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Ventricular Pressure-volume Loop in Normal Heart

Updated: Jun 1

Ventricular Pressure-volume Diagram in Normal Heart
Ventricular Pressure-volume Diagram in Normal Heart

The volume-pressure loop of the heart, also known as the left ventricular pressure-volume loop, is a graphical representation of the relationship between the pressure and volume in the left ventricle during one cardiac cycle. It is divided into several distinct phases that illustrate the mechanical function of the heart.


The first phase, isovolumetric contraction, begins with the closure of the mitral valve and ends with the opening of the aortic valve. During this phase, the volume within the left ventricle remains constant as the ventricle contracts, leading to a rapid increase in pressure. This phase is represented by a vertical line moving upwards on the right side of the loop. Key events in this phase include the closure of the mitral valve and the maintenance of a closed aortic valve, resulting in a rapid rise in ventricular pressure.

Following isovolumetric contraction is the ventricular ejection phase. This phase starts with the opening of the aortic valve and ends with its closure. The volume of the ventricle decreases as blood is ejected into the aorta, with the pressure initially rising to a peak before beginning to decrease. This phase forms the top curved part of the loop, moving from right to left. Key events during this phase include the opening of the aortic valve, the ejection of blood from the ventricle, the attainment of peak systolic pressure, and the subsequent closure of the aortic valve.


The next phase, isovolumetric relaxation, begins with the closure of the aortic valve and ends with the opening of the mitral valve. During this phase, the volume of the ventricle remains constant as it relaxes, causing the pressure to drop sharply. This phase is represented by a vertical line moving downwards on the left side of the loop. Important events in this phase include the closure of the aortic valve and a rapid decrease in ventricular pressure while the mitral valve remains closed.


The final phase of the loop is ventricular filling. This phase begins with the opening of the mitral valve and ends with its closure. During ventricular filling, the volume of the ventricle increases as blood flows in from the left atrium, while the pressure remains relatively low and constant. This phase forms the bottom curved part of the loop, moving from left to the right. Key events in this phase include the opening of the mitral valve, passive filling of the ventricle (initially rapid then slower), atrial contraction, and the eventual closure of the mitral valve.


Stroke volume (SV) and stroke work (SW) are key parameters derived from the pressure-volume loop that provide insights into the mechanical performance of the heart.

Stroke Volume (SV)

Stroke volume is the amount of blood ejected by the left ventricle during each cardiac cycle. It is calculated as the difference between the end-diastolic volume (EDV) and the end-systolic volume (ESV):

𝑆𝑉=𝐸𝐷𝑉−𝐸𝑆𝑉

In the pressure-volume loop, stroke volume is represented by the horizontal distance between the points corresponding to the end of diastole and the end of systole on the volume axis. A larger stroke volume indicates a greater amount of blood being pumped out of the ventricle with each heartbeat, which is crucial for maintaining adequate cardiac output and tissue perfusion.


Stroke Work (SW)

Stroke work is the amount of work performed by the heart to eject blood during each cardiac cycle. It is represented by the area enclosed within the pressure-volume loop. Stroke work can be calculated by integrating the ventricular pressure over the change in volume during systole.


This area represents the mechanical energy generated by the ventricle to overcome both the resistive and elastic components of the arterial system. Stroke work is an important indicator of the heart's efficiency and energy expenditure. Higher stroke work signifies a more energetically demanding cardiac cycle, which can be seen in conditions with increased afterload, such as hypertension.


End-diastolic Pressure-volume Relationship

The End-Diastolic Pressure-volume Relationship (EDPVR) curve is a graphical representation that illustrates the relationship between the volume in the left ventricle at the end of diastole (end-diastolic volume or EDV) and the pressure within the ventricle at that same point (end-diastolic pressure or EDP). This curve is crucial for understanding ventricular compliance and diastolic function. The key Aspects of the EDVPR curve are:

  • Diastolic Filling Phase: During diastole, the heart muscle relaxes, allowing the ventricles to fill with blood from the atria. The volume of blood in the ventricle at the end of this filling phase is the end-diastolic volume. As the ventricle fills, the pressure within it gradually increases.

  • Ventricular Compliance: The slope of the EDVPR curve reflects the compliance of the ventricular muscle. Compliance refers to the ability of the ventricle to expand in response to increased volume. A steep slope indicates low compliance (stiffer ventricle), meaning that even small increases in volume result in significant increases in pressure. Conversely, a shallow slope indicates high compliance (more elastic ventricle), where large increases in volume result in relatively small increases in pressure.

  • Clinical Significance: In a healthy heart, the EDVPR curve is relatively shallow, indicating that the ventricle can accommodate increased volumes of blood with only slight increases in pressure. This reflects good compliance and effective diastolic function.  In conditions such as left ventricular hypertrophy or restrictive cardiomyopathy, the ventricular walls are stiffer, and the EDVPR curve becomes steeper. This means that small increases in end-diastolic volume result in large increases in end-diastolic pressure, reflecting poor compliance and impaired diastolic function.  Conversely, conditions that lead to increased ventricular compliance, such as dilated cardiomyopathy, result in a flatter EDVPR curve. The ventricle can hold more blood without a significant rise in pressure, although this can sometimes be maladaptive, leading to inefficient systolic function.


End-systolic Pressure-volume Relationship

The End-Systolic Pressure-Volume Relationship (ESPVR), is a crucial graphical representation in cardiac physiology. It illustrates the relationship between the volume in the left ventricle at the end of systole (end-systolic volume or ESV) and the pressure within the ventricle at that same point (end-systolic pressure or ESP). This curve provides insight into the contractile properties and systolic function of the heart. The key aspects of the ESVPR Curve are:

  • Systolic Ejection Phase: During systole, the heart muscle contracts, ejecting blood from the ventricles into the aorta and pulmonary artery. The volume of blood remaining in the ventricle after this contraction is the end-systolic volume. The pressure in the ventricle at this point is the end-systolic pressure.


  • Ventricular Contractility: The slope of the ESVPR curve is a measure of ventricular contractility, independent of preload and afterload. A steeper slope indicates higher contractility, meaning the ventricle can generate higher pressure at a given volume. A less steep slope indicates lower contractility.


  • Linearity of the Curve: The ESVPR is often depicted as a straight line, which suggests that the relationship between end-systolic pressure and volume is linear over the physiological range. This linearity is important for understanding how changes in contractility affect the heart’s ability to pump blood.


  • Clinical Significance: The ESVPR curve is an essential tool for assessing ventricular contractility. It helps distinguish between different types of cardiac dysfunction. For instance, a flatter ESVPR curve suggests systolic dysfunction, commonly seen in heart failure with reduced ejection fraction (HFrEF). On the other hand, a steeper curve might be seen with increased contractile states, such as during stress or with certain pharmacological interventions.



Arterial Elastance

The arterial elastance (Ea) curve is a graphical representation used to assess the relationship between the arterial system's properties and ventricular function. Arterial elastance is a measure of the arterial system's ability to accept and transmit the blood ejected from the left ventricle during systole. It reflects the combined effects of arterial resistance, compliance, and characteristic impedance. Understanding the Ea curve is crucial for evaluating cardiovascular performance and the interaction between the heart and the arterial system. The key aspects of the arterial elastance curve are:

  • Calculation of Arterial Elastance: Arterial elastance (Ea) is calculated as the ratio of end-systolic pressure (ESP) to stroke volume (SV). It provides a simplified index of the afterload, or the load against which the heart must eject blood. Mathematically, it is expressed as: 𝐸𝑎=𝐸𝑆𝑃/𝑆𝑉 where ESP is the pressure in the ventricle at the end of systole, and SV is the volume of blood ejected during systole.


  • Relationship with Ventricular Function: The Ea curve is typically plotted alongside the end-systolic pressure-volume relationship (ESPVR) to evaluate ventricular-arterial coupling. The slope of the Ea line reflects the afterload imposed by the arterial system. Changes in arterial properties, such as increased arterial stiffness or resistance, affect the Ea and thus influence ventricular performance.


  • Slope and Position of the Ea Curve: The slope of the Ea curve indicates the effective arterial load. A steeper slope (higher Ea) represents increased arterial load, which can result from increased arterial resistance or decreased arterial compliance. Conversely, a flatter slope (lower Ea) indicates a lower arterial load, associated with lower resistance and higher compliance.

  • Increased Arterial Load: Conditions such as hypertension or arteriosclerosis increase arterial stiffness, resulting in a steeper Ea slope. This reflects a higher afterload, making it more challenging for the ventricle to eject blood, and may lead to increased myocardial workload and potential systolic dysfunction.


  • Decreased Arterial Load: In conditions where arterial resistance is reduced or compliance is increased, the Ea slope becomes flatter. This reflects a lower afterload, which can be seen in situations such as vasodilation or improved arterial compliance.


Ventricular-arterial Coupling

The ratio of arterial elastance (Ea) to end-systolic elastance (Ees) is an important index known as the ventricular-arterial coupling ratio. This ratio provides a comprehensive measure of the interaction between the left ventricle and the arterial system. The Ea/Ees ratio reflects the efficiency of energy transfer from the heart to the arterial system during each cardiac cycle. An optimal Ea/Ees ratio typically falls within a range (0.6-1.3) that maximizes cardiac efficiency and minimizes myocardial oxygen consumption. When the ratio is optimal, the heart operates efficiently, ensuring adequate perfusion with minimal energy expenditure. The key points about the Ea/Ees Ratio are:

  • Optimal Range (0.6 to 1.3): A ratio within this range indicates a well-matched ventricular-arterial coupling, where the heart and arterial system are functioning in harmony. This balance is crucial for maintaining optimal cardiac efficiency and minimizing the workload on the heart.


  • Ratios Above 1.3: A higher Ea/Ees ratio suggests increased arterial load relative to ventricular contractility. This condition can lead to increased myocardial stress and reduced cardiac efficiency. It is often seen in conditions like hypertension or heart failure with preserved ejection fraction (HFpEF), where the arterial system imposes a significant load on the heart.


  • Ratios Below 0.6: A lower Ea/Ees ratio indicates a relatively lower arterial load compared to ventricular contractility. This can occur in situations where arterial resistance is reduced, such as in vasodilation or in conditions with enhanced ventricular contractility. While this may seem advantageous, excessively low ratios can also indicate maladaptive conditions where the arterial system is not providing sufficient resistance, potentially leading to inefficient cardiac function.


Conclusion

The pressure-volume loop and its associated parameters—End-Diastolic Pressure Volume Relationship (EDPVR), End-Systolic Pressure Volume Relationship (ESPVR), arterial elastance (Ea), and the Ea/Ees ratio—provide comprehensive insights into the mechanical and functional status of the heart. The EDVPR curve illustrates ventricular compliance and diastolic function, while the ESVPR curve offers a measure of ventricular contractility and systolic performance. The Ea curve reflects the arterial system's load on the heart, and the Ea/Ees ratio indicates the efficiency of ventricular-arterial coupling. Stroke volume (SV) and stroke work (SW), derived from the pressure-volume loop, are critical for assessing the heart’s performance and energy expenditure during each cardiac cycle. Together, these parameters enable a detailed evaluation of cardiac function, guiding clinical decision-making and therapeutic interventions. Understanding these relationships helps optimize cardiac efficiency, manage cardiovascular diseases, and ultimately improve patient outcomes.



References

  1. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine

  2. Guyton and Hall Textbook of Medical Physiology

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