Physiology, Starling Relationships - StatPearls - NCBI Bookshelf
Afterload is the pressure against which the heart must work to eject blood during systole. Disease processes pathology that include indicators such as an increasing left ventricular afterload include elevated blood "Afterload mismatch and preload reserve: A conceptual framework for the analysis of ventricular function". The normal cardiac cycle, showing pressure relationships between the left-sided Loading Conditions -- Preload and Afterload: The terms "preload" and . heart disease, cardiomyopathies, pericardial disease, ischemic heart disease and. Preload and afterload are intimately related. . If ventricular contractility is constant, the end-systolic P-V relationship is not . PDE inhibitors are also commonly used for afterload reduction in pediatric patients with congenital heart disease.Preload and afterload simplified
The remainder of ventricular filling occurs at the very end of diastole at which time there is atrial contraction followed immediately by closure of the mitral valve. In "stiff" or non-compliant hearts, the "atrial kick" component of left ventricular filling is proportionately higher. A major influence on how well the left ventricle fills is the "compliance" of the left ventricle. Left ventricular compliance is described using left ventricular filling curves which plot change in volume versus change in pressure.
The slope of the curve reflects the myocardial stiffness at any given point during left ventricular filling. Note that at low filling pressures, the left ventricular compliance curve is almost linear but that at higher volume and pressures it begins to curve upward more steeply. Note that the upper of these two curves represents a less compliant left ventricle, in which a higher left ventricular end-diastolic pressure is present at a given volume load.
A patient may be brought from point B to point A or from D to C by giving a diuretic to decrease intravascular volume or by giving a venous vasodilator -- thereby increasing the capacitance of the venous system and reducing volume entering the heart. Left ventricular systole occurs when the mitral valve closes and the left ventricle begins to contract, first through a brief period of "isovolumic contraction", immediately followed by opening of the aortic valve and the main portion of systole: This in turn is followed by closure of the aortic valve.
Systole can be considered the active phase of the cardiac cycle where myocardial contractility becomes the key to left ventricular performance. Left ventricular systolic performance can be graphed on a "Frank-Starling performance curve" which plots left ventricular performance, i. A sample curve is included below: The cardiac output, simply defined, is the net volume ejected by the left ventricle per minute, and is equal to the stroke volume times the heart rate, expressed in units of liters per minute.
In turn, the stroke volume the volume of blood ejected by the heart with each beat is determined by a number of factors, as diagrammed below: Each of these terms is defined in the table below, as taken from the textbook, page The ventricular wall tension at the end of diastole.
In clinical terms, it is the stretch on the ventricular fibers just prior to contraction, often approximated by the end-diastolic volume or end-diastolic pressure.
The ventricular wall tension during contraction; the resistance that must be overcome in order for the ventricle to eject its contents.
It is often approximated by the systolic ventricular or arterial pressure. A measurement of the magnitude of contractile force at a given resting fiber length. Loading Conditions -- Preload and Afterload: The terms "preload" and "afterload" are defined as the wall tension or wall stress during diastole and during systole, respectively.
Understanding cardiac output
What does this mean in real terms? It is for this reason that, clinically, we relate preload to the degree of volume which is loading the ventricle.
We therefore relate afterload to the pressure which the ventricle is pumping against, i. Note that any factor which lowers blood pressure will therefore lower afterload. Likewise, any factor that lowers left ventricular end-diastolic volume will lower preload.
Preload and pressure (video) | Khan Academy
Also, note that a compensatory increase in left ventricular wall thickness i. During systole, often thought of as the active phase of the cardiac cycle, the left ventricle contracts forcefully, ejecting approximately two-thirds of its contents with each beat.
The force of contraction is determined by the "contractility" of the ventricle, which, in turn, varies with the length of the individual sarcomere. In general, the farther each individual sarcomere is stretched, the greater the force of contraction. There is a limit, of course, to the length which each sarcomere can be stretched, and there is a point beyond which no further incremental force will be generated. To demonstrate the relationship between loading conditions and LV performance, a curve called a Frank-Starling performance curve can be created by plotting left ventricular end-diastolic volume or pressure -- i.
The position and slope of the curve reflect the contractile state of the individual ventricle at the point in time that the curve is drawn. Factors that augment the contractile state of the ventricle i.
Measurement of Cardiac Output: Well, the above curves sure look nice, but how on Earth do we obtain the values to create such a curve -- i.
So far, the most reliable way to do both is to place a balloon-tipped flexible tube called a Swan-Ganz catheter into a vein, and thread it through the right side of the heart to the pulmonary artery. There, inflation of the balloon allows us to measure the "pulmonary capillary wedge pressure" which, in turn, reflects the left atrial pressure.
Since the mitral valve is open during diastole, the left atrial pressure equals the left ventricular diastolic pressure barring any mitral valve stenosis. The left ventricle is filled with blood from the pulmonary veins.
As the ventricle contracts, it will eject blood more rapidly because the Frank-Starling mechanism will be activated by the increased preload. With no change in afterload or inotropy, the ventricle will eject blood to the same end-systolic volume despite the increase in preload.
Interdependent Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops
This ability to contract to the same end-systolic volume is a property of cardiac muscle that can be demonstrated using isolated cardiac muscle and studying isotonic shortening contractions under the condition of constant afterload.
When muscle preload length is increased, the contracting muscle shortens to the same minimal length as found before the preload was increased see Effects of Preload on Cardiac Fiber Shortening. If pulmonary venous flow decreases, then the ventricle will fill to a smaller end-diastolic volume decreased preload; green loop in figure. To summarize, changes in preload alter the stroke volume; however, end-systolic volume is unchanged if afterload and inotropy are held constant.
There is, however, a caveat to this discussion. For example, increasing end-diastolic volume leads to a small increase in end-systolic volume because of increased wall stress afterload at end-diastole. Therefore, ejection begins at a higher aortic diastolic pressure. If preload end-diastolic volume and inotropy are held constant, this will result in a smaller stroke volume and an increase in end-systolic volume red loop in figure. Stroke volume is reduced because increased afterload reduces the velocity of muscle fiber shortening and the velocity at which the blood is ejected see force-velocity relationship.