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
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
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
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
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
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
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
