Pressure-Volume Loops: Foundations and Frameworks
Does a decrease in contractility result in an increase or decrease in stroke volume?
It results in a decrease in stroke volume.
Let's look at the valvular and volume changes shown in Figure 1 in more detail: Opening of the aortic valve (2):
Opening of the aortic valve (2): Once the pressure of the left ventricle exceeds the afterload of the aorta, blood is rapidly ejected into the aorta, resulting in the decrease in left ventricular volume observed travelling right to left on the graph during phase 2.
What phases occur when the aortic and mitral valves are closed?
The isovolumetric contraction and isovolumetric relaxation periods occur when both valves are closed.
The phases of the pressure-volume relationships as illustrated in Figure 1 include
The phases of the pressure-volume relationships as illustrated in Figure 1 include isovolumetric contraction (1), systolic ejection (2), isovolumetric relaxation (3), rapid ventricular filling (4), and final ventricular filling with atrial systole (5). The major difference among these phases involves the opening and closing of the aortic and mitral valves and the flow of blood.
stroke work is equivalent to?
This means that stroke work is equivalent to the area under the pressure-volume loop curve, or the integral of pressure multiplied by the derivative of volume. Stroke work can therefore be estimated as stroke volume (the horizontal displacement) multiplied by the mean arterial pressure (the average vertical displacement).
How do you calculate the stroke volume from the pressure-volume loop?
You can calculate the SV by subtracting the ESV from the EDV on the x-axis.
Afterload describes ?
Afterload describes the resistance to ejection from the left ventricle. This is the resistance that must be overcome to eject the stroke volume. Such increased afterload, as in aortic stenosis or arterial hypertension, for example, will decrease stroke volume, which ultimately results in increased end-systolic volume (Figure 3). As the diagonal line demonstrates, afterload changes don't affect contractility, and the innate ability of the cardiac myocytes to contract is maintained. However, the ventricle is working against an increased resistance and its efficiency will decrease. Clinically, afterload is estimated by the total peripheral resistance, or more roughly by the mean arterial pressure, but the presence of aortic stenosis will also increase afterload regardless of these measurements. **Afterload has an indirect [inverse] relationship with stroke volume. Also, does not change the contractility.
Let's look at the valvular and volume changes shown in Figure 1 in more detail: Aortic and mitral valves closed (1):
Aortic and mitral valves closed (1): During this phase of isovolumetric contraction, both the mitral valve and aortic valve are closed, as the contracting ventricle generates enough pressure to overcome the pressure in the aorta (the afterload). The force exerted by contraction of cardiac myocytes against closed valves results in a dramatic increase in intraventricular pressure during this phase.
What Are Pressure Volume Loops?
As the heart moves through each cycle of contraction (systole) and relaxation (diastole) to create a heartbeat, pressure and volume changes occur in the ventricles. Visually, these changes can be shown on graphs known as pressure-volume loops: pressure is indicated on the y-axis, volume is indicated on the x-axis, Measurements taken from the pressure-volume loops can then be used to calculate other parameters, including stroke volume and ejection fraction, all of which can be used to assess cardiac performance.
Let's look at the valvular and volume changes shown in Figure 1 in more detail: Closure of the aortic valve (3):
Closure of the aortic valve (3): After the ejection is complete, the heart relaxes during diastole, at which time the pressure in the left ventricle decreases. During this phase of isovolumetric relaxation, there is no transfer of volume into or out of the ventricle since the aortic and mitral valves are both closed.
Contractility (inotropy) is
Contractility (inotropy) is the contractile force generated by myocytes independent of preload and afterload. It is typically due to changes in calcium availability to the myofilaments and contributes to the ability of the heart to accommodate blood ejection to meet the oxygen demand of the body. This is illustrated as a steady state in Figure 2 and Figure 3 and as the shifting diagonal line in Figure 4. A change in contractility, or inotropy, is a change in the intrinsic function of the myocytes themselves. With increased inotropy, at a constant preload and afterload, as illustrated by the leftward displacement and the increased slope of the diagonal line, greater pressure is generated and results in a greater ejection fraction. Thus, a change in contractility causes a change in the position and slope of the end-systolic pressure volume relationship curve. ***Intropy has a direct relationship with ejection fraction thus stroke volume. *here afterload and preload are held constant.
Ejection fraction is?
Ejection fraction is the percentage of EDV ejected from the ventricle with each beat. It is calculated as a ratio between the stroke volume and EDV. In a normally functioning heart, this fraction should be approximately 55%-60%.
Let's look at the valvular and volume changes shown in Figure 1 in more detail: Opening of the mitral valve (4, 5):
Opening of the mitral valve (4, 5): Ever since the closure of the mitral valve, the atria have been filling with blood. As left atrial pressure exceeds the pressure in the left ventricle, the mitral valve opens, and the ventricles begin to rapidly fill, as represented by phase 4. Atrial contraction, represented by phase 5, results in the final filling of the ventricles ("atrial kick"). Together, this increase in ventricular volume is represented by phases 4 and 5. So the early part of left ventricular diastolic filling is rapid and passive (due to mitral valve opening). The latter part, phase 5, is due to atrial contraction, near the end of ventricular filling.
Preload is related to ?
Preload is related to the amount of stretch of myocytes as a result of the end-diastolic volume (EDV) in the left ventricle as indicated by the lateral (rightward) displacement of the "base" line in Figure 2. If contractility is held constant (as indicated by the diagonal line), an increase in preload corresponds to larger stroke volume, as illustrated by the volume change on the x-axis of Figure 2. In practice, this usually occurs with increases in venous return to the heart, or slowing of the heart rate (which allows more time for ventricular filling with an increased EDV). Clinically, preload is estimated by the central venous pressure. Such changes in EDV are the basis for the Starling law of the heart and indicate changes in sarcomere length. Preload has a direct relationship with stroke volume
Returning to the pressure-volume loop, the three important variables that affect its shape are ?
Returning to the pressure-volume loop, the three important variables that affect its shape are 1) preload, 2) afterload, 3) contractility (sympathetic stimulation).
Stroke volume is the volume of blood that is successfully ejected out of the left ventricle to the rest of the body (systemic circulation). It can be calculated as the difference between end-diastolic and end-systolic volumes and is seen in the horizontal displacement of the loop.
Stroke volume is the volume of blood that is successfully ejected out of the left ventricle to the rest of the body (systemic circulation). It can be calculated as the difference between end-diastolic and end-systolic volumes and is seen in the horizontal displacement of the loop.
