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__NOTOC__
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{{CMG}}
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Rim Halaby|Rim Halaby]]


{{SK}} Pressure-volume loop; P-V diagram;  volume-pressure loop
{{SK}} Pressure-volume loop; P-V diagram;  volume-pressure loop


==Overview==
==Overview==
A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot ([[pressure volume diagram]]). A number of [[Pv loop experiments|methods]] have been determined for measuring PV-loop values experimentally.
*A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart.
*Real time left ventricular (LV) pressure-volume loops provide a framework for understanding cardiac mechanics; in fact, a considerable amount of information on cardiac performance can be determined from the pressure versus volume plot (also known as [[pressure volume diagram]]).
*Several physiologically relevant hemodynamic parameters such as [[stroke volume]], [[cardiac output]], [[ejection fraction]], myocardial contractility can be determined from these loops.
*To generate a [[pressure volume loop]] for the left [[ventricle]], the left ventricular pressure is plotted against left ventricular volume at multiple time points during a single [[cardiac cycle]].


;Below is an image of typical process depicting various changes and returning to initial state.
== Cardiac Pressure-Volume Loop==
*The left ventricular pressure-volume loop (PV loop) represents the different events of the [[cardiac cycle]].
*To generate a PV loop for the left [[ventricle]], the left ventricular pressure is plotted against the left ventricular volume at multiple time points during a single cardiac cycle.
*The left ventricular pressure-volume illustrates the four phases of the [[cardiac cycle]] with respect to pressure and volume changes:
**'''Phase I: Diastolic ventricular filling'''
***The [[mitral valve]] is open while the [[aortic valve]] is closed.
***The volume increases to reach the maximal ventricular capacity known as end diastolic volume '''EDV'''.
***The pressure slightly increases.
**'''Phase II: Isovolumetric contraction'''
***The mitral and aortic valves are both closed.
***The volume of the blood is unchanged as the [[ventricles]] are contracting.
***The pressure inside the ventricles significantly increases.
**'''Phase III: Ventricular ejection'''
***The [[aortic valve]] opens as the pressure inside the ventricles exceeds that of the [[aorta]].
***The blood volume inside the left [[ventricle]] decreases because it is pumped into the systemic circulation.
**'''Phase IV: Isovolumetric relaxation'''
***The aortic and mitral valves are closed.
***The volume inside the left [[ventricle]] is unchanged and it corresponds to the volume remaining in the ventricle after systole, known as end systolic volume '''ESV'''.
***The pressure inside the ventricle tremendously decreases as the ventricles are relaxing.


[[Image:Cyclic_process.PNG|center]]
; Below is an image showing idealized pressure-volume diagram featuring cardiac cycle events.
[[Image:Normal_Pressure_Volume_Loop.png‎|600px|Normal pressure volume loop]]


== Cardiac pressure-volume loops==
== Pressure-Volume Parameters ==
=== Stroke Volume ===
*[[Stroke volume]] (SV) is the amount of blood pumped by the left [[ventricle]] in a single cardiac cycle.
**At the start of systole, the left [[ventricle]] is filled with blood to the capacity known as end diastolic volume EDV.
**During systole, the left [[ventricle]] contracts and ejects blood until it reaches its minimum capacity known as end systolic volume ESV.
**'''Stroke Volume (SV) = EDV – ESV'''
* The stroke volume is an indicator the left ventricular function which is mainly affected by the preload, afterload and contractility of the heart.


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 physiologically relevant hemodynamic parameters such as stroke volume, cardiac output, ejection fraction, myocardial contractility, etc. can be determined 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 single cardiac cycle.
=== Stroke Work ===
*Ventricular stroke work (SW) is defined as the work performed by the left or right ventricle to eject the stroke volume into the aorta or pulmonary artery, respectively.
*The area enclosed by the PV loop is a measure 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.


; Below is an image demonstrating idealized pressure-volume diagram featuring cardiac cycle events.
=== Cardiac Output ===
[[File:Cardiac Presure Volume Loop.jpg|600px|center]]
*[[Cardiac output]] (CO) is defined as the amount of blood pumped by the left [[ventricle]] in unit time.
** '''CO = Stroke Volume x Heart Rate'''
**The normal cardiac output is '''5-6L/min''' and it can increase up to 5 times during exercise.
**CO is an indicator of the left ventricular function.


== Cardiac terminology ==
=== Ejection Fraction ===
=== Afterload ===
*[[Ejection fraction]] (EF) is defined as the fraction of end diastolic volume that is ejected out of the ventricle during each contraction.
[[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 large vessel compliance, wave reflection and small vessel resistance (LV afterload) or similar pulmonary artery parameters (RV afterload).
*'''Ejection Fraction = Stroke volume/end diastolic volume'''
* Healthy ventricles typically have ejection fractions greater than 0.55.
* [[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 as heart failure.
**Low EF usually indicates [[systolic dysfunction]] and severe heart failure can result in EF lower than 0.2.


Left ventricular afterload is affected by various disease conditions. Hypertension increases the afterload since the LV has to work harder to overcome the elevated arterial peripheral resistance and decreased compliance. Aortic valve diseases like aortic stenosis and insufficiency also increase the afterload whereas [[mitral regurgitation|mitral valve regurgitation]] decreases the afterload.
=== dP/dt<sub>min</sub> and dP/dt<sub>max</sub> ===


=== Preload ===
*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. However, it is known to be load dependent and inferior to hemodynamic parameters defined by the PV plane.
[[Preload (cardiology)|Preload]] is described as the stretching of a single cardiac myocyte immediately 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.
*An increase in contractility 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.
Quantitatively, preload can be calculated as


:preload = (LVEDP×LVEDR)/2h
*Similarly, an increase in diastolic function or an increase in relaxation ([[lusitropy]]) causes increased dP/dtmin during isovolumic relaxation. Hence, dP/dtmin has been used as a valuable tool in the analysis of isovolumic relaxation. However, studies have shown that this parameter may not be a valid measure of LV relaxation rate, especially during acute alterations in contractility or afterload.
where
:* LVEDP = left ventricular end diastolic pressure
:* LVEDR = left ventricular end diastolic radius (at midpoint of ventricle)
:* h = thickness of ventricle
 
== Pressure-volume parameters ==
=== Stroke volume ===
 
[[Stroke volume]] (SV) is the volume of blood ejected by the right/left ventricle in a single 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.
 
=== Stroke work ===
 
Ventricular stroke work (SW) is defined as the work performed by the left or right ventricle to eject the stroke volume into the aorta or pulmonary artery, respectively. The area enclosed by the PV loop is a measure 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.
 
=== Cardiac output ===
[[Cardiac output]] (CO) is defined as the amount of blood pumped 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 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.
 
Physiologic 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 physiology as it provides for improved diagnosis of abnormalities, and can be used to guide the development of new treatment strategies. However, CO is dependent upon loading conditions and is inferior to hemodynamic parameters defined by the PV plane.
 
=== Ejection fraction ===
 
[[Ejection fraction]] (EF) is defined as the fraction of end diastolic volume that is ejected out of the ventricle during each contraction.
 
Mathematically, EF = SV/EDV


Healthy ventricles typically have ejection fractions greater than 0.55. However, EF is also dependent on loading conditions and inferior to hemodynamic parameters defined by the PV plane.
=== Isovolumic Relaxation Constant (Τau) ===


Physiologic relevance
*Tau 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.
 
*Calculation of Tau (Glantz method)
[[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 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.
 
=== dP/dt<sub>min</sub> & dP/dt<sub>max</sub> ===
 
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. However, it is known to be load dependent and inferior to hemodynamic parameters defined by the PV plane.
 
An increase in contractility 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 ([[lusitropy]]) causes increased dP/dtmin during isovolumic relaxation. Hence, dP/dtmin has been used as a valuable tool in the analysis of isovolumic relaxation. However, studies have shown that this parameter may not be a valid measure of LV relaxation rate, especially during acute alterations in contractility or afterload.
 
=== Isovolumic relaxation constant (Τau) ===
 
Tau 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 (Glantz method)


P(t)= P<sub>0</sub>e<sup>-t⁄τ<sub>E</sub></sup> +P<sub>α</sub>
P(t)= P<sub>0</sub>e<sup>-t⁄τ<sub>E</sub></sup> +P<sub>α</sub>
Line 98: Line 79:
:* P<sub>α</sub> = non zero asymptote due to pleural and pericardial pressure
:* P<sub>α</sub> = non zero asymptote due to pleural and pericardial pressure


; Below is an image depicting the calculation of Tau using Glantz Method.
; Below is an image showing the calculation of Tau using Glantz Method.


[[File:Calculation of Tau.jpg|center]]
[[File:Calculation of Tau.jpg|center]]


== PV loop analysis  ==
==Determinants of Left Ventricular Function==
Due to the load dependency of the previous parameters, more accurate measures of ventricular function are available in the PV plane.
*'''1- Preload:'''
**The preload is the '''volume''' that fills in the [[heart]] during diastole, and it is referred to as the end diastolic volume (EDV).
**According to '''Frank Starling's law''', the larger the blood volume filling the heart is, the larger the degree of cardiac stretching is and consequently  more [[blood]] is pumped.
**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 myocyte. 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.
;Below is an image showing Frank Starling's law according to which the left ventricular function increases as the preload increases.
[[Image:Frank_Starling_Law_of_the_Heart.png|350px|Frank starling law of the heart: as the preload increases, the cardiac output increases]]
*'''2- Afterload:'''
**The afterload is the '''pressure''' corresponding to the mean arterial pressure that the heart needs to overcome when pumping blood.
**When the afterload increases, it makes it harder for the heart to pump the [[blood]], and thus the volume remaining in the ventricles after ventricular contraction (end systolic volume) will increase and the stroke volume will be low.
*'''3- Contractility:'''
**The contractility of the heart is defined as the intrinsic force with which the heart contracts.
**Factors that increase the contractility of the heart (positive '''ionotropy''') are: [[catecholamines]], xanthines (caffeine), medications ([[Digitalis]]).
**Factors that decrease the contractlity of the heart (negative '''ionotropy''') are: hypercapnea, hypoxia, acidosis, medications ([[quinidine]], [[procainamide]], barbiturates), heart failure.<ref ="Ganong">Barrett KE, Barman SM, Boitano S, Brooks HL. Chapter 30. The Heart as a Pump. In: Barrett KE, Barman SM, Boitano S, Brooks HL, eds. Ganong's Review of Medical Physiology. 24th ed. New York: McGraw-Hill; 2012.</ref>
;Below is an image showing various curves illustrating different states of contractlity of the heart.
[[Image:Variation_in_the_Contractility_of_the_Heart.png‎|400px|Variation in the contractility of the heart: note that each curve represents a state of contractility of the heart but any point on each curve represents the same state of contractility.]]


=== End systolic pressure volume relationship ===
== Pressure-Volume Loop Analysis  ==
[[File:End Systolic Pressure Volume Relationship .jpg|thumb|250px|alt=|Pressure-Volume loops showing end systolic pressure volume relationship]]
=== End Systolic Pressure Volume Relationship ESPVR===
End systolic pressure volume relationship (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 line defining ESPVR for any given contractile state.
*End systolic pressure volume relationship ('''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 line defining 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 hemodynamic parameters like ejection fraction, cardiac output and stroke volume.
**The ESPVR becomes steeper and shifts to the left as inotropy (contractility) increases.
**The ESPVR becomes flatter and shifts to the right as inotropy decreases.


The slope of ESPVR (Ees) 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 hemodynamic parameters like ejection fraction, cardiac output and stroke volume.
;Below is an image showing a pressure-volume loop with a steeper ESPVR that shifts to the left in the case of increased inotropy or contractility.
[[Image:Increased_Contractility.png|250px|Pressure- Volume loop showing a steeper ESPVR that shifts to the left as inotropy (contractility) increases. Note that the normal pressure volume diagram is in dotted line.]]


The ESPVR becomes steeper and shifts to the left as inotropy (contractility) increases. The ESPVR becomes flatter and shifts to the right as inotropy decreases.
=== End Diastolic Pressure Volume Relationship EDPVR===
{{Clear}}
*End diastolic pressure volume relationship (EDPVR) describes the passive filling curve for the ventricle and thus the passive properties of the myocardium.
*The slope of the EDPVR at any point along this curve is the reciprocal of ventricular compliance (or ventricular stiffness).
**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):
***The EDV may be very high but the EDP may not be greatly elevated.
;Below is an image showing a pressure volume loop with changes in the EDPVR's part resulting from variations in the ventricular compliance.


=== End diastolic pressure volume relationship  ===
[[Image:Variation_in_the_compliance.png‎|300px|Changes in the EDPVR's part of pressure-volume loop with variations in the ventricular compliance.]]
[[File:End Diastolic Pressure Volume Relationship.jpg|thumb|250px|alt=|End diastolic pressure volume relationship.]]
End diastolic pressure volume relationship (EDPVR) describes the passive filling curve for the ventricle and thus the passive properties of the myocardium. 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.
=== Pressure Volume Area ===
*The Pressure-volume  area (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).
**PVA = PE + SW


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.
== Pressure- Volume Loop Changes in Cardiac Abnormalities ==
{{Clear}}
===Variation in Preload and Afterload===
*When preload increases the following changes are observed:
**Increased end diastolic volume
**Increased stroke volume
**No changes in pressure


=== Pressure-volume area ===
*When afterload increases the following changes are observed:
**Increased end systolic volume
**Decreased stroke volume
**Increased ventricular pressure because the ventricles need to contract more in order to overcome the afterload


The Pressure-volume area (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).
;Below is an image showing the pressure volume graph in case of changes in preload and afterload.
[[Image:Variation_in_the_Preload_and_Afterload.png|300px|The variation in the pressure volume loop in case of increased preload and in the case of increased afterload. Note that the normal pressure volume diagram is in dotted line.]]
=== Dilated Cardiomyopathy ===
*In [[dilated cardiomyopathy]], the ventricle becomes dilated without compensatory thickening of the wall and consequently the following changes are observed:
**Decreased contractility of the left ventricle that is illustrated by a shift to the right of the ESPVR curve
**Decreased ventricular compliance illustrated by the shift to the right of the EDPVR curve
**Decreased stroke volume leading to an increase in the end systolic volume
**Increased end diastolic volume due to the dilatation of the ventricles
**Decreased cardiac output
**No change in the ventricular pressures accompanies the changes in the volume.


Mathematically, PVA = PE + SW
;Below is an image showing the pressure volume graph in case of dilated cardiomyopathy.
[[Image:Dilated_Cardiomyopathy.png‎|300px|The pressure volume loop in dilated cardiomyopathy. Note that the normal pressure volume diagram is in dotted line]]
<br clear=left>


also,
=== Left Ventricular Hypertrophy ===
:PE = PES(VES – V0)/2 – PED(VED – V0)/4
*[[Left ventricular hypertrophy]] (LVH) is an increase in the thickness and mass of the myocardium.
where
*The thickening of the ventricular muscle results in decreased chamber compliance and consequently the following changes are observed:
* PES – end systolic pressure
**Elevated left ventricular pressures
* PED – end diastolic pressure
**Increased ESV
* VES – end systolic volume
**Decreased EDV
* VED – end diastolic volume
**Decreased cardiac output
* V0 – theoretical volume when no pressure is generated
;Below is an image showing the pressure volume curve in case of left ventricular hypertrophy (LVH) with associated reduced stroke volume (SV), end diastolic volume (EDV) and increased left ventricular pressure (LVP).
[[Image:Left_Ventricular_Hypertrophy.png‎|300px|The pressure volume loop in left ventricular hypertrophy. Note that the normal pressure volume diagram is in dotted line.]]


==== Physiologic relevance ====
*There are two exceptions to these changes, where moderate hypertrophy allows for a lower heart rate, increased diastolic volume, and thus higher stroke volume:
[[File:Pressure Volume Area.jpg|thumb|250px|alt=|Pressure-volume area plot.]]
**Increased left ventricular hypertrophy with increased EDV and SV seen with athletes<ref>{{cite web|last=Scharhag|first=J.ürgen|title=Athlete’s heart|url=http://content.onlinejacc.org/cgi/content/figsonly/40/10/1856|work=Athlete’s heart}}</ref>  
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 (MVO<sub>2</sub>) 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. MVO<sub>2</sub> is also used in the calculation of cardiac efficiency, which is the ratio of cardiac stroke work to MVO<sub>2</sub>.
**Increased left ventricular hypertrophy in healthy normal elderly individuals.
{{Clear}}


=== Preload recruitable stroke work ===
=== Restrictive Cardiomyopathy ===
Preload recruitable stroke work (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.
*[[Restrictive cardiomyopathy]] includes a group of heart disorders in which the walls of the ventricles become stiff (but not necessarily thickened) and resist normal filling with blood between heartbeats.
*This condition occurs when heart muscle is gradually infiltrated or replaced by scar tissue or when abnormal substances accumulate in the heart muscle and consequently the following changes are observed:
**Normal ventricular systolic pressure
**Elevated diastolic pressure
**Reduced cardiac output
;Below is an image showing the pressure volume curve in case of restrictive cardiomyopathy with associated reduced stroke volume.
[[Image:Restrictive_Cardiomyopathy.png|300px|The pressure volume curve in restrictive cardiomyopathy. Note that the normal pressure volume diagram is in dotted line.]]


==== Physiologic relevance ====
=== Valvular Diseases ===
[[File:Preload Recruitable Stroke Work .jpg|thumb|250px|alt=|Preload recruitable stroke work.]]
==== Aortic Stenosis ====
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.
*[[Aortic valve stenosis]] is the abnormal narrowing of the aortic valve.
{{Clear}}
*This results in the left ventricle pressures being much greater than the aortic pressures during left ventricular ejection. The magnitude of the pressure gradient is determined by the severity of the stenosis and the flow rate across the valve.


=== Frank–Starling curve ===
*The following changes are observed in severe aortic stenosis:
[[File:Frank-Starling Curve.jpg‎|thumb|250px|alt=|Frank–Starling curve.]]
** Reduced ventricular stroke volume due to increased afterload (which decreases ejection velocity)
''“The heart will pump what it receives”- Starling’s law of the heart''
** Increased end-systolic volume
** Compensatory increase in end-diastolic volume and pressure


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.
; Below is an image showing a pressure volume diagram in case of aortic stenosis depicting increased end systolic pressure and reduced stroke volume.
[[Image:Pressure_Volume_Loop_Aortic_Stenosis.png‎|300px|Pressure-volume loop in aortic stenosis. Note that the normal pressure volume diagram is in dotted line.]]


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 myocyte. This stretches the muscle fibers, increasing the affinity of troponin C to Ca<sup>2+</sup> 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.
==== Mitral Stenosis ====
*Mitral stenosis is the abnormal narrowing of the mitral valve orifice.
*The following changes are observed in[[mitral stenosis]]:
**Decreased end-diastolic volume (preload) due to impaired left ventricular filling
**Decreased stroke volume resulting from the decreased preload according to the Frank–Starling mechanism
**Decreased cardiac output and aortic pressure (afterload) as the stroke volume is decreased
**Slightly decreased end-systolic volume due to the decrease in the afterload


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.
;Below is an image showing a pressure volume curve in case of mitral stenosis depicting reduced end diastolic volume and reduced stroke volume.
{{Clear}}
[[Image:Pressure_Volume_Loop_Mitral_Stenosis.png|300px|Pressure-volume loop in mitral stenosis. Note that the normal pressure volume loop is in dotted line.]]


=== Arterial elastance ===
==== Aortic Regurgitation ====
[[File:Arterial Elastance .jpg|thumb|250px|alt=|Arterial elastance]]
*[[Aortic insufficiency]] (AI) or regurgitation is the failure of the valve to close completely at the end of systolic ejection, causing leakage of blood back through the valve during LV diastole.
Arterial elastance (Ea) is a measure of arterial load and is calculated as the simple ratio of ventricular end-systolic pressure to stroke volume.
*The following changes are observed in aortic regurgitation:
**Increased end diastolic volume (preload) because the LV volume is greatly increased due to the enhanced ventricular filling from the constant backflow of blood through the leaky valve
**Increased systolic pressure and stroke volume due to the elevated preload according to the Frank–Starling mechanism
* Not that when the LV begins to contract and develop pressure, blood is still entering the LV from the aorta (since aortic pressure is higher than LV pressure), implying that there is no true isovolumic contraction. Once the LV pressure exceeds the aortic diastolic pressure, the LV begins to eject blood into the aorta.


Mathematically, Ea = ESP/SV
;Below is an image showing the pressure volume curve in case of aortic regurgitation  depicting increased end diastolic volume, increased stroke volume and increased LV systolic pressure.
[[Image:Pressure_Volume_Loop_Aortic_Regurgitation.png‎|300px|Pressure-volume loop in aortic regurgitation. Note that the normal pressure-volume diagram is in dotted line.]]


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).
==== Mitral Regurgitation ====
{{Clear}}
*[[Mitral regurgitation]] (MR) is the failure of the mitral valve to close completely, causing blood to flow back into the left atrium during ventricular systole.
*The increased ventricular
*The following changes are observed in mitral regurgitation:
**Decreased end systolic volume due to the constant back flow of blood through the leaky valve
**Increased left ventricular end diastolic volume as the volume and pressure of atria are higher than normal
**Increased stroke volume in such a way that the ejection into the aorta (forward flow) is reduced as the stroke volume in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium


== PV loop changes for diverse cardiac abnormalities ==
;Below is an image showing the pressure volume curve in case of mitral regurgitation depicting increased end diastolic volume and increased stroke voume.
=== Dilated cardiomyopathy ===
[[Image:Pressure_Volume_Loop_Mitral_Regurgitation.png‎|300px|Pressure volume loop in case of mitral regurgitation. Note that the normal pressure volume loop is in dotted line.]]
[[File:Dilated Cardiomyopathy.jpg|thumb|250px|alt=|Dilated Cardiomyopathy]]
In [[dilated cardiomyopathy]], the ventricle becomes dilated without compensatory thickening of the wall. The LV is unable to pump enough blood to meet the metabolic demands of the organism.


The end systolic and diastolic volumes increase and the pressures remain relatively unchanged. The ESPVR and EDPVR curves are shifted to the right.
==References==
{{Clear}}
{{reflist|2}}
 
=== Left ventricular hypertrophy ===
[[File:Left Ventricular Hypertrophy.jpg|thumb|250px|alt=|Left Ventricular Hypertrophy]]
[[Left ventricular hypertrophy]] (LVH) is an increase in the thickness and mass of the myocardium. This could be a normal reversible response to cardiovascular conditioning (athletic heart) or an abnormal irreversible response to chronically increased volume load (preload) or increased pressure load (afterload). Shown is a diagram of pathological hypertrophy reducing EDV and SV.
 
The thickening of the ventricular muscle results in decreased chamber compliance. As a result, LV pressures are elevated, the ESV is increased and the EDV is decreased, causing an overall reduction in cardiac output.
<br />
:There are two exceptions to this. Increased left ventricular hypertrophy with increased EDV and SV is seen with athletes<ref>{{cite web|last=Scharhag|first=J.ürgen|title=Athlete’s heart|url=http://content.onlinejacc.org/cgi/content/figsonly/40/10/1856|work=Athlete’s heart}}</ref>  and in healthy normal elderly individuals.<ref>http://www.medscape.com/viewarticle/450564_4</ref> Moderate hypertrophy allows for a lower heart rate, increased diastolic volume, and thus higher stroke volume.
 
{{Clear}}
 
=== Restrictive cardiomyopathy ===
[[File:Restrictive cardiomyopathy.jpg‎|thumb|250px|alt=|Restrictive cardiomyopathy]]
[[Restrictive cardiomyopathy]] includes a group of heart disorders in which the walls of the ventricles become stiff (but not necessarily thickened) and resist normal filling with blood between heartbeats.
 
This condition occurs when heart muscle is gradually infiltrated or replaced by scar tissue or when abnormal substances accumulate in the heart muscle. The ventricular systolic pressure remains normal, diastolic pressure is elevated and the cardiac output is reduced.
{{Clear}}
 
=== Valve diseases ===
==== Aortic stenosis ====
[[File:Aortic stenosis.jpg‎|thumb|250px|alt=|Aortic stenosis‎]]
[[Aortic valve stenosis]] is abnormal narrowing of the aortic valve. This results in the LV pressures being much greater than the aortic pressures during LV ejection. The magnitude of the pressure gradient is determined by the severity of the stenosis and the flow rate across the valve.
 
Severe aortic stenosis results in
#    reduced ventricular stroke volume due to increased afterload (which decreases ejection velocity)
#    increased end-systolic volume
#    compensatory increase in end-diastolic volume and pressure
{{Clear}}
 
==== Mitral stenosis ====
[[File:Mitral stenosis.jpg|thumb|250px|alt=|Mitral stenosis]]
This is a narrowing of the mitral valve orifice when the valve is open. [[Mitral stenosis]] impairs LV filling so that there is a decrease in end-diastolic volume (preload). This leads to a decrease in stroke volume by the Frank–Starling mechanism and a fall in cardiac output and aortic pressure. This reduction in afterload (particularly aortic diastolic pressure) enables the end-systolic volume to decrease slightly, but not enough to overcome the decline in end-diastolic volume. Therefore, because end-diastolic volume decreases more than end-systolic volume decreases, the stroke volume decreases.
{{Clear}}
 
==== Aortic regurgitation  ====
[[File:Aortic regurgitation.jpg|thumb|250px|alt=|Aortic regurgitation]]
[[Aortic insufficiency]] (AI) is a condition in which the aortic valve fails to close completely at the end of systolic ejection, causing leakage of blood back through the valve during LV diastole.
 
The constant backflow of blood through the leaky aortic valve implies that there is no true phase of isovolumic relaxation. The LV volume is greatly increased due to the enhanced ventricular filling.
 
When the LV begins to contract and develop pressure, blood is still entering the LV from the aorta (since aortic pressure is higher than LV pressure), implying that there is no true isovolumic contraction. Once the LV pressure exceeds the aortic diastolic pressure, the LV begins to eject blood into the aorta.
 
The increased end-diastolic volume (increased preload) activates the Frank–Starling mechanism to increase the force of contraction, LV systolic pressure, and stroke volume.
{{Clear}}
 
==== Mitral regurgitation ====
[[File:Mitral regurgitation.jpg|thumb|250px|alt=|Mitral regurgitation]]
[[Mitral regurgitation]] (MR) occurs when the mitral valve fails to close completely, causing blood to flow back into the left atrium during ventricular systole.
 
The constant backflow of blood through the leaky mitral valve implies that there is no true phase of isovolumic contraction. Since the afterload imposed on the ventricle is reduced, end-systolic volume can be smaller than normal.
 
There is also no true period of isovolumic relaxation because some LV blood flows back into the left atrium through the leaky mitral valve. During ventricular diastolic filling, the elevated atrial pressure is transmitted to the LV during filling so that LV end-diastolic volume (and pressure) increases.  This would cause the afterload to increase if it were not for the reduced outflow resistance (due to mitral regurgitation) that tends to decrease afterload during ejection. The net effect of these changes is that the width of the PV loop is increased (i.e., ventricular stroke volume is increased). However, ejection into the aorta (forward flow) is reduced.  The increased ventricular stroke volume in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium.


{{Cardiovascular physiology}}
{{Cardiovascular physiology}}


[[Category:Cardiology]]
[[Category:Cardiology]]
[[Category:Physiology]]


{{WH}}
{{WS}}


==See also==
==Related Chapters==
* [[Wiggers diagram]]
* [[Stroke volume]]
* [[stroke volume]]
* [[cyclic process]]
* [[cyclic process]]


==References==
<references/>


[[Category:Thermodynamics|Thermodynamics]]
[[Category:Cardiology]]
[[Category:Cardiology]]


Latest revision as of 15:00, 26 October 2012

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-in-Chief: Rim Halaby

Synonyms and keywords: Pressure-volume loop; P-V diagram; volume-pressure loop

Overview

  • A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart.
  • Real time left ventricular (LV) pressure-volume loops provide a framework for understanding cardiac mechanics; in fact, a considerable amount of information on cardiac performance can be determined from the pressure versus volume plot (also known as pressure volume diagram).
  • Several physiologically relevant hemodynamic parameters such as stroke volume, cardiac output, ejection fraction, myocardial contractility can be determined from these loops.
  • To generate a pressure volume loop for the left ventricle, the left ventricular pressure is plotted against left ventricular volume at multiple time points during a single cardiac cycle.

Cardiac Pressure-Volume Loop

  • The left ventricular pressure-volume loop (PV loop) represents the different events of the cardiac cycle.
  • To generate a PV loop for the left ventricle, the left ventricular pressure is plotted against the left ventricular volume at multiple time points during a single cardiac cycle.
  • The left ventricular pressure-volume illustrates the four phases of the cardiac cycle with respect to pressure and volume changes:
    • Phase I: Diastolic ventricular filling
      • The mitral valve is open while the aortic valve is closed.
      • The volume increases to reach the maximal ventricular capacity known as end diastolic volume EDV.
      • The pressure slightly increases.
    • Phase II: Isovolumetric contraction
      • The mitral and aortic valves are both closed.
      • The volume of the blood is unchanged as the ventricles are contracting.
      • The pressure inside the ventricles significantly increases.
    • Phase III: Ventricular ejection
      • The aortic valve opens as the pressure inside the ventricles exceeds that of the aorta.
      • The blood volume inside the left ventricle decreases because it is pumped into the systemic circulation.
    • Phase IV: Isovolumetric relaxation
      • The aortic and mitral valves are closed.
      • The volume inside the left ventricle is unchanged and it corresponds to the volume remaining in the ventricle after systole, known as end systolic volume ESV.
      • The pressure inside the ventricle tremendously decreases as the ventricles are relaxing.
Below is an image showing idealized pressure-volume diagram featuring cardiac cycle events.

Normal pressure volume loop

Pressure-Volume Parameters

Stroke Volume

  • Stroke volume (SV) is the amount of blood pumped by the left ventricle in a single cardiac cycle.
    • At the start of systole, the left ventricle is filled with blood to the capacity known as end diastolic volume EDV.
    • During systole, the left ventricle contracts and ejects blood until it reaches its minimum capacity known as end systolic volume ESV.
    • Stroke Volume (SV) = EDV – ESV
  • The stroke volume is an indicator the left ventricular function which is mainly affected by the preload, afterload and contractility of the heart.

Stroke Work

  • Ventricular stroke work (SW) is defined as the work performed by the left or right ventricle to eject the stroke volume into the aorta or pulmonary artery, respectively.
  • The area enclosed by the PV loop is a measure 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.

Cardiac Output

  • Cardiac output (CO) is defined as the amount of blood pumped by the left ventricle in unit time.
    • CO = Stroke Volume x Heart Rate
    • The normal cardiac output is 5-6L/min and it can increase up to 5 times during exercise.
    • CO is an indicator of the left ventricular function.

Ejection Fraction

  • Ejection fraction (EF) is defined as the fraction of end diastolic volume that is ejected out of the ventricle during each contraction.
  • Ejection Fraction = Stroke volume/end diastolic volume
  • Healthy ventricles typically have ejection fractions greater than 0.55.
  • 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 as heart failure.
    • Low EF usually indicates systolic dysfunction and severe heart failure can result in EF lower than 0.2.

dP/dtmin and 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. However, it is known to be load dependent and inferior to hemodynamic parameters defined by the PV plane.
  • An increase in contractility 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 (lusitropy) causes increased dP/dtmin during isovolumic relaxation. Hence, dP/dtmin has been used as a valuable tool in the analysis of isovolumic relaxation. However, studies have shown that this parameter may not be a valid measure of LV relaxation rate, especially during acute alterations in contractility or afterload.

Isovolumic Relaxation Constant (Τau)

  • Tau 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.
  • Calculation of Tau (Glantz method)

P(t)= P0e-t⁄τE +Pα

where

  • P = pressure at time t
  • P0 = amplitude constant
  • τE = Glantz relaxation constant
  • Pα = non zero asymptote due to pleural and pericardial pressure
Below is an image showing the calculation of Tau using Glantz Method.

Determinants of Left Ventricular Function

  • 1- Preload:
    • The preload is the volume that fills in the heart during diastole, and it is referred to as the end diastolic volume (EDV).
    • According to Frank Starling's law, the larger the blood volume filling the heart is, the larger the degree of cardiac stretching is and consequently more blood is pumped.
    • 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 myocyte. 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.
Below is an image showing Frank Starling's law according to which the left ventricular function increases as the preload increases.

Frank starling law of the heart: as the preload increases, the cardiac output increases

  • 2- Afterload:
    • The afterload is the pressure corresponding to the mean arterial pressure that the heart needs to overcome when pumping blood.
    • When the afterload increases, it makes it harder for the heart to pump the blood, and thus the volume remaining in the ventricles after ventricular contraction (end systolic volume) will increase and the stroke volume will be low.
  • 3- Contractility:
    • The contractility of the heart is defined as the intrinsic force with which the heart contracts.
    • Factors that increase the contractility of the heart (positive ionotropy) are: catecholamines, xanthines (caffeine), medications (Digitalis).
    • Factors that decrease the contractlity of the heart (negative ionotropy) are: hypercapnea, hypoxia, acidosis, medications (quinidine, procainamide, barbiturates), heart failure.[1]
Below is an image showing various curves illustrating different states of contractlity of the heart.

Variation in the contractility of the heart: note that each curve represents a state of contractility of the heart but any point on each curve represents the same state of contractility.

Pressure-Volume Loop Analysis

End Systolic Pressure Volume Relationship ESPVR

  • End systolic pressure volume relationship (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 line defining 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 hemodynamic parameters like ejection fraction, cardiac output and stroke volume.
    • The ESPVR becomes steeper and shifts to the left as inotropy (contractility) increases.
    • The ESPVR becomes flatter and shifts to the right as inotropy decreases.
Below is an image showing a pressure-volume loop with a steeper ESPVR that shifts to the left in the case of increased inotropy or contractility.

Pressure- Volume loop showing a steeper ESPVR that shifts to the left as inotropy (contractility) increases. Note that the normal pressure volume diagram is in dotted line.

End Diastolic Pressure Volume Relationship EDPVR

  • End diastolic pressure volume relationship (EDPVR) describes the passive filling curve for the ventricle and thus the passive properties of the myocardium.
  • The slope of the EDPVR at any point along this curve is the reciprocal of ventricular compliance (or ventricular stiffness).
    • 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):
      • The EDV may be very high but the EDP may not be greatly elevated.
Below is an image showing a pressure volume loop with changes in the EDPVR's part resulting from variations in the ventricular compliance.

Changes in the EDPVR's part of pressure-volume loop with variations in the ventricular compliance.

Pressure Volume Area

  • The Pressure-volume area (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).
    • PVA = PE + SW

Pressure- Volume Loop Changes in Cardiac Abnormalities

Variation in Preload and Afterload

  • When preload increases the following changes are observed:
    • Increased end diastolic volume
    • Increased stroke volume
    • No changes in pressure
  • When afterload increases the following changes are observed:
    • Increased end systolic volume
    • Decreased stroke volume
    • Increased ventricular pressure because the ventricles need to contract more in order to overcome the afterload
Below is an image showing the pressure volume graph in case of changes in preload and afterload.

The variation in the pressure volume loop in case of increased preload and in the case of increased afterload. Note that the normal pressure volume diagram is in dotted line.

Dilated Cardiomyopathy

  • In dilated cardiomyopathy, the ventricle becomes dilated without compensatory thickening of the wall and consequently the following changes are observed:
    • Decreased contractility of the left ventricle that is illustrated by a shift to the right of the ESPVR curve
    • Decreased ventricular compliance illustrated by the shift to the right of the EDPVR curve
    • Decreased stroke volume leading to an increase in the end systolic volume
    • Increased end diastolic volume due to the dilatation of the ventricles
    • Decreased cardiac output
    • No change in the ventricular pressures accompanies the changes in the volume.
Below is an image showing the pressure volume graph in case of dilated cardiomyopathy.

The pressure volume loop in dilated cardiomyopathy. Note that the normal pressure volume diagram is in dotted line

Left Ventricular Hypertrophy

  • Left ventricular hypertrophy (LVH) is an increase in the thickness and mass of the myocardium.
  • The thickening of the ventricular muscle results in decreased chamber compliance and consequently the following changes are observed:
    • Elevated left ventricular pressures
    • Increased ESV
    • Decreased EDV
    • Decreased cardiac output
Below is an image showing the pressure volume curve in case of left ventricular hypertrophy (LVH) with associated reduced stroke volume (SV), end diastolic volume (EDV) and increased left ventricular pressure (LVP).

The pressure volume loop in left ventricular hypertrophy. Note that the normal pressure volume diagram is in dotted line.

  • There are two exceptions to these changes, where moderate hypertrophy allows for a lower heart rate, increased diastolic volume, and thus higher stroke volume:
    • Increased left ventricular hypertrophy with increased EDV and SV seen with athletes[2]
    • Increased left ventricular hypertrophy in healthy normal elderly individuals.

Restrictive Cardiomyopathy

  • Restrictive cardiomyopathy includes a group of heart disorders in which the walls of the ventricles become stiff (but not necessarily thickened) and resist normal filling with blood between heartbeats.
  • This condition occurs when heart muscle is gradually infiltrated or replaced by scar tissue or when abnormal substances accumulate in the heart muscle and consequently the following changes are observed:
    • Normal ventricular systolic pressure
    • Elevated diastolic pressure
    • Reduced cardiac output
Below is an image showing the pressure volume curve in case of restrictive cardiomyopathy with associated reduced stroke volume.

The pressure volume curve in restrictive cardiomyopathy. Note that the normal pressure volume diagram is in dotted line.

Valvular Diseases

Aortic Stenosis

  • Aortic valve stenosis is the abnormal narrowing of the aortic valve.
  • This results in the left ventricle pressures being much greater than the aortic pressures during left ventricular ejection. The magnitude of the pressure gradient is determined by the severity of the stenosis and the flow rate across the valve.
  • The following changes are observed in severe aortic stenosis:
    • Reduced ventricular stroke volume due to increased afterload (which decreases ejection velocity)
    • Increased end-systolic volume
    • Compensatory increase in end-diastolic volume and pressure
Below is an image showing a pressure volume diagram in case of aortic stenosis depicting increased end systolic pressure and reduced stroke volume.

Pressure-volume loop in aortic stenosis. Note that the normal pressure volume diagram is in dotted line.

Mitral Stenosis

  • Mitral stenosis is the abnormal narrowing of the mitral valve orifice.
  • The following changes are observed inmitral stenosis:
    • Decreased end-diastolic volume (preload) due to impaired left ventricular filling
    • Decreased stroke volume resulting from the decreased preload according to the Frank–Starling mechanism
    • Decreased cardiac output and aortic pressure (afterload) as the stroke volume is decreased
    • Slightly decreased end-systolic volume due to the decrease in the afterload
Below is an image showing a pressure volume curve in case of mitral stenosis depicting reduced end diastolic volume and reduced stroke volume.

Pressure-volume loop in mitral stenosis. Note that the normal pressure volume loop is in dotted line.

Aortic Regurgitation

  • Aortic insufficiency (AI) or regurgitation is the failure of the valve to close completely at the end of systolic ejection, causing leakage of blood back through the valve during LV diastole.
  • The following changes are observed in aortic regurgitation:
    • Increased end diastolic volume (preload) because the LV volume is greatly increased due to the enhanced ventricular filling from the constant backflow of blood through the leaky valve
    • Increased systolic pressure and stroke volume due to the elevated preload according to the Frank–Starling mechanism
  • Not that when the LV begins to contract and develop pressure, blood is still entering the LV from the aorta (since aortic pressure is higher than LV pressure), implying that there is no true isovolumic contraction. Once the LV pressure exceeds the aortic diastolic pressure, the LV begins to eject blood into the aorta.
Below is an image showing the pressure volume curve in case of aortic regurgitation depicting increased end diastolic volume, increased stroke volume and increased LV systolic pressure.

Pressure-volume loop in aortic regurgitation. Note that the normal pressure-volume diagram is in dotted line.

Mitral Regurgitation

  • Mitral regurgitation (MR) is the failure of the mitral valve to close completely, causing blood to flow back into the left atrium during ventricular systole.
  • The increased ventricular
  • The following changes are observed in mitral regurgitation:
    • Decreased end systolic volume due to the constant back flow of blood through the leaky valve
    • Increased left ventricular end diastolic volume as the volume and pressure of atria are higher than normal
    • Increased stroke volume in such a way that the ejection into the aorta (forward flow) is reduced as the stroke volume in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium
Below is an image showing the pressure volume curve in case of mitral regurgitation depicting increased end diastolic volume and increased stroke voume.

Pressure volume loop in case of mitral regurgitation. Note that the normal pressure volume loop is in dotted line.

References

  1. ↑ Barrett KE, Barman SM, Boitano S, Brooks HL. Chapter 30. The Heart as a Pump. In: Barrett KE, Barman SM, Boitano S, Brooks HL, eds. Ganong's Review of Medical Physiology. 24th ed. New York: McGraw-Hill; 2012.
  2. ↑ Scharhag, J.ürgen. "Athlete's heart". Athlete’s heart.

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