.
• Local tissue flow varies over 100-fold.

Series and Parallel Circuits

Vascular beds organize into series and parallel circuits. Series arrangements connect sequential vascular divisions. Arteries, arterioles, capillaries, venules, and veins form series systems. Total series resistance equals individual resistances summed together.

Parallel circuits branch blood flow to separate organs. Parallel organization allows independent organ flow regulation. Adding parallel vessels reduces total circuit resistance. Organ removals eliminate parallel pathways and elevate resistance.

• Systemic vessels form series and parallel circuits.
• Sequential vessel divisions form series circuits.
• Flow stays equal through all series vessels.
• Series resistance equals sum of individual resistances.
• Total peripheral resistance sums all sequential segments.
• Branching organ circuits form parallel circuits.
• Parallel circuits permit independent organ flow control.
• Parallel resistance formula sums reciprocal resistances.
• Total parallel resistance is less than single vessels.
• Individual parallel flows depend on local resistance.
• Adding parallel vessels reduces total circuit resistance.
• Extra vessels provide additional flow pathways.
• Total parallel conductance equals sum of pathways.
• Major body organs operate as parallel circuits.
• Surgical organ removal reduces total conductance.
• Organ removal increases total peripheral vascular resistance.

Blood Hematocrit and Viscosity

Viscosity represents a critical factor in Poiseuille's law. Higher fluid viscosity reduces vascular blood flow. Whole blood viscosity equals three times water viscosity. Red blood cells create primary viscosity through drag.

Polycythemia elevates hematocrit to extreme levels. Elevated hematocrit drastically increases overall blood viscosity. Plasma protein concentrations exert minor viscosity influences. Plasma alone maintains 1.5 times water viscosity.

• Viscosity inversely affects vessel blood flow.
• Normal blood viscosity equals three times water.
• Normal blood requires triple water's forcing pressure.
• Suspended red blood cells create primary viscosity.
• Cells exert drag against adjacent cellular structures.
• Cells exert drag against vessel endothelial walls.
• Polycythemia raises hematocrit to 60 or 70.
• High hematocrit elevates viscosity ten times water.
• High blood viscosity greatly retards overall flow.
• Plasma protein concentration affects viscosity slightly.
• Plasma protein types affect viscosity minimally.
• Plasma viscosity equals 1.5 times water viscosity.

Autoregulation and Passive Beds

Pressure increases normally drive increased vascular flow. Autoregulation limits pressure-induced flow changes in tissues. Tissues adjust vascular resistance within seconds. Normal flow persists between 70 and 175 mmHg.

Passive vascular beds lack active autoregulatory mechanisms. Elevated pressure distends elastic vessels to lower resistance. Falling pressure permits vessel collapse at critical points. Sympathetic stimulation modulates passive pressure-flow curves.

• Autoregulation attenuates arterial pressure effects.
• Pressure increases initiate rapid resistance increases.
• Pressure drops trigger rapid local vasodilation.
• Autoregulation maintains constant flow from 70-175 mmHg.
• Sympathetic stimulation constricts vessels to reduce flow.
• Hormonal vasoconstrictors transiently decrease blood flow.
• Norepinephrine, angiotensin II, and vasopressin constrict vessels.
• Local mechanisms eventually override sustained vasoconstriction.
• Passive beds lack acute blood flow autoregulation.
• High pressure distends elastic vessels to lower resistance.
• Low pressure increases resistance via elastic collapse.
• Critical closing pressure causes complete vessel collapse.
• Flow ceases entirely below critical closing pressure.
• Sympathetic inhibition dilates passive vessels twofold.
• Strong sympathetic stimulation can decrease flow zero.
• Sustained pressure changes invoke long-term tissue control.