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Heart lung
interaction
8EDLGXU 5DKDPDQ
6HQLRU 5HVLGHQW
&&0 6*3*,06
/XFNQRZ ,QGLD
“The primary function of the cardiovascular- pulmonary system is
to link metabolizing cells with energy sources in the environment”

“Mother Nature is the meanest management Guru
in terms of cost effectiveness”

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Relatonship between FLOW and PRESSURE

P1

intra mural pressure

P2

P1> P2
Pressure gradient (∆P) = P1-P2
At a constant ∆P flow depends upon
RESISTANCE
to that flow

Resistance

(Poiseuille equation)

ⁿ= viscosity of fluid, L= length of tube, r= radius of tube

Force driving flow (F) = ∆P/ R
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Relatonship between FLOW and PRESSURE

Radius (r) of any collapsible tube depends on
distending pressure
TRANSMURAL PRESSURE
Psur

Pim

Psur

Transmural Pressure = intramural pressure – surrounding pressure
(Ptm = Pim – Psur)
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
In a collapsible tube if volume is not allowed to change

Change in Psur will bring about similar change in Pim
so that Ptm will remain unchanged

4

1

10

7

4

1

Ptm = 10-4=6

Ptm = 7-1=6

Volume will remain unchanged only when Ptm remains unchanged
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Analogous scenario

if lung volume is not allowed to change,
then transpulmonarypressure will not change
and relationship between airway pressure and pleural pressure
will remain constant

muller’s maneuver or valsalva maneuver
change in pleural pressure
will bring identical change in airway pressure
so that lung volume remains constant

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Surround pressure for intrathoracic vascular structures
outside the alveoli and their vessels is
JUXTACARDIAC PLEURAL PRESSURE
which is defined as
INTRATHORACIC PRESSURE (ITP)
changes in ITP will bring about similar changes in Pim of vascular structures
(so that Ptm remains constant)
and this change
will be measured by device (which measure it relative to Patm)
this is easily appreciable in patients with arterial line
during coughing (causing increased ITP) increased arterial pressure
could be seen on monitor
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
another analogy

“Ship in the water appearing to rise and fall
as it is acted upon by passive waves when viewed from shore.
The same ship, however does not change its relationship to water,
and as for as the ship is concerned is quiet stable in the sea,
and is not forever sinking and rising again”

Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
What we routinely measure
Pim in relation to Patm

ITP
Pim
ITP

Arterial Pressure
Central venous pressure
Ppa/Ppao

For Transmural pressure
We need Pleural pressure or pericardial pressure
Measurement of Pleural pressure or pericardial pressure is difficult and tricky

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
For heart Psur is pericardial pressure (Ppc)
Ttm = Pim – Ppc
Pericardium
high extensibility at lowlevel of stress
with an abrupt transition to relative inextensibility at higher stress
therefore it exerts a restraining effect on volume of heart

Physiologic role of normal pericardium
Matthew W. Watkins, Martin M. LeWinter, annu. Rev. Med 993;44:171-180
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
When heart is not distended and pericardium is not diseased
Ppc = Ppl
but
Ppc >> Ppl
if

heart is distended
primarycardiac disease or ventricular interdependence)
(pericardium exerts restraining effect)
pericardium is diseased
pericardial fluid or decreased pericardial compliance
overdistension of lung or massive pleural effusion or tension pneumothorax
compressing heart in cardiac fossa
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
All we talked about is mechanical factors
but
there are other factors which simultaneously and dependently
play role

Mural smooth muscle ( vascular, cardiac)
Neuro-humoral factors effecting these smooth muscles

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Transient effects: mechanical
Periodic changes induced by respiratory cycle (phasic effects)
or unsustained effects of various respiratory manoeuvres like
coughing, straining, recruitment manoeuvre

Steady state effects: mechanical and neuro-humoral
Impact of sustained alterations of respiratory conditions:
PEEP, CPAP, weaning

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Changes In Lung Volume
Neuro-humoral interactions

Autonomic tone
Respiratorysinus arrhythmia (normal autonomic responsiveness)
Lung inflation at Vt >15 ml/kg ↓ heart rate by sympathetic withdrawal
Reflex vasodilation with lung hyperinflation
Humoral factors
Sustained hyperinflation induces fluid retention by
↑ plasma norepinephrine and renin and↓ Atrial natriuretic peptide (ANP)
Mechanical interactions

compression of heart in cardiac fossa by
juxtacardiac ITP and Lung Volume
↑PVR (by hyperinflation)

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Primary difference in NPV and PPV

Negative pressure ventilation
primary change is in pleural pressure which leads to
change in airway pressure

Positive pressure ventilation
primary change is in airway pressure which leads to
change in pleural pressure

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Surrounding Pressures of Circulatory System

Ppl

Ppl
Palv
Ppc

Patm

Patm
Ppl

Ppl
Pabd
Pabd

Patm
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

Patm= 0
Ppl= -2 to -5
Pabd = <5
PLEURAL PRESSURE

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
P-V curve of Lung, Chest wall and Respiratory system
Chest wall

Lung

TLC

Vital capacity %

100
Chest wall and Lung
( respiratory system)
75
50

25

FRC
RV

0
-20

0

20

Pressure ( cm H2O)
Ppl, Pcw, Prs
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Resting Volume of Respiratory system
Negative pleural pressure

Elastic force of LUNG

=

Elastic force of CHEST WALL

At End Expiration
Functional Residual Capacity
(FRC)

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Pleural space is only a potential space
Pressure is difficult to measure
But can be estimated from distal esophageal pressure
( in posterior mediastinum where esophagus lies between two pleural recesses)

Pleural pressure is not uniform throughout the pleural space

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Effect of gravity
+
weight of lung

Vertical gradient
in
Ppl and TTP

Dependent alveoli have lesser volume
than non dependent alveoli
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
This truth remains true
when lung volume is increasing
Change in Pleural Pressure is
NOT UNIFORM
When lung is inflating

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Heart and great vessels
In cardiac fossa
TRAPPED AND COMPRESSED
Greater change in Ppl

Lateral chest wall moves outward
Less change in Ppl

Diaphragm most compliant
Least change in Ppl

Pleural pressure change
juxta cardiac > lateral chest wall > diaphragm
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
In different pathological states

Obesity
compliance of lateral chest wall decreases
Greater change in Ppl
Intra abdominal hypertension
compliance of diaphragmatic pleura decreases
Greater change in Ppl

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Change = +3

Change = +2

Change = +5

Change = +10

Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Pleural pressure has to be defined accordingly

Lung compliance
lateral chest wall pleural pressure

Hemodynamic
juxta cardiac pleural pressure

Diaphragmatic work
diaphragmatic pleural pressure

Eosophageal pressure estimates diaphragmatic pleural pressure
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Relationship between
PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Relation betweenAlveolar pressure and Pleural pressure
∆ITP / ∆Palv = 1/(1+Ccw/CL )
In healthy subjects, Ccw=CL, during normal tidal volumes
∆ITP / ∆Palv = ½
Half of applied PEEP would be expected to be transmitted to
ITP
Decrease in CL will decrease the transmission

Clinical review: positive end expiratory pressure and cardiac output
Thomas Luecke, Palolo Pelosi. Crit Care 2005,9:607-621
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Relationship between
PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE
in normal and diseased lung

ALI

control

Cardiopulmonary effect of positive pressure ventilation during acute lung injury.
Romand JA, Shi W, Pinsky MR. Chest 1995;108:1041-1048
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Relationship between
PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE
in normal and diseased lung
ALI
control

Cardiopulmonary effect of positive pressure ventilation during acute lung injury.
Romand JA, Shi W, Pinsky MR. Chest 1995;108:1041-1048
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Primary determinant of increases in Pleural Pressure during PPV is
change in LUNG VOLUME,
not change in airway pressure

If tidal volume is kept constant, pleural pressure will increase equally,
independent of the mechanical properties of lung
Decreased compliance/ higher airway resistance
higher Paw required to generate similar tidal volume
Presumably pericardial pressure does not increase as much as ITP
because increasing lung volume reduces filling of ventricles,
decreasing their size inside cardiac fossa

It is difficult to estimate changes in pleural pressure or pericardial pressure
that will occur in patient as PEEP is increased.

Heart lung interactions.
Pinsky MR, Textbook of Critical Care, 5th edition, Elsvier Saunders
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Surrounding Pressures of Circulatory System

Patm

Patm

Ptm = Pim - Patm

Ppl

Ppl

Ptm = Pim - Ppl

RA

LV

RV

LA

Ppl

Ppl

Ptm = Pim - Ppl
Ppl

Ppl

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Change in ITP independent of change in lung volume

Changes in Ptm will be similar with any change in ITP
for all intrathoracic structures
No change in
RV afterload
gradient to flowin Pulmonarycirculation
LV preload

Except
those continuing as extra thoracic structureAorta and great veins
Gradient to flow
Venous return and cardiac ejection

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
VR and ITP

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
VR and ITP
Increased ITP
Increased MSFP

increased Pim of RA
Increased Resistance to VR

Decreased VR
Decreased Pim of RA

Decreased Ptm of RA

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Trend recording of
RA pressure, juxta cardiac Pleural pressure and RA transmural pressure

Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
LV afterload and ITP

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
LV afterload and ITP
increase ITP---- increase Pim Aorta

Intrathoracic aorta
Ptm unchanged ( Ptm= Pim – ITP)

Extrathoracic aorta
Ptm increased (Ptm=Pim- Patm)
sensed by carotid baroreceptors

Decreased Pim
Intrathoracic aorta

Decreased Ptm of intrathoracic aorta

LV Ptm required to open A also decreased
V

Decreased LV wall stress

vasodialation

Decreased Pim
Ptm
came to baseline value

Decreased LV afterload

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Reflex vasodilatation

Reflex vasoconstriction

Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Concept of AFTERLOAD
Wall tension = Transmural pressure radius of curvature / wall thickness
T = Ptm r / h
( Laplace’s Law)

Of any given volume, geometrical shape, with smallest radius of curvature is
SPHERE
Most stable geometrical shape, of any volume
Air bubbles acquire spherical shape

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
LV ejects blood into Aorta when A opens
V
A opens when LV Ptm exceeds Aortic Ptm
V
LV Ptm is generated (isovolumetric contraction)
To generate this Ptm, tension is generated in muscle fibre (isometric contraction)
This Tension generation requires ATP
WORK OF PUMPING
Increased ITP
Aortic Ptm is decreased

AFTERLOAD IS DECREASED
STROKE VOLUME IS INCREASED

LV Ptm required, to open A also decreased
V,
DEREASESD WORK OF PUMPING

Tension generated in muscle fibre also decreased

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
LV PRESSURE VOLUME CURVE

d-AVC
150

C-AVO

LVESPVR

b-MVC
d

a-MVO

50

Isovolemic contraction

c
isovolemic relaxation

LV Pressure

100

a

LVESDVR

b
LV volume

50

130

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
CARDIAC MUSLCE LENGTH TENSION CURVE

Isometric contraction

Isometric relaxation

Muscle tension

End systolic length

End diastolic length

Muscle length

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
LV PRESSURE VOLUME CURVE

LVESPVR

150

Afterload = 90 mm Hg
SV
= 80 ml
Afterload = 70 mm Hg

LV Pressure

100

SV

= 105 ml

50
LVESDVR

LV volume
25

50

130

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
CARDIAC MUSLCE LENGTH TENSION CURVE

Muscle tension

Peak isometric tension

Resting tension

Muscle length

Decreased muscle tension
Decreased wall stress
Decreased work
Decreased oxygen requirement

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Clinical implications

This increase or decrease in afterload will have marked
effect in

LV dysfunction
poor frank starling curve
Marked variation in pleural pressure esp negative
lung airway and parenchymal disease

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
RV afterload, Pulmonary circulation,
LV preload
&

Lung volume
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
PVR

lung volume and PVR (RV afterload)
(bimodal relation)

RV

FRC
Lung volume

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

TLC
West zones of pulmonary
circulation

Pa=Pulmonary arterial pressu
PA=Alveolar pressure
Pv=Pulmonary venous pressu

PA >Pa >Pv

Pa >PA >Pv

Pa >Pv >PA

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Ventricular
Interdependence

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
pericardium

RV

LV

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
For heart Psur is pericardial pressure (Ppc)
Ttm = Pim – Ppc
Pericardium
high extensibility at lowlevel of stress
with an abrupt transition to relative inextensibility at higher stress
therefore it exerts a restraining effect on volume of heart

Physiologic role of normal pericardium
Matthew W. Watkins, Martin M. LeWinter, annu. Rev. Med 993;44:171-180
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
RV & LV mechanically coupled
common septum & circumferential fibres
expansion of both ventricles constrained by a common pericardium
(pericardial constraint)
Diastolic filling of one ventricle has to be at the cost of another
diastolic filling of one ventricle will affect the geometry and stiffness of another

PARELLEL INTERDEPENDENCE

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Changes in RVEDV, changed LV diastolic compliance

RV end diastolic volume
50

LV pressure (mmHg)

20

35

10

5

10

20

30

40

LV end diastolic volume (ml)

Heart lung interactions.
Pinsky MR, Textbook of Critical Care, 5th edition, Elsvier Saunders
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

20

0
Output of RV is preload of LV

SERIES INTERDEPENDENCE

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
Myocardial contractility is not
significantly affected by ITP

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
So
This was ……

heart…….

.lung………………

Is our interaction still preserved?

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

interaction
Heart lung interaction
Heart lung interaction
……..Thank You

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Heart lung interaction

  • 1. Heart lung interaction 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW &&0 6*3*,06 /XFNQRZ ,QGLD
  • 2. “The primary function of the cardiovascular- pulmonary system is to link metabolizing cells with energy sources in the environment” “Mother Nature is the meanest management Guru in terms of cost effectiveness” Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 3. Relatonship between FLOW and PRESSURE P1 intra mural pressure P2 P1> P2 Pressure gradient (∆P) = P1-P2 At a constant ∆P flow depends upon RESISTANCE to that flow Resistance (Poiseuille equation) ⁿ= viscosity of fluid, L= length of tube, r= radius of tube Force driving flow (F) = ∆P/ R Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 4. Relatonship between FLOW and PRESSURE Radius (r) of any collapsible tube depends on distending pressure TRANSMURAL PRESSURE Psur Pim Psur Transmural Pressure = intramural pressure – surrounding pressure (Ptm = Pim – Psur) Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 5. In a collapsible tube if volume is not allowed to change Change in Psur will bring about similar change in Pim so that Ptm will remain unchanged 4 1 10 7 4 1 Ptm = 10-4=6 Ptm = 7-1=6 Volume will remain unchanged only when Ptm remains unchanged Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 6. Analogous scenario if lung volume is not allowed to change, then transpulmonarypressure will not change and relationship between airway pressure and pleural pressure will remain constant muller’s maneuver or valsalva maneuver change in pleural pressure will bring identical change in airway pressure so that lung volume remains constant Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 7. Surround pressure for intrathoracic vascular structures outside the alveoli and their vessels is JUXTACARDIAC PLEURAL PRESSURE which is defined as INTRATHORACIC PRESSURE (ITP) changes in ITP will bring about similar changes in Pim of vascular structures (so that Ptm remains constant) and this change will be measured by device (which measure it relative to Patm) this is easily appreciable in patients with arterial line during coughing (causing increased ITP) increased arterial pressure could be seen on monitor Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 8. another analogy “Ship in the water appearing to rise and fall as it is acted upon by passive waves when viewed from shore. The same ship, however does not change its relationship to water, and as for as the ship is concerned is quiet stable in the sea, and is not forever sinking and rising again” Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 9. What we routinely measure Pim in relation to Patm ITP Pim ITP Arterial Pressure Central venous pressure Ppa/Ppao For Transmural pressure We need Pleural pressure or pericardial pressure Measurement of Pleural pressure or pericardial pressure is difficult and tricky Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 10. For heart Psur is pericardial pressure (Ppc) Ttm = Pim – Ppc Pericardium high extensibility at lowlevel of stress with an abrupt transition to relative inextensibility at higher stress therefore it exerts a restraining effect on volume of heart Physiologic role of normal pericardium Matthew W. Watkins, Martin M. LeWinter, annu. Rev. Med 993;44:171-180 Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 11. When heart is not distended and pericardium is not diseased Ppc = Ppl but Ppc >> Ppl if heart is distended primarycardiac disease or ventricular interdependence) (pericardium exerts restraining effect) pericardium is diseased pericardial fluid or decreased pericardial compliance overdistension of lung or massive pleural effusion or tension pneumothorax compressing heart in cardiac fossa Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 12. All we talked about is mechanical factors but there are other factors which simultaneously and dependently play role Mural smooth muscle ( vascular, cardiac) Neuro-humoral factors effecting these smooth muscles Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 13. Transient effects: mechanical Periodic changes induced by respiratory cycle (phasic effects) or unsustained effects of various respiratory manoeuvres like coughing, straining, recruitment manoeuvre Steady state effects: mechanical and neuro-humoral Impact of sustained alterations of respiratory conditions: PEEP, CPAP, weaning Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 14. Changes In Lung Volume Neuro-humoral interactions Autonomic tone Respiratorysinus arrhythmia (normal autonomic responsiveness) Lung inflation at Vt >15 ml/kg ↓ heart rate by sympathetic withdrawal Reflex vasodilation with lung hyperinflation Humoral factors Sustained hyperinflation induces fluid retention by ↑ plasma norepinephrine and renin and↓ Atrial natriuretic peptide (ANP) Mechanical interactions compression of heart in cardiac fossa by juxtacardiac ITP and Lung Volume ↑PVR (by hyperinflation) Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 15. Primary difference in NPV and PPV Negative pressure ventilation primary change is in pleural pressure which leads to change in airway pressure Positive pressure ventilation primary change is in airway pressure which leads to change in pleural pressure Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 16. Surrounding Pressures of Circulatory System Ppl Ppl Palv Ppc Patm Patm Ppl Ppl Pabd Pabd Patm Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India Patm= 0 Ppl= -2 to -5 Pabd = <5
  • 17. PLEURAL PRESSURE Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 18. P-V curve of Lung, Chest wall and Respiratory system Chest wall Lung TLC Vital capacity % 100 Chest wall and Lung ( respiratory system) 75 50 25 FRC RV 0 -20 0 20 Pressure ( cm H2O) Ppl, Pcw, Prs Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 19. Resting Volume of Respiratory system Negative pleural pressure Elastic force of LUNG = Elastic force of CHEST WALL At End Expiration Functional Residual Capacity (FRC) Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 20. Pleural space is only a potential space Pressure is difficult to measure But can be estimated from distal esophageal pressure ( in posterior mediastinum where esophagus lies between two pleural recesses) Pleural pressure is not uniform throughout the pleural space Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 21. Effect of gravity + weight of lung Vertical gradient in Ppl and TTP Dependent alveoli have lesser volume than non dependent alveoli Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 22. This truth remains true when lung volume is increasing Change in Pleural Pressure is NOT UNIFORM When lung is inflating Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 23. Heart and great vessels In cardiac fossa TRAPPED AND COMPRESSED Greater change in Ppl Lateral chest wall moves outward Less change in Ppl Diaphragm most compliant Least change in Ppl Pleural pressure change juxta cardiac > lateral chest wall > diaphragm Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 24. In different pathological states Obesity compliance of lateral chest wall decreases Greater change in Ppl Intra abdominal hypertension compliance of diaphragmatic pleura decreases Greater change in Ppl Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 25. Change = +3 Change = +2 Change = +5 Change = +10 Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 26. Pleural pressure has to be defined accordingly Lung compliance lateral chest wall pleural pressure Hemodynamic juxta cardiac pleural pressure Diaphragmatic work diaphragmatic pleural pressure Eosophageal pressure estimates diaphragmatic pleural pressure Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 27. Relationship between PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 28. Relation betweenAlveolar pressure and Pleural pressure ∆ITP / ∆Palv = 1/(1+Ccw/CL ) In healthy subjects, Ccw=CL, during normal tidal volumes ∆ITP / ∆Palv = ½ Half of applied PEEP would be expected to be transmitted to ITP Decrease in CL will decrease the transmission Clinical review: positive end expiratory pressure and cardiac output Thomas Luecke, Palolo Pelosi. Crit Care 2005,9:607-621 Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 29. Relationship between PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE in normal and diseased lung ALI control Cardiopulmonary effect of positive pressure ventilation during acute lung injury. Romand JA, Shi W, Pinsky MR. Chest 1995;108:1041-1048 Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 30. Relationship between PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE in normal and diseased lung ALI control Cardiopulmonary effect of positive pressure ventilation during acute lung injury. Romand JA, Shi W, Pinsky MR. Chest 1995;108:1041-1048 Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 31. Primary determinant of increases in Pleural Pressure during PPV is change in LUNG VOLUME, not change in airway pressure If tidal volume is kept constant, pleural pressure will increase equally, independent of the mechanical properties of lung Decreased compliance/ higher airway resistance higher Paw required to generate similar tidal volume Presumably pericardial pressure does not increase as much as ITP because increasing lung volume reduces filling of ventricles, decreasing their size inside cardiac fossa It is difficult to estimate changes in pleural pressure or pericardial pressure that will occur in patient as PEEP is increased. Heart lung interactions. Pinsky MR, Textbook of Critical Care, 5th edition, Elsvier Saunders Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 32. Surrounding Pressures of Circulatory System Patm Patm Ptm = Pim - Patm Ppl Ppl Ptm = Pim - Ppl RA LV RV LA Ppl Ppl Ptm = Pim - Ppl Ppl Ppl Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 33. Change in ITP independent of change in lung volume Changes in Ptm will be similar with any change in ITP for all intrathoracic structures No change in RV afterload gradient to flowin Pulmonarycirculation LV preload Except those continuing as extra thoracic structureAorta and great veins Gradient to flow Venous return and cardiac ejection Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 34. VR and ITP Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 35. VR and ITP Increased ITP Increased MSFP increased Pim of RA Increased Resistance to VR Decreased VR Decreased Pim of RA Decreased Ptm of RA Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 36. Trend recording of RA pressure, juxta cardiac Pleural pressure and RA transmural pressure Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 37. LV afterload and ITP Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 38. LV afterload and ITP increase ITP---- increase Pim Aorta Intrathoracic aorta Ptm unchanged ( Ptm= Pim – ITP) Extrathoracic aorta Ptm increased (Ptm=Pim- Patm) sensed by carotid baroreceptors Decreased Pim Intrathoracic aorta Decreased Ptm of intrathoracic aorta LV Ptm required to open A also decreased V Decreased LV wall stress vasodialation Decreased Pim Ptm came to baseline value Decreased LV afterload Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 39. Reflex vasodilatation Reflex vasoconstriction Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 40. Concept of AFTERLOAD Wall tension = Transmural pressure radius of curvature / wall thickness T = Ptm r / h ( Laplace’s Law) Of any given volume, geometrical shape, with smallest radius of curvature is SPHERE Most stable geometrical shape, of any volume Air bubbles acquire spherical shape Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 41. LV ejects blood into Aorta when A opens V A opens when LV Ptm exceeds Aortic Ptm V LV Ptm is generated (isovolumetric contraction) To generate this Ptm, tension is generated in muscle fibre (isometric contraction) This Tension generation requires ATP WORK OF PUMPING Increased ITP Aortic Ptm is decreased AFTERLOAD IS DECREASED STROKE VOLUME IS INCREASED LV Ptm required, to open A also decreased V, DEREASESD WORK OF PUMPING Tension generated in muscle fibre also decreased Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 42. LV PRESSURE VOLUME CURVE d-AVC 150 C-AVO LVESPVR b-MVC d a-MVO 50 Isovolemic contraction c isovolemic relaxation LV Pressure 100 a LVESDVR b LV volume 50 130 Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 43. CARDIAC MUSLCE LENGTH TENSION CURVE Isometric contraction Isometric relaxation Muscle tension End systolic length End diastolic length Muscle length Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 44. LV PRESSURE VOLUME CURVE LVESPVR 150 Afterload = 90 mm Hg SV = 80 ml Afterload = 70 mm Hg LV Pressure 100 SV = 105 ml 50 LVESDVR LV volume 25 50 130 Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 45. CARDIAC MUSLCE LENGTH TENSION CURVE Muscle tension Peak isometric tension Resting tension Muscle length Decreased muscle tension Decreased wall stress Decreased work Decreased oxygen requirement Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 46. Clinical implications This increase or decrease in afterload will have marked effect in LV dysfunction poor frank starling curve Marked variation in pleural pressure esp negative lung airway and parenchymal disease Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 47. RV afterload, Pulmonary circulation, LV preload & Lung volume Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 48. PVR lung volume and PVR (RV afterload) (bimodal relation) RV FRC Lung volume Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India TLC
  • 49. West zones of pulmonary circulation Pa=Pulmonary arterial pressu PA=Alveolar pressure Pv=Pulmonary venous pressu PA >Pa >Pv Pa >PA >Pv Pa >Pv >PA Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 50. Ventricular Interdependence Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 51. pericardium RV LV Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 52. For heart Psur is pericardial pressure (Ppc) Ttm = Pim – Ppc Pericardium high extensibility at lowlevel of stress with an abrupt transition to relative inextensibility at higher stress therefore it exerts a restraining effect on volume of heart Physiologic role of normal pericardium Matthew W. Watkins, Martin M. LeWinter, annu. Rev. Med 993;44:171-180 Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 53. RV & LV mechanically coupled common septum & circumferential fibres expansion of both ventricles constrained by a common pericardium (pericardial constraint) Diastolic filling of one ventricle has to be at the cost of another diastolic filling of one ventricle will affect the geometry and stiffness of another PARELLEL INTERDEPENDENCE Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 54. Changes in RVEDV, changed LV diastolic compliance RV end diastolic volume 50 LV pressure (mmHg) 20 35 10 5 10 20 30 40 LV end diastolic volume (ml) Heart lung interactions. Pinsky MR, Textbook of Critical Care, 5th edition, Elsvier Saunders Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India 20 0
  • 55. Output of RV is preload of LV SERIES INTERDEPENDENCE Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 56. Myocardial contractility is not significantly affected by ITP Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India
  • 57. So This was …… heart……. .lung……………… Is our interaction still preserved? Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India interaction