Information about Frank Starling Law Of The Heart
The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
This means that the force of contractions will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fiber. In particular, such increased load stretches further the myocardium and enhances the affinity of troponin C for Calcium, hence increasing the contractile force. The force that any single muscle fibre generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibres is related to the end-diastolic volume of the ventricle. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in the normal heart. Initial lengths larger or smaller than this optimal value will drop the force of the muscle owing to: less overlap of the thin and thick filaments for larger values and more overlap of the thin filaments for smaller values.
This can be seen most dramatically in the case of a 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 increases, increasing preload, this will increase stroke volume. The heart will pump what it receives.
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.
Long before the development of the sliding filament hypothesis and our understanding that active tension depends on the sarcomere's length, in 1914 Ernest Starling hypothesized 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." Therefore, the initial length of myocardial fibers determines the work done during the cardiac cycle.
Otto Frank (June 21, 1865 - 1944) was a German physiologist. He was educated at Munich, Kiel, Heidelberg, Glasgow and Strassburg.
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Chronotropic effects (from chrono-, meaning time) are those that change the heart rate.
Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.
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This means that the force of contractions will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fiber. In particular, such increased load stretches further the myocardium and enhances the affinity of troponin C for Calcium, hence increasing the contractile force. The force that any single muscle fibre generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibres is related to the end-diastolic volume of the ventricle. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in the normal heart. Initial lengths larger or smaller than this optimal value will drop the force of the muscle owing to: less overlap of the thin and thick filaments for larger values and more overlap of the thin filaments for smaller values.
This can be seen most dramatically in the case of a 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 increases, increasing preload, this will increase stroke volume. The heart will pump what it receives.
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.
History
The law is 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 sarcomere's length, in 1914 Ernest Starling hypothesized 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." Therefore, the initial length of myocardial fibers determines the work done during the cardiac cycle.
See also
External links
Cardiovascular system, physiology: cardiovascular physiology | |
|---|---|
| Volumes | Preload - Afterload - End-systolic volume - End-diastolic volume - Frank-Starling law of the heart |
| Interactions | Cardiac output - Wiggers diagram - Pressure volume diagram |
| Tropism | Chronotropic - Dromotropic - Inotropic |
| Hemodynamics | Baroreflex - Kinin-kallikrein system - Renin-angiotensin system - Vasoconstrictors - Vasodilators - Compliance - Vascular resistance |
| Other | Electrical conduction system of the heart (Cardiac action potential) |
In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in a ventricle at the end of filling (diastole). Because greater EDVs cause greater distention of the ventricle, EDV is often used synonymously with preload
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Stroke volume is the amount of blood pumped by the left ventricle of the heart in one contraction.
The stroke volume is not all of the blood contained in the left ventricle. The heart does not pump all the blood out of the ventricle.
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The stroke volume is not all of the blood contained in the left ventricle. The heart does not pump all the blood out of the ventricle.
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A sarcomere is the basic unit of a muscle's cross-striated myofibril. Sarcomeres are multi-protein complexes composed of three different filament systems.
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- The thick filament system is composed of myosin protein which is connected from the M-line to the Z-disc by Titin
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preload is the pressure stretching the ventricle of the heart, after passive filling and atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
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Premature ventricular contraction
Classification & external resources
Premature ventricular contraction in an ECG (arrows)
ICD-10 I 49.3
ICD-9 427.
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Classification & external resources
Premature ventricular contraction in an ECG (arrows)
ICD-10 I 49.3
ICD-9 427.
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The left ventricle is one of four chambers (two atria and two ventricles) in the human heart. It receives oxygenated blood from the left atrium via the mitral valve, and pumps it into the aorta via the aortic valve.
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The aorta (generally pronounced [eɪˈɔːtə] or "ay-orta") is the largest artery in the human body, originating from the left ventricle of the heart and bringing oxygenated blood to all parts of the body in the systemic circulation.
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Heart failure
Classification & external resources
ICD-10 I 50.0
ICD-9 428.0
DiseasesDB 16209
MedlinePlus 000158
eMedicine med/3552
MeSH D006333
Congestive heart failure (CHF), also called
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Classification & external resources
ICD-10 I 50.0
ICD-9 428.0
DiseasesDB 16209
MedlinePlus 000158
eMedicine med/3552
MeSH D006333
Congestive heart failure (CHF), also called
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Laplace's law or The law of Laplace may refer to several concepts,
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- Biot-Savart law, in electromagnetics, it describes the magnetic field set up by a steady current density.
- Young-Laplace equation, describing pressure difference over an interface in fluid mechanics.
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- For the father of Anne Frank, see Otto Frank.
Otto Frank (June 21, 1865 - 1944) was a German physiologist. He was educated at Munich, Kiel, Heidelberg, Glasgow and Strassburg.
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Ernest Starling was an English physiologist born on April 17 1866, in London, and died on May 2 1927. He worked mainly at University College London, although he also worked for many years in Germany and France.
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Formulated in 1896 by the British physiologist Ernest Starling, the Starling equation illustrates the role of hydrostatic and oncotic forces (the so-called Starling forces) in the movement of fluid across capillary membranes.
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Who Named It? is an English-language dictionary of medical eponyms and the people associated with their identification. Though this is a dictionary, many eponyms and persons are presented in extensive articles with comprehensive bibliographies.
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GPnotebook is a British medical database for general practitioners (GPs).[1] It is an online encyclopaedia of medicine that provides an immediate reference resource for clinicians worldwide. The database consists of over 30,000 pages of information.
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Circulatory System is a psychedelic rock musical ensemble formed by musician/painter Will Cullen Hart, and featuring Hannah Jones, Derek Almstead, Peter Erchick, John Fernandes, and Heather McIntosh.
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Human physiology is the science of the mechanical, physical, and biochemical functions of humans in good health, their organs, and the cells of which they are composed. The principal level of focus of physiology is at the level of organs and systems.
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Cardiovascular physiology is the study of the circulatory system. More specifically, it addresses the physiology of the heart ("cardio") and blood vessels ("vascular").
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preload is the pressure stretching the ventricle of the heart, after passive filling and atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
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afterload is used to mean the tension produced by a chamber of the heart in order to contract. If the chamber is not mentioned, it is usually assumed to be the left ventricle. However, the strict definition of the term relates to the properties of a single cardiac myocyte.
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End-systolic volume (ESV) is the volume of blood in the ventricles just after systole. The amount of blood in the ventricle at the end of the cardiac ejection period and immediately preceding the beginning of ventricular relaxation; a measurement of the adequacy of cardiac
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In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in a ventricle at the end of filling (diastole). Because greater EDVs cause greater distention of the ventricle, EDV is often used synonymously with preload
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Cardiac output (CO) is the volume of blood being pumped by the heart, in particular by a ventricle in a minute.
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Normal Output
Cardiac output is equal to the stroke volume (SV) multiplied by the heart rate (HR)...... Click the link for more information.
Wiggers diagram is a standard diagram used in cardiac physiology.
The X axis is used to plot time, while the Y axis contains all of the following on a single grid:
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The X axis is used to plot time, while the Y axis contains all of the following on a single grid:
- Blood pressure
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A pressure volume diagram (or P-V diagram, or volume-pressure loop)[1]) is used to describe a thermal cycle involving the following two variables:
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- Volume (on the X axis)
- Pressure (on the Y axis)
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Chronotropic effects (from chrono-, meaning time) are those that change the heart rate.
Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.
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A dromotropic agent is one which affects the conduction velocity of the AV node, and subsequently the rate of electrical impulses in the heart.[1][2]
Agents that are dromotropic are often (but not always) inotropic and chronotropic.
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Agents that are dromotropic are often (but not always) inotropic and chronotropic.
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An inotrope (IPA: [ˈaɪnətrop]) is an agent which increases or decreases the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions.
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Hemodynamics, meaning literally "blood movement", is the study of blood flow or the circulation.
All animal cells require oxygen (O2) for the conversion of carbohydrates, fats and proteins into carbon dioxide (CO2), water and energy in a process known as aerobic respiration.
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All animal cells require oxygen (O2) for the conversion of carbohydrates, fats and proteins into carbon dioxide (CO2), water and energy in a process known as aerobic respiration.
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In cardiovascular physiology, the baroreflex or baroreceptor reflex is one of the body's homeostatic mechanisms for maintaining blood pressure. It provides a negative feedback loop in which an elevated blood pressure reflexively causes blood pressure to decrease; similarly,
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The kinin-kallikrein system or simply kinin system is a poorly delineated system of blood proteins that plays a role in inflammation, blood pressure control, coagulation and pain. Its important mediators bradykinin and kallidin are vasodilators and act on many cell types.
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