Newtonian Pipe Flow Turbulence.(1) Turbulent forward flow appears as fast-moving “jet streams” (shown in red) that form along the inner walls of pipes and force slow-moving fluid to the center, where it moves backward (shown in blue), causing increased viscosity (flow resistance). A, C and E are laser photographs that show “fast (A), faster (C) and fastest (E)” flow acceleration that produce “small (A), medium (C) and large (E)” increases in turbulent intensity. B, D and F are computer simulations that predicted the experimental results shown by A, C and E. Similar arterial turbulence during diastole mobilizes particulate deposits from arterial walls to prevent atherosclerosis. It also generates lateral forces that press on the inner walls of the vessel, which explains blood pressure and the palpable pulse.
 

1. B. Hof et al., Experimental observation of nonlinear traveling waves in turbulent pipe flow. Science 305, 1594-1598 (2004).

 

The Turbulence Mechanism

“Big whirls have little whirls, That feed on their velocity; 
And little whirls have lesser whirls, 
And so on to viscosity.” 

---Lewis Fry Richardson 


The turbulence mechanism works in conjunction with the capillary gate mechanism. It explains the nature of  blood pressure, the palpable pulse, atherosclerosis, and arterial thrombosis. The key to understanding hemodynamic physiology is the non-Newtonian nature of blood, which abolishes turbulence during systolic blood acceleration. Red cell "aggregates" form spontaneously during systolic blood acceleration and abolish systolic turbulence, so that the heart expels its contents with extreme efficiency. The elastic arterial tree expands to accommodate the increased volume. At the conclusion of systole, the heart relaxes and blood flow briefly reverses direction in the aorta to close the aortic valve. The decreased diameter of the distal aorta exaggerates the flow reversal, disrupts the aggregate formations, and initiates a burst of pulsatile turbulence that speeds throughout the arterial tree, briefly halting forward flow as it travels. The turbulence prevents atherosclerosis and thrombosis, and generates lateral forces that explain blood pressure. In the wake of the pulse wave, the muscular arterial tree acts as a "secondary heart" that efficiently propels laminar blood flow to perfuse capillary beds, but the force is so small that it cannot be measured by conventional instruments. 

The turbulent lateral force that explains blood pressure is exponentially altered by several factors including vessel diameter, length, bifurcations and strictures; body temperature; and blood viscosity (flow resistance). Mammalian physiology maintains body temperature above the threshold of lipoprotein liquefaction to prevent lipoprotein solidification that exaggerates blood viscosity. Opening the capillary gate lowers blood viscosity, enhances tissue perfusion, and reduces blood pressure, as in normal sleep. Closing the capillary gate increases blood viscosity, decreases tissue perfusion, and exaggerates blood pressure. Thus blood pressure is a counterintuitive and counterproductive means of medical management. 

 

 

 Aortic turbulence in a dog. Blood accelerates from 0 to 100 cm/sec and the heart empties itself in less than a tenth of a second. Mammalian systolic flow simultaneously inhibits atherosclerosis and optimizes flow efficiency, tissue perfusion, tissue oxygenation, and exercise tolerance.