Clinical applications of the areas under ESPVR
Indexes of cardiac performance
It has long been observed that the use of the ejection fraction (EF) to assess the condition of the heart offers serious limitations (1). It is estimated that half of the patients presenting with symptoms of cardiomyopathies and heart failure (HF) have preserved EF defined as EF >50%. It was shown in (2) that the areas under the end-systolic pressure-volume relation (ESPVR) in the heart ventricles are sensitive indexes to reflect the state of the myocardium, a review of some clinical applications of indexes derived from the ESPVR can be found in (3). An objective of the study by Doyle et al. (4) is precisely to show that areas under the ESPVR, or bivariate combination of areas with another index, can be used as a prognostically useful tool for studying cases of women with suspected myocardial ischemia.
The ESPVR is the relation between pressure and volume in the left or right ventricle when the myocardium reaches its maximum state of activation near end-systole (2,3). There have been several studies on the ESPVR (3,5-7), most of these studies have focused on the use of the maximum slope Emax and the volume axis intercept Vom of the ESPVR in order to assess the state of the myocardium. Because of the difficulty to calculate Vom, some researchers have tried to neglect Vom and to approximate Emax ≈ (end-systolic pressure/end-systolic volume) (4). Such an approximation can only be justified if it is proven that the results obtained contain useful reliable clinical information. In what follows we introduce some relations that reflect the way the energetic of cardiac contraction is related to the areas under the ESPVR, and how the EF is also influenced by these areas. It may provide some background for the study published in (4).
Mathematical formalism
PVR
As in previous publications (8-11), the left ventricle is represented as a thick-walled cylinder contracting symmetrically (Figure 1). A radial active force Dr (force per unit volume of the myocardium) is developed by the myocardium during the contraction phase. The active pressure on the inner surface of the myocardium (endocardium) is given by ∫ab Dr dr=Piso, where a = inner radius of the myocardium, b = outer radius of the myocardium. We neglect inertia and viscous forces since they are relatively small. The equilibrium of forces on the endocardium can then be expressed in the form:
Piso–P = E (Ved–V) [1]
P is the left ventricular pressure, V is the corresponding left ventricular volume, Ved is the end-diastolic volume (the largest volume when dV/dt =0). The right-hand side of Equations [1] is the pressure on the endocardium resulting from the elastic deformation of the myocardium. When the elastance E reaches its maximum value Emax near end-systole (maximum state of activation of the myocardium), we can write Equations [1] as follows:
Pisom–Pm = Emax (Ved–Vm) [2]
We take Vm ≈ Ves the end-systolic volume when dV/dt = 0.
ESPVR
Equations [1] and [2] are represented graphically in a simplified way in Figure 2. The ESPVR is a relation between Pm and Vm when the peak isovolumic pressure Pisom is kept constant, it is represented by the line d3Vom with slope Emax.
During a normal ejecting contraction the PVR is represented by the rectangle Vedd2d1Vm. Equations [2] can be split into the following form:
Pm = Emax (Vm–Vom) [3]
Pisom = Emax (Ved–Vom) [4]
We can distinguish the following cases described by the ratio Emax/eam (maximum ventricular elastance/maximum arterial elastance) and the stroke volume SV ≈ Ved–Vm (see Figure 2).
(I) Normal physiological state of the heart, with d1 below d5 on the line d3Vom. In this case we have SV > (Ved–Vom)/2, with Emax/eam ≈2 and Pisom/Pm ≈3. This case corresponds to maximum efficiency for O2 consumption by the myocardium.
(II) Mildly depressed state of the heart, with d1 and d5 coinciding. In this case we have SV ≈ (Ved–Vom)/2, with Emax/eam ≈1 and Pisom/Pm ≈2. The stroke work SW reaches its maximum value SWmax.
(III) Severely depressed state of the heart, with d1 above d5 on the line d3Vom. In this case we have SV ed–Vom)/2, with Emax/eamisom/Pm
Notice from Figure 2 that in cases (II) and (III) an increase in pressure Pm causes a decrease of the stroke work SW, resulting in cardiac insufficiency.
Experimental verification of these results can be found in (5) (left ventricle) and in (6) (right ventricle) for experiments on dogs, and in (7) for results obtained from patients.
We have the following areas under the ESPVR:
(I) SW = Pm (SV), energy delivered to the systemic circulation;
(II) PE = Pm(Vm–Vom)/2, potential energy apparently related to the internal metabolism of the myocardium;
(III) CW = (Pisom–Pm) SV/2, energy apparently absorbed by the passive medium of the myocardium;
(IV) SWR = SWmax–SW, stroke work reserve. It is the reserve energy that can be delivered to the systemic circulation when afterload represented by Pm is increased.
We have SW + PE + CW = TW the total area under ESPVR. One can derive the following relation for the stroke volume:
SV = (CW/TW)1/2 (Ved –Vom) [5]
Which shows how SV (and EF = SV/Ved) is determined by the areas under the ESPVR. When CW/TW = 1/4 (d1 and d5 coincide in Figure 2), we get from Equations [5] SV = (Ved-Vom)/2. Experimental verification is shown in Figure 3. We also have:
Emax/eam =2×CW/SW [6]
Acknowledgements
Disclosure: The author declares no conflict of interest.
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