Dr. Dibbendhu Khanra, SR2
1
The lost world
2
The wind of change
3
Tools of the trade
4
 Numbers
 Formulas
 Graphs
 Relations
5
6
7
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
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
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
Ventricular Arterial
Diastole Pr rises Pr falls
Baseline touch Yes No
Dicrotic notch Absent Present
A bump Present Absent
Shape Rectangular Triangular
11
12
 LA
 LV
 RA
 RV
 PA
TR: ventricularization
RAP = RVEDP
13
 LA
 LV
 RA
 RV
 PA
MR: tall v
Severe PAH mPCWP = dPAP
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
 LVDD
 MS
 CP
 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
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
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
Qp/Qs = Ao – MVO2/ PV-PA = 96 – 78/ 98 – 83 = 18 / 15 = 1.2 (small L-R)
PDA (L-R)
PAH
CoA
TAPVC
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
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
Bidirectional shunt
Eisenmenger’s
systemic = pulmonary pr
PVR>SVR (PVR> 5)
Qp<Qs (Qp/Qs <1) 22
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
Qp
Qs
Qeff
PVR
25
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
 AS
 HOCM
 technical error
AS HOCM
Always rule out error in zeroing
Peripheral artery
-Pressure elevated
-No dicrotic notch
- delayed
28
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
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
Echo gradient Higher
AVA less
Aortic root<3cm
AR
AVA
= Q/√PG
Pseudo severe AS
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
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
CI 1.6 HR 55 EF 40% PA o2sat 55% BP 130/80
35
CI 3 HR 78 EF 40% PA o2sat 73%
True severe AS
36
End hole
 Wedge
 Wire manipulation
- Pulmonary wedge catheter
 Pressure monitoring
 Blood sampling
- Berman catheter
- Multipurpose catheter
- Pigtail catheter
Side hole
37
AS HOCM
38
 AS
 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 39
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
 vulvular AS
 supravulvular AS
 subvulvular AS
 CoA
 pressure recovery
CoA CoA +AS CoA + AR
Gradient
>20 mmHg
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
 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
 Acute severe AR
 chronic compensated AR
 chronic decompensated AR
-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
Rest Dobutamine stress
MVA 1.6
mPG 3.8
PCWP 18
PAP 41
MVA 0.85
mPG 13
PCWP 22
PAP 66
CABG + MVR
 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
 chambers?
 wave?
 diagnosis?
49
 LV/ PCWP
 Absent A, tall V
 AF, severe MR
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
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
 RCMP
 RVF
 CP
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
 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
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
W pattern
Severe RVF
57Tamponade
v
a
x
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
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
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
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
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
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
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
 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
The legend of fall
66
Misguided faith in catheter 67
Then & Now
68
 no subjective error
 hemodynamics in paper
 decision making
69
70

interpretation of hemodynamic data

  • 1.
  • 2.
  • 3.
    The wind ofchange 3
  • 4.
    Tools of thetrade 4
  • 5.
     Numbers  Formulas Graphs  Relations 5
  • 6.
  • 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  Twopeaks/ 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 Prrises 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>meanPCWP+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.
  • 16.
     LVEDP  Abump  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% RA75% 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 upD/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: 0.5-1woods 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  PA70/40/50  PCWP 10 100% o2 VO2 220 Hb 15 45 mmHg 80 mmHg 450 mmHg 100 mmHg PA 55/32/39  PCWP 10
  • 24.
  • 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 ruleout error in zeroing Peripheral artery -Pressure elevated -No dicrotic notch - delayed 28
  • 29.
    Vena Contracta (Ao prlesser) 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% CO4CI 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 AVAless 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 HR55 EF 40% PA o2sat 55% BP 130/80
  • 35.
    35 CI 3 HR78 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.
  • 38.
  • 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: LVpr 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 +ASCoA + AR Gradient >20 mmHg
  • 43.
    Acute AR Chronic compensatedAR 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 severeAR  chronic compensated AR  chronic decompensated AR
  • 46.
    -Severe PAH - largeV 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 MVA1.6 mPG 3.8 PCWP 18 PAP 41 MVA 0.85 mPG 13 PCWP 22 PAP 66 CABG + MVR
  • 48.
     Echo - meanPG 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 compensatedMR 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 HighPCWP 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.
  • 53.
    Chamber pressures arehigh & 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 Discordantsystolic 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.
  • 57.
  • 58.
    Tamponade Constriction Early diastole Laterpart 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 Precapillary 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 - meanPAP 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 Cardiactamponade 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; CI3.3 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 andabnormals  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.
  • 67.
    Misguided faith incatheter 67
  • 68.
  • 69.
     no subjectiveerror  hemodynamics in paper  decision making 69
  • 70.

Editor's Notes

  • #3 Sceince is based on objective evidence
  • #4 Objective findings Hemodynamics in paper Decision making At the cost of invasive procedure
  • #5 Swan ganj cathter was first to be introduced for hemodynamic monitoring Transducers transforms pressure signas to electrical signals Importance of equalization of pressure to atmosphere to get a proper curve Wiggers diagram Once thought to be the best way to decipher hemodynamics
  • #6 Understanding science is easier than understanding philosophy Abnormal is more attractive and romantic than the naïve normal
  • #9 Abnormal values Normal relations Equality Inequals get equal (eisenmenger/ CP)// equal get inequal is a problem Inequality Pericardial pressure is measured by RAP In CP, LVEDP is elevated..but if RAP is substacted..true transmural pressure will be obtained..and that wl be low due to low filling
  • #20 Qp/Qs = Ao – MVO2/ PV-PA = 96 – 78/ 98 – 83 = 18 / 15 = 1.2 (small L-R)
  • #27 Hakki area lesser than gorlin area Hakki area: not validated for tachycardia or bradycardia Hakki area: angel’s correction: <75 in MS, >90 in AS, multiply with 1.35 Hakki area: Mean grad in MS, peak instantaneous grad in AS
  • #68 But not free of fallacies
  • #70 Exams/ quiz Mathemetical Composite data f clin findings/ echo/ ecg