Heart lung interaction

drurehman 5,500 views 60 slides Feb 09, 2014
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About This Presentation

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Slide Content

Heart lung
interaction
Heart lunagaiac


“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, Luc know, India

P1 P2
P1> P2
Pressure gradient (∆P) = P1-P2
Relatonship between FLOW and PRESSURE
At a constant ∆P flow depends upon
RESISTANCE
intra mural pressure
RESISTANCE
to that flow
(Poiseuille equation)Resistance
ⁿ= viscosity of fluid, L= length of tube, r= radius of tube
Force driving flow (F) = ∆P/ R
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Psur
Relatonship between FLOW and PRESSURE
TRANSMURAL PRESSURE
Radius (r) of any collapsible tube depends on
distending pressure
Transmural Pressure = intramural pressure – surrounding pressure
(Ptm = Pim – Psur)
Pim
Psur
Psur
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

In a collapsible tube if volume is not allowed to change
so that Ptmwill remain unchanged
Change in Psurwill bring about similar change in Pim
10
4
4
Ptm= 10-4=6
1
7
1
Ptm= 7-1=6
Volume will remain unchanged only when P tmremains unchanged
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Analogous scenario
if lung volume is not allowed to change,
then transpulmonary pressure 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, Luc know, India

Surround pressure for intrathoracic vascular structures
outside the alveoli and their vessels is
JUXTACARDIAC PLEURAL PRESSURE
changes in ITP will bring about similar changes in Pim of vascular structures
INTRATHORACIC PRESSURE (ITP)
which is defined as
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, Luc know, 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, Luc know, India

ITP
ITP
What we routinely measure
Pim
Arterial Pressure
Central venous pressure
Pim in relation to Patm
ITP
Measurement of Pleural pressure or pericardial pressure is difficult and tricky
Central venous pressure
Ppa/Ppao
For Transmural pressure
We need Pleural pressure or pericardial pressure
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

For heart Psur is pericardial pressure (Ppc)
Ttm = Pim –Ppc
Pericardium
high extensibility at low level 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, Luc know, India

When heart is not distended and pericardium is not diseased
Ppc = Ppl
Ppc >> Ppl
heart is distended
primary cardiac disease or ventricular interdependence)
but
if
primary cardiac 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, Luc know, 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, Luc know, India

Transient effects:mechanical
Periodic changes induced by respiratory cycle (phasic effects)
or unsustained effects of various respiratory manoeuvres like
coughing, straining, recruitment manoeuvrecoughing, 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, Luc know, India

Autonomic tone
Respiratory sinus 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
Changes In Lung Volume
Neuro-humoral interactions
Sustained hyperinflation induces fluid retention by
↑ plasma norepinephrine and renin and↓ Atrial natriuretic peptide (ANP)
compression of heart in cardiac fossa by
juxtacardiac ITP and Lung Volume
↑PVR (by hyperinflation)
Mechanical interactions
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, 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, Luc know, India

Palv
Ppl Ppl
Patm
Patm
Ppc
Surrounding Pressures of Circulatory System
Ppl
Ppl
Pabd
Pabd
Patm
Patm= 0
Ppl= -2 to -5
Pabd = <5
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

PLEURAL PRESSURE
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

50
75
100
Chest wall
Lung
Chest wall and Lung
( respiratory system)
Vital capacity %
TLC
P-V curve of  Lung, Chest wall and Respiratory system
0
25
50
0-20 20
FRC
RV
Pressure ( cm H2O)
Ppl, Pcw, Prs
Vital capacity %
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Resting Volume of Respiratory system
At End Expiration
Elastic force of LUNG Elastic force of CHEST WALL=
Negative pleural pressure
Functional Residual Capacity
(FRC)
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, 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, Luc know, India

Effect of gravity
+
weight of lung
Vertical gradient
inin
Ppl and TTP
Dependent alveoli have lesser volume
than non dependent alveoli
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, 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, Luc know, India

Lateral chest wall moves outward
Less change in Ppl
Heart and great vessels
In cardiac fossa
TRAPPED AND COMPRESSED
Greater change in Ppl
Diaphragm most compliant
Least change in Ppl
Less change in Ppl
Pleural pressure change
juxta cardiac > lateral chest wall > diaphragm
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Obesity
compliance of lateral chest wall decreases
Greater change in Ppl
In different pathological states
Greater change in Ppl
Intra abdominal hypertension
compliance of diaphragmatic pleura decreases
Greater change in Ppl
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Change = +2
Change = +3
Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders
Change = +5
Change = +10
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, 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
juxta cardiac pleural pressure
Eosophageal pressure estimates diaphragmatic pleural pressure
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Relationship between
PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSUREPLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

∆ITP / ∆Palv = 1/(1+Ccw/CL )
In healthy subjects, Ccw=CL, during normal tidal volumes
∆ITP / ∆Palv = ½
Relation betweenAlveolar pressure and Pleural pressure
Half of applied PEEP would be expected to be transmitted to
ITP
Decrease in CLwill 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, Luc know, India

Relationship between
PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE
in normal and diseased lung
control
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, Luc know, India

control
ALI
Relationship between
PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE
in normal and diseased lung
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, Luc know, 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
Heart lung interactions. 
Pinsky MR, Textbook of Critical Care, 5
th
edition, Elsvier Saunders
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.
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

LVRA
Patm
Patm Ptm = Pim - Patm
Ppl Ppl Ptm = Pim - Ppl
Surrounding Pressures of Circulatory System
LA
LVRA
RV
Ptm = Pim - Ppl
Ppl
Ppl
Ppl
Ppl
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Changes in Ptm will be similar with any change in ITP
for all intrathoracic structures
No changein
RV afterload
gradient to flow in Pulmonary circulation
LV preload
Change in ITP independent of change in lung volume
Except
those continuing as extra thoracic structure-
Aorta and great veins
Gradient to flow
Venous return and cardiac ejection
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

VR and ITP VR and ITP
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Increased ITP
Increased MSFP
Increased Resistance to VR
VR and ITP
increased Pim of RA
Decreased VR
Decreased Pim of RA
Decreased Ptm of RA
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, 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, Luc know, India

LV afterload and ITP LV afterload and ITP
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

increase ITP---- increase Pim Aorta
Intrathoracic aorta
Ptm unchanged( Ptm= Pim – ITP)
Extrathoracic aorta
Ptm increased (Ptm=Pim- Patm)
sensed by carotid baroreceptors
vasodialation
Decreased Pim
Intrathoracic aorta
LV afterload and ITP
vasodialationIntrathoracic aorta
Decreased Pim
Ptm
came to baseline value
Decreased Ptm of intrathoracic aorta
LV Ptm required to open AV also decreased
Decreased LV wall stress Decreased LV afterload
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Reflex vasodilatation Reflex vasoconstriction
Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. Saunders
Reflex vasodilatation Reflex vasoconstriction
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Concept of AFTERLOAD
Wall tension = Transmural pressure Uradius of curvature / wall thickness
T = Ptm Ur / 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, Luc know, India

LV ejects blood into Aorta when AV opens
AV opens when LV Ptm exceeds Aortic Ptm
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
LV Ptm required, to open AV, also decreased
Tension generated in muscle fibre also decreased
AFTERLOAD IS DECREASED
STROKE VOLUME IS INCREASED
DEREASESD WORK OF PUMPING
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

c
d
LVESPVR
100
150 C-AVO
d-AVC
a-MVO
b-MVC
LV PRESSURE VOLUME CURVE
LV volume
a
b
c
50 130
50
isovolemic relaxation
Isovolemic contraction
LVESDVR
LV  Pressure
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Isometric relaxation
Isometric contraction
Muscle tension
End systolic length
CARDIAC MUSLCE LENGTH TENSION CURVE
Muscle length
Isometric relaxation
Isometric contraction
Muscle tension
End diastolic length
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

LVESPVR
100
150
LV PRESSURE VOLUME CURVE
Afterload = 90 mm Hg
SV           = 80 ml
Afterload = 70 mm Hg
SV          = 105 ml
LV volume
50
130
50
LVESDVR
LV  Pressure
25
SV          = 105 ml
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Muscle tension
CARDIAC MUSLCE LENGTH TENSION CURVE
Peak isometric tension
Muscle length
Muscle tension
Resting tension
Decreased muscle tension
Decreased wall stress
Decreased work
Decreased oxygen requirement
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Clinical implications
This increase or decrease in afterload will have marked
effect in
LV dysfunctionLV dysfunction
poor frank starling curve
Marked variation in pleural pressure esp negative
lung airway and parenchymal disease
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

RV afterload, Pulmonary circulation,
LV preload LV preload
&
Lung volume
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

lung volume and PVR (RV afterload)
(bimodal relation)
PVR PVR
Lung volume
RV TLCFRC
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

West zones of pulmonary
circulation
PA >Pa >Pv
Pa=Pulmonary arterial pressu
PA=Alveolar pressure
Pv=Pulmonary venous pressu
Pa >Pv >PA
Pa >PA >Pv
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Ventricular Ventricular
Interdependence
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

LVRV
pericardium
LVRV
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

For heart Psur is pericardial pressure (Ppc)
Ttm = Pim –Ppc
Pericardium
high extensibility at low level 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, Luc know, India

common septum & circumferential fibres
expansion of both ventricles constrained by a common pericardium
(pericardial constraint)
RV & LV mechanically coupled
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, Luc know, India

050 35 20
LV pressure (mmHg)
RV end diastolic volume
10
20
Changes in RVEDV, changed LV diastolic compliance
10 20 30
LV end diastolic volume (ml)
LV pressure (mmHg)
40
5
Heart lung interactions. 
Pinsky MR, Textbook of Critical Care, 5
th
edition, Elsvier Saunders
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

Output of RV is preload of LV
SERIES INTERDEPENDENCE
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

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

So
This was …… heart……. .lung……………… interaction
Is our interaction still preserved?
Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Luc know, India

……..Thank You