The document discusses ventricular pressure-volume loops and cardiac physiology. It begins by introducing ventricular pressure-volume loops and their use in assessing cardiac function. It then covers the normal cardiac cycle and mechanics, including the isovolumic contraction and relaxation phases. Key concepts like preload, afterload, contractility, compliance, and indices of cardiac function such as ejection fraction, fractional shortening, and Tei index are defined and their clinical significance explained. Older indices assessed by biplane cineangiography are also mentioned.

1. VENTRICULAR
PRESSURE VOLUME LOOP
Dr Dipak Patade

2. VENTRICULAR PRESSURE VOLUME LOOP
• Introduction
• Basic physiologic concepts
• Generation of pressure volume loop
• Abnormal pressure volume loop
• PV loop in common pathologic states

3. CARDIAC CYCLE

4. CARDIAC CYCLE

5. cardiac cycle describes pressure, volume and flow phenomena in the ventricles as
a function of time.
Similar for both LV and RV except for the timing, levels of pressure.
Mechanical events in Cardiac cycle :
Systole :
• Isovolumic contraction
• Maximal ejection
• Reduced ejection
Diastole :
• Isovolumic relaxation
• Rapid filling phase
• Slow filling phase /diastasis
• Atrial systole

6. •The pulmonary valve remains open for some time even after the right ventricular
pressure becomes equal to pulmonary artery pressure at end of systole this time
interval is known as hangout interval
Why does pulmonary valve remain open even after pressure equilisation?
•According to Newton’s first law of motion, every body continues to move at
constant speed unless acted upon by an external force .In this case, the blood
continues to flow from the right ventricle even after the the pressure in the right
ventricle and the pulmonary artery becomes equal ,Just like a rolling ball is
stopped by the friction offered by the ground, the ejection of blood is stopped by
the resistance offered by the pulmonary vasculature.Since the pulmonary
vascular resistance is low compared to the systemic vascular resistance, it takes
some time for the blood flow from the right ventricle to stop This corresponds to
the hangout interval.
Significance of hangout interval
•Hangout interval is shortened in cases of increased pulmonary vascular
resistance such as pulmonary vasospasm, obliteration of pulmonary vessels etc
Does the aortic valve have a hangout interval?
•Due to high systemic vascular resistance, the aortic valve closes almost
immediately Hence hangout interval is negligible
hangout interval

7. LV contraction
Actin myosin contraction triggered by arrival of Calcium ions
at contractile proteins.
ECG – peak of R wave
LV pressure >LA pressure (10-15mm Hg) Followed approx.
50msec by M1.
Delay of M1 – inertia of the blood flow – valve is kept open.
Isovolumic contraction as volume is fixed.
Increased pressure as more fibers enter contractile state.
LV pressure >Aorta – Aortic valve opens – silent event
clinically.

8. LV RELAXATION
Isovolumic relaxation(e)
Start of relaxation in reduced ejection (d)
Rapid phase(f)
Slow filling (diastasis)(g)
Atrial systole or booster
LV RELAXATION

9. Rapid filling phase – active diastolic relaxation of LV.
• LA- LV pressures equalize - diastasis.
• LA booster atrial systole – important in exercise and LVH.
• First phase of diastole –isovolumic phase – no ventricular
filling.
Most of ventricular filling 80% –rapid filling phase.
Diastasis -5%
Final atrial booster phase -15%.
The sucking effect of ventricle – myosin is pulled into the
space between the two anchoring segments of titin.
Dominant backward pressure wave –diastolic coronary
filling.
LV filling

10. • Wall stress at the end of diastole – maximum resting
length of sarcomere.
• Increasing LVEDV increases SV in ejecting
beats,increases LV pressure in isovolumic beats.
• Modulation of ventricular performance by changes
in preload with constant afterload –heterometric
autoregulation,
operates on a beat –to beat basis
Preload

11. Exact definition – wall stress during LV ejection.
Tension in the LV wall that resists ventricular ejection
or as the arterial input impedance.
In clinical practice the arterial blood pressure is often
taken as synonymous with afterload while ignoring
aortic compliance (increase in stiff aorta).
Afterload

12. • Frank Starling – venous pressure in RA – heart volume
Within physiological limits – the larger the volume of the heart –greater
the energy of its contraction – the greater the amount of chemical change
at each contraction.
LV volume – Cardiac Output Stroke volume related to LVEDV – modern
version Real time 3D ECHO – global LV volume,endocardial function LV
volume surrogate markers – LVEDP ,PCWP.
Frank – greater the initial LV volume – more rapid rate of rise
greater the peak pressure reached –faster the rate of relaxation.
An important compensatory mechanism that maintains stroke volume
,when there is myocardial dysfunction or excessive afterload. Atria also
exhibit frank starling curve – exercise.(resistance to early diastolic filling).
Frank Starling mechanism

13. Hemodynamic variables
•stroke volume -the quantity of blood expelled from the
ventricle per beat
•cardiac output -multiply stroke volume by heart represents
the volume of ejected blood per minute
•cardiac index :when you divide cardiac output by body
surface area you obtain the cardiac index.

14. dP/dt is a parameter of
myocardial contractility.
Dp/dt represents the ratio of pressure
change in the ventricular cavity during
the isovolemic contraction period.
LV dP/dt is estimated by using time
interval between 1 and 3 m/sec on
MR velocity spectrum.(because
velocities represent pressure
gradients -by applying the
Bernoulli equation of 4v2).
The faster the ventricle is able to
build up pressure, the better it
functions. As pressure in the left
atrium during early systole may
be neglected, the MR velocity is
the instantaneous systolic
pressure in the left ventricle
(which resembles systolic blood
pressure).
Contractility - dP/dt

15. It is the inherent capacity of the myocardium to
contract independently of changes in the preload and
afterload.
An increased contractile function –assosciated with
greater degree of relaxation – LUSITROPIC effect
Important regulator of My02 uptake
Increased contractile function by exercise,adrenergic
stimulation,digitalis,other inotropic agents
Contractility

16. The term compliance is used to describe how easily a chamber of the heart or the
lumen of a blood vessel expands when it is filled with a volume of blood.
Physically, compliance (C) is defined as the change in volume (ΔV) divided by
the change in pressure (ΔP).
C = ΔV / ΔP
compliance
The slope of the curve at any given pressure and volume (dV/dP) represents the
compliance of the vessel at that pressure and volume.
at higher volumes and pressures there is a larger change in pressure for a given
change in volume.
Another way to think of this is that the "stiffness" of the vessel wall (reciprocal of
compliance) increases at higher volumes and pressures.
This non-linearity in the relationship between volume and pressure is common in
biological tissues.

17. Compliance is a
fundamental property of
a tissue; however, the
compliance can be
modified by histological
changes in the tissue.
This occurs, for
example, when a heart
structurally remodels in
response to chronic
volume or pressure
overload conditions. In a
blood vessel,
compliance can also be
altered by contraction of
smooth muscle in the
vessel wall, which
decreases the
compliance of the
vessel.
compliance

19. The compliance of the ventricle is determined by the structural properties of
the cardiac muscle (e.g., muscle fibers and their orientation, and connective
tissue) as well as by the state of ventricular contraction and relaxation.
For example, in ventricular hypertrophy the ventricular compliance is
decreased (i.e., the ventricle is "stiffer") because the thickness of the
ventricular wall increases;
therefore, ventricular end-diastolic pressure (EDP) is higher at any given end-
diastolic volume (EDV)
compliance

20. The Tei index : myocardial performance index (MPI)
It is a parameter for global ventricular performance.
The Tei index consists of 3 variables which are derived from Doppler spectrum.
The formula is: MPI = (IVCT + IVRT) / ET
When systolic dysfunction is present in patients IVCT will increase and ET decrease.
Normal range is considered at 0,39+/-0,05. An MPI over 0,5 is considered abnormal.
Tei index / Myocardial performance index

21. Fractional shortning
• percentage of "size reduction" of the left ventricle :is fractional
shortening
•does not express ejection fraction because we are not
computing volumes
formula:
(LVEDD - LVESD / LVEDD) x 100

22. Fractional shortning
• fractional shortening has limited application, cannot be used
in all patients, and only provides a rough approximation of
left ventricular function.
• Limitations-
• LBBB / Dyssynchrony
• Regional wall motion abnormalities
• Poor image quality
• Abnormal septal motion
• Inadequate MMode orientation

23. Ejection fraction
• Ejection fraction (EF) refers to how
well your left ventricle (or right
ventricle) pumps blood with each
heart beat.
• It is the ratio of blood ejected during
systole (stroke volume) to blood in
the ventricle at the end of diastole
(end-diastolic volume).
• LVEF = stroke volume (EDV - ESV)
÷ EDV

24. In patients in whom satisfactory biplane cineangiograms were obtained, three indices
were determined:
a) ejection fraction
b) two normalized velocity measurements:
1. mean velocity of circumferential fiber shortening (mVcf)
2. mean systolic ejection rate.( mSER)
Ejection fraction (EF) was calculated as the difference between left ventricular end-
diastolic and end-systolic volumes, divided by end-diastolic volume.
Mean velocity of circumferential fiber shortening (mVcf) was calculated as the
difference between the minor axis of the left ventricle (L2) in end diastole and end
systole, divided by L2 in end diastole, divided by ejection time.
L2 was calculated from the area of the frontal projection (AF) and the long axis (LJ) by
the formula: L2 = 4AF/rL,. Values were expressed in circumferences/second.
Mean systolic ejection rate (mSER) was calculated as the difference between end-
diastolic and end systolic left ventricular volumes, divided by end diastolic volume,
divided by ejection time; or as ejection fraction divided by ejection time. Values were
expressed in volumes/second.
Old indices on biplane cineangiography

26. 200
100
0
0 100 200
LVpressure(mmHg)
LV volume (ml)
AoV
closes
AoV opens
MV closes
MV
opens
ESPVR
EDPVR
VENTRICULAR PRESSURE VOLUME LOOP
No time representation
PRESSURE &
VOLUME MEASUREMENT
Conductance catheter
Volume by echo
Pressure by high fidelity manometer
APPLICATION
Clinical tool;

27. • Best of the current approaches to the assessment of the
contractile behaviour of the intact heart. Es,the pressure –
volume relation
Changes in the slope of this line joining the different Es
points are generally good load independent index of the
contractile performance of the heart.
Enhanced inotropic effect, Es shifted upward and to the
left. Lusitropic effect shifted Es downward and to right.
The P-V relationship is linear in smooth muscle,curvilinear
in cardiac muscle(exponential).
Pressure volume loop

28. LEFT ATRIAL PRESSURE VOLUME LOOP

29. VENTRICULAR PRESSURE VOLUME LOOP
INCA PV LOOP SYSTEM CD LEYCOM CONDUCTANCE CATHETER

30. DETERMINANTS OF VENTRICULAR FUNCTION
Preload: wall tension at the end of diastole;
clinical index: end diastolic volume or end diastolic pressure
Afterload: the load against which the ventricle ejects
clinical index: Aortic pressure (in the absence of LVOT obstruction)
or precisely wall stress
Contractility: the intrinsic ability of a cardiac muscle fibre to contract at a
given fibre length.
Heart rate

31. BASIC PHYSIOLOGIC CONCEPTS
1.FRANK-STARLING CURVE
(VENTRICULAR FUNCTION CURVE)
2. FORCE – VELOCITY RELATIONSHIP
3. DIASTOLIC PRESSURE VOLUME
RELATIONSHIP
4. SYSTOLIC PRESSURE VOLUME
RELATIONSHIP

32. FRANK-STARLING CURVE
A
B
INCREASED
VENOUS
RETURN
100
50
0 0 10 20
SV
(ml)
LVEDP (mmHg)
100
50
0 0 10 20
SV
(ml)
DECREASED
VENOUS
RETURN
C
normal
‘Stroke volume increases proportionately with preload within physiologic limits’

33. 100
50
0
0 10 20
SV
(ml)
LVEDP (mmHg)
100
50
0
0 10 20
SV
(ml)
FAMILY OF FRANK STARLING CURVES
 Afterload
 Inotropy
 Afterload
 Inotropy
‘Increased afterload and decreased inotropy shifts the curve downward – SV decreases’
‘Decreased afterload and increased inotropy shifts the curve upwards – SV increases’

34. INOTROPY & FORCE VELOCITY RELATIONSHIP
Afterload (force)
Shorteningvelocity
Normal
Decreased
inotropy
Increased
inotropy
As afterload increases; shortening velocity decreases -- SV decreases;
As afterload decreases, shortening velocity increases – SV increases;
At a given afterload; increasing inotropy increases shortening velocity;

35. Shorteningvelocity
Afterload (Force)
Increasing preload a c
a
b
c
PRELOAD & FORCE VELOCITY RELATIONSHIP
As afterload increases; shortening velocity decreases -- SV decreases;
As afterload decreases, shortening velocity increases – SV increases;
At a given afterload; increasing preload increases shortening velocity;

36. EDV
0 100 200
EDP
LVpressure(mmHg)
100
50
0
Decreased
compliance
normal
VENTRICULAR COMPLIANCE CURVE
Increased
compliance
DIASTOLIC PRESSURE VOLUME RELATIONSHIP
‘Slope of the curve is stiffness dP/dV;
Compliance is the inverse of the slope dV/dP’
‘As compliance decreases; filling pressure increases’

37. 200
100
0
0 100 200
LVpressure(mmHg)
LV volume (ml)
ESPVR
EDPVR
END SYSTOLIC PRESSURE VOLUME RELATIONSHIP
normal
 inotropy
 inotropy

38. 200
100
0
0 100 200
LVpressure(mmHg)
LV volume (ml)
AoV
closes
AoV opens
MV closes
MV
opens
4
1
2
3
a
b
c
d
1 = MV closing point
2 = AV opening point
3 = AV closing point
4 = MV opening point
a = Diastole
b = Isovolumic
contraction
c = Systole
d = Isovolumic
relaxation
GENERATION OF PRESSURE VOLUME LOOP
stroke volume

39. NORMAL PRESSURE VOLUME LOOP
200
100
0
0 100 200
LVpressure(mmHg)
LV volume (ml)
AoV
closes
AoV opens
MV closes
MV
opens
ESPVR
EDPVR
systole
diastole
IVC
IVR
Normal IVR & IVC
Abnormal IVR & IVC

40. CHANGES IN PRELOAD AND STROKE VOLUME
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV EDV
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV EDV
INCREASED PRELOAD DECREASED PRELOADINCREASED PRELOAD DECREASED PRELOAD
EDV increases; Cardiac output increases;
Afterload minimally increases:
Net effect : SV increases
EDV decreases; Cardiac output decreases;
Afterload minimally decreases
Net effect : SV decreases

41. CHANGES IN AFTERLOAD AND STROKE VOLUME
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV EDV
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV EDV
INCREASED AFTERLOAD DECREASED AFTERLOADINCREASED AFTERLOAD DECREASED AFTERLOAD
ESV increases; Cardiac output decreases;
Preload minimally increases:
Net effect : SV decreases
ESV decreases; Cardiac output increases;
Preload minimally decreases:
Net effect : SV increases

42. CHANGES IN INOTROPY AND STROKE VOLUME
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV EDV
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV EDV
INCREASED INOTROPY DECREASED INOTROPY
ESV increases; SV decreases
EDV increases minimally
ESV decreases; SV increases
EDV decreases minimally

43. PRELOAD, AFTER LOAD & STROKE VOLUME
PRELOAD = END DIASTOLIC VOLUME
Increasing Preload Increases End Diastolic Volume
‘Stroke volume is directly proportional to end diastolic volume’
AFTERLOAD ~ END SYSTOLIC VOLUME
Increasing Afterload Increases End Systolic Volume
‘Stroke volume is inversely related to after load’
INOTROPIC STATE IS RELATED TO END SYSTOLIC VOLUME
Increasing Inotropy Decreases End Systolic Volume
‘Stroke volume is directly proportional to inotropic state’

44. ABNORMAL PRESSURE VOLUME LOOP
200
100
0
0 100 200
LVpressure(mmHg)
LV volume (ml)
AoV
closes
AoV opens
MV closes
MV
opens
ESPVR
EDPVR
Identified by
• Change in EDPVR & EDP
• Change in ESPVR & pressure
at which AoV closes
• Change in Stroke volume
• Curved IVC & IVR line
• Overall shape of PV loop
systole
diastole
IVC
IVR

45. SYSTOLIC DYSFUNCTION
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV EDV
NORMAL
SYSTOLIC
DYSFUNCTION
Strokevolume(ml)
LV EDP (mm Hg)
0 10 20 30
100
50
0
loss of
inotropy
VASODILATORS
Loss of inotropy shifts ESPVR downwards; ESV increases, Compensatory increase in
EDV to some extent; However SV decreases.
Frank Starling curve : shifts downwards; EDP increases. SV falls;
With vasodilator therapy, afterload & preload decrease; EDP is reduced, SV increases

46. DIASTOLIC DYSFUNCTION
LV volume (ml)
LVpressure(mmHg)
200
100
0 0 100
200 ESV EDVEDV
0 100 200
EDP
LVpressure(mmHg)
100
50
0
Decreased
compliance
normal
LV volume (ml)
eg. LVH; compliance curve shifts up. EDP increases and SV decreases.
Careful use of diuretics will be of use; because some degree of raised venous pressure
is necessary to fill less compliant ventricle.

47. LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV
EDV
MITRAL STENOSIS
Decrease in EDV since there
is reduced filling.
SV decreases, fall in CO and
Aortic pressure.
Afterload is decreased so
ESV also decreases to some
extent, not enough to
overcome decrease in EDV.

48. LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV
EDV
AORTIC STENOSIS
Afterload is very much
increased, so ESV increases
and SV decreases
As ESV increases, residual
volume is added to venous
return, so EDV increases.
Increased preload increases
force of contraction and
maintains SV to some extent
esp. in mild aortic stenosis.
Diuretics are deleterious in
this situation

49. LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV
EDV
CHRONIC AORTIC REGURGITATION
No true Isovolumic contraction
and relaxation
EDV increases greatly.
This increases Stroke volume
and cardiac output.
Afterload increases hence
ESV also increases to some
extent.
Once systolic dysfunction
sets in, ESV increases
progressively and peak
systolic pressure & SV fall

50. LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV
EDV
CHRONIC MITRAL REGURGITATION
No true isovolumic contraction
and relaxation
EDV increases
Afterload is reduced, so ESV
is reduced
Net effect = SV increases
With systolic dysfunction; ESV
increases, forward stroke
volume decreases

51. ACUTE AORTIC REGURGITATION
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV
EDV
Ventricular diastolic volume
increases suddenly
EDV and EDP increases
PV loop appears small
No true isovolumic relaxation
SV falls

52. LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV
EDV
ACUTE MITRAL REGURGITATION
Ventricular volume increases
abruptly
No true isovolumic
contraction
EDP rapidly increases
PV loop appears small

53. CARDIAC TAMPONADE
LV volume (ml)
LVpressure(mmHg)
200
100
0
0 100 200
ESV
EDV
Unique PV loop
Preload is greatly decreased;
EDP is elevated
ESV is also decreased
Stroke volume is decreased

54. TAKE HOME POINTS
Pressure volume loop is an excellent clinical tool to understand pathologic cardiac
conditions
Interaction between preload, afterload and contractility determines the shape and size
of pressure volume loop
Increased preload increases end diastolic volume and vice versa
Increased afterload increases end systolic volume and vice versa
Increased inotropy decreases end systolic volume and vice versa
Increased compliance increases end diastolic volume and vice versa
Isovolumic contraction line and isovolumic relaxation line are not straight in
regurgitant lesions

55. ‘