This cardiac response to changes in venous return and ventricular filling pressure is intrinsic to the heart and does not depend on extrinsic neurohumoral mechanisms although such mechanisms can modify the intrinsic cardiac response. In honor of these two early pioneers, the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism or Starling's Law of the heart.
There is no single Frank-Starling curve on which the ventricle operates. Instead, there is a family of curves, each of which is defined by the afterload and inotropic state of the heart. In the figure showing multiple curves, the red dashed curve represents a "normal" ventricular Frank-Starling curve.
Increasing afterload or decreasing inotropy shifts the curve down and to the right. Decreasing afterload and increasing inotropy shifts the curve up and to the left. At a given state of ventricular inotropy and afterload, the ventricle responds to changes in venous return and ventricular filling based on the unique curve for those conditions. To summarize, changes in venous return cause the ventricle to move up or down along a single Frank-Starling curve; however, the slope of that curve is defined by the existing conditions of afterload and inotropy.
Frank-Starling curves show how changes in ventricular preload lead to changes in stroke volume. This type of graphical representation, however, does not show how changes in venous return affect end-diastolic and end-systolic volumes. In order to do this, it is necessary to describe ventricular function in terms of pressure-volume diagrams. When venous return is increased, there is increased filling of the ventricle along its passive pressure curve leading to an increase in end-diastolic volume see Figure.
The functional importance of the Frank-Starling mechanism lies mainly in adapting left to right ventricular output. During upright physical exercise an increase in end-diastolic volume due to the action of the peripheral muscle pump and increased venous tone can assist in enhancing stroke volume. Reduced contractility leads to a shift of the operating point to the right in the pressure-volume diagram, thus tending to prevent a decrease in stroke volume.
However, the consequences of increased circulating blood volume in chronic heart failure are, as a rule, mainly detrimental congestive symptoms; myocardial component of coronary resistance; cardiac energetics. This chapter is relevant to Section G3 i of the CICM Primary Syllabus , which asks the exam candidate to "explain the Frank-Starling mechanism and its relationship to excitation-contraction coupling". Remarkably, the college examiners have never attempted to directly weaponise this section of the syllabus, though it does appear as shrapnel in the casing of other questions.
This is mainly surprising because the subject matter is fundamental to cardiovascular physiology, and because there is a diagram which makes for easy question-writing just ask them to draw and label it. For the effects of pathophysiology on the Frank-Starling relationship, the best free offering is Jacob et al , which is comprehensive and contains lovely diagrams.
Mann's chapter from Data Interpretation in Anaesthesia is also excellent as it is presented in a question and answer format, like a viva station. There is also a series of about ten articles titled " Studies on Starling's law of the heart", published in Circulation between and , which contains even more permutations on this theme i. It would be pointless also, probably harmful to actually consume all of this literature in the course of exam preparation, and it is being left here for a purely decorative purpose, like a bowl of plastic fruit.
It is probably misnamed, as neither Ernest Frank nor Otto Frank discovered this thing. It was probably first noted either thirty or sixty years earlier. Apparently, in Elias Cyon first noticed it in the frog heart he was molesting, but he didn't write anything down and so it didn't happen. The greater the length of the fibre and therefore the greater amount of the surface of its longitudinal contracule elements at the moment when it begins to contraxct, the greater will be the energy in the form of contractile stress set up in its contraction, and the more extensive wull be the chemical changes involved.
This relation between the length of the heart fibre and the power of contraction I have called "the law of the heart".
The editor of the Journal of Physiology clearly made Starling and Visscher cut it down to a more easily digestible form, which resembles the modern version:.
There are, unfortunately, as many modern versions as there are writers in the field of physiology; but at least they only vary the wording slightly. No group of authors has given any evidence that any specific choice of language matters, which means that you can literally plot them in a grid and pick any combination of terms at random:.
In any case, it all boils down to the relationship between cardiac filling and cardiac contraction. The Frank-Starling law is the observation that cardiac input and cardiac output are matched; it is a description of an intrinsic cardiac autoregulatory mechanism.
It is a fundamental and ancient property of the myocardium; all vertebrate hearts and probably also insect hearts possess this ability, which probably makes it an essential engineering specification for building any circulatory system. In an exam scenario, the unprepared trainee who is confronted with a question like "define the Frank-Starling law" should immediately grab a piece of paper and scribble this diagram:.
These are "ventricular function curves" and are discussed elsewhere. Here it will suffice to say that:.
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