Heart lung interaction

Heart lung

interaction

��

“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

P1 P2

P1> P2Pressure gradient (∆P) = P1-P2

Relatonship between FLOW and PRESSURE

At a constant ∆P flow depends uponRESISTANCE

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


Psur

Relatonship between FLOW and PRESSURE

TRANSMURAL PRESSURE

Radius (r) of any collapsible tube depends ondistending pressure

Transmural Pressure = intramural pressure – surrounding pressure

(Ptm = Pim – Psur)

Pim

Psur

Psur


In a collapsible tube if volume is not allowed to change

so that Ptm will remain unchanged

Change in Psur will 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 Ptm remains unchanged


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 pressureso that lung volume remains constant


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 changewill be measured by device (which measure it relative to Patm)

this is easily appreciable in patients with arterial lineduring coughing (causing increased ITP) increased arterial pressure

could be seen on monitor


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


ITP

ITP

What we routinely measure

Pim

Arterial PressureCentral venous pressure

Pim in relation to Patm

ITP

Measurement of Pleural pressure or pericardial pressure is difficult and tricky

Central venous pressurePpa/Ppao

For Transmural pressureWe need Pleural pressure or pericardial pressure


For heart Psur is pericardial pressure (Ppc)Ttm = Pim – Ppc

Pericardiumhigh extensibility at low level of stress

with an abrupt transition to relative inextensibility at higher stresstherefore it exerts a restraining effect on volume of heart

Physiologic role of normal pericardiumMatthew W. Watkins, Martin M. LeWinter, annu. Rev. Med 993;44:171-180


When heart is not distended and pericardium is not diseased Ppc = Ppl

Ppc >> Ppl

heart is distendedprimary cardiac disease or ventricular interdependence)

but

if

primary cardiac disease or ventricular interdependence) (pericardium exerts restraining effect)

pericardium is diseasedpericardial fluid or decreased pericardial compliance

overdistension of lung or massive pleural effusion or tension pneumothoraxcompressing heart in cardiac fossa


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


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


Autonomic toneRespiratory sinus arrhythmia (normal autonomic responsiveness)

Lung inflation at Vt >15 ml/kg ↓ heart rate by sympathetic withdrawalReflex vasodilation with lung hyperinflation

Humoral factorsSustained 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


Primary difference in NPV and PPV

Negative pressure ventilationprimary change is in pleural pressure which leads to

change in airway pressure

Positive pressure ventilationprimary change is in airway pressure which leads to

change in pleural pressure


Palv

Ppl Ppl

Patm Patm

Ppc

Surrounding Pressures of Circulatory System

Ppl Ppl

Pabd

Pabd

Patm

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


PLEURAL PRESSURE


50

75

100

Chest wallLung

Chest wall and Lung( respiratory system)

Vita

l cap

acity

%

TLC

P-V curve of Lung, Chest wall and Respiratory system

0

25

50

0-20 20

FRCRV

Pressure ( cm H2O)Ppl, Pcw, Prs

Vita

l cap

acity

%


Resting Volume of Respiratory system

At End Expiration

Elastic force of LUNG Elastic force of CHEST WALL=

Negative pleural pressure

Functional Residual Capacity(FRC)


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


Effect of gravity+ weight of lung

Vertical gradientinin

Ppl and TTP

Dependent alveoli have lesser volumethan non dependent alveoli


This truth remains truewhen lung volume is increasing

Change in Pleural Pressure is NOT UNIFORM

When lung is inflating


Lateral chest wall moves outwardLess change in Ppl

Heart and great vessels In cardiac fossa

TRAPPED AND COMPRESSEDGreater change in Ppl

Diaphragm most compliantLeast change in Ppl

Less change in Ppl

Pleural pressure change juxta cardiac > lateral chest wall > diaphragm


Obesitycompliance of lateral chest wall decreases

Greater change in Ppl

In different pathological states


Intra abdominal hypertensioncompliance of diaphragmatic pleura decreases



Change = +2

Change = +3


Change = +5

Change = +10


Pleural pressure has to be defined accordingly

Lung compliancelateral chest wall pleural pressure

Hemodynamic juxta cardiac pleural pressure

Diaphragmatic workdiaphragmatic pleural pressure

juxta cardiac pleural pressure

Eosophageal pressure estimates diaphragmatic pleural pressure


Relationship between PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSUREPLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSURE


∆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 CL will decrease the transmission

Clinical review: positive end expiratory pressure and cardiac outputThomas Luecke, Palolo Pelosi. Crit Care 2005,9:607-621


Relationship between PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSUREin 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


control

ALI

Relationship between PLEURAL PRESSURE, LUNG VOLUME and AIRWAY PRESSUREin 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


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 resistancehigher Paw required to generate similar tidal volume

Heart lung interactions. Pinsky MR, Textbook of Critical Care, 5th 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.


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


Changes in Ptm will be similar with any change in ITP for all intrathoracic structures

No change inRV 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 flowVenous return and cardiac ejection


VR and ITPVR and ITP


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


Trend recording of RA pressure, juxta cardiac Pleural pressure and RA transmural pressure

Cardiopulmonary interaction, Pinsky, Cardiopulmonary Critical Care, W.B. SaundersUbaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

LV afterload and ITPLV afterload and ITP


increase ITP---- increase Pim Aorta

Intrathoracic aortaPtm unchanged ( Ptm= Pim – ITP)

Extrathoracic aortaPtm increased (Ptm=Pim- Patm)

sensed by carotid baroreceptors

vasodialationDecreased Pim

Intrathoracic aorta

LV afterload and ITP

vasodialationIntrathoracic aorta

Decreased Pim

Ptmcame to baseline value

Decreased Ptm of intrathoracic aorta

LV Ptm required to open AV also decreased

Decreased LV wall stress Decreased LV afterload


Reflex vasodilatation Reflex vasoconstriction


Reflex vasodilatation Reflex vasoconstriction


Concept of AFTERLOAD

Wall tension = Transmural pressure � radius of curvature / wall thicknessT = Ptm � r / h( Laplace’s Law)

Of any given volume, geometrical shape, with smallest radius of curvature isSPHERE

Most stable geometrical shape, of any volume

Air bubbles acquire spherical shape


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


c

d

LVESPVR

100

150 C-AVO

d-AVC

a-MVO

b-MVC

LV PRESSURE VOLUME CURVE

LV volume

ab

c

50 130

50

isov

olem

ic re

laxa

tion

Isov

olem

ic c

ontr

actio

n

LVESDVR

LV P

ress

ure


Isom

etric

rela

xatio

n

Isom

etric

con

trac

tion

Mus

cle

tens

ion

End systolic length

CARDIAC MUSLCE LENGTH TENSION CURVE

Muscle length

Isom

etric

rela

xatio

n

Isom

etric

con

trac

tion

Mus

cle

tens

ion

End diastolic length


LVESPVR

100

150

LV PRESSURE VOLUME CURVE

Afterload = 90 mm HgSV = 80 ml

Afterload = 70 mm Hg

SV = 105 ml

LV volume

50 130

50

LVESDVR

LV P

ress

ure

25

SV = 105 ml


Mus

cle

tens

ion

CARDIAC MUSLCE LENGTH TENSION CURVE

Peak isometric tension

Muscle length

Mus

cle

tens

ion

Resting tension

Decreased muscle tensionDecreased wall stressDecreased workDecreased oxygen requirement


Clinical implications

This increase or decrease in afterload will have marked effect in

LV dysfunctionLV dysfunctionpoor frank starling curve

Marked variation in pleural pressure esp negativelung airway and parenchymal disease


RV afterload, Pulmonary circulation, LV preload LV preload

&Lung volume


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

PVR

PVR

Lung volume

RV TLCFRC


West zones of pulmonary circulation

PA >Pa >Pv

Pa=Pulmonary arterial pressuPA=Alveolar pressurePv=Pulmonary venous pressu

Pa >Pv >PA

Pa >PA >Pv


Ventricular Ventricular Interdependence


LVRV

pericardium

LVRV


For heart Psur is pericardial pressure (Ppc)Ttm = Pim – Ppc

Pericardiumhigh extensibility at low level of stress

with an abrupt transition to relative inextensibility at higher stresstherefore it exerts a restraining effect on volume of heart

Physiologic role of normal pericardiumMatthew W. Watkins, Martin M. LeWinter, annu. Rev. Med 993;44:171-180Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, 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 anotherdiastolic filling of one ventricle will affect the geometry and stiffness of another

PARELLEL INTERDEPENDENCE


050 35 20

LV p

ress

ure

(m

mH

g)

RV end diastolic volume

10

20

Changes in RVEDV, changed LV diastolic compliance

10 20 30

LV end diastolic volume (ml)

LV p

ress

ure

(m

mH

g)

40

5

Heart lung interactions. Pinsky MR, Textbook of Critical Care, 5th edition, Elsvier Saunders


Output of RV is preload of LV

SERIES INTERDEPENDENCE


Myocardial contractility is not Myocardial contractility is not significantly affected by ITP


So

This was …… heart……. .lung……………… interaction

Is our interaction still preserved?


……..Thank You

Education

Heart lung interaction