Ventricular Pressure-Volume Loop

Introduction

• The cardiac cycle of the left ventricle (LV) begins with electrical excitation of the myocardium and proceeds through a sequence of mechanical events that generate a pressure gradient, eject the stroke volume, and drive forward blood flow.¹
• The most practical depiction of the cardiac cycle is the pressure-volume (PV) loop. This continuous, two-dimensional trace shows the relationship between pressure and volume as the heart muscle contracts (systole) and relaxes (diastole).¹
• Unlike isolated measurements (e.g., blood pressure, heart rate), PV loops integrate critical hemodynamic parameters (pressure, volume, and time) into a single, dynamic visualization that reflects both systolic and diastolic function.
• While traditional hemodynamic monitoring provides valuable data, PV loop analysis offers unparalleled insight into intrinsic myocardial contractility, ventricular-arterial coupling, preload, and afterload, often identifying subtle changes that standard metrics miss.

Method of Obtaining the PV loop

• PV loops are obtained using invasive cardiac catheterization. A specialized catheter with a pressure sensor is advanced into the left ventricle via a blood vessel.
• The catheter simultaneously measures ventricular pressure and volume throughout the cardiac cycle. Volume is typically measured using electrical conductivity from a conductance catheter.
• A computer plots pressure and volume data in real time to generate the characteristic PV loop.²

The Normal Pressure-Volume Loop

• Figure 1A shows a normal left ventricular PV loop. The x-axis represents ventricular volume, and the y-axis represents ventricular pressure.
• The loop is rectangular in shape. The black line traces the pressure and volume changes throughout one complete cardiac cycle. The direction of the cycle is counterclockwise.¹

Phases

• A. Ventricular filling (D → A): The mitral valve opens (D), and the ventricle fills with blood from the atrium. The volume increases significantly while the pressure rises only slightly. This phase ends when the mitral valve closes (A).
• B. Isovolumetric contraction (A → B): With both the mitral and aortic valves closed, the ventricle contracts. The volume remains constant, but the pressure rises sharply until it’s high enough to open the aortic valve (B).
• C. Ejection (B → C): The aortic valve opens (B), and the ventricle ejects blood into the aorta. The volume decreases, while the pressure initially rises and then falls. This phase ends when the aortic valve closes (C).
• D. Isovolumetric relaxation (C → D): With both the aortic and mitral valves closed, the ventricle relaxes. The volume remains constant, but the pressure drops sharply until it’s low enough for the mitral valve to open (D), starting the next cycle.¹

Key Parameters

• A. End-diastolic volume (EDV): The volume at the end of filling (point A) represents preload.
• B. End-systolic volume (ESV): The volume remaining in the ventricle after ejection (point C).
• C. Stroke volume (SV): The difference between EDV and ESV. It represents the volume of blood ejected with each beat. This is represented by the loop’s width.¹

Factors Affecting the Pressure-Volume Loop

Increased Contractility

• The red loop in Figure 2(B) shows the effect of increased contractility.
• The loop becomes wider.
• The ESV decreases (the loop’s left border shifts to the left). This is because a more forceful contraction ejects more blood.
• Subsequently, a reduced amount of residual blood, combined with venous return, results in a slightly lower left ventricular EDV.
• Because the decrease in ESV is greater than the decrease in EDV, the overall SV increases (the loop widens).
• The ejection fraction (EF) increases. EF is SV/EDV. Since SV increases and EDV is mostly unchanged, EF increases.³

Increased Preload

• The blue loop in Figure 2C shows the effect of increased preload, which is the volume of blood in the ventricle at the end of diastole (EDV). This is typically caused by a larger volume of blood returning to the heart.
• The loop becomes wider.
• The EDV increases (the loop’s right border shifts to the right).
• In a healthy heart, this leads to a more forceful contraction (the Frank-Starling mechanism), which increases the amount of blood ejected.
• The ESV increases only slightly. This is due to a minor increase in the heart’s afterload (aortic pressure) as it pumps a larger volume of blood.
• The SV increases (the loop becomes wider).³

Increased Afterload

• The purple loop in Figure 2D shows the effect of increased afterload, which is the resistance the heart must overcome to eject blood. This is often due to hypertension or a stiff aortic valve.
• The loop is taller and narrower.
• The ESV increases. This is because the heart has to work against greater resistance, so it cannot eject as much blood; consequently, more blood remains in the ventricle after systole.
• This larger residual volume, combined with venous return, leads to a greater left ventricular end-diastolic volume (LVEDV).
• According to Starling’s Law, an increase in LVEDV stretches the heart muscle, leading to a more forceful contraction. This stronger contraction increases SV, helping return the LVEDV towards a normal level.
• Despite compensation, the overall increase in LVESV is typically greater than that in LVEDV. The overall SV is slightly decreased, resulting in a taller, narrower PV loop.³

Comparison of Left and Right Ventricular PV Loops

• The LV and right ventricle (RV) loops also differ in the pressures they operate under and the work they perform.
• The pressure in the RV is significantly lower than in the LV because the RV pumps against a much lower afterload, resulting from low pulmonary vascular resistance and pressure.
• While both ventricles pump the same volume of blood, the RV’s stroke work (the area of the loop) is only 20-25% of the LV’s.
• Blood ejection from the RV begins early in systole, causing the ventricular volume to decrease shortly after the pressure rises.³

Cardiac Work and the PV Loop

• The LV operates within the limits defined by two key relationships: the end-systolic pressure-volume relationship (ESPVR) and the end-diastolic pressure-volume relationship (EDPVR).⁴
• The ESPVR represents the maximum pressure the ventricle can generate at a given volume at the end of systole (contraction). It’s a measure of the heart’s contractility.⁴
• The EDPVR describes the passive stiffness of the ventricle at the end of diastole (relaxation). It shows how much pressure is needed to fill the ventricle to a certain volume.⁴

• The mechanical work of the heart is a measure of the energy it expends during a cardiac cycle. This work can be divided into two main components, both of which are represented on the PV loop.³
  • External work (stroke work): This is the mechanical energy used to eject blood from the ventricle. It is represented by the area enclosed within the PV loop and measures the work done during a single cardiac cycle.³
  • Internal work (pressure work): This is the energy expended during the isovolumetric contraction phase. Since no blood is being ejected (no myofilament shortening), this energy is potential energy that is ultimately converted to heat. On the PV loop, this is the area bounded by the ESPVR, the EDPVR, and the isovolumetric relaxation line.³
  • Total work (pressure-volume area [PVA]): This is the sum of external and internal work. PVA is an excellent indicator of the heart’s total energy expenditure and correlates closely with myocardial oxygen consumption.³
• Factors affecting cardiac workload³
  • Impact of preload: An increase in preload results in a larger PV loop area, leading to increased external work and higher myocardial oxygen demand.
  • Impact of afterload: An increase in afterload may not significantly increase external work, but it dramatically increases internal work as the heart has to build up more pressure. This leads to a substantial increase in myocardial oxygen demand.
  • Impact of contractility: Increased contractility primarily increases external work by ejecting more blood, which also increases myocardial oxygen consumption.

Pressure-Volume Loops in Pathological Conditions

Heart Failure¹

• Heart failure can be visualized using PV analysis, which helps distinguish between systolic and diastolic dysfunction.

Pure LV Systolic Dysfunction

• Reduced contractility: The ESPVR slope decreases, indicating the heart’s pumping ability is weakened.
• Compensation: The PV loop shifts to the right, showing an increase in preload (end-diastolic volume). This is a compensatory mechanism that maintains stroke volume despite reduced contractility.

Pure LV Diastolic Dysfunction

• Reduced compliance: The EDPVR rises, indicating the ventricle has become stiffer and less compliant. This requires a higher pressure to fill the ventricle with the same volume of blood.
• Preserved contractility: The ESPVR slope remains normal, so the heart’s ability to contract is not impaired.

Combined LV Systolic and Diastolic Dysfunction

• Dual impairment: This condition is characterized by a reduced ESPVR slope (systolic dysfunction) and an elevated EDPVR (diastolic dysfunction).
• Compromised performance: The ventricle operates within a very narrow pressure-volume range, leading to a significant decrease in stroke volume and cardiac output.

Valvular Heart Disease

Mitral Stenosis

• Reduced preload (Underloading): The mitral stenosis loop is notably shifted to the left, indicating a diminished EDV. This signifies LV “underloading” due to impaired diastolic filling caused by the stenotic mitral valve.
• Decreased stroke volume and work: The reduced width and area of the mitral stenosis loop reflect a substantial decrease in both SV and stroke work, consistent with reduced forward flow.
• Preserved systolic function: While stroke work is reduced, intrinsic LV contractility (ESPVR) is typically preserved or even augmented as a compensatory mechanism.⁵

Mitral Regurgitation

• Absent isovolumetric contraction: The hallmark of mitral regurgitation is the absence of a defined isovolumetric contraction phase, as immediate regurgitant flow into the left atrium prevents a pressure rise at constant volume.
• Reduced effective afterload: The low-pressure regurgitant pathway decreases effective LV afterload, thereby enhancing ejection.
• Increased preload and chamber dilation: The loop shifts rightward, indicating increased EDV due to augmented venous return and reflecting LV volume overload.
• Increased total stroke work: The enlarged loop area signifies increased total stroke volume and stroke work, driven by combined forward and regurgitant output.
• Lower peak systolic pressure: Despite increased work, peak systolic pressure may be reduced due to the low-resistance regurgitant pathway.⁵

Aortic Stenosis

• Elevated afterload and systolic pressure: The loop in aortic stenosis exhibits markedly increased peak systolic pressure, reflecting severe afterload imposed by the stenotic aortic valve.
• Reduced stroke volume: The narrower loop width indicates a decreased SV due to impaired ejection against high resistance.
• Increased diastolic stiffness: The upward-shifted diastolic pressure-volume relationship (LVDPVR) signifies reduced LV compliance and increased diastolic stiffness, a common sequela of chronic pressure overload.
• Increased myocardial work: The enlarged loop area, particularly its height, denotes a substantial increase in myocardial work and oxygen demand.
• Preserved contractility (early compensation): Intrinsic LV contractility (ESPVR) may initially be maintained or augmented as a compensatory response to chronic afterload elevation.⁵

Aortic Regurgitation

• Absence of isovolumetric relaxation: A defining feature of AR is the lack of a distinct isovolumetric relaxation phase. As the LV begins to relax, immediate backflow from the aorta into the LV prevents a rapid pressure drop at a constant volume.
• Acute AR (Smaller, Right-Shifted Loop):
  • Rapid volume overload: The LV is acutely volume overloaded, leading to increased EDV and elevated end-diastolic pressure (EDP).
  • Limited compensation: The LV has not had time to dilate, resulting in a steeper diastolic pressure-volume relationship (DPVR) and a relatively higher pressure for a given volume.
  • Reduced forward flow: The overall loop size and shape reflect the acute volume load, often with compromised forward stroke volume due to the immediate regurgitant volume.
• Chronic AR (Larger, markedly right-shifted loop):
  • Compensatory dilation: The LV undergoes eccentric hypertrophy and significant dilation, leading to a greatly increased EDV and SV.
    • Preserved diastolic compliance: Despite increased volume, the DPVR is often maintained (not markedly shifted upwards as in acute AR or stenosis), indicating preserved LV compliance in the compensated state.
    • Increased stroke work: The substantially larger loop area signifies significantly increased total stroke work (forward plus regurgitant) as the LV handles a much larger volume.⁵