mm Hg - SRLF

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Is Volume-Responsiveness
the Same as Preload?
Michael R. Pinsky, MD, Dr hc
Department of Critical Care Medicine
University of Pittsburgh
No
Not Now
Not Ever
Is cardiac output responsive to
intravascular fluid loading?
• Assumes that venous return and LV preload are
the primary determinants of cardiac output
(Starling’s Law of the Heart)
• Assumes low LV end-diastolic volume (EDV)
equals preload-responsiveness
• Attempts to assess EDV through surrogate
measures
– CVP, Ppao, LV end-diastolic area, RV EDV,
intrathoracic blood volume
CVP before volume expansion in Responders (R)
and Non-Responders (NR)
*
12
Pra (mm Hg)
10
*
8
6
4
2
0
Calvin
1981
Schneider
1988
Reuse
Wagner
Michard
1990
1998
2000
Michard & Teboul. Chest 121: 2000-8, 2002
Changes in stroke volume (%)
CVP does not predict volume responsiveness
r = 0.45
Baseline PRA (mm Hg)
Wagner et al. Chest 1998
Ppao (mm Hg) before volume expansion in
Responders (R) and Non-responders (NR)
R
Calvin (Surgery 81)
Schneider (Am Heart J 88)
Reuse (Chest 90)
Diebel (J Trauma 94)
Tavernier (Anesthesiology 98)
Michard (AJRCCM 00)
2
Wagner (Chest 98)
Tousignant (Anesth Analg 00)
8±1
10 ± 2
10 ± 4
16 ± 6
10 ± 4
10 ± 3
NR
7±2
10 ± 2
10 ± 3
15 ± 5
12 ± 3
11 ±
p < 0.05
10 ± 3
12 ± 3
14 ± 4
16 ± 3
p < 0.05
Michard & Teboul. Chest 121: 2000-8, 2002
Ppao does not predict preload-responsiveness
Non-responders
Ppao (mm Hg)
Responders
$
$
Pre Post
*
Pre Post
Tousignant et al. Anesth Analg 90:351-5, 2000
Neither DCVP or DPpao Mirror DSV
Lichtwarck-Aschoff et al. Intensive Care Med 18: 142-7, 1992
Changes in global EDV
predict DSV
But individual subjects have markedly different relations
Lichtwarck-Aschoff et al. Intensive Care Med 1992; 18: 142-7
RVEDV (mL/m2) before volume expansion in
Responders (R) and Non-responders (NR)
*
150
120
*
90
60
30
0
Calvin
1981
Schneider
1988
Reuse
1990
Diebel
1992
Diebel
1994
Wagner
1998
Michard & Teboul. Chest 121: 2000-8, 2002
Echocardiographic LVEDA (cm2/m2)
R
Feissel (Chest 01)
10 ± 4
NR
10 ± 2
Tavernier (Anesthesiology 98) 9 ± 3
12 ± 4 *
Tousignant (Anesth Analg 00) 15 ± 5
20 ± 5 *
(cm2)
* p < 0.05
LV EDV in Responders and Non-responders
of fluid resuscitation
16
LVEDA
14
before fluid infusion
12
_
10
(cm2/m2)
8
6
_
4
responders
non responders
Feissel et al. Chest 119:867-73, 2001
End-diastolic Area (EDA) to Predict Preload-Responsiveness
Non-responders
Responders
EDA cm2
*
Pre Post
**
Pre Post
Tousignant et al. Anesth Analg 90:351-5, 2000
End-expiration: The pressure which is
important to a distensible structure is
the transmural pressure
Inside pressure minus outside pressure
Transmural pressures determine
Starling’s forces across capillaries
Ventricular preload
5
10
5
5
15
10
0
10
Transmural Pressure is the Amount Above the Surface
Pra, Ppao, RVEDV and LVEDA are not
always accurate indicators of preload
1- Pra and Ppao are rarely expressed as transmural pressures
2- Even transmural Ppao depends on LV compliance
3- RVEDV measures are influenced by tricuspid regurgitation
4- LVED Area may not reflect LVED Volume
5- All these parameters are supposed to give information on the
preload of one ventricle but not on the global cardiac preload
Or……
Neither CVP or Ppao reflect Ventricular
Volumes or Tract Preload-Responsiveness
Preload  Preload Responsiveness
Kumar et al. Crit Care Med 32:691-9, 2004
Starling’s Law of the Heart Lives!
Kumar et al. Crit Care Med 32:691-9, 2004
Hemodynamic Truths
•
•
•
•
•
Tachycardia is never a good thing
Hypotension is always pathological
There is no normal cardiac output
CVP is only elevated in disease
Peripheral edema is of cosmetic concern
Hemodynamic Effects of Changes
in Intrathoracic Pressure
Venous
Return
Thorax
LV
Ejection
Spontaneous Ventilation
Positive-Pressure
Ventilation
SVrv
(ml/kg)
Time (sec)
Pratm
(mm Hg)
Ppl
(mm Hg)
CVP
(mm Hg)
Pinsky. J Appl Physiol 56:1237-45, 1984
Effect of IPPV on LV Pressure and Volume
IPPV 20 ml/kg
IPPV 20 ml/kg
190
170
150
Stroke
Volume Variation
LV pressure (mm Hg)
130
110
90
70
Cardiac
Compression
50
30
10
-10
15
20
25
30
LV volume (ml)
35
40
PPV and SVV Predict Preload-Responsiveness
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Jardin et al. Circulation 83: 266-27, 1983 IPPV
Perel et al. Anesthesiology 67: 498-502, 1987 SPV-IPPV
Tavernier et al. Anesthesiology 89: 1313-1321, 1998 SPV-IPPV
Ornstein et al. J Clin Anesth 10:137-140, 1998 SPV-IPPV
Michard et al. Am J Respir Crit Care Med 159:935-939, 1999
Dalibon et al. Brit J Anaesth 82:97-103, 1999
Michard et al. Am J Respir Crit Care Med 162: 134-138, 2000
Michard & Teboul JL Crit Care 4: 282-289, 2000
Feissel et al. Chest 119: 867-873, 2001
Berkenstadt et al. Anesth Analg 92: 984-989, 2001 SPV-IPPV
Reuter et al. Intensive Care Med 28: 392-398, 2002
Boulain et al. Chest 121:1245-52, 2002
Reuter et al. British J Anaesth 88: 124-126, 2002
Slama et al. Am J Physiol 283:H1729-33, 2002
Reuter et al. Crit Care Med 31: 1399-1404, 2003
Vieillard-Baron et al. American J Resp Crit Care Med 168:671-676, 2003
Marx et al. European J Anaesth 21: 132-138, 2004
Systolic pressure variations correlate with stroke
volume variations measured by the pulse contour
technique
In general: SPV under estimates SVV
by 5%
Reuter et al. Brit J Anaesth 88:124-6, 2002.
Practical Limitations of PPV
• Requires fixed HR
– Atrial fibrillation, frequent PVCs
• Requires no spontaneous ventilatory efforts
– Can not use during CPAP, PSV
• Magnitude of PPV or SVV will change with
changing tidal volume
• Heart failure may give false positive
response!
Spontaneous Ventilation Alters LV Filling
by Ventricular Interdependence
Taylor et al. Am J Physiol 213:706-10, 1967
Effect of ventilation on
RV and LV Output
Spontaneous inspiration
Ventricular
Interdependence
Minimal
Ventricular
Interdependence
Positive-pressure
Inspiration
Pinsky et al. J Appl Physiol 58:1189-98, 1985
Effect of Positive-Pressure Ventilation on Dynamic LV Volumes and Pressure
ECG
(m v)
0 .8
0 .6
0 .4
0 .2
Pa
(m m H g)
140
120
Protocol:
100
80
40
Ppa
30
(m m H g)
20
Measured LV areas
using
echocardiographic
imaging IPPV during
closed and open chest
Pre and post CPB
10
20
P ra
15
(m m H g)
10
8
6
L V A rea
(cm ²)
4
2
P aw
(cm H 2 O )
20
10
0
0
2
4
T im e
(se co n d s)
6
8
Denault et al. Chest 116:176-86, 1999
C h a n g e s in S
1
0
-1
Changes in SAP can not be explained
by changes in LV Volumes
-1
-2
-2
-3
-3
-4
-2
0
2
4
6
8
10
-4
-1 2 -1 0
2
2
1
1
0
0
-1
-1
-2
-2
-3
-3
-4
-4
C h a n g e s in E S A (cm ²)
Neither end-diastolic
volume or end-systolic
volume changes
parallel SPV
C h a n g e s in E D A (cm ²)
-4
-2
0
2
4
6
8
10 12
-4
-1 2 -1 0
1
1
0
0
-1
-1
-2
-2
-3
-4
-2
0
2
4
6
8
% C h a n g e in S A P
10 12

-3
-1 2 -1 0
-8
-6
-4
-2
0
2
-8
-6
-4
-2
0
2
-8
-6
-4
-2
0
2
% F a ll in S A P
Denault et al. Chest 1999; 116:176-86
There is no relation between pulse
pressure variation and initial LV enddiastolic area (EDA) in patients
during CABG surgery
EDA (cm2)
20
15
Preload  Preload Responsiveness
10
n=9
r2 = 0.11
5
0
0%
2%
4%
6%
8%
10%
12%
14%
16%
PPV (%)
Gunn et al. Crit Care & Shock 5: 170-6, 2002
T IM E S S E R IE S
FREQUENCY
A rte ria l P re s s u re
Fourier Analysis:
1 .0 0
500
0 .7 5
400
0 .5 0
300
0 .2 5
200
0 .0 0
The changes in SAP
poorly reflect airway
pressure induced
changes in LV volumes,
but reflect very well
changes in airway
pressure
100
-0 .2 5
-0 .5 0
0
0
500
1000
1500
2000
0
1
2
3
4
5
A irw a y P re s s u re
1 .0
500
0 .8
400
0 .6
0 .4
300
Primary harmonic
0 .2
200
0 .0
-0 .2
100
-0 .4
0
0
500
1000
1500
2000
0
1
2
3
4
5
4
5
E c h o c a rd io g ra p h ic L V A re a
1 .0
500
400
0 .5
300
0 .0
200
-0 .5
100
-1 .0
0
0
500
1000
1500
2000
0
1
2
3
Denault et al. Chest 1999; 116:176-86
Asynchronous High Frequency Jet Ventilation in Acute Ventricular Failure
SVrv
SVlv
PAo
Platm
Ppatm
Pratm
Paw
Ppl
Pinsky et al. J Appl Physiol 58:1189-98, 1985
Asynchronous High Frequency Jet Ventilation in Acute Ventricular Failure
Pinsky et al. J Appl Physiol 58:1189-98, 1985
Cardiac cycle-specific increases in ITP
during Acute Ventricular Failure
SVlv
ml/kg
QAo
PAo
mm Hg
early
systolic
late
systolic
early
systolic
late
systolic
Pinsky et al. J Appl Physiol 60:604-12, 1986
Pressure-Volume Loops During Positive Pressure Ventilation
End systole
Transmural
Pressure
Airway
Pressure
Left Ventricular
Volume
Denault et al . J Appl Physiol 91:298-308, 2001
Positive-Pressure Ventilation Alters
Both Preload and Afterload
Denault et al. J Appl Physiol 91:298-308, 2001
CPAP 5 mm Hg
160
160
140
140
120
120
LV Pressure (mm Hg)
LV Pressure (mm Hg)
IVC occlusion
100
80
60
40
100
80
60
40
20
20
0
0
-20
-20
15
20
25
30
35
40
15
20
LV Volume (ml)
140
140
LV Pressure (mm Hg)
LV Pressure (mm Hg)
160
120
100
80
60
40
100
80
60
40
20
0
0
-20
-20
25
30
40
120
20
LV Volume (ml)
35
CPAP 15 mm Hg
160
20
30
LV Volume (ml)
CPAP 10 mm Hg
15
25
35
40
15
20
25
30
35
40
LV Volume (ml)
Kim et al. Proc Am Thorac Soc 3:A297, 2006
Effect of Tidal Volume on LV Pressure and Volume
190
190
170
170
5 ml/kg
150
15 ml/kg
150
130
130
110
110
90
90
70
70
50
50
30
30
10
10
-10
-10
15
20
25
30
35
15
40
20
25
30
35
40
190
190
170
170
10 ml/kg
20 ml/kg
150
150
130
130
110
110
90
90
70
70
50
50
30
30
10
10
-10
15
20
25
30
35
40
-10
15
20
25
30
35
40
Kim et al. Proc Am Thorac Soc 3:A297, 2006
PPV and SVV during IPPV
• Reflect complex interactions between preload and
afterload
• Potential false positive PPV with inspiration
– Severe CHF-Reverse Bernheim Effect
– Cor pulmonale- Minimize ventricular interdependence
• Potential false positive SVP with inspiration
– Stiff chest wall + large tidal volume: Valsalva Maneuver
– Whenever ITP increases rapidly
• These limitations dissolve with passive leg raising
Limits of Preload-Responsiveness
• Preload  Preload-responsiveness
• Preload-responsiveness  Need for fluids
• The means of altering preload matters
– Size of Vt, passive leg raising, spontaneous breaths
• Different measures of pressure or flow
variation will have different calibrations
• Pinsky Intensive Care Med 30: 1008-10, 2004
Thank You
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