HISTORICAL BRIEF: ERNEST HENRY STARLING AND THE LAW OF THE HEART Corresponding Author Hector O. Ventura, MD From the Department of Cardiology, Cardiomyopathy and Heart Transplantation Center Ochsner Clinic Foundation
English physiologist Ernest Henry Starling was born on April 17, 1866, in London. He worked mainly at the University College in London with his brother-in-law William Maddock Bayliss and both made many important contributions to medical science. Starling’s importance on the understanding of heart failure stems from his articulation of the Law of the Heart, published in 1918. He wrote, “The behaviour of the muscle tissue of the heart thus resembles that of muscular tissue generally, whether skeletal or unstriated, in which the contractile stress set up by each contraction is a function of the length of the bre. The greater the length of the bre, and therefore the greater amount of surface of its longitudinal contractile elements at the moment when it begins to contract, the greater will be the energy in the form of contractile stress set up in its contraction, and the more extensive will be the chemical changes involved. This relation between the length of the heart bre and its power of contraction I have called ‘the law of the heart.” (1) Starling designed an experimental model of heart failure that utilized a canine heart preparation and had a series of manometers to measure the various pressures of the system. By varying the venous pressure and measuring the cardiac output, Starling created the well-known curve that explained heart function and viewed heart failure as a hemodynamic syndrome. He stated “…The longer the muscle (within physiological limits) the greater the amount of chemical energy, heat production and tension set up when the muscle passes from the resting to the active condition…the law of the heart…is the same as that for skeletal muscle, namely that the mechanical energy set free on passage from the resting to the contracted state depends on the area of chemically active surface, i.e. on the length of the muscle bers…If for any reason the heart fails in its pumping action, the blood will remain in the auricles and ventricles and will prevent the
further entry of blood from the reservoir. The heart will dilate more and more after each ine cient systole, while the pressure in the great veins will rise steadily; but this rise of pressure will be associated not with increased output from the ventricles but with diminished output. We have therefore to distinguish between a rise in venous pressure which is e ective in dilating the heart during diastole and increasing its output and a rise of venous pressure which is passively induced by failure of the pumping action of the heart…” (2,3) The concept from Starling and his co-workers paved the way to cardiac hemodynamics as the principal mechanism for the development of heart failure. This clinical thinking dominated the knowledge of the concept of heart failure for more than 70 years. As an example, Tinsley Harrison in 1936, in his book Failure of the Circulation (4) utilized Starling principles to explain the clinical syndrome of heart failure and more recently in 1970, Jeremy Swan, William Ganz, James Forrester and coworkers reported their technique of bedside hemodynamic monitoring incorporating principles that Starling articulated early in the 1900’s. (5)
Ernest Starling after a very productive career died in Kingston Jamaica on May 2, 1927.
References 1) Starling EH: On the circulatory changes associated with exercise. J R Army Med Corps 1920; 34: 265–266 2) Patterson SW, Starling EH. On the mechanical factors which determine the output of the ventricles. J Physiol 1914; 48:357 3) Patterson SW, Piper H, Starling EH. The regulation of the heart beat. J Physiol 1914;48: 465 4) Harrison TR: Failure of the Circulation. Baltimore: Williams & Wilkins Co., 1936 5) Swan HJC, GanzW, Forrester J, Marcus J, Diamond G, Chonette D: Catheterization of the heart inman with use of a ow-directed balloontipped catheter. N Engl J Med 1970; 283: 447–451
11 J LA MED SOC | VOL 172 | NO. 1
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