10/27/2017 CV Physiology | Turbulent Flow

Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD

Introduction
Acknowledgements

Topics:

Arrhythmias
Cardiac Valve Disease
Coronary Artery Disease
Edema
Heart Failure
Hypertension
Hypotension
Peripheral Artery Disease

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CVpharmacology.com

Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2012)

Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)

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Turbulent Flow
Generally in the body, blood flow is laminar. However, under conditions of high flow, particularly in the
ascending aorta, laminar flow can be disrupted and become turbulent. When this occurs, blood does not flow
linearly and smoothly in adjacent layers, but instead the flow can be described as being chaotic. Turbulent
flow also occurs in large arteries at branch points, in diseased and narrowed (stenotic) arteries (see figure
below), and across stenotic heart valves.

Turbulence increases the energy required to drive blood flow because turbulence increases the loss of energy
in the form of friction, which generates heat. When plotting a pressure-flow relationship (see figure to right),
turbulence increases the perfusion pressure required to drive a given flow. Alternatively, at a given perfusion
pressure, turbulence leads to a decrease in flow.

Turbulence does not begin to occur until the velocity of flow becomes high enough that the flow lamina
break apart. Therefore, as blood flow velocity increases in a blood vessel or across a heart valve, there is not
a gradual increase in turbulence. Instead, turbulence occurs when a critical Reynolds number (Re) is
exceeded. Reynolds number is a way to predict under ideal conditions when turbulence will occur. The
equation for Reynolds number is:

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10/27/2017 CV Physiology | Turbulent Flow

Where v = mean velocity, D = vessel diameter, = blood density, and = blood viscosity

As can be seen in this equation, Re increases as velocity increases, and decreases as viscosity increases.
Therefore, high velocities and low blood viscosity (as occurs with anemia due to reduced hematocrit) are
more likely to cause turbulence. An increase in diameter without a change in velocity also increases Re and
the likelihood of turbulence; however, the velocity in vessels ordinarily decreases disproportionately as
diameter increases. The reason for this is that flow (F) equals the product of mean velocity (V) times cross-
sectional area (A), and area is proportionate to radius squared; therefore, the velocity at constant flow is
inversely related to radius (or diameter) squared. For example, if radius (or diameter) is doubled, the velocity
decreases to one-fourth its normal value, and Re decreases by one-half.

Under ideal conditions (e.g., long, straight, smooth blood vessels), the critical Re is relatively high. However,
in branching vessels, or in vessels with atherosclerotic plaques protruding into the lumen, the critical Re is
much lower so that there can be turbulence even at normal physiological flow velocities.

Turbulence generates sound waves (e.g., ejection murmurs, carotid bruits) that can be heard with a
stethoscope. Because higher velocities enhance turbulence, murmurs intensify as flow increases. Elevated
cardiac outputs, even across anatomically normal aortic valves, can cause physiological murmurs because of
turbulence. This sometimes occurs in pregnant women who have elevated cardiac output and who may also
have anemia, which decreases blood viscosity. Both factors increase the Reynolds number, which increases
the likelihood of turbulence.

Revised 04/10/07

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-
making advice.

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