presented in 23.11.16 LPS institute of cardiology, kanpur

1. Dr. Dibbendhu Khanra, SR2
1

2. The lost world
2

3. The wind of change
3

4. Tools of the trade
4

5.  Numbers
 Formulas
 Graphs
 Relations
5

6. 6

7. 7

8. PP>60
RVF
PAH
Impaired
LV
compliance
Impaired
LA
compliance
MR
AR
Low SVR
High output
states
CI <2.2
Cardiogenic shock
>8
>8
8
= =
>
>
= dPAP
RVSP= sPAPLVSP= SBP >
= pericardial pressure

9. PA systolic pressure = RV systolic pressure
mean PCWP = PA diastolic pressure (+5)
Mean PCWP = LVEDP
RVEDP = RA pressure
PCWP>RA pressure
LVEDP>RVEDP
Pressure
equalize in
CP, RVF, RCMP9
Atrial Ventricular Arterial

10. 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) 10

11. Ventricular Arterial
Diastole Pr rises Pr falls
Baseline touch Yes No
Dicrotic notch Absent Present
A bump Present Absent
Shape Rectangular Triangular
11

12. 12
 LA
 LV
 RA
 RV
 PA
TR: ventricularization
RAP = RVEDP

13. 13
 LA
 LV
 RA
 RV
 PA
MR: tall v
Severe PAH mPCWP = dPAP

14. Tall V
 V>mean PCWP+10
 decompensated LVF
 Severe 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
PC-PA hybrid pressure
14

15. 15
 LVDD
 MS
 CP

16.  LVEDP
 A bump
 Diastolic slope
 LVEDP normal/ low in MS
 LVEDP high in CP, AR, LVDD
 Absent A bump in MS, AF
 Prominent in HOCM, LVDD
LVEDP = mPCWP
Except
1. MS
2. MR
3. PAH
16
Flat slope in chronic ARSharp slope in acute AR

17. LA 95% RA 75%
LV 95% RV 75%
AO 95% PA 75%
SVO2/ MVO2
SVC 74%
SCVO2
IVC 78%
PV 98%
Normal: SVO2> SCVO2
In shock relation reverses
MVO2 sat< 65%
Low CO 17

18. Chambers 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 RV
RV to PA >= 5% PDA, APW
SVC to PA >= 8% L-R shunt
RA 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
18

19. 19
Qp/Qs = Ao – MVO2/ PV-PA = 96 – 78/ 98 – 83 = 18 / 15 = 1.2 (small L-R)
PDA (L-R)
PAH
CoA
TAPVC

20. Fick
 Gold standard
 True Fick
 O2 challenge
 Not accurate in
- Low output state
- Shunt
- Regurgitation lesion
Thermodilution
SV = CO/ HR CI = CO/ BSA SVI = SV/ BSA = CI/ HR 20

21. SVR
 N: 0.5-1 woods unit
 High in PAH
- <3: passive PAH
- 3-5: mixed PAH
- >5: reactive PAH
• In shunt: Qp
PVR
 MAP = 1SBP+2DBP/3
 N: <700 dyn cm /sec5
 Low SVR in septic shock
 High SVR in ionotrps
W (mmHg/ L/min) = 80 dyn cm /sec5 21

22. Bidirectional shunt
Eisenmenger’s
systemic = pulmonary pr
PVR>SVR (PVR> 5)
Qp<Qs (Qp/Qs <1) 22

23. 23
Room O2
 PA 70/40/50
 PCWP 10
100% o2
VO2 220
Hb 15
45
mmHg
80
mmHg
450
mmHg
100
mmHg PA 55/32/39
 PCWP 10

24. 24
Qp
Qs
Qeff
PVR

25. 25

26. 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
AVA in AS
Peak to
peak PG
= mean PG
mean PG
= 70% of Peak
instantaneous
PG
26
Area α Q
Gradient α Q2
A = Q/ √PG
Area α 1/ √PG

27. 27
 AS
 HOCM
 technical error

28. AS HOCM
Always rule out error in zeroing
Peripheral artery
-Pressure elevated
-No dicrotic notch
- delayed
28

29. Vena Contracta
(Ao pr lesser)
Aortic root<3cm
Pressure reco ery
Echo gradient
Higher
AVA less
In aortic root<3cm
catheter gradient accurate
Downstream to valve
(Ao pr higher)
HTN, LVDD
catheter gradient
Lower
AVA high
HTN, LVDD
Echo gradient accurate
29
Area
= Q/ √PG
LV load
SBP+PG/ SVI
= SBP+PG/ CI (ml) X HR
(> 4.5 abnormal)

30. 30
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

31. 31
Echo gradient Higher
AVA less
Aortic root<3cm
AR
AVA
= Q/√PG
Pseudo severe AS

32. 32
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

33. 33
True severe
AS
Pseudosevere
AS
DCM+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

34. 34
CI 1.6 HR 55 EF 40% PA o2sat 55% BP 130/80

35. 35
CI 3 HR 78 EF 40% PA o2sat 73%
True severe AS

36. 36
End hole
 Wedge
 Wire manipulation
- Pulmonary wedge catheter
 Pressure monitoring
 Blood sampling
- Berman catheter
- Multipurpose catheter
- Pigtail catheter
Side hole

37. 37
AS HOCM

38. 38
 AS
 HOCM

39. • 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 39

40. Brokenborough
sign
AS HOCM
PAC: LV pr increase Increase
PAC: Ao Pr Increase Decrease (CO low)
PAC: LV-Ao grad low high
Ao: pr upslope Delay Rapid
Dicrotic pulse - +
LV/Ao pr peak discordant Concordant
40

41. 41
 vulvular AS
 supravulvular AS
 subvulvular AS
 CoA
 pressure recovery

42. CoA CoA +AS CoA + AR
Gradient
>20 mmHg

43. Acute AR Chronic
compensated AR
Chronic
decompensated AR
LV 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
Q = 2 X CO (severe AR)
Area= Q/ √PG= 2CO/ √PG
Otherwise Gorlin AVA falsely low
43
Severe AR
- L/O dicrotic notch
- LVEDP = DBP
- Q = 2CO
- LVEDP elevated
- Flat rise of LVEDP

44. 44
 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

45. 45
 Acute severe AR
 chronic compensated AR
 chronic decompensated AR

46. -Severe PAH
- large V wave
-High PCWP (>25)
- mitral prosthesis
Mild MS + Stress test (2/3)
- Gradient >15
- mPAP>60
- PCWP>25
Low PG
Low MVA
High PG
High MVA
MVA = 220/ PHT
-Impaired LV compliance
- severe AR
High gradient
Low MVA
46

47. 47
Rest Dobutamine stress
MVA 1.6
mPG 3.8
PCWP 18
PAP 41
MVA 0.85
mPG 13
PCWP 22
PAP 66
CABG + MVR

48.  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
48 Increased LVEDP

49.  chambers?
 wave?
 diagnosis?
49
 LV/ PCWP
 Absent A, tall V
 AF, severe MR

50. 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
50
Q = 2 X CO (severe MR)
Q = 1.5 X CO (moderate MR)
Gorlin MVA false low

51. LVEDP >16
Impaired
LA
compliance
Myocardial
disease
Aortic
valve
disease
LVDD
MS, MR
High PCWP
Tall V
DCM
CI low
High PCWP
Tall A
Dicrotic aortic tracing
LVDD
LVEDP >20
Prominent A bump
Steep diastolic slope
PCWP normal
AR
Flat diastole
Wide PP
L/O dicrotic notch
51

52. 52
 RCMP
 RVF
 CP

53. Chamber pressures are high & equalises in early diastole
M or W pattern RA pr = mPCWP LVEDP = RVEDP
Square root
(dip & plateu)
D/D
RVF
RCMP
RVEDP > LVEDP +5
PA pressure high
Better seen
in volume loading 53

54.  Ventricular interdependance
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
54

55. Dissociation of intracardiac / intrathorasic pressure
>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
55

56. 56
W pattern
Severe RVF

57. 57Tamponade
v
a
x

58. Tamponade Constriction
Early diastole
Later part of diastole
Compressed
Compressed (no Y)
Expands
Constrained (y)
Elevation & equalization of pressure + +
Dissociation of
intracardiac / intrathorasic pressure
- +
RAP Deep x flat y Deep x deep y
Early 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
58
Pulsus paradoxus absent in
1. ASD
2. AR

59. Post capillary Pre capillary
Prevalence Common Less common
Mechanism Passive Reactive
Causes Mitral valve disease
LVF
Vascular dis (ASD, SSC)
Chr thromboembolism
Lung disease
Eisenmengers
PCWP >15 <15 (may be high)
Diast PA pr <5+ PCWP >5+ PCWP
PVR <3 >5
Transpulmonary gradient <12 >12
Chronic PAH
-PAP may be normal
-PVR>5
- >50 mmHg
59
 Rule out shunt
 Vasoreactivity

60. 60
CO 4
CI 1.9
mPCWP= 15
PVR = 55 – 15/ 4 = 10
mPAP – PCWP = 40
dPAP> mPCWP+5
Money.Monster.2016.720p.BluRay.x264.YIFY

61. Positive when
- mean PAP drops by >10 (to a value<40)
- PVR drops by >20% (to a value <5)
- PCWP <15
-Role of CCB
- safety of CCB
- long term prognosis
- shunt reversibility
61

62. 62
CO 4
CI 1.9
mPCWP= 15
PVR = 55 – 15/ 4 = 10
mPAP – PCWP = 40
dPAP> mPCWP+5
SVC/IVC/PA 58/62/58 (5%): no o2 step up: no L-R shunt
Vasoreactivity test negative

63. Pulmonary embolism Cardiac tamponade
CVP High (>PCWP) High (=PCWP)
PAP High N
<700
Fluid response: leg rising
-CO increase by >10%
- IVC diameter >12mm
- pulse pressure >9%
Fluid challenge
Risky if PCWP>15
63
 Mean BP<80
 Dicrotic pulse
 high PCWP (A)
 High RAP
 SVR >700
 CI<2.2
 PA sat <65%
 SVO2< SCVO2
Septic

64. 64
CO 8; CI 3.3
PA o2sat 53%
SPO2 93%
Hb 11
High filling pressure
Dicrotic pulse
Normal CI
Low SVR
SVO2 53%
SVC SO2 63%
Cardiogenic shock on ionotrops
Septic shock

65.  Normal and abnormals
 Traces & relations
 Shunt / o2 challenge/ resistance
 Grdaient –area mismatch of severe AS
 AS/ HOCM/ CoA
 Severe MS/ stress test
 Compensated/ decompensated AR/MR
 RVF/ LVF
 Contriction/ RVF/ tamponade
 Passive/ reactive PAH/ vasoreactivity
 Shock
65

66. The legend of fall
66

67. Misguided faith in catheter 67

68. Then & Now
68

69.  no subjective error
 hemodynamics in paper
 decision making
69

70. 70