Ventricular Pressure-Volume Relationship
The cardiac cycle diagram depicts changes in ventricular pressure and volume as a function of time. This information can be obtained by placing a catheter inside the left ventricle and measuring changes in intraventricular pressure as the heart beats. This same catheter can also be used to inject a radiopaque contrast agent into the left ventricular chamber, thereby permitting fluoroscopic imaging of the ventricular chamber from which estimates of ventricular volume can be obtained. Alternatively, ventricular volume changes can be assessed in real time using echocardiography or radionuclide imaging. While measurement of pressure and volume changes as a function of time can provide important insights into ventricular function, another powerful tool for analyzing ventricular function is constructing pressure-volume loops from ventricular volume and pressure data.
Pressure-volume (PV) loops are generated by plotting left ventricular pressure (LVP) against left ventricular volume at many time points during a complete cardiac cycle. When this is done, a PV loop is generated (bottom panel of figure). In the figure, the letters represent the cardiac cycle phases of ventricular filling (a), isovolumetric contraction (b), ejection (c), and isovolumetric relaxation (4). The end-diastolic volume (EDV) is the maximal volume achieved at the end of filling, and end-systolic volume (ESV) is the minimal volume (i.e., residual volume) of the ventricle found at the end of ejection. The width of the loop, therefore, represents the difference between EDV and ESV, which is by definition the stroke volume (SV). The filling phase moves along the end-diastolic pressure-volume relationship (EDPVR), or passive filling curve for the ventricle. The slope of the EDPVR is the reciprocal of ventricular compliance. The maximal pressure that can be developed by the ventricle at any given left ventricular volume is the end-systolic pressure-volume relationship (ESPVR), which represents the inotropic state of the ventricle. The pressure-volume loop, therefore, cannot cross over the ESPVR, because it defines the maximal pressure that can be generated under a given inotropic state. The end-diastolic and end-systolic pressure-volume relationships are analogous to the passive and total tension curves used to analyze muscle function.
Ventricular Pressure-Volume Loop Changes in Valve Disease
Cardiac valve disease significantly alters ventricular pressure and volume relationships during the cardiac cycle. A convenient way to analyze cardiac pressure and volume changes is by using ventricular pressure-volume loops. The following describes pressure-volume changes that occur during:
Mitral stenosis impairs left ventricular filling so that there is a decrease in end-diastolic volume (preload). This leads to a decrease in stroke volume by the Frank-Starling mechanism and a fall in cardiac output and aortic pressure. This reduction in afterload (particularly aortic diastolic pressure) enables the end-systolic volume to decrease slightly, but not enough to overcome the decline in end-diastolic volume. These changes just described do not include cardiac and systemic compensatory mechanisms that attempt to maintain cardiac output and arterial pressure. These compensatory responses include, but are not limited to, systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy.
In aortic stenosis, left ventricular emptying is impaired because of high outflow resistance. The stenosis leads to an increase in ventricular afterload, a decrease in stroke volume, and an increase in end-systolic volume. Stroke volume decreases because the velocity of fiber shortening is decreased by the increased afterload (see force-velocity relationship). Because end-systolic volume is elevated, the excess residual volume added to the incoming venous return causes the end-diastolic volume to increase. This increases preload and activates the Frank-Starling mechanism to increase the force of contraction to help the ventricle overcome, in part, the increased outflow resistance. In mild aortic stenosis, this can be adequate to maintain normal stroke volume, but in moderate and severe stenosis, the stroke volume falls as shown in the figure because the end-systolic volume increases more than the end-diastolic volume increases. These changes just described do not include cardiac and systemic compensatory mechanisms that attempt to maintain cardiac output and arterial pressure. These compensatory responses include, but are not limited to, systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy.
In mitral valve regurgitation, as the left ventricle contracts, blood is not only ejected into the aorta but also back up into the left atrium. This causes left atrial volume and pressure to increase during ventricular systole. Note in the pressure-volume loop that there is no true isovolumetric contraction phase because blood begins to flow across the mitral valve and back into the atrium before the aortic valve opens. Because of mitral regurgitation, the afterload on the ventricle is reduced (total outflow resistance is reduced) so that end-systolic volume can be smaller than normal; however, end-systolic volume can increase if the heart also goes into systolic failure. There is no true isovolumetric relaxation because as the ventricle begins to relax, the mitral valve is never closed completely so blood flows back into the left atrium as long as intraventricular pressure is greater than left atrial pressure. During diastole, the elevated pressure within the left atrium is transmitted to the left ventricle during filling so that left ventricular end-diastolic volume increases. This would cause wall stress (afterload) to increase if it were not for the reduced outflow resistance that tends to decrease afterload during ejection. The net effect of these changes is that the width of the pressure-volume loop is increased; however, ejection into the aorta is reduced. The increased ventricular "stroke volume" in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium. These changes just described do not include cardiac and systemic compensatory mechanisms that attempt to maintain cardiac output and arterial pressure. These compensatory responses include, but are not limited to, systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy.
In aortic valve regurgitation, the aortic valve does not close completely at the end of systolic ejection. As the ventricle relaxes during diastole, blood flows from the aorta back into the ventricle. Therefore, there is no true phase of isovolumetric relaxation because as the ventricle relaxes, even before the mitral valve opens, blood is entering the ventricle from the aorta thereby increasing ventricular volume. Once the mitral valve opens, filling occurs from the left atrium; however, blood continues to flow from the aorta into the ventricle throughout diastole because aortic pressure is higher than ventricular pressure during diastole. This greatly enhances ventricular filling so that end-diastolic volume is increased as shown in the pressure-volume loop. The increased end-diastolic volume (increased preload) activates the Frank-Starling mechanism to increase the force of contraction and therefore stroke volume as shown by the increased width of the pressure-volume loop. Left ventricular peak pressure also increases because of the large stroke volume ejected into the aorta. As long as the ventricle is not in failure, normal end-systolic volumes are observed However, once the ventricle goes into systolic failure, then end-systolic volume increases. These changes just described do not include cardiac and systemic compensatory mechanisms that attempt to maintain cardiac output and arterial pressure. These compensatory responses include, but are not limited to, systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy.