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Cardiac Pressure-Volume (PV) 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 clinically relevant hemodynamic parameters such as stroke volume, cardiac output, ejection fraction, myocardial contractility, etc. can be estimated 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 complete cardiac cycle.

Glossary of terms

• 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 pressure (LV afterload) or pulmonary artery pressure (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 aortic pressure. 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 initial stretching of a single cardiac myocyte 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.

Quantitatively, preload can be calculated as

where
     LVEDP = left ventricular end diastolic pressure
     LVEDR = left ventricular end diastolic radius (at midpoint of ventricle)
     h = thickness of ventricle

Pressure-Volume parameters

1. Stroke Volume (SV)

   Stroke volume is the volume of blood pumped out by the right/left ventricle in one contraction. It is the difference between the end diastolic volume (EDV) and the end systolic volume (ESV).

   Mathematically, SV = EDV – 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.

2. Stroke Work (SW)

   Ventricular stroke work is defined as the work done by the right/left ventricle to eject the stroke volume into the aorta or pulmonary artery. The area enclosed by the PV loop is an approximation 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.

   The area within pressure-volume loops only provides an estimate of cardiac stroke work due to the following factors.

   • PV loops fail to account for the heart rate (which has an effect on myocardial oxygen consumption, which in turn is proportional to cardiac work)
   • PV loops fail to account for changes in resting wall tension, which may also alter oxygen consumption.
   
   
3. Cardiac Output (CO)

   Cardiac output is defined as the amount of blood pumped out by the ventricle in unit time.

   Mathematically, CO = SV x heart rate

   CO is an indicator of how well the heart is performing its function of transporting the 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.

   Clinical 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 clinical medicine as it provides for improved diagnosis of abnormalities, and can be used to guide appropriate treatment strategies.

4. Ejection Fraction (EF)

   Ejection fraction is defined as the fraction of end diastolic volume that is ejected out of the ventricle during each contraction.

   Mathematically, EF = SV/EDV

   Healthy individuals typically have ejection fractions greater than 0.55. However, normal values depend upon the modality being used to calculate the ejection fraction.

   Clinical 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 clinically 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, while decreasing inotropy decreases EF.

5. dP/dtmin & dP/dtmax

   These represent the minimum and maximum rate of pressure change in the ventricle. Peak dP/dt has historically been used as an index of ventricular performance that is not influenced by afterload, wall motion abnormalities, or the variations in ventricular anatomy and morphology commonly encountered in diseased hearts.

   An increase in contractility as well as the ability to contract faster (chronotropy) is manifested as an increase in dP/dtmax during isovolumic contraction. However, dP/dtmax is also influenced by preload, afterload, heart rate and myocardial hypertrophy. Hence the relationship between ventricular end-diastolic volume and dP/dt is a more accurate index of contractility than dP/dt alone.

   Similarly, an increase in diastolic function or an increase in relaxation (lusotropy) causes increased dP/dtmin during isovolumic relaxation. Hence, dP/dtmin has been used as a valuable tool in the analysis of isovolumic relaxation. However, recent studies have shown that this parameter may not be a valid measure of LV relaxation rate, especially during acute alterations in contractility or afterload.

6. Isovolumic Relaxation Constant (Tau)

   This represents the exponential decay of the ventricular pressure during isovolumic relaxation. Several studies have shown that Tau is a preload independent measure of isovolumic relaxation.

   The accurate estimation of Tau is highly dependent on the accuracy of ventricular pressure measurements. Thus, high fidelity pressure transducers are required to obtain real time instantaneous ventricular pressures.

   Calculation of Tau (Raff and Glantz method)

   

   

   where
   P = pressure at time t
   P0 = amplitude constant
   τE = Glantz relaxation constant
   Pα = non zero asymptote due to pleural and pericardial pressure

PV Loop Analysis

1. End Systolic Pressure Volume Relationship (ESPVR)

   The ESPVR describes the maximal pressure that can be developed by the ventricle at any given LV volume. This implies that the PV loop cannot cross over the ESPVR for any given contractile state.

   The slope of ESPVR represents the end-systolic elastance, which provides an index of myocardial contractility. The ESPVR is relatively insensitive to changes in preload, afterload and heart rate. This makes it an improved index of systolic function over other PV loop parameters like ejection fraction, cardiac output and stroke volume.

   The ESPVR curve becomes steeper and shifts to the left as inotropy (contractility) increases.

   
   
2. End Diastolic Pressure Volume Relationship (EDPVR)

   The EDPVR describes the passive filling curve for the ventricle. The slope of the EDPVR at any point along this curve is the reciprocal of ventricular compliance (or ventricular stiffness).

   For example, if ventricular compliance is decreased (such as in ventricular hypertrophy), the ventricle is stiffer. This results in higher ventricular end-diastolic pressures (EDP) at any given end-diastolic volume (EDV). Alternatively, for a given EDP, a less compliant ventricle would have a smaller EDV due to impaired filling.

   If ventricular compliance increases (such as in dilated cardiomyopathy where the ventricle becomes highly dilated without appreciable thickening of the wall), the EDV may be very high but the EDP may not be greatly elevated.

   
   
3. Pressure-Volume  Area (PVA)

   The 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).

    Mathematically, PVA = PE + SW

   also,    PE = PES(VES – V0)/2 – PED(VED – V0)/4
   where PES – end systolic pressure
                     PED – end diastolic pressure
                     VES – end systolic volume
                     VED – end diastolic volume
                     V0 – theoretical volume when no pressure is generated

   Clinical Relevance

   There is a highly linear correlation between the PVA and cardiac oxygen consumption per beat. This relationship holds true under a variety of loading and contractile conditions. This estimation of myocardial oxygen consumption (MVO2) is used to study the coupling of mechanical work and the energy requirement of the heart in various disease states, such as diabetes, ventricular hypertrophy and heart failure. MVO2 is also used in the calculation of cardiac efficiency, which is the ratio of cardiac stroke work to MVO2.

   
   
4. Preload Recruitable Stroke Work (PRSW)

   PRSW is determined by the linear regression of stroke work with the end diastolic volume. The slope of the PRSW relationship is a highly linear index of myocardial contractility that is insensitive to preload and afterload.

   Clinical Relevance

   During heart failure, myocardial contractility is reduced which decreases the slope of the PRSW relationship. Recent studies also indicate that the volume axis intercept of the PRSW relationship (not the slope) may be a better indicator of the severity of contractile dysfunction.

5. Frank-Starling Curve

   “The heart will pump what it receives”- Starling’s law of the heart

   The Frank-Starling mechanism describes the ability of the heart to change its force of contraction (and hence stroke volume) in response to changes in venous return. In other words, if the end diastolic volume increases, there is a corresponding increase in stroke volume.

   The Frank-Starling mechanism can be explained on the basis of preload. As the heart fills with more blood than usual, there is an increase in the load experienced by each muscle fiber. This stretches the muscle fibers, increasing the affinity of troponin C to Ca2+ ions causing a greater number of cross-bridges to form within the muscle fibers. This increases the contractile force of the cardiac muscle, resulting in increased stroke volume.

   

   Frank Starling curves can be used as an indicator of muscle contractility (inotropy). However, there is no single Frank-Starling curve on which the ventricle operates, but rather a family of curves, each of which is defined by the afterload and inotropic state of the heart. Increased afterload or decreased inotropy shifts the curve down and to the right. Decreased afterload and increased inotropy shifts the curve up and to the left.

   
   
6. Arterial Elastance (Ea)

   This is a measure of arterial load and is calculated as the simple ratio of ventricular end-systolic pressure to stroke volume.

   

   Mathematically, Ea = ESP/SV

   By characterizing both the ventricular and arterial systems in terms of pressure and stroke volume, it is possible to study the ventriculo-arterial coupling (the interaction between the heart and the arterial system).