Windkessel effect

From Wikipedia, the free encyclopedia

Windkessel effect is the term used in medicine to describe the recoiling effect of large arteries (Windkessel vessels). Windkessel in German means elastic reservoir.[1] The walls of large arteries (eg. aorta, common carotid, subclavian, and pulmonary arteries and their larger branches) contain elastic fibers in their walls. These arteries increase their diameters when the blood pressure rises during systole and decrease their diameters when the blood pressure falls during diastole. The diameter changes result in the large arteries containing more blood during systole than during diastole. That additional blood is discharged peripherally during the next diastole. This compliance effect of the Windkessel prevents excessive rises in blood pressure during systole. One result is a lower fluid mechanical load on the heart than otherwise would have occurred. Pressure wave reflections in the arterial system (a distributed system, as contrasted with a lumped system) can and do alter this effect.

The Windkessel effect becomes diminished with age. This occurs because the walls of the aorta and other arteries become less elastic as a result of arteriosclerosis or atherosclerosis. Then, for the same amount of blood ejected from the heart during systole of the same duration, an excess rise of pressure does occur in the large arteries, as the vessel walls are no longer able to absorb and dissipate forces in the same way. Elevated systolic pressures have increasingly been shown to be associated with strokes, cardiac enlargement, heart failure and other undesirable events.

The blood pressure against which the heart ejects – the systolic load, normally diminished by the Windkessel effect - is similarly increased when long, synthetic, non-elastic grafts are used to replace a major portion of the thoracic aorta. [2]

Blood flow in the arterial system began to be viewed, perhaps beginning in the early 1950's, as much more dynamic and more complicated than the Windkessel concept describes .[3][4]. Blood being ejected from the heart has at the aortic root a flow waveform and a pressure waveform. Flow and pressure waveforms change in shape and amplitude as the blood flows distally in the arteries. The changes occur because of interactions between arterial wall elasticity (capacitance effect), blood mass (inertial effect), and frictional (resistive) effects. In the more distal arteries frictional (resistive) effects on blood flow become increasingly important.

The interaction of the capacitance, inertial and frictional effects on blood flow often results in blood pressure wave reflections. These occur at arterial branch sites and from distal arteries. These stand in contrast to the passive Windkessel concept. The pressure wave reflections occur in some instances with timing so that, when systole begins, it begins at the same instant a negative pressure wave reflection reaches the aortic root. The result is a decrease in the fluid mechanical and thus also in the metabolic load on the heart. This effect and other dynamic properties of blood flow in the arterial system stand in contrast to the relatively static properties inherent in the original Windkessel concept.

[edit] References

  1. ^ Ganong M.D., William F. (2005): Review of Medical Physiology, Twenty-Second Edition, page 587. The McGraw-Hill Companies, Inc.
  2. ^ Shepard, R.B. (1992). Invited Letter to the Editor on The Effect of Extra-Anatomic Bypass on Aortic Input Impedance Studies in Open Chest Dogs: Should the Vascular Prosthesis Be Compliant to Unload the Left Ventricle? J Thorac Cardiovasc Surg 104(4):1175-1177, October, 1992.
  3. ^ McDonald D.A. (1960). Blood Flow in Arteries. Monographs of the Physiological Society. Baltimore: Williams and Wilkins Company
  4. ^ Nichols W.W., O'Rourke M.F. (2005). McDonald's Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. Hodder Arnold Publication