VENTRICULAR PRESSURE VOLUME LOOP

42
VENTRICULAR PRESSURE VOLUME LOOP Dr. G. Gnanavelu, MD, DM Associate Professor and Head Department of Cardiology Kilpauk Medical College Chennai

description

VENTRICULAR PRESSURE VOLUME LOOP. Dr. G. Gnanavelu , MD, DM Associate Professor and Head Department of Cardiology Kilpauk Medical College Chennai. CARDIAC CYCLE. VENTRICULAR PRESSURE VOLUME LOOP. ESPVR. AoV closes. LV pressure (mmHg). AoV opens. MV closes. MV opens. EDPVR. - PowerPoint PPT Presentation

Transcript of VENTRICULAR PRESSURE VOLUME LOOP

VENTRICULAR PRESSURE VOLUME LOOP

Dr. G. Gnanavelu, MD, DM

Associate Professor and Head

Department of Cardiology

Kilpauk Medical College

Chennai

CARDIAC CYCLE

200

100

0

0 100 200

LV p

ress

ure

(mm

Hg)

LV volume (ml)

AoV

closesAoV opens

MV closesMV

opens

ESPVR

EDPVR

VENTRICULAR PRESSURE VOLUME LOOP

PRESSURE &

VOLUME MEASUREMENT

Conductance catheter

Volume by echo

Pressure by high fidelity manometer

APPLICATION

Clinical tool;

Experimental

LEFT ATRIAL PRESSURE VOLUME LOOP

VENTRICULAR PRESSURE VOLUME LOOP

200

100

0

0 100 200

LV p

ress

ure

(m

mH

g)

LV volume (ml)

AoV

closesAoV opens

MV closesMV

opens

41

23

a

b

c

d

1 = MV closing point2 = MV opening point3 = Ao V closing point4 = Ao V opening point

a = Diastoleb = Isovolumic

contractionc = Systoled = Isovolumic

relaxation

GENERATION OF PRESSURE VOLUME LOOP

stroke volume

DETERMINANTS OF VENTRICULAR FUNCTION

Preload: initial stretching of the cardiac myocytes prior to contraction.

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

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’

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’

INOTROPY & FORCE VELOCITY RELATIONSHIP

Afterload (force)

Sho

rten

ing

velo

city 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;

Sho

rten

ing

velo

city

Afterload (Force)

Increasing preload a c

ab

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;

EDV0 100 200

EDP

L

V p

ress

ure

(mm

Hg)

100

50

0

Decreased compliance

normal

VENTRICULAR COMPLIANCE CURVE

Increased compliance

DIASTOLIC PRESSURE VOLUME RELATIONSHIP

‘Slope of the curve is stiffness; Compliance is the inverse of the slope’‘As compliance decreases; filling pressure increases’

200

100

0

0 100 200

LV p

ress

ure

(m

mH

g)

LV volume (ml)

ESPVR

EDPVR

END SYSTOLIC PRESSURE VOLUME RELATIONSHIP

normal

inotropy

inotropy

NORMAL PRESSURE VOLUME LOOP

200

100

0

0 100 200

LV p

ress

ure

(mm

Hg)

LV volume (ml)

AoV

closesAoV opens

MV closesMV

opens

ESPVR

EDPVR

systole

diastole

IVC

IVR Normal IVR & IVC

Abnormal IVR & IVC

CHANGES IN PRELOAD AND STROKE VOLUME

LV volume (ml)

L V

pre

ssur

e (m

m H

g)

200

100

0

0 100 200ESV EDV

LV volume (ml)

L V

pre

ssur

e (m

m H

g)

200

100

0

0 100 200ESV EDV

INCREASED PRELOAD DECREASED PRELOADINCREASED PRELOAD DECREASED PRELOAD

Primary change: EDV increases; SV increases

Secondary change : ESV increases minimally

Primary change: EDV decreases; SV dereases

Secondary change : ESV decreases minimally

CHANGES IN AFTERLOAD AND STROKE VOLUME

LV volume (ml)

L V

pre

ssur

e (m

m H

g)

200

100

0

0 100 200ESV EDV

LV volume (ml)

L V

pre

ssur

e (m

m H

g)

200

100

0

0 100 200ESV EDV

INCREASED AFTERLOAD DECREASED AFTERLOADINCREASED AFTERLOAD DECREASED AFTERLOAD

Primary change: ESV increases; SV decreases

Secondary change : EDV increases minimally

Primary change: ESV decreases; SV increases

Secondary change : EDV decreases minimally

CHANGES IN INOTROPY AND STROKE VOLUME

LV volume (ml)

L V

pre

ssur

e (m

m H

g)

200

100

0

0 100 200ESV EDV

LV volume (ml)

L V

pre

ssur

e (m

m H

g)

200

100

0

0 100 200ESV EDV

INCREASED INOTROPY DECREASED INOTROPY

Primary change: ESV decreases; SV increases

Secondary change : EDV decreases minimally

Primary change: ESV increases; SV decreases

Secondary change : EDV increases minimally

ABNORMAL PRESSURE VOLUME LOOP

200

100

0

0 100 200

LV p

ress

ure

(mm

Hg)

LV volume (ml)

AoV

closesAoV opens

MV closesMV

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

SYSTOLIC DYSFUNCTION

LV volume (ml)

L V

pre

ssur

e (m

m H

g)

200

100

0

0 100 200ESV EDV

NORMAL

SYSTOLIC DYSFUNCTION

Str

oke

volu

me

(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; SV decreases.

Frank Starling curve : shifts downwards; EDP increases. SV falls; With vasodilator therapy, SV improves; EDP is reduced.

DIASTOLIC DYSFUNCTION

LV volume (ml)

L V

pre

ssur

e (m

m

Hg)

200

100

0

0 100 200 ESV EDVEDV

0 100 200

EDP

L

V p

ress

ure

(mm

Hg)

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.

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV 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.

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV 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

Diuretics are deleterious in this situation

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV 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

ACUTE AORTIC REGURGITATION

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

Ventricular diastolic volume increases suddenly

EDV and EDP increases

PV loop appears small

No true isovolumic relaxation

SV falls

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

CHRONIC MITRAL REGURGITATION

EDV increases

No true isovolumic contraction and relaxation

Afterload is reduced, so ESV is reduced

Net effect = SV increases

With systolic dysfunction; ESV increases, forward stroke volume decreases

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

ACUTE MITRAL REGURGITATION

Ventricular volume increases abruptly

No true isovolumic contraction

EDP rapidly increases

PV loop appears small

CARDIAC TAMPONADE

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

Unique PV loop

Preload is greatly decreased;

EDP is elevated

ESV is also decreased

Stroke volume is decreased

PV LOOP - QUIZ

Where does Aortic valve close?

1. Point 1

2. Point 2

3. Point 3

4. Point 4

200

100

0

0 100 200

LV p

ress

ure

(m

mH

g)

LV volume (ml)

41

23

a

b

c

d

PV LOOP - QUIZ

200

100

0

0 100 200

LV p

ress

ure

(m

mH

g)

LV volume (ml)

41

23

a

b

c

d

Where does Mitral valve open?

1. Point 1

2. Point 2

3. Point 3

4. Point 4

200

100

0

0 100 200

LV p

ress

ure

(mm

Hg)

LV volume (ml)

PV LOOP - QUIZ

Which portion of the loop issystole

1. Shaded area

2. Unshaded area

200

100

0

0 100 200

LV p

ress

ure

(mm

Hg)

LV volume (ml)

PV LOOP - QUIZ

What is the abnormality ?

Why ?

PV LOOP - QUIZ

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

What does the blue line with arrows indicate?

1. Cardiac output

2. Stroke volume

3. Stroke work

4. Kinetic energy

INTERPRETING PV LOOP

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

30 yr old male

Hb 8 gms%

C/o SOB & palpitation

BP 130/70

What is the abnormality?

INTERPRETING PV LOOP

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

What has caused the change in the shaded pressure

volume loop?

1. Intravenous fluids

2. Diuretics

3. ACE inhibitors

4. Dobutamine

INTERPRETING PV LOOP

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

What has caused the change in the shaded pressure

volume loop?

1. Intravenous fluids

2. Diuretics

3. ACE inhibitors

4. Dobutamine

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

INTERPRETING PV LOOP

30 yr old male

With acute gastroenteritis

Pulse thready and rapid

BP 80 systolic

Clear lungs

What is the abnormality in PV loop ?

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

50 yr old male

Hypertensive

Old ASMI

c/o SOB Class III

BP 150/100

ECHO: RWMA; EF 38%

What are the changes seen in

Colored PV Loop?

INTERPRETING PV LOOP

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV

EDV

After drugs

Before drugs

INTERPRETING PV LOOP

Same patient

After three months of drugs

SOB Class III

BP 120/80

ECHO: RWMA; EF 45%

What are the drugs which have caused the changes in PV loop?

INTERPRETING PV LOOP

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

65 yr. old female

Hypertensive

c/o SOB Class III

BP 160/100

S4

Bil. basal rales

ECHO: Mod. Conc. LVH EF 60%

Why is the patient dyspneic on exertion?

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

INTERPRETING PV LOOP

25 yr. old male

Bicuspid aortic valve

No RF delay

BP 140/70

What are the hemodynamic

changes seen in PV loop?

What are the lesions?

INTERPRETING PV LOOP

LV volume (ml)

L V

pr

essu

re (

mm

Hg)

200

100

0

0 100 200ESV EDV

60 year old male

Calcific aortic stenosis – severe (blue PV loop)

After 3 years – (green PV loop)

What are the changes?

What will be the clinical findings?