Preload

Heart during ventricular diastole.

In cardiac physiology, preload is the end diastolic volume that stretches the right or left ventricle of the heart to
its greatest dimensions under variable physiologic demand.[1] In other words, it is the initial stretching of
the cardiomyocytes prior to contraction; therefore, it is related to the sarcomere length at the end of diastole.
Parameters such as ventricular end diastolic volume or pressure are used to measure preload since the ideal
length of the cardiac sarcomere cannot be measured. Passive filling of the (heart) ventricle and subsequent
atrial contraction thus allows an echocardiographically volumetric measurement. Preload is theoretically most
accurately described as the initial stretching of a single cardiomyocyte prior to contraction. This cannot be
measured in vivo and therefore other measurements are used as estimates. Estimation may be inaccurate, for
example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the
relaxed ventricle to appear enlarged. The term end-diastolic volumeis better suited to the clinic, although not
exactly equivalent to the strict definition of preload. Atrial pressure is a surrogate for preload.

Calculation[edit]
Quantitatively, preload can be calculated as

where LVEDP = Left ventricular end diastolic pressure, LVEDR = Left ventricular end diastolic radius (at the
ventricle's midpoint), and h = thickness of the ventricle. This calculation is based on the Law of
Laplace which states that,
(wall stress) = Hence, preload is the wall stress. Preload is measured
in pressure units (mm Hg).

Factors affecting preload[edit]

Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous
tone and volume of circulating blood.
Preload is related to the ventricular end-diastolic volume; a higher end-diastolic volume implies a higher
preload. However, the relationship is not simple because of the restriction of the term preload to single
myocytes. Preload can still be approximated by the inexpensive echocardiographic measurement end
diastolic volume or EDV.
Preload increases with exercise (slightly), increasing blood volume (overtransfusion, polycythemia) and
neuroendocrine excitement (sympathetic tone).
An arteriovenous fistula can increase preload.[2]
Preload is also affected by two main body "pumps." The Respiratory pump - Intrathoracic pressure
decreases during inspiration and abdominal pressure increases, squeezing local abdominal veins, allowing
thoracic veins to expand and increase blood flow towards the right atrium. Skeletal muscle pump - In the
deep veins of the legs, surrounding muscles squeeze veins and pump blood back towards the heart. This
occurs most notably in the legs. Once blood flows past valves it cannot flow backwards and therefore blood
is milked towards the heart.
https://en.wikipedia.org/wiki/Preload_(cardiology)
Afterload
Ventricular systole. Red arrow is path from left ventricle to aorta. Afterload is largely dependent
upon aortic pressure.

Afterload is the stress in the wall of the left ventricle during ejection. In other
words, it is the end load against which the heart contracts to eject blood.
Afterload is readily broken into components: one factor is the aortic pressure
the left ventricular muscle must overcome to eject blood. The greater the
aortic/pulmonary pressure, the greater the after load on the left/right ventricle,
respectively. Following Laplace's law, the tension upon the muscle fibers in
the heart wall is the pressure within the ventricle multiplied by the volume
within the ventricle divided by the wall thickness (this ratio is the other factor
in setting the afterload). Therefore, when comparing a normal heart to a heart
with a dilated left ventricle, if the aortic pressure is the same in both hearts,
the dilated heart must create a greater tension to overcome the same aortic
pressure to eject blood because it has a larger internal radius and volume.
Thus, the dilated heart has a greater total load (tension) on the myocytes, i.e., has a
higher afterload. This is also true in the eccentric hypertrophy consequent to high intensity aerobic training.
Conversely, a concentrically hypertrophied left ventricle may have a lower afterload for a given aortic pressure.
When contractility becomes impaired and the ventricle dilates, the afterload rises and limits output. This may
start a vicious circle, in which cardiac output is reduced as oxygen requirements are increased.[1]
Afterload can also be described as the pressure that the chambers of the heart must generate in order to eject
blood out of the heart and thus is a consequence of the aortic pressure (for the left ventricle) and pulmonic
pressure or pulmonary artery pressure (for the right ventricle). The pressure in the ventricles must be greater
than the systemic and pulmonary pressure to open the aortic and pulmonic valves, respectively. As afterload
increases, cardiac output decreases. Cardiac imaging is a somewhat limited modality in defining afterload
because it depends on the interpretation of volumetric data.[citation needed]

Pathology[edit]
Disease processes pathology that include indicators such as an increasing left ventricular afterload include
elevated blood pressure and aortic valve disease.
Systemic hypertension (HTN) (elevated blood pressure) increases the left ventricular (LV) afterload because the
LV must work harder to eject blood into the aorta. This is because the aortic valve won't open until the pressure
generated in the left ventricle is higher than the elevated blood pressure in the aorta.[2]
Pulmonary hypertension (PH) is increased blood pressure within the right heart leading to the lungs. PH
indicates a regionally applied increase in afterload dedicated to the right side of the heart, divided and isolated
from the left heart by the interventricular septum.
In the natural aging process, aortic stenosis often increases afterload because the left ventricle must overcome
the pressure gradient caused by the calcified and stenotic aortic valve in addition to the blood pressure in order
to eject blood into the aorta. For instance, if the blood pressure is 120/80, and the aortic valve stenosis creates a
trans-valvular gradient of 30 mmHg, the left ventricle has to generate a pressure of 110 mmHg in order to open
the aortic valve and eject blood into the aorta.
Due to the increased afterload, the ventricle has to work harder to accomplish its goal of ejecting blood into the
aorta. Thus in the long-term, the increased afterload (due to the stenosis) will result in hypertrophy of the left
ventricle to account for the increased work required.
Aortic insufficiency (Aortic Regurgitation) increases afterload because a percentage of the blood that is ejected
forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure. The
diastolic blood pressure in the aorta would fall, due to regurgitation. This would result in an increase in pulse
pressure.
Mitral regurgitation MR decreases afterload. In ventricular systole under MR, regurgitant blood flows
backwards/retrograde back and forth through a diseased and leaking mitral valve. The remaining blood loaded
into the LV is then optimally ejected out through the aortic valve. With an extra pathway for blood flow through
the mitral valve, the left ventricle does not have to work as hard to eject its blood, i.e. there is a decreased
afterload.[3] Afterload is largely dependent upon aortic pressure.
https://en.wikipedia.org/wiki/Afterload
FrankStarling law
(Redirected from FrankStarling law of the heart)

Cardiac function curve In diagrams illustrating the FrankStarling 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 FrankStarling law of the heart (also known as Starling's law and the FrankStarling
mechanism) 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[edit]
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.[citation needed]
Due to the intrinsic property of myocardium that is responsible for the Frank-Starling mechanism, the heart can
automatically accommodate an increase in venous return, at any heart rate.[1][6] The mechanism is of functional
importance because it serves to adapt left ventricular output to right ventricular output.[3] If this mechanism did
not exist and the right and left cardiac outputs were not equivalent, blood would accumulate throughout
circulation.[1]

Clinical examples[edit]
Premature ventricular contraction[edit]
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 FrankStarling 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]

Diastolic dysfunction heart failure[edit]

Diastolic dysfunction is associated with a reduced compliance, or increased stiffness, of the ventricle wall. This
reduced compliance results in an inadequate filling of the ventricle and a decrease in the end-diastolic volume.
The decreased end-diastolic volume then leads to a reduction in stroke volume because of the Frank-Starling
mechanism.[1]

History[edit]
The FrankStarling law is named after the 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.[4] 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" .[7][8][9][10][11][12][13][14][15][16][17][18][19]
Otto Frank's contributions are derived from his 1895 experiments 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.[4]
Starling experimented on intact mammalian hearts, such as from dogs, to understand why variations in arterial
pressure, heart rate, and temperature do not affect the relatively constant cardiac output.[4]More than 30 years
before the development of sliding filament model of muscle contractionand 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.[20]

https://en.wikipedia.org/wiki/Frank%E2%80%93Starling_law