User:Mczachor1/sandbox

Evaluation Notes on Physiology Article

• The sentence about the Noble Prize in Physiology does not seem to fit in the introduction and is not cited
• The sentence defining a physiologic state could be integrated better in another place
• Not all facts are cited, such as the sentence about The American Physiological Society
• The sentences about the American Physiological Society are plagiarized
• It may read better if all of the achievements from the history section were added together under a different title or under subtitle of the history section
• References 5 and 22 may not be reliable sources
• The Human Physiology section seems to jump from point to point and a short summary that reads better is needed
• Other sections like how physiology contributes to modern medicine may make the page stronger

Edits I Plan on Making to Frank-Starling Law Article

The article has very little citations throughout so I am planning on increasing the reliability of the article by adding more sources. The history section and the physiology section of the article also need to be expanded. In the history section, I think it would be beneficial to talk specifically about Frank and Starling's finding separately and then how both of their findings together were used to formulate the Frank-Starling Law. In the physiology section, I am planning on expanding the information about the cellular basis of the mechanism by including information about all the cellular processes that contribute to the mechanism. I would also like to add more about why this mechanism is significant in the human heart. Some sentences in the article also use words like we, our, etc. and I think it would help make the article sound more encyclopedic if the wording of those sentences were changed. The first paragraph also seems a little repetitive and jumps around a little. Rewording it and adding a little bit more information may help it flow better.

Possible Sources

• http://www.clinsci.org/content/ppclinsci/54/1/1.full.pdf
• http://jeb.biologists.org/content/211/13/2005
• http://ccnmtl.columbia.edu/projects/heart/exercises/set1-3.html
• http://pie.med.utoronto.ca/CA/CA_content/CA_cardiacPhys_preload.html
• http://circres.ahajournals.org/content/90/1/11

EDITS ARE IN BOLD ITALICS

Frank–Starling law

From Wikipedia, the free encyclopedia

  (Redirected from Frank-Starling law) Cardiac function curve In diagrams illustrating the Frank–Starling law of the heart, the y-axis often describes the stroke volume, stroke work, or cardiac output. The x-axis often describes end-diastolic volume, right atrial pressure, or pulmonary capillary wedge pressure. The three curves illustrate that shifts along the same line indicate a change in preload, while shifts from one line to another indicate a change in afterload or contractility.

The Frank–Starling law of the heart (also known as Starling's law or the Frank–Starling mechanism or Maestrini heart's law) states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant. In other words, as a larger volume of blood flows into the ventricle, the blood will stretch the walls of the heart, causing a greater expansion during diastole, which in turn increases the force of the contraction and thus the quantity of blood that is pumped into the aorta during systole. The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully (the so-called Frank–Starling mechanisms). The stroke volume may also increase as a result of greater contractility of the cardiac muscle during exercise, independent of the end-diastolic volume. The Frank–Starling mechanism appears to make its greatest contribution to increasing stroke volume at lower work rates, and contractility has its greatest influence at higher work rates.

The Frank-Starling law of the heart (also known as Starling's law, the Frank-Starling mechanism and Maestrini heart's law) represents the relationship between stroke volume and end-diastolic volume . The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant . As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction. The mechanism occurs automatically, at any given heart rate, without depending upon external regulation (book). The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, without depending upon external regulation to make alterations (citation in actual article). The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.

Physiology[edit]

The Frank-Starling mechanism is the result of the length-tension relationship observed in skeletal muscles. As a muscle fiber is stretched, active tension is created by altering the overlap of thick and thin filaments. The greatest isometric active tension is developed when a muscle is at its optimal length. In most relaxed skeletal muscle fibers, passive elastic properties maintain the muscle fibers length near optimal. In contrast, the normal point of cardiac muscle cells, in a resting individual, is lower than the optimal length for contraction. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in a normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For larger sarcomere lengths, this is the result of less overlap of the thin and thick filaments; for smaller sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments. (citation needed, I can't find where this is from) An increase in filing of the ventricle increases the load experienced by each cardiac muscle fiber, stretching the fibers toward their optimal length.

The stretching of the muscle fibers augments cardiac muscle contraction by increasing the calcium sensitivity of the myofibrils, causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. (citation in actual article) Specifically, the sensitivity of troponin for binding Ca²⁺ increases and there is an increased release of Ca²⁺ from the sarcoplasmic reticulum. In addition, there is a decrease in the spacing between thick and thin filaments, when a cardiac muscle fiber is stretched, allowing an increased number of cross-bridges to form. The force that any single cardiac muscle fiber generates is proportional to the initial sarcomere length (known as preload), and the stretch of the individual fibers is related to the end-diastolic volume of the left and right ventricles.(citation in actual article)

A more forceful contraction occurs in a stretched cardiac muscle cell because more cross-bridges are able to bind due to a decrease in the spacing between thick and thin filaments. In addition, the sensitivity of troponin for binding when cardiac muscle cells are stretched.

As the heart fills with more blood than usual, the force of cardiac muscular contractions increases. This is a result of an increase in the load experienced by each muscle fiber due to the extra blood load entering the heart.

Clinical examples[edit]

Edited this section directly on the mainspace.

Shifting along the line[edit]

• A blood volume increase would cause a shift along the line to the right, which increases left ventricular end diastolic volume (x axis), and therefore also increases stroke volume (y axis) (because the line curves upwards).

This can be seen most dramatically in the case of premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Because of the Frank–Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.

For example, during vasoconstriction the end diastolic volume (EDV) will increase due to an increase in TPR (total peripheral resistance) (increased TPR causes a decrease in the stroke volume which means that more blood will be left in the ventricle upon contraction – an increased end systolic volume (ESV). ESV + normal venous return will increase the end diastolic volume). Increased EDV causes the stretching of the ventricular myocardial cells which in turn use more force when contracting. Cardiac output will then increase according to the Frank–Starling graph. (The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.) The S3, or third heart sound can be heard due to this increase in volume which can be pathognomic for heart failure.

• By contrast, pericardial effusion would result in a shift along the line to the left, decreasing stroke volume.

History[edit]

The Frank-Starling law is named after two physiologists, Otto Frank and Ernest Henry Starling. However, neither Frank nor Starling was the first to describe the relationship between the end-diastolic volume and the regulation of cardiac output.Indeed, the first formulation of the law was theorized by the Italian physiologist Dario Maestrini, who on December 13, 1914, started the first of 19 experiments that led him to formulate the "legge del cuore".

Otto Frank's contributions are derived from his 1895 experiment on frog hearts. In order to relate the work of the heart to skeletal muscle mechanics, Frank observed changes in diastolic pressure with varying volumes of the frog ventricle. His data was analyzed on a pressure-volume diagram, which resulted in his description of peak isovolumic pressure and its affects on ventricular volume.

Starling experimented on intact mammalian hearts, such as from dogs, to understand why variations in arterial pressure, heart rate, and temperature does not affect the relatively constant cardiac output. More than 30 years before the development of sliding filament model of muscle contraction and the understanding of the relationship between active tension and sarcomere length, Starling hypothesized in 1914, "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." Starling used a volume-pressure diagram to construct a length-tension diagram from his data.Starling's data and associated diagrams, provided evidence that the length of the muscle fibers, and resulting tension, altered the systolic pressure.

Long before the development of the sliding filament hypothesis and the understanding that active tension depends on the maximum load on a single cardiac sarcomere or Cardiomyocyte, Ernest Starling hypothesized in 1918 that "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." (Citation Needed). We now have a technological glimpse of the It is now possible to observe the powerful mechanical/molecular basis of the sliding filament theory perhaps unforeseen by Frank or Starling. We still lack a There is still no working mathematical construct that shows a link between the sliding filament theory and the Frank–Starling mechanism. Initial length of myocardial fibers determines the initial work done during the cardiac cycle.

Professor Ernest Henry Starling, (most famous at the time), was the holder of the Physiology chair at London University and traced Maestrini theories in 1918. Despite the sudden death of Starling, whose great fame was the driving motive of the proposed award of the Nobel Prize, Maestrini never received due recognition, and today the "law of the heart" is known worldwide as "Starling's Law," though, among the Italian doctors, it is known by the nickname "Legge di Maestrini".

In 1974 an editorial comment in The Lancet briefly mentioned that "Starling’s law [of the heart] was no complete novelty, and, like many others, he built on the work of notable predecessors".

See also[edit]

• Starling equation

References[edit]

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3. Jump up ^ Klabunde, Richard E. "Cardiovascular Physiology Concepts". Lippincott Williams & Wilkins, 2011, p. 74.
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