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Frank–Starling law

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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. 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).

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.[1] 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.[1] 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 Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length,[2] without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.[1][3]

Physiology

The Frank-Starling mechanism occurs as the result of the length-tension relationship observed in skeletal muscles.[4] 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.[1] 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] An increase in filling of the ventricle increases the load experienced by each cardiac muscle fiber, stretching the fibers toward their optimal length.[1]

The stretching of the muscle fibers augments cardiac muscle contraction by increasing the calcium sensitivity of the myofibrils,[5] causing a greater number of actin-myosin cross-bridges to form within the muscle fibers. 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.[1] The force that any single cardiac muscle fiber generates is proportional to the initial sarcomere length, and the stretch on the individual fibers is related to the end-diastolic volume of the left and right ventricles.

Clinical Examples

Premature Ventricular Contraction

premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction occurs at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Due to the Frank–Starling mechanism, the next ventricular contraction is more forceful, leading to the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.[citation needed]

Heart Failure

History

The law was named after the two physiologists, Otto Frank and Ernest Starling, who first described it.

Long before the development of the sliding filament hypothesis and our 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." We now have a technological glimpse of the powerful mechanical/molecular basis of the sliding filament theory perhaps unforeseen by Frank or Starling. We still lack a working mathematical construct that proves a link between sliding filament theory and Frank–Starling. Initial length of myocardial fibers determines the initial work done during the cardiac cycle.

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" .[6][7][8][9][10][11][12][13][14][15][16][17][18]

Professor Ernest Henry Starling,[19] (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".[20][21][22][23][24]

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".[25]

See also

References

  1. ^ a b c d e f Widmaier, E. P., Hershel, R., & Strang, K. T. (2016). Vander's Human Physiology: The Mechanisms of Body Function (14th ed.). New York, NY: McGraw-Hill Education. ISBN 978-1-259-29409-9
  2. ^ Costanzo, Linda S. (2007). Physiology. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 81. ISBN 0-7817-7311-3.
  3. ^ R., Jacob,; B., Dierberger,; G., Kissling, (1992-11-01). "Functional significance of the Frank-Starling mechanism under physiological and pathophysiological conditions". European Heart Journal. 13 (suppl_E). doi:10.1093/eurheartj/13.suppl_E.7. ISSN 0195-668X.
  4. ^ Katz, Arnold M. (2002-12-03). "Ernest Henry Starling, His Predecessors, and the "Law of the Heart"". Circulation. 106 (23): 2986–2992. doi:10.1161/01.CIR.0000040594.96123.55. ISSN 0009-7322. PMID 12460884.
  5. ^ Klabunde, Richard E. "Cardiovascular Physiology Concepts". Lippincott Williams & Wilkins, 2011, p. 74.
  6. ^ Spadolini, Igino (1946). Trattato di Fisiologia,. Vol. 2. Torino. {{cite book}}: Unknown parameter |editors= ignored (|editor= suggested) (help)CS1 maint: location missing publisher (link)
  7. ^ Berne, Robert M. (2004). Fisiologia. Milano. {{cite book}}: Cite has empty unknown parameter: |capitolo= (help); Unknown parameter |editors= ignored (|editor= suggested) (help)CS1 maint: location missing publisher (link)
  8. ^ "www.ancecardio.it" (PDF) (in Italian). pp. 29–31. Retrieved 6 August 2010. {{cite web}}: Cite has empty unknown parameters: |opera=, |wkautore=, and |urlarchivio= (help)
  9. ^ MAESTRINI, D. (February 1951). "[Genesis of the so-called insufficient contractions of the heart in decompensation.]". Policlinico Prat. 58 (9): 257–68. PMID 14833944.
  10. ^ MAESTRINI, D. (July 1951). "[The importance of the altered organic exchange (fatigue), of the structure and colloidal state of the fiber, for the genesis of the so-called small, insufficient contractions of the heart in failure.]". Policlinico Prat. 58 (30): 933–45. PMID 14864102.
  11. ^ MAESTRINI, D. (November 1951). "[The law of the heart in biology and clinical medicine.]". Minerva Med. 42 (80): 857–64. PMID 14919226.
  12. ^ MAESTRINI, D. (June 1952). "[A new theory of cardiac decompensation.]". Policlinico Prat. 59 (24): 797–814. PMID 14957592.
  13. ^ MAESTRINI, D. "[Not Available.]". Gazz Sanit. 18 (5): 162–4. PMID 18859625.
  14. ^ PENNACCHIO, L.; D. MAESTRINI (September 1952). "[Comment on a new theory of cardiac insufficiency.]". Policlinico Prat. 59 (37): 1223–4. PMID 13026471.
  15. ^ MAESTRINI, D. (January 1958). "[The law of the heart from its discovery to the present time.]". Minerva Med. 49 (3–4): Varia, 28–36. PMID 13516733.
  16. ^ MAESTRINI, D. (December 1958). "[Variations of cardiac volume dynamics in clinical practice, examined in the light of the law of the heart.]". Minerva Cardioangiol. 6 (12): 657–67. PMID 13643787.
  17. ^ MAESTRINI, D. (February 1959). "[S. Baglioni and the law of the heart.]". Policlinico Prat. 66 (7): 224–30. PMID 13645276.
  18. ^ MAESTRINI, D. (October 1959). "[On cardiac dynamics in the phase preceding right hypertrophy and on its electrocardiographic aspect in man.]". Policlinico Prat. 66: 1409–13. PMID 13853750.
  19. ^ Katz, AM.; EH. Starling (December 2002). "Ernest Henry Starling, his predecessors, and the "Law of the Heart"". Circulation. 106 (23): 2986–92. doi:10.1161/01.CIR.0000040594.96123.55. PMID 12460884.
  20. ^ Dario, Maestrini, ed. (1925), "La legge del cuore in clinica", Comunicazione Soc. Med. Chirur. Osp. Abruzzesi, seduta del 30 Agosto 1925, Cuore e Circolazione, p. 506{{citation}}: CS1 maint: location missing publisher (link)
  21. ^ "Maestrini biografie" (PDF). Retrieved 6 August 2010. {{cite web}}: Cite has empty unknown parameters: |opera=, |wkautore=, and |urlarchivio= (help)
  22. ^ Maestrini, Dario (1967). Nuove vedute e nuove realtà in Cardiologia 1911-1967. Roma. p. 279. {{cite book}}: Unknown parameter |editors= ignored (|editor= suggested) (help)CS1 maint: location missing publisher (link)
  23. ^ Italo Farnetani Italo, Farnetani; Farnetani, Francesca (2002). "È ad Arezzo il giallo della "Legge di Maestrini-Starling,". Il Cisalpino. 3: 57–62.
  24. ^ Massimo Pandolfi,; Francesco De Tommasi. ANALECTA HISTORICO MEDICA (ed.). "www.profpaolovanni.it" (PDF). pp. 185–187. Retrieved 6 August 2010. {{cite web}}: Cite has empty unknown parameters: |wkautore=, |opera=, and |urlarchivio= (help)CS1 maint: extra punctuation (link)
  25. ^ "Editorial: Starling's law survives". Lancet. 304 (7884): 818. October 1974. doi:10.1016/S0140-6736(74)91080-0. PMID 4138723.
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