Pressure–volume loop analysis in cardiology
A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot (pressure–volume diagram).
Real-time left ventricular (LV) pressure–volume loops provide a framework for understanding cardiac mechanics in experimental animals and humans.
Several physiologically relevant hemodynamic parameters such as stroke volume, cardiac output, ejection fraction, myocardial contractility, etc.
Hypertension increases the afterload, since the LV has to work harder to overcome the elevated arterial peripheral resistance and decreased compliance.
Preload is described as the stretching of a single cardiac myocyte immediately prior to contraction and is, therefore, related to the sarcomere length.
Since sarcomere length cannot be determined in the intact heart, other indices of preload such as ventricular end-diastolic volume or pressure are used.
Cardiac output (CO) is defined as the amount of blood pumped by the ventricle in unit time.
CO is an indicator of how well the heart is performing its function of transporting blood to deliver oxygen, nutrients, and chemicals to various cells of the body and to remove the cellular wastes.
Hence, the ability to accurately measure CO is important in physiology, as it provides for improved diagnosis of abnormalities, and can be used to guide the development of new treatment strategies.
However, CO is dependent upon loading conditions and is inferior to hemodynamic parameters defined by the PV plane.
However, EF is also dependent on loading conditions and inferior to hemodynamic parameters defined by the PV plane.
However, studies have shown that this parameter may not be a valid measure of LV relaxation rate, especially during acute alterations in contractility or afterload.
The accurate estimation of Tau is highly dependent on the accuracy of ventricular pressure measurements.
where Due to the load dependency of the previous parameters, more accurate measures of ventricular function are available in the PV plane.
This implies that the PV loop cannot cross over the line defining ESPVR for any given contractile state.
The slope of ESPVR (Ees) represents the end-systolic elastance, which provides an index of myocardial contractility.
This makes it an improved index of systolic function over other hemodynamic parameters like ejection fraction, cardiac output, and stroke volume.
Alternatively, for a given EDP, a less compliant ventricle would have a smaller EDV due to impaired filling.
The Pressure-volume area (PVA) represents the total mechanical energy generated by ventricular contraction.
This is equal to the sum of the stroke work (SW), encompassed within the PV loop, and the elastic potential energy (PE).
The slope of the PRSW relationship is a highly linear index of myocardial contractility that is insensitive to preload and afterload.
During heart failure, myocardial contractility is reduced, which decreases the slope of the PRSW relationship.
As a result, LV pressures are elevated, the ESV is increased, and the EDV is decreased, causing an overall reduction in cardiac output.
Restrictive cardiomyopathy includes a group of heart disorders in which the walls of the ventricles become stiff (but not necessarily thickened) and resist normal filling with blood between heartbeats.
The magnitude of the pressure gradient is determined by the severity of the stenosis and the flow rate across the valve.
Mitral stenosis impairs LV 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.
The constant backflow of blood through the leaky aortic valve implies that there is no true phase of isovolumic relaxation.
The constant backflow of blood through the leaky mitral valve implies that there is no true phase of isovolumic contraction.
There is also no true period of isovolumic relaxation because some LV blood flows back into the left atrium through the leaky mitral valve.
