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 (pressure–volume diagram). A number of methods have been determined for measuring PV-loop values experimentally.
Cardiac pressure–volume loops
Real-time left ventricular (LV) pressure–volume loops provide a framework for understanding cardiac mechanics in experimental animals and humans. Such loops can be generated by real-time measurement of pressure and volume within the left ventricle. Several physiologically relevant hemodynamic parameters such as stroke volume, cardiac output, ejection fraction, myocardial contractility, etc. can be determined from these loops. To generate a PV loop for the left ventricle, the LV pressure is plotted against LV volume at multiple time points during a single cardiac cycle.
Cardiac terminology
Afterload Afterload is the mean tension produced by a chamber of the heart in order to contract. It can also be considered as the ‘load’ that the heart must eject blood against. Afterload is, therefore, a consequence of aortic large vessel compliance, wave reflection, and small vessel resistance (LV afterload) or similar pulmonary artery parameters (RV afterload). Left ventricular afterload is affected by various disease conditions. Hypertension increases the afterload, since the LV has to work harder to overcome the elevated arterial peripheral resistance and decreased compliance. Aortic valve diseases like aortic stenosis and insufficiency also increase the afterload, whereas mitral valve regurgitation decreases the afterload.
Preload 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. As an example, preload increases when venous return is increased. This is because the end-diastolic pressure and volume of the ventricle are increased, which stretches the sarcomeres. Preload can be calculated as
preload = LVEDP × LVEDR 2 h {\displaystyle {\text{preload}}={\frac {{\text{LVEDP}}\times {\text{LVEDR}}}{2{\text{h}}}}}
where
LVEDP = left ventricular end-diastolic pressure LVEDR = left ventricular end-diastolic radius (at midpoint of ventricle) h = thickness of ventricle
Pressure–volume parameters
Stroke volume Stroke volume (SV) is the volume of blood ejected by the right/left ventricle in a single contraction. It is the difference between the end-diastolic volume (EDV) and the end-systolic volume (ESV). In mathematical terms, SV = EDV − ESV {\displaystyle {\text{SV}}={\text{EDV}}-{\text{ESV}}}
The stroke volume is affected by changes in preload, afterload, and inotropy (contractility). In normal hearts, the SV is not strongly influenced by afterload, whereas, in failing hearts, the SV is highly sensitive to afterload changes. Stroke volume relative to EDV is Ejection Fraction.
Stroke work Ventricular stroke work (SW) is defined as the work performed by the left or right ventricle to eject the stroke volume into the aorta or pulmonary artery, respectively. The area enclosed by the PV loop is a measure of the ventricular stroke work, which is a product of the stroke volume and the mean aortic or pulmonary artery pressure (afterload), depending on whether one is considering the left or the right ventricle.
Cardiac output Cardiac output (CO) is defined as the amount of blood pumped by the ventricle in unit time. In mathematical terms, CO = SV × Heart Rate {\displaystyle {\text{CO}}={\text{SV}}\times {\text{Heart Rate}}} . 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. CO is regulated principally by the demand for oxygen by the cells of the body.
Physiologic relevance Diseases of the cardiovascular system, such as hypertension and heart failure, are often associated with changes in CO. Cardiomyopathy and heart failure cause a reduction in cardiac output, whereas infection and sepsis are known to increase cardiac output. 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. Further reading: Bramwel's book of physiology
Ejection fraction Ejection fraction (EF) is defined as the fraction of end-diastolic volume that is ejected out of the ventricle during each contraction. In mathematical terms, EF = SV EDV {\displaystyle {\text{EF}}={\frac {\text{SV}}{\text{EDV}}}}
Healthy ventricles typically have ejection fractions greater than 0.55. However, EF is also dependent on loading conditions and inferior to hemodynamic parameters defined by the PV plane.
Physiologic relevance Myocardial infarction or cardiomyopathy causes damage to the myocardium, which impairs the heart's ability to eject blood and, therefore, reduces ejection fraction. This reduction in the ejection fraction can manifest itself as heart failure. Low EF usually indicates systolic dysfunction, and severe heart failure can result in EF lower than 0.2. EF is also used as a clinical indicator of the inotropy (contractility) of the heart. Increasing inotropy leads to an increase in EF, whereas decreasing inotropy decreases EF.
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