In a world of binary decision there remains little room for applied maths and physiology. Or maybe not... Parkin's approach brings out a forgotten tool-the volume state. Although reductionistic as well as Guyton's entire view, it might be a better language for us, for clinicians and for all those lost in translation when they've stumbled across loose binary decisions such as SVV,PPV,SPV etc. Mean systemic filling pressure has been resurrected. Parkin, Maas, Pinsky and Geerts have come a long way from Versprille.

1. SHOCK
A GUYTONIAN
APPROACH
2013
Bucharest-SUUB

2. POISEUILLE’S LAW
 I = ↑ / R (τhm’s law)
 Q = (P1- P2) / R
 CO = (MAP - PRA) / SVR
 VR = (PMS - PRA) / RV

3. ARCHETYPAL REDUCTIONISTIC NEED OF A
FUNCTIONAL VENOUS HEMODYNAMIC POLE
Weber E. 1850

4. BASIC THEORETICAL IMPLICATIONS
OF A HEMODYNAMIC VENOUS POLE
 Small changes (as absolute values) in PRA, RV,
PMS determine large changes in VR
 Steady state - CO = VR ĺ CO (for constant
dp/dt) depends on Pms (VR) and is adjusted
(for variable dp/dt) through pump performance
(inotropism,lusitropism,cronotropism)
 ↑R’s physiology ĺ PMS / stressed blood
volume + unstressed / RV

5. MEAN SYSTEMIC FILLING PRESSURE
 Stopped flow ĺ mean arterial pressure Ļ and
large venous vessels pressure Ĺ ĺ as these
two come closer to each other ĺ PMS
 PMS = VS / CMS
 PMS ≠ MAP

6. BASIC BICOMPARTMENTAL MODEL OF
Qr=5
Cv
Pv=2
Pump
Resistance
Qh=5
Pa=102
Ca
Qr=5
Cv
Pv=2
Qh=0
Pa=102
Ca
Qh=0
Pa=7
Ca Cv
Pv=6
Qh=1
Pa=26
Ca
Qr =1
MSFP
Pump
Resistance
Pump Pump
Resistance
Resistance
Cv
Qr=0
Pv=7
• Pa-Pv=R∙Q
• Pms=V/Cs
• V=Va+Vv
• Cs=Ca+Cv
• Va=Pa∙Ca
• Vv=Pv∙Cv
• ΔPa=Pa-Pms=Vtr/Ca
• ΔPv=Pms-Pv=Vtr/Cv
• Cv/Ca=19
0
120
7
0
2
6
Pv
7
26
102 Pa
Pa
Pv
0
CO
C O = 0 C O =1 CO=5
Modified from Levy 2007

7. STRESSED / UNSTRESSED BLOOD
VOLUME
 V0 = blood volume needed to fill up the circulatory
system just to the point where stress ( transmural
pressure ) would be created
 VS = blood volume that would begin to create stress (
transmural pressure ) if it were added up to V0
Modified from Jacobsohn 2013

8. COMPLIANCE vs CAPACITANCE
 Pms = VT - V0 / C ( ΔP= ΔV/C ) C = static, mechanical item,
almost unadjustable
 Pms = VT / Cp ( ΔP= VT / Cp ) Cp = dynamic, tone dependent -
variable, sympathetically mediated item  VS►◄ V0
 Pms is influenced by spontaneous (Δtemperature ) / therapeutic
variation of Cp ( nitroglycerine ) ( VS ►◄ V0) or of VT
 One easy example – vasopressors Ĺ VS by adjusting the
capacitance (Ĺ Pms) of the reservoir compartment - splanchnic
compartment ĺ Ĺ VR
 VS ≈ 20-30 % (1,5 L)
 C ≈ 0.187L∙mmHg-1
 Pms ≈ 8-10 mmHg
Modified from Jacobsohn 2013

9. COMPLIANCE vs CAPACITANCE
Elastance=tgı=ΔP/ΔV
Compliance=1/tgı=ΔV/ΔP=V2-V1
=Vt-Vo=Vs/P
Capacitance=Vt/P
Modified from Jacobsohn 2013
σ

10. Gelman’s

11. Gelman’s

12. Gelman’s

13. VENOUS RESISTANCE
RV = 8ηl / πr4
RV is influenced by the size of the venous
circulation ĺ venous circ. time constant is
determined by vascular volume / flux ( L∙min∙L-1 =
min ) - (IJ = C∙R)
Vasopressors could ĺ redistribute blood from one
teritory to another ĺ from IJslow la IJfast ĺ Ļ RV si Ĺ
VR
Modified from Jacobsohn 2013

14. STARLING RESISTOR

15. VENOUS RETURN ON GRAPHS
Starling
Resistor
Thoracic-
Abdominal
interface
Pabd>Ppl
Pleuro-vascular interface – PPVent.
Modified from Jacobsohn 2013

16. VENOUS RETURN ON GRAPHS
tg α = slope
α

17. VASCULAR FUNCTION CURVES IN A
BUNDLE
Ȗ
α ȕ α α
Pms↑
Rv↓
Normal
Rv↑
Pms↓
RIGHT ATRIAL PRESSURE
VENOUS RETURN

18. FRANK STARLING CURVE
0
inotropism ↓
afterload↑
RIGHT ATRIAL PRESSURE
CARDIAC OUTPUT

19. DIDACTICISM WITH A TASTE OF
MATHEMATICAL COMPROMISE
Y Y
O X
O X
Y
O
X
CO
RAP ivasc
Pms
CO
RAP tm
CO
RAP ?
Pms
Right shift in case of increasing Pextramural
but with constant inotropism.
RIGHT

20. TREATMENTS AND THEIR
HEMODYNAMIC CONSEQUENCES
A
B
C
↓ Rv
↑ Pms
D
↑Vt,↑Vs
normal
ȕ
α α
RIGHT ATRIAL PRESSURE
CO / VR
BLOOD vs CRISTALOID / COLOID
0
1
2
1
2
3
Modified from
Jacobsohn 2013

21. normal
↑Rv+↑Pms(↑Vs)
↑Rv
A
C
B
D
RIGHT ATRIAL PRESSURE
CO / VR
0
VASOPRESSORS
ȕ α α
1
2
3
1
2
Modified from
Jacobsohn 2013

22. RIGHT ATRIAL PRESSURE
CO / VR
0
↓Rv
↓Rv+↓Pms
↓Vs
normal
C
A
B
D
α α ȕ
INODILATORS
1
2
1
2
3
Modified from
Jacobsohn 2013

23. ↑Rv+↑Pms (↑Vs)
normal
↑Rv
B
A
C
D
INOVASOPRESSORS
0 RIGHT ATRIAL PRESSURE
CO / VR
α α ȕ
1
2
3
1
2
Modified from
Jacobsohn 2013

24. HYPOVOLEMIC SHOCK
Mixed hemodynamic impact: inotropism and capacitance
Starting point sensibility ( SIRS – increasing incidence )
Lusitropism might get affected during prolonged illness
MSFP is maintained through capacitive recruitment and
interstitial shift

25. A
B
C
3
D
E
↓Rv
normal
fluid shift
↓Pms (↓Vt)
α α α ȕ
RIGHT ATRIAL PRESSURE
CO / VR
0
1
2
3
1
2
4
Modified from
Jacobsohn 2013

26. CARDIOGENIC SHOCK
Primary hemodynamic impact: inotropism
SIRS as a negative prognostic factor – hyperdynamic phenotype
( dynamic elastance PPV/SVV ↓ )
MSFP modulation is of secondary importance in favour of inotropic
modulators
Lusitropism has become a hallmark and requires therapeutic attitude
Catecholaminergic spareness when possible ( levosimendan ?,
omecamtiv mecarbil ?, istaroxime ?, metabolic modulation – HDI )

27. Rv↓and Pms ↓(Dtx/Mil)
+ fluid shift+adm.
Pms↑ through
fluid shift+adm.
normal
A
B
C
D
E
α ȕ α
RIGHT ATRIAL PRESSURE
CO / VR
0
1
2
3
1
2
3
4
Modified from
Jacobsohn 2013

28. SEPTIC SHOCK
Most complex hemodynamic impact: cardiogenic as well as vascular
Cardiogenic impact: inotropism,lusitropism
Vascular impact: capacitance, SVR/Eadyn and the reflection coefficient
(glycocalyx)
variable hemodynamic MSFP dependent phenotype
Hemorheological consequences opening new therapeutic targets (Kenyeres)
Microvascular - macrohemodynamics dissociation
Unveiling guytonian reductionism

29. RIGHT ATRIAL PRESSURE
CO / VR
A
C
B
D
E
F
Pms-N Rv-↓
normal
Pms-↓ Rv-↓
Pms-↓ Rv-N
0
1
2
3
4
1
2
3
4
Modified from
Jacobsohn 2013

30. OBSTRUCTIVE SHOCK
TENSION PTX
Vascular hemodynamic impact – Starling resistor at the pleural-vascular
interface or at the pericardial-vascular/heart interface
Secondary cardiac impact – RV afterload
Therapeutics – typically mechanical

31. normal
Plateau shift
Rv↑ Pms↑(fluid,SS)
plateau shift
plateau shift
Rv↑
afterload ↑
A
A1
B
C
D
E
F
0 RIGHT ATRIAL PRESSURE
CO / VR
SHIFT PLATEAU
Ppl
α ȕ α
1
2
3
4
1
2
3
4
Modified from
Jacobsohn 2013

32. HEART LUNG INTERACTION
in very few words
Vascular plateau shift similar to obstructive shock
Hemodynamic profile related to MSFP and the crossing point on the
vascular-cardiac graph
ESPVR dependent hemodynamic impact
PVR dependent impact ( West zone profile )
Ecw ( IAP included ) relative to El dependent hemodynamic impact
Prone position impact
Lung-heart-kidney cross - talk
Energy shift by lessening WOB

33. Rv↑ Pms↑
(fluid,SS)
normal
Rv↑
Rv↑ Pms↓
dehydration
Right shift
SHIFT PLATEAU
Right shift ++
1
2
A
B
E
C
D
F
1
2
3
4
3
0 Ppl+ Ppl++ RIGHT ATRIAL PRESSURE
CO / VR
α α ȕ α
4
Modified from
Jacobsohn 2013

35. 1959
Ca
V

Ca Cv
Ra
Pms


V

Ca Cv
Pms


Ca
C
P

Rv Ra
D
 

Heart
Lung
Rv
Cv
Ra Rv
Ca Cv
Pa
Pra
  

Va Vv
Ca Cv
Pms

  
Ca Pa Cv Pv
Ca Cv
Pms


Pv
  
Pa Pv Ra D
  
Pv RAP Rv D
      
Ca (Pv Ra D) Cv (RAP Rv D)
Ca Cv
Pms


RAP
      
Ca (Pv Ra D) Cv (RAP Rv D)
Pms RAP 

Ca Cv
 
       
Ca (Pv RAP) Cv Rv D Ca Ra D
Ca Cv
Pms RAP

 
       
Ca Rv D Cv Rv D Ca Ra D
Ca Cv
Pms RAP

 
Rv C Ca Ra
C
Pms RAP D
  
  
Ca
C
P

Rv Ra
D
 


36. 1959
Ca
C
P

Rv Ra
D
 

Cv
Ra,Ca
Rv
VR
ml/min
%∙initial value
50 100 150

37. 1993
Rc
Ra
LV RV
Rv
Rc
Ca
Ra
Cv
Rv
Ca Cv
Model parameters
Ees mmHg/ml
Vo ml
Tes ms
Τ ms
Ra dyn∙s∙cm-5
Rc dyn∙s∙cm-5
Rv dyn∙s∙cm-5
Rt dyn∙s∙cm-5
Ca ml/mmHg
Cv ml/mmHg
Hr beat/min
Vt ml
Vs ml
Vu ml
Why does pulmonary venous pressure rise after
onset of LV dysfunction: a theoretical analysis

38. Gelman’s again favouring Tyberg

39. Gelman’s…

40. UNICORNS IN ICU
VOLEMIA

42. PPV
IVCI SVV
ΔVpeak
PEPV
SVCI
PLR
SPV
Hold Exp
RSVT
Fluid responsiveness is function of system performance.
ΔABF
Volemia is just a (VOLUME) state. Volemia is linked to TBW.

43. Searching for performance (fluid responsiveness) in statics…
REDV
LEDA
PAOP LVEDP PVC
LEDV
ITBV
GEDV
REDA
Or reductionism at its absolute funniest.

44. P
R
E
S
S
U
R
E
V
O
L
U
M
E
DYNAMIC STATIC
VOLEMIA

45. DAXOR
-volume/static-
Albumin I 131
Vx
Vy
Cx
dCx/dt

46. t
Radioisotope
DAXOR
Regression to time 0
Blood volume Injecting Measuring
tgα
+
+
_ _
Mixing
BV PV RBCV CLI

48. Guytonian view on volemia
-pressure/dynamic-functional-
active-effective (Parkin)
-RVR and Cv/Ca dependent-
‘anatomical’-passive (Pinsky)

49. AMERICAN MSFP
 MSFP-Pcv=Rv•Dc
 MSFP-Pcv1=Rv•Dc1
 MSFP-Pcvβ=Rv•Dcβ
 2 unknowns Rv and MSFP
 2 equations
 Rv=(Pcv2-Pcv1)/(Dc1-Dc2)
Maas,Pinsky 2009
 MSFP-Pcv1=Rv•Dc1
Dc1
Pcv1

50. AMERICAN COMPLIANCE
 C= ΔV/ΔP
 C= ΔV/Pmsfa
 C= (ΔV+Vx)/Pmsfb
 C= Vx/(Pmsfb-Pmsfa)
Vx
Pmsf
a
Pmsfb
Maas,Pinsky 2009
α
α

51. AUSTRALIAN MSFP
-modified demonstration-
Pa  Pv  Ra Q
Pv  RAP  Rv Q
Pa Ca  Pv Cv  Pms  (Ca Cv)
Flux equations
Volume equation
C
v
C
a
x 
Ra  RvQ RAPCa  (Rv Q RAP) Cv  Pms  (Ca Cv)
(Ra  Rv) QCa Cv Rv Q RAP(Ca Cv)  Pms(Ca Cv)
x  24 :1
RAP
   
C (R R ) C R
a a v v v
ms 
  
(R R ) R x
 
Q R x
Q SVR
1
MAP
 
Q R x
 
Pmsa  0,96RAP  0,04MAP  c CO
1 : 25
R
v
R
a

 
R v R a
SVR
c0.3,1.2
C
P Q
tot
 
RAP
1 x
P Q
a V v
ms 

 
RAP
x 1
x 1
P
v
ms 





)
x 1
RAP(1
x 1
x 1
P
v
ms 





52. AUSTRALIAN MSFP
Pmsa  0,96RAPact  0,04MAPact  c COact

R x
x 1
c
v


1
25
R
v 24 
R
a
C
v  
C
x
a

c     
SVRst 0.038 SVRst
1
26
0.96
24 SVR

25 26


53. AUSTRALIAN MSFP
SVRst
st
MAP
CO
st
MAPst = 94.17+0.19γ•age
CI  4.50.99
CIst=4.5•(0.99age-15)=COst/BSA
BSA=0.007184•(height0.725)•(weight0.425)

0.038 MAP
CI BSA
  
c 0.038 SVR
st
st
st 

54. Parkin’s EH

55. HEART
PERFORMANCE
STATE
ARTERIAL
TONE
STATE
VOLUME
STATE

56. Circulatory dynamic variables
Volume state Tone state Performance state
Blood volume
Unstressed volume
Stressed volume
Compliance
Venous resistance
Chronotropy
Dromotropy
Inotropy
Lusitropy
SVR
MAP-RAP=Pms•Eh•SVR/RVR

57. MSFP
MCFP
There ain’t no time for summertime blues

63. Fluid unresponsiveness-you
do not want to go there
AP↓
N
Microcirculation Microcirculation
VD
N
VC VP↑
P
mmHg P
mmHg
A V A V

65. Bakker’s case

71. In a world of PPV or SVV…
is there any room left for
basic physiology?

72. Trending MSFP and Eh in PPV’s
world
 Is the patient ventilated without spontaneous efforts?
 Is the patient ventilated in nonprotective ventilation (TV at least 8ml/kg)?
 Is the patient in sinus rhythm ( or other regulated rhythm)?
 How is Ecw versus El?
 Is the patient unaffected by serious valvular disease?
 Is the patient unaffected by right ventricle dysfunction or severe left ventricle
dysfunction?
 How is the patient’s IAP ?
 Which treshhold will you use for your binary decision?
 Have you established your patient’s compliance in order to standardize the VE?
 Have you established that the patient’s heart rate/respiratory rate ratio is > 3.6?