Cardiac function curve

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A cardiac function curve is a graph showing the relationship between right atrial pressure (x-axis) and cardiac output (y-axis).[ citation needed ] Superimposition of the cardiac function curve and venous return curve is used in one hemodynamic model. [1]

Contents

Shape of curve

The horizontal axis of Guyton diagram represents right atrial pressure or central venous pressure, and the vertical axis represents cardiac output or venous return. The red curve sloping upward to the right is the cardiac output curve, and the blue curve sloping downward to the right is the venous return curve. A steady state is formed at the point where the two curves meet. Starling RAP combined.svg
The horizontal axis of Guyton diagram represents right atrial pressure or central venous pressure, and the vertical axis represents cardiac output or venous return. The red curve sloping upward to the right is the cardiac output curve, and the blue curve sloping downward to the right is the venous return curve. A steady state is formed at the point where the two curves meet.
Cardiac function curve in Frank-Starling's law, illustrating stroke volume (SV) as a function of preload Frank Starling's curve.png
Cardiac function curve in Frank–Starling's law, illustrating stroke volume (SV) as a function of preload
The cardiac function curve expresses how systemic flow changes as a function of the central venous pressure; it represents the Frank-Starling mechanism. The vascular function curve expresses how "central venous pressure" changes as a function of "systemic flow". Note that, for cardiac function curve, "central venous pressure" is the independent variable and "systemic flow" is the dependent variable; for vascular function curve, the opposite is true. Cardiac and vascular function curves.png
The cardiac function curve expresses how systemic flow changes as a function of the central venous pressure; it represents the Frank-Starling mechanism. The vascular function curve expresses how "central venous pressure" changes as a function of "systemic flow". Note that, for cardiac function curve, "central venous pressure" is the independent variable and "systemic flow" is the dependent variable; for vascular function curve, the opposite is true.

It shows a steep relationship at relatively low filling pressures and a plateau, where further stretch is not possible and so increases in pressure have little effect on output. The pressures where there is a steep relationship lie within the normal range of right atrial pressure (RAP) found in the healthy human during life. This range is about -1 to +2 mmHg. The higher pressures normally occur only in disease, in conditions such as heart failure, where the heart is unable to pump forward all the blood returning to it and so the pressure builds up in the right atrium and the great veins. Swollen neck veins are often an indicator of this type of heart failure.[ citation needed ]

At low right atrial pressures this graph serves as a graphic demonstration of the Frank–Starling mechanism, [2] that is as more blood is returned to the heart, more blood is pumped from it without extrinsic signals.

Changes in the cardiac function curve

In vivo however, extrinsic factors such as an increase in activity of the sympathetic nerves, and a decrease in vagal tone cause the heart to beat more frequently and more forcefully. This alters the cardiac function curve, shifting it upwards. This allows the heart to cope with the required cardiac output at a relatively low right atrial pressure. We get what is known as a family of cardiac function curves, as the heart rate increases before the plateau is reached, and without the RAP having to rise dramatically to stretch the heart more and get the Starling effect.[ citation needed ]

In vivo sympathetic outflow within the myocardium is probably best described by the time honored description of the sinoatrial tree branching out to Purkinges fibers. Parasympathetic inflow within the myocardium is probably best described by influence of the vagus nerve and spinal accessory ganglia.[ citation needed ]

See also

Related Research Articles

<span class="mw-page-title-main">Frank–Starling law</span> Relationship between stroke volume and end diastolic volume

The Frank–Starling law of the heart 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, when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, 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, without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.

<span class="mw-page-title-main">Diastole</span> Part of the cardiac cycle

Diastole is the relaxed phase of the cardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.

<span class="mw-page-title-main">Atrial septal defect</span> Human heart defect present at birth

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<span class="mw-page-title-main">Jugular venous pressure</span> Blood pressure in a vein of the neck

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<span class="mw-page-title-main">Cardiac catheterization</span> Insertion of a catheter into a chamber or vessel of the heart

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<span class="mw-page-title-main">Atrium (heart)</span> Part of the human heart

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<span class="mw-page-title-main">Preload (cardiology)</span> Heart muscle stretch at rest

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<span class="mw-page-title-main">Cardiac cycle</span> Performance of the human heart

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<span class="mw-page-title-main">Central venous pressure</span> Blood pressure in vein near the heart

Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure.

The Bainbridge reflex or Bainbridge effect is a cardiovascular reflex causing an increase in heart rate in response to increased stretching of the wall of the right atrium due to increased filling of the right atrium with venous blood. It is detected by stretch receptors embedded within the wall of the right atrium, and regulated by a center in the medulla oblongata of the brain.

Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.

<span class="mw-page-title-main">Right atrial pressure</span>

Right atrial pressure (RAP) is the blood pressure in the right atrium of the heart. RAP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system. RAP is often nearly identical to central venous pressure (CVP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when venous tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure.

<span class="mw-page-title-main">Volume overload</span>

Volume overload refers to the state of one of the chambers of the heart in which too large a volume of blood exists within it for it to function efficiently. Ventricular volume overload is approximately equivalent to an excessively high preload. It is a cause of cardiac failure.

In medicine, the mean systemic pressure (MSP) or mean systemic filling pressure (MSFP) is defined as the mean pressure that exists in the circulatory system when there is no blood motion. A similar term, mean circulatory filling pressure, (MCFP) is defined as the mean pressure that exists in the combined circulatory system & pulmonary system when there is no blood motion. The value of MSP in animal experimental models is approximately 7 mm Hg. It is an indicator of how full the circulatory system is, and is influenced by the volume of circulating blood and the smooth muscle tone in the walls of the venous system.

Low pressure baroreceptors are baroreceptors that relay information derived from blood pressure within the autonomic nervous system. They are stimulated by stretching of the vessel wall. They are located in large systemic veins and in the walls of the atria of the heart, and pulmonary vasculature. Low pressure baroreceptors are also referred to as volume receptors and cardiopulmonary baroreceptors.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

<span class="mw-page-title-main">Heart development</span> Prenatal development of the heart

Heart development, also known as cardiogenesis, refers to the prenatal development of the heart. This begins with the formation of two endocardial tubes which merge to form the tubular heart, also called the primitive heart tube. The heart is the first functional organ in vertebrate embryos.

<span class="mw-page-title-main">Pathophysiology of heart failure</span>

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

  1. Brengelmann GL (March 2003). "A critical analysis of the view that right atrial pressure determines venous return". J. Appl. Physiol. 94 (3): 849–59. doi:10.1152/japplphysiol.00868.2002. PMID   12391065.
  2. "Cardiac Basic Physiology". Archived from the original on 2008-10-11.