heart-lung interactions: insights from pleural pressure · heart-lung interactions: insights from...
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Heart-lung interactions:
insights from pleural pressure
S Magder
Department of Critical Care,
McGill University Health Centre
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Outline:• Basics of heart-lung interaction
– Venous return/cardiac function relationship
– Importance of transmural pressure
• Does heart function decrease with PEEP
• Mueller maneuver
• Lessons from Peso
1. Forced expiration
2. Inspiratory load on RV
3. Ventilator triggered breaths.
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Pra
Q
-1/Rv
Pra = MCFP
A
Pra < MCFP
B
MCFP
Rv
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Right Atrial Pressure
Cardiac function curve C
ardia
c ou
tput
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Q
PraCardiac
Preload
Cardiac limited
“Wasted preload”
Maximal return
“Cardiac independent”
Pra/CVP
Gradient
for VR
Cardiac output
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Effect of decrease in Ppl
Q
Pra
↓ Ppl
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Cardiac Function determines change in
VR during inspiration
Return function intersects plateau of
cardiac function curve
Q
Pra
No change in
Pra
No change in
RV filling
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Effect of increase in Ppl
Q
Pra
↑ Ppl
“O”
transmural
is
normally
at –ve Pra
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What happens when the Return Curve intersects plateau
of Cardiac Function Curve?
Q
Pra
No change in Q
(or SV)
↑ Ppl
But, if
↑ Ppl is
large
enough
Reduced TM
diastolic
wall tension
- less
“wasted”
preload
TM TM
Cardiac output falls
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2nd Effect of increase in Ppl
Q
Pra
“Collapse”
pressure occurs
at +v Pra
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Principle :The pressure that determines
the volume or filtration across an elastic
structure is the Transmural Pressure
(ie PTM = Pinside- Poutside)
Eg. -Starling’s forces across capillaries
-Ventricular preload
V
P
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A
B
Problem of the reference point for
thoracic structures
C
Says V increasedSays V decreased
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Right Atrial Pressure
Q
Does positive pressures “depress”
cardiac function?
Observed fall
?
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Marini, Culver, Butler J Appl Physiol 51:1367,1981
LATM RATM (cmH2O)
LA ( cmH2O) RA ( cmH2O)
Str
oke
volu
me
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Mueller Maneuver (Magder AJC 1983)
ΔTransmural Pw = -10-(-40) = +30 mmHg !
-40
+5
-5
mmHg
Pw
Mouth
Aorta
mmHg
Aorta
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Insp Insp InspInsp
PS = 6 cmH2O
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Insp (VC) Insp (VC)
12
4.5
VC = 650 ml
dPpao is greater than dPeso
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CA
A
A AA
AA
C
C
C
CC
CA
A
AA
A
AA
C
C
C
CC
Increased filling of left heart with lung
inflation
Inter-alveolar vessels (corners) do not
expand when Pla> ~ 3 mmHg
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Insp (VC) Insp (VC)
12
4.5
VC = 650 ml
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20
6
0
20
30
25
11
10
25
810
Lung inflation can load the RV by creating
“zone II conditions”
It then directly impedes RV ejection
+5 +5
Palv < PLAPalv > PLA
ExpirationInspiration
Zone III
Zone II
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Insp (VC) Insp (VC) Insp (VC)Paw
Ppao
CVP
Peso
1 2 3
VC = 650 mlVentilator triggered breaths
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0-
30-
15-
PS = 6 Possible insp non-zone III?
Ppao
Peso
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A B
C D
E F
25-
0-
PpaoPesoCVP
Paw7 mmHg
12 mmHg
10 min
15 mmHg
11 min
20 mmHg
14 mmHg
12 min11 min
20 min 9 mmHg21 min
8 mmHg
Note effort
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Summary
• Intrathoracic transmural pressures in the
chest are relative to pleural pressure
• Inspiratory and expiratory activity can
dramatically change the “apparent”
transmural pressure
• These efforts also can have significant
hemodynamic effects.
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VC Ppao
Average dPao and dPeo (mmHg)
0 1 2 3 4 5 6 7 8
dP
eo
-dP
pa
o
-10
-8
-6
-4
-2
0
2
4
6VC CVP
Average dCVP and dPeo (mmHg)
0 2 4 6 8
dP
eo
-dC
VP
-10
-8
-6
-4
-2
0
2
4
6
dPpao
0 2 4 6 8
dP
eo
0
2
4
6
8
dCVP
0 1 2 3 4 5 6 7 8
dP
eo
0
1
2
3
4
5
6
7
8
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PS Ppao
Average Ppao and Peo (mmHg)
-16 -12 -8 -4 0 4 8
dP
eo
- d
Pp
ao
-10
-8
-6
-4
-2
0
2
4
6 PS CVP
Average dCVP and dPeo (mmHg)
-16 -12 -8 -4 0 4 8d
Pe
o -
dC
VP
-10
-8
-6
-4
-2
0
2
4
6
dPpao
-16 -12 -8 -4 0 4 8
dP
eo
-16
-12
-8
-4
0
4
8
dCVP
-16 -12 -8 -4 0 4 8
dP
eo
-16
-12
-8
-4
0
4
8
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Insp (VC) Insp (VC)
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40-
0-
PpaoCVP
mmHg
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28 mmHg
40-
0-
mmHg
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Increase in abdominal pressure on
circuit function curve
Q
Pra
↑ PP
E10
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How does positive pressure effect
outflow from the right heart?
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Does lung inflation increase PVR?
Permutt et al 1962
Vascular waterfall effectWhittenberg et al 1960
Increase in resistance
Change in Palv
Re
sis
tan
ce
Change in Palv
Re
sis
tan
ce
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? Rise in pulmonary vascular resistance?
+20
+8
Increase afterload on RV through rise in PVR
+8
+3
+1
TP = 12
Inspiration (Paw = 20 cmH20)
But this does not occur because fluids are not compressible
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Permutt et al 1962
Vascular waterfall effect
Pu
lmonary
Art
ery
Pre
ssure
Re
sis
tan
ce
Change Palv
Cardiac Output
PLA
Wittenberg
Permutt
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LV
P
V
RV
P
V
Time
PartCyclic “insp”
+ve pressure
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Pulmonary vascular reservoir and buffer
Alv
L R
MSFP
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Key points:
• Dominant factor in heart-lung
interaction is change in pleural
pressure (Ppl) relative to atmosphere
– Increase Ppl decreases venous return
and cardiac output
–Decreased Ppl increases venous return
and cardiac output
– Transpulmonary pressure becomes important
when West Zone II conditions are present
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Conclusions 2:
• Left heart can only put out what the right
heart gives it (in the steady state)
• Do not get fooled by pressures relative to
atmosphere
• Effects of ventilation on the heart are
dependent upon blood volume (systemic
and pulmonary) and cardiac function
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Part
Time
Part
Time
Decreasing Cardiac function decreased PP variation
8.3 mmHg
11.7 mmHgN Eeslv
Depressed
Eeslv
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-40
100
mmHg
100mmHg TM = 140mmHg (100 + 40)
A B
TM =
0
100 140
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Vieillard-Baron A et al J Appl Physiol 87:1644-1650, 1999
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PA –velocity Jardin & Vieillard-Baron 2003
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End-expiration (PEEP = 5 cmH20)
+1
+3
RV LV
PalvTP = 2+1
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Royal Victoria Hospital 1893