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pV Diagram

End systolic elastance

End-systolic elastance shows the slope angle of the End-systolic pressure volume relation (ESPVR). It is a measure of the heart contractility, resulting in a steeper slope when contractility is enhanced.

Total vascular resistance

Total vascular resistance is a sum of alveolar and extra-alveolar resistances that resists the flow of blood and generates pressure.

Heart rate

The heart rate is an intrinsic quality of the heart. It directly shows how many electric signals the heart's internal pacemaker produces that result in heart contraction in one minute.

End-diastolic volume

End-diastolic volume is a variable that represents the hearts ability to extend and fill with blood. It show the maximal ventricle volume prior to contraction.


Pressure-volume diagram

If one looks at how the heart performs its main task, which is moving blood through the body to supply oxygen and metabolic substrates to the peripheral tissues [1], one quickly understands that it accomplishes this through generating pressure with contractions. To display this mechanism, researchers have plotted a pressure-volume loop diagram to depict this process in graph form.

Understanding the graph

The graph shows two different linear functions. The line (shown in blue) represents the ventricular contraction and is also termed the end-systolic pressure volume relationship (ESPVR), whilst the line (shown in red) represents the arterial elastance. They intersect at the end-systolic pressure value. The independent variable is the blood volume measured in millilitres (mL) (represented on the x-axis) and the dependent variable is the pressure measured in mmHg (represented on the y-axis). There are two points illustrated on the x-axis: the unstressed ventricle volume, which also marks the starting point of the line, and end-diastolic volume, which also marks the starting point of the line. The difference between the end-diastolic volume and end-systolic volume, which corresponds with the volume at the end-systolic pressure value, results in stroke volume. If one connects the end-diastolic volume point and end-systolic pressure point with the adjacent points to form a rectangle, one gets and approximation of the pressure volume loop. The right side of the rectangle represents isovolumetric contraction, the top side systolic ejection, the left side isovolumetric relaxation and the bottom side diastolic filling.

The cardiac cycle

The cardiac cycle can be divided into two main phases: systole and diastole, which can further be divided into two more parts. The four sides of the rectangle shown in the graph correspond with the four parts and indicate the timing of four valvular events, which terminate each of the four phases. Phase 1 is comprised of ventricular filling during diastole and ends with atrioventricular valve closure. Phase 2 depicts isovolumetric contraction of ventricles, where the ventricle volume does not change, because all valves are closed, which results in pressure build-up (from about 8 mmHg to 80 mmHg) and ends with semilunar valve opening. As the semilunar valves open, phase 3 also known as the ejection phase begins. During phase 3 ventricular pressure continues to rise to reach a maximum at the systolic blood value pressure value, followed by a fall in the pressure ending with the end-systolic pressure value when the semilunar valves close. The reason for the pressure fall and semilunar valves not closing at the uppermost pressure is inertia of blood flow, which imparts considerable kinetic energy to the blood. The cardiac cycle ends with phase 4 also termed isovolumetric relaxation, which marks the beginning of diastole and ends with the atrioventricular valves opening [1, 2, 3]. If one looks at the graph, this cardiac cycle and all the changes that occur is also termed the pressure-volume loop.


Preload can be defined as the stretching of cardiac muscle prior to systole imposed on the heart by initial sarcomere length and end diastolic volume. Starling’s law that states that a greater fiber length causes the heart to deliver more mechanical energy, i.e. to contract more, focuses on preload [2]. The direct effect of preload on the heart can be seen by regulating the end diastolic volume in our graph, where a higher end diastolic volume, i. e. more blood in the ventricle, results in a higher stroke volume and higher generated pressure. Yet one cannot simply raise the end diastolic volume endlessly, but one must adhere to the end diastolic pressure volume relation (see below), which limits ventricular distention.


Afterload portrays forces that the contracting myocytes must overcome [2]. It may be defined as the tension or stress developed in the ventricle wall during ejection [1]. A convenient index of the opposing forces is arterial pressure that opposes blood flow from the ventricles. Myocytes that try to overcome a greater afterload do so with a higher tension and contract more slowly than myocytes overcoming a lower afterload [2].

End-systolic pressure-volume relation

If one would measure the pressure in the ventricle after systole (end-systolic pressure) for multiple cardiac cycles with different end-diastolic volumes, provided other physiological parameters such as contractility would not change, the end systolic pressure values would fall along a line when plotted in a graph. This line is also termed the end-systolic pressure-volume relation (ESPVR), because it represents the relationship between pressure and volume at an instant of maximal activation – end-systole. The steepness of the slope represents cardiac contractility, where a steeper slope shows higher contractility, stroke volume and blood pressure generated [2, 4].

End-diastolic pressure volume relation

End-diastolic pressure-volume relationship is a relationship between pressure and volume in the ventricle at the instant of complete relaxation (end-diastole). One could imagine the heart as an empty balloon, even when there is no pressure on the wall, there is still some volume left in the opening. The volume at pressure 0 is often referred to as V0 or unstressed volume. Then when the heart slowly begins to fill with blood the pressure remains constantly low, until at some point begins to rise rapidly. This point is dependent on the heart’s intrinsic properties such as compliance. The EDPVR limits the distention of the heart’s ventricles [4].

Intersection of the ESPVR and EDPVR

Sunagawa et al. measured how the end systolic and end-diastolic pressure-volume relation curves course in the negative pressure region, and found that the two curves converge with a negative pressure of -15 to -20 mmHg at a volume only mildly less than V0 (different V0 than in the EDPVR segment - volume at zero pressure after systole - ESPVR). At this pressure the ventricle cannot develop any systolic pressure [5, 6].

“Pumping work” done by the heart

The heart’s main role is to generate pressure to enable blood to circulate. The work that it does is by imparting momentum to the blood and propelling it against the resistance of the periphery. If we examine this from a purely physical perspective, the external work done by the heart is the pressure generated multiplied by the change in volume ejected from the ventricle [2]. The main problem with this approach is that the pressure generated is not constant. That is why Sunagawa et al. have used the concept of end-systolic elastance to measure the total work and the concept of arterial elastance to measure the effective arterial elastance. By comparing both entities they calculated a ratio which represents the efficiency of the energy transfer and found out that that the heart reaches its maximal stroke work when the ratio equals 0.25 – when the end-systolic elastance and arterial elastance are the same [7]. In healthy individuals with an ejection fraction (ratio between stroke volume and end-diastolic volume) of about 60% the arterial elastance is always lower than the systolic elastance, but in slightly failing heart, ejection fraction of about 50%, the end-systolic elastance and arterial elastance are nearly equal, reaching the heart’s maximal stroke work [8].



  1. Fukuta H, Little CW. The Cardiac Cycle and the Physiological Basis of Left Ventricular Contraction, Ejection, Relaxation and Filling. Heart Fail Clin. 2008; 4(1):1-11.
  2. Boulpaep EL. The Heart as a Pump. In: Boron WF, Boulpaep EL. Medical physiology. 2nd ed. Philadelphia: Saunders/Elsevier; 2012. p. 529-53.
  3. Hall JE. Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves. In: Hall JE. Guyton and Hall textbook of medical physiology. 13th ed. Philadelphia: Elsevier; 2016. p.115-22.
  4. Burkhoff D. Mechanical properties of the heart and its interaction with the vascular system. [Internet] Available at: [Accessed on 3. 5. 2017]
  5. Sagawa K. The end-systolic pressure-volume relation of the ventricle: definition, modifications and clinical use. Circ Res. 1981;63(6):1223-7.
  6. Sunagawa K, Maughan WL, Friesinger GC, Chang M, Sagawa K: Coronary perfusion pressure and left ventricular end systolic pressure-volume relation. Circ. 1980; 62(suppl III):111-203
  7. Sunagawa K, Sagawa K, Maughan WL. Ventricular interaction with the loading system. Ann Biomed Eng. 1984;12(2):163-89
  8. Asanoi H, Sasayama S, Kameyama T. Ventriculoarterial coupling in normal and failing heart in humans. Circ Res. 1989;65(2):483-93.

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