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

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.

Pra

Q

-1/Rv

Pra = MCFP

A

Pra < MCFP

B

MCFP

Rv

Right Atrial Pressure

Cardiac function curve C

ardia

c ou

tput

Q

PraCardiac

Preload

Cardiac limited

“Wasted preload”

Maximal return

“Cardiac independent”

Pra/CVP

Gradient

for VR

Cardiac output

Effect of decrease in Ppl

Q

Pra

↓ Ppl

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

Effect of increase in Ppl

Q

Pra

↑ Ppl

“O”

transmural

is

normally

at –ve Pra

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

2nd Effect of increase in Ppl

Q

Pra

“Collapse”

pressure occurs

at +v Pra

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

A

B

Problem of the reference point for

thoracic structures

C

Says V increasedSays V decreased

Right Atrial Pressure

Q

Does positive pressures “depress”

cardiac function?

Observed fall

?

Marini, Culver, Butler J Appl Physiol 51:1367,1981

LATM RATM (cmH2O)

LA ( cmH2O) RA ( cmH2O)

Str

oke

volu

me

Mueller Maneuver (Magder AJC 1983)

ΔTransmural Pw = -10-(-40) = +30 mmHg !

-40

+5

-5

mmHg

Pw

Mouth

Aorta

mmHg

Aorta

Insp Insp InspInsp

PS = 6 cmH2O

Insp (VC) Insp (VC)

12

4.5

VC = 650 ml

dPpao is greater than dPeso

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

Insp (VC) Insp (VC)

12

4.5

VC = 650 ml

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

Insp (VC) Insp (VC) Insp (VC)Paw

Ppao

CVP

Peso

1 2 3

VC = 650 mlVentilator triggered breaths

0-

30-

15-

PS = 6 Possible insp non-zone III?

Ppao

Peso

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

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.

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

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

Insp (VC) Insp (VC)

40-

0-

PpaoCVP

mmHg

28 mmHg

40-

0-

mmHg

Increase in abdominal pressure on

circuit function curve

Q

Pra

↑ PP

E10

How does positive pressure effect

outflow from the right heart?

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

? 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

Permutt et al 1962

Vascular waterfall effect

Pu

lmonary

Art

ery

Pre

ssure

Re

sis

tan

ce

Change Palv

Cardiac Output

PLA

Wittenberg

Permutt

LV

P

V

RV

P

V

Time

PartCyclic “insp”

+ve pressure

Pulmonary vascular reservoir and buffer

Alv

L R

MSFP

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

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

Part

Time

Part

Time

Decreasing Cardiac function decreased PP variation

8.3 mmHg

11.7 mmHgN Eeslv

Depressed

Eeslv

-40

100

mmHg

100mmHg TM = 140mmHg (100 + 40)

A B

TM =

0

100 140

Vieillard-Baron A et al J Appl Physiol 87:1644-1650, 1999

PA –velocity Jardin & Vieillard-Baron 2003

End-expiration (PEEP = 5 cmH20)

+1

+3

RV LV

PalvTP = 2+1

Royal Victoria Hospital 1893