interpretation of hemodynamic data

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Dr. Dibbendhu Khanra, SR2 Interpretation of hemodynamics data 1

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Page 1: interpretation of hemodynamic data

1

Dr. Dibbendhu Khanra, SR2

Interpretation of hemodynamics

data

Page 2: interpretation of hemodynamic data

2

The lost world

Page 3: interpretation of hemodynamic data

3

The wind of change

Page 4: interpretation of hemodynamic data

4

Tools of the trade

Page 5: interpretation of hemodynamic data

5

Numbers

Formulas

Graphs

Relations

ABC of interpretation

Page 6: interpretation of hemodynamic data

6

The systole & the diastole

Page 7: interpretation of hemodynamic data

7

The normals

Page 8: interpretation of hemodynamic data

8

The abnormals

PP>60

RVF

PAH

Impaired LV

compliance

Impaired LA

complianceMR

ARLow SVR

High output states

CI <2.2Cardiogenic

shock

>8

>8

= =>

>

= dPAP

RVSP= sPAPLVSP= SBP >

= pericardial pressure

Page 9: interpretation of hemodynamic data

9

Relations

PA systolic pressure = RV systolic pressure

mean PCWP = PA diastolic pressure (+5)Mean PCWP = LVEDPRVEDP = RA pressurePCWP>RA pressure

LVEDP>RVEDP

Pressure equalize in

CP, RVF, RCMP

Atrial Ventricular

Arterial

Page 10: interpretation of hemodynamic data

10

Atrial pressure

TP

V A

Two peaks/ QRS v=T; a=P PCWP: v>a; CVP: a>v (ASD a=v) rises in diastole falls in systole end expiration (on ventillation: substract half of PEEP)

Page 11: interpretation of hemodynamic data

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Ventricular trace vs arterial trace

Ventricular Arterial Diastole Pr rises Pr falls

Baseline touch Yes No Dicrotic notch Absent Present

A bump Present AbsentShape Rectangular Triangular

Page 12: interpretation of hemodynamic data

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Problem: SOB, edema, PSM LA LV RA RV PA

TR: ventricularization RAP = RVEDP

Page 13: interpretation of hemodynamic data

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Problem: DOE LA LV RA RV PA

MR: tall vSevere PAH mPCWP =

dPAP

Page 14: interpretation of hemodynamic data

14

Tall V

V>mean PCWP+10decompensated LVFSevere MR (early diastole slow downslope)

Severe MS (early diastole sharp downslope)

A=P, V=T (PA peaks before T)V-V horizontal (downsloping)No dicrotic notch PV sat >95%, PA sat 75% Mean PCWP = diast PA pr (+5) < PASP

PCWPPC-PA hybrid pressure

Page 15: interpretation of hemodynamic data

15

Problem: DOE, normal EF

LVDD MS CP

Page 16: interpretation of hemodynamic data

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LVEDPA bumpDiastolic slope

LVEDP normal/ low in MS LVEDP high in CP, AR, LVDD Absent A bump in MS, AF Prominent in HOCM, LVDD

LVEDP

LVEDP = mPCWPExcept1. MS2. MR3. PAH

Flat slope in chronic ARSharp slope in acute AR

Page 17: interpretation of hemodynamic data

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Saturations

LA 95% RA 75%

LV 95% RV 75%

AO 95%

PA 75%SVO2/ MVO2

SVC 74%

SCVO2

IVC 78%

PV 98%

Normal: SVO2> SCVO2In shock relation reverses MVO2 sat< 65%

Low CO

Page 18: interpretation of hemodynamic data

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Step upChambers Step up D/D

SVC/IVC to RA >= 7% OS ASD, TAPVC, RSOV, CMF to RA

RA to RV >= 5% VSD, OP ASD, CMF to RVRV to PA >= 5% PDA, APWSVC to PA >= 8% L-R shuntRA to PA >= 6% L-R shunt

PV to arterial SO2 >5% R-L shunt

MVO2= O2 saturation in chamber proximal to shunt= ASD: 3SVC+1IVC/4 (=SVC O2)= VSD: RA SO2= PDA: RV SO2

Page 19: interpretation of hemodynamic data

19

Problem

Qp/Qs = Ao – MVO2/ PV-PA = 96 – 78/ 98 – 83 = 18 / 15 = 1.2 (small L-R)

PDA (L-R)PAHCoA

TAPVC

Page 20: interpretation of hemodynamic data

20

Fick

Gold standardTrue FickO2 challenge

Not accurate in- Low output state- Shunt- Regurgitation lesion

Cardiac outputThermodilution

SV = CO/ HR CI = CO/ BSA SVI = SV/ BSA = CI/ HR

Page 21: interpretation of hemodynamic data

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SVR

N: 0.5-1 woods unitHigh in PAH- <3: passive PAH- 3-5: mixed PAH- >5: reactive PAH• In shunt: Qp

Resistance = Pressure/ flowPVR

MAP = 1SBP+2DBP/3

N: <700 dyn cm /sec5

Low SVR in septic shock

High SVR in ionotrpsW (mmHg/ L/min) = 80 dyn cm /sec5

Page 22: interpretation of hemodynamic data

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Shunts Bidirectional shunt

Eisenmenger’s systemic = pulmonary pr

PVR>SVR (PVR> 5)Qp<Qs (Qp/Qs <1)

Page 23: interpretation of hemodynamic data

23

Room O2

PA 70/40/50 PCWP 10

ASD: bidirectional shunt in EchoRepair or not?

100% o2

VO2 220Hb 15

45 mmH

g

80 mmH

g

450 mmH

g

100 mmH

gPA 55/32/39 PCWP 10

Page 24: interpretation of hemodynamic data

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Rest

QpQs

QeffPVR

Page 25: interpretation of hemodynamic data

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100% o2

Repair

Page 26: interpretation of hemodynamic data

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MVA in MS

AF: 10 sec…X6 (avg over 10 beats)Hakki area = CO/√PG Mean grad in MS, peak instantaneous grad in AS not validated for tachycardia or bradycardia

Gorlin’sValve area

AVA in AS

Peak to peak PG = mean

PG

mean PG = 70% of

Peak instantaneo

us PG

Area α QGradient α Q2

A = Q/ √PG

Area α 1/ √PG

Page 27: interpretation of hemodynamic data

27

Problem:

AS HOCM technical error

Page 28: interpretation of hemodynamic data

28

AS

Aortic stenosisHOCM

Always rule out error in zeroing

Peripheral artery- Pressure

elevated- No dicrotic

notch- delayed

Page 29: interpretation of hemodynamic data

29

LV – Aorta gradient: doppler vs catheter

Vena Contracta(Ao pr lesser)

Aortic root<3cm

Pressure reco ery

Echo gradientHigher

AVA less

In aortic root<3cmcatheter gradient

accurate

Downstream to valve

(Ao pr higher)HTN, LVDD

catheter gradientLower

AVA highHTN, LVDD

Echo gradient accurate

Area= Q/ √PG

LV loadSBP+PG/ SVI

= SBP+PG/ CI (ml) X HR

(> 4.5 abnormal)

Page 30: interpretation of hemodynamic data

30

Severe AS, mPG 27mmHg, AVA 0.9 cm2

EF 55% CO4 CI 2 HR 80 SBP 178 mPG22

EF 55% CO4 CI 2 HR 80 SBP 138 mPG42

total LV load 8

total LV load 4.51 week

True severe AS

Page 31: interpretation of hemodynamic data

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Asympt, normal EF, PG 43, AVA 1.25

Echo gradient Higher

AVA less

Aortic root<3cmAR

AVA = Q/√PG

Pseudo severe AS

Page 32: interpretation of hemodynamic data

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Low gradient (<40mmHg) severe AS (AVA<1 cm2)

Gradient α Q2

EF <40%

EF >40%

low volume status RAP, LVEDP low fluid load - gradient rises uncontrolled HTN

total LV load>4.5 control HTN- gradient rises severe MS or MR low forward flow PCWP>15

Pseudosevere AS True severe AS

DCM+ AS

Dobutamine stress

test

fluid load

RAP, LVEDP low

Page 33: interpretation of hemodynamic data

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Low gradient severe AS with low EFTrue

severe ASPseudoseve

re ASDCM+AS

SV increase

>20% >20% <20%

PG increase

>50% (>40)

<50% (<40) <50% (<40)

AVA increase

<0.3 (<1.2)

>0.3 (>1.2) >0.3 (>1.2)

PG ++++ Area +

PG + Area +++

+

True severe AS

Pseudo severe AS

Page 34: interpretation of hemodynamic data

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severe AS, mPG 26mmHg, AVA 0.85 cm2

CI 1.6 HR 55 EF 40% PA o2sat 55% BP 130/80

Page 35: interpretation of hemodynamic data

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Dobutamine stress: mPG 45, AVA 1.1

CI 3 HR 78 EF 40% PA o2sat 73%

True severe AS

Page 36: interpretation of hemodynamic data

36

End holeWedge Wire manipulation- Pulmonary wedge

catheter

Pressure monitoring

Blood sampling- Berman catheter- Multipurpose

catheter- Pigtail catheter

Choosing Catheter Side hole

Page 37: interpretation of hemodynamic data

37

AS HOCM

Page 38: interpretation of hemodynamic data

38

Problem: LV to aorta pull back

AS HOCM

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HOCM• ASH (anterior)• LVOT narrows• increased velocity • SAM (MR)• LVOT further narrows• gradient increases- Low preload- high contractility (dobu CIed)- low afterload• gradient max in late systole• dicrotic pulse (Low CO)•early systolic pr peak in aorta• LV pressure peaks later

Spike and dome

Page 40: interpretation of hemodynamic data

40

Brokenborough sign

AS HOCMPAC: LV pr increase IncreasePAC: Ao Pr Increase Decrease (CO

low)PAC: LV-Ao grad low highAo: pr upslope Delay Rapid Dicrotic pulse - +LV/Ao pr peak discordant Concordant

Page 41: interpretation of hemodynamic data

41

Level of obstruction

vulvular AS supravulvular AS subvulvular AS CoA pressure recovery

Page 42: interpretation of hemodynamic data

Level of obstruction

CoA CoA +AS

CoA + AR

Gradient>20

mmHg

Page 43: interpretation of hemodynamic data

43

Acute AR Chronic compensated

AR

Chronic decompensated

ARLV vol Normal Increased Increased

EF (SV) Normal Very high Falls LVEDP Steep Rise Normal to

high Flat rise

LV-LA gradient

(end of diastole)

Present (Austin Flint

murmer)

No No

Pulse pressure

Normal Wide Wide

Aortic regurgiatation

Q = 2 X CO (severe AR) Area= Q/ √PG= 2CO/ √PG

Otherwise Gorlin AVA falsely low

Severe AR- L/O dicrotic notch

- LVEDP = DBP- Q = 2CO

- LVEDP elevated- Flat rise of LVEDP

Page 44: interpretation of hemodynamic data

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Problem: Bicuspid AV, severe AR, LVF

EF 15% LVEDD 75 CO 3.6 mPG 31 AVA 0.65

Area= Q/ √PG

= 2CO/ √PG= 1.3 cm2

chronic severe decompensated AR

L/O dicrotic notch

Page 45: interpretation of hemodynamic data

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Severe AR, sudden LVF

Acute severe AR chronic compensated AR chronic decompensated AR

Page 46: interpretation of hemodynamic data

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Mitral stenosis [PCWP: high a, high v; LVEDP: low, absent A]

- Severe PAH- large V wave

- High PCWP (>25)- mitral prosthesis

Mild MS + Stress test (2/3)

- Gradient >15- mPAP>60- PCWP>25

Low PGLow MVA

High PGHigh MVA

MVA = 220/ PHT

- Impaired LV compliance

- severe AR

High gradientLow MVA

Page 47: interpretation of hemodynamic data

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Rest

TVD, DOE, Echo: mild MS, EF =55%

Dobutamine stress

MVA 1.6mPG 3.8PCWP 18PAP 41

MVA 0.85mPG 13PCWP 22PAP 66

CABG + MVR

Page 48: interpretation of hemodynamic data

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Echo - mean PG 15 mmHg - MVA 2.2 cm2 (PHT)

• Cath study - CO 4 ltr/ min - mean PG 16 mmHg - Gorlin MVA 4/√16 =

1 cm2

Problem: long mid diastolic mumer

Increased LVEDP

Page 49: interpretation of hemodynamic data

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chambers?

wave?

diagnosis?

Problem: SOB, PSM

LV/ PCWPAbsent A, tall VAF, severe MR

Page 50: interpretation of hemodynamic data

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Mitral regurgiatation Acute MR Chronic

compensated MR

Chronic decompensated MR

v 3 x mPCWP Normal High PCWP High Normal High (>10 + mean

PCWP)LV vol Normal High High EF High High Lower

Q = 2 X CO (severe MR) Q = 1.5 X CO (moderate

MR)Gorlin MVA false low

Page 51: interpretation of hemodynamic data

51

Left ventricular failure

LVEDP >16

Impaired LA

compliance

Myocardial disease

Aortic valve diseaseLVDD

MS, MR High

PCWPTall V

DCMCI low

High PCWP Tall A

Dicrotic aortic tracing

LVDDLVEDP >20Prominent A

bumpSteep diastolic

slopePCWP normal

AR Flat diastole

Wide PPL/O dicrotic

notch

Page 52: interpretation of hemodynamic data

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Problem: SOB, swelling, raised JVP

RCMP RVF CP

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Chamber pressures are high & equalises in early diastole

Constriction

M or W pattern RA pr = mPCWP

LVEDP = RVEDP

Square root(dip & plateu)

D/DRVF

RCMPRVEDP > LVEDP

+5PA pressure high

Better seen in volume loading

Page 54: interpretation of hemodynamic data

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Ventricular interdependance

Constriction

Discordant systolic peak

CP

Concordant systolic peak RCMP , RVF

Better seen in low volume

status Also in COPD

RVEDP rises in inspiration

but not >LVEDP

RVEDP rises in inspiration

>LVEDP

Page 55: interpretation of hemodynamic data

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Dissociation of intracardiac / intrathorasic pressure

Constriction

>5

RAP does not decrease in inspiration

(kussmaul’s sign)D/D COPD

Inspiration Lack of transmission of

-ve intrathorasic pressure to LV

RV is sucked by LV

Page 56: interpretation of hemodynamic data

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Problem: Anasacrca, LVF, RVF, normal EF

W pattern

Severe RVF

Page 57: interpretation of hemodynamic data

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Problem: SOB, low BP, elevated JVP

Tamponade

v

a

x

Page 58: interpretation of hemodynamic data

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Tamponade Tamponade Constriction

Early diastole Later part of diastole

CompressedCompressed

(no Y)

ExpandsConstrained (y)

Elevation & equalization of pressure

+ +

Dissociation of intracardiac / intrathorasic

pressure

- +

RAP Deep x flat y Deep x deep yEarly diastolic dip Abesnt Present

RAP decreases in inspiration Yes No Kussmaul’s sign in JVP - +

Ventricular interdependance + (RV pushes LV)

+ (RV sucked by LV)

CO Low Maintained

Pulsus paradoxus(Inspiratory decrease of SBP> 10

mmHg)

Present Absent usually

Pulsus paradoxus absent in1. ASD2. AR

Page 59: interpretation of hemodynamic data

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PAH (mPAP>25 in rest, >30 in exercise)

Post capillary Pre capillary Prevalence Common Less commonMechanism Passive Reactive Causes Mitral valve

diseaseLVF

Vascular dis (ASD, SSC)Chr thromboembolismLung diseaseEisenmengers

PCWP >15 <15 (may be high)Diast PA pr <5+ PCWP >5+ PCWPPVR <3 >5Transpulmonary gradient

<12 >12

Chronic PAH-PAP may be

normal- PVR>5

- >50 mmHg

Rule out shunt Vasoreactivity

Page 60: interpretation of hemodynamic data

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Severe PAH

CO 4CI 1.9

mPCWP= 15PVR = 55 – 15/ 4 =

10mPAP – PCWP = 40dPAP> mPCWP+5

Money.Monster.2016.720p.BluRay.x264.YIFY

Severe precapillary PAH

Page 61: interpretation of hemodynamic data

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Positive when - mean PAP drops by >10 (to a value<40)

- PVR drops by >20% (to a value <5)- PCWP <15

Vasoreactivity test

- Role of CCB- safety of CCB

- long term prognosis- shunt

reversibility

Precapillary /reactive PAH

Page 62: interpretation of hemodynamic data

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Severe PAH

CO 4CI 1.9

mPCWP= 15PVR = 55 – 15/ 4 =

10mPAP – PCWP = 40dPAP> mPCWP+5

SVC/IVC/PA 58/62/58 (5%): no o2 step up: no L-R shunt

Vasoreactivity test negative

Page 63: interpretation of hemodynamic data

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Pulmonary embolism

Cardiac tamponade

CVP High (>PCWP) High (=PCWP)

PAP High N

ShockMAP<60, SBP<90, SBP decrease by >40

<700

Fluid response: leg rising- CO increase by >10%- IVC diameter >12mm- pulse pressure >9%

Fluid challengeRisky if PCWP>15

Mean BP<80 Dicrotic

pulse high PCWP

(A) High RAP

SVR >700 CI<2.2

PA sat <65% SVO2<

SCVO2

Septic

Page 64: interpretation of hemodynamic data

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Post PTCA, CA stomach, DCM (EF 20%), refractory shock, on ionotrops,

on ventillation

CO 8; CI 3.3 PA

o2sat 53% SPO2 93%

Hb 11High filling pressure

Dicrotic pulseNormal CILow SVR

SVO2 53%SVC SO2

63%Cardiogenic shock on ionotrops

Septic shock

Page 65: interpretation of hemodynamic data

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Normal and abnormalsTraces & relations Shunt / o2 challenge/ resistanceGrdaient –area mismatch of severe ASAS/ HOCM/ CoASevere MS/ stress testCompensated/ decompensated AR/MRRVF/ LVFContriction/ RVF/ tamponade Passive/ reactive PAH/ vasoreactivity Shock

Summary

Page 66: interpretation of hemodynamic data

66

The legend of fall

Page 67: interpretation of hemodynamic data

67Misguided faith in catheter

Page 68: interpretation of hemodynamic data

68

Then & Now

Page 69: interpretation of hemodynamic data

69

no subjective error

hemodynamics in paper

decision making

Page 70: interpretation of hemodynamic data

70Thank you