SHOCK
A GUYTONIAN
APPROACH
2013 Bucharest-SUUB
POISEUILLE’S LAW
I = ↑ / R (τhm’s law)
Q = (P1- P2) / R
CO = (MAP - PRA) / SVR
VR = (PMS - PRA) / RV
ARCHETYPAL REDUCTIONISTIC NEED OF A FUNCTIONAL VENOUS HEMODYNAMIC POLE
Weber E. 1850
Small changes (as absolute values) in PRA, RV, PMS determine large changes in VR
Steady state - CO = VR 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 PMS / stressed blood volume + unstressed / RV
BASIC THEORETICAL IMPLICATIONS OF A HEMODYNAMIC VENOUS POLE
MEAN SYSTEMIC FILLING PRESSURE
Stopped flow mean arterial pressure and large venous vessels pressure as these two come closer to each other PMS
PMS = VS / CMS
PMS ≠ MAP
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
BASIC BICOMPARTMENTAL MODEL OF MSFP
Pump
Pump Pump
Resistance
Resistance
Resistance
Cv
Pv=7
Qr=0
• 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
7
0
120
2
6
Pv
7
26
102 Pa Pa
Pv
0
CO
CO=5 CO=1 CO=0
Modified from Levy 2007
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
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 VS by adjusting the capacitance ( Pms) of the reservoir compartment - splanchnic compartment VR
COMPLIANCE vs CAPACITANCE
VS ≈ 20-30 % (1,5 L)
C ≈ 0.187L∙mmHg-1
Pms ≈ 8-10 mmHg
Modified from Jacobsohn 2013
Elastance=tg =ΔP/ΔV
Compliance=1/tg =ΔV/ΔP=V2-V1
=Vt-Vo=Vs/P
Capacitance=Vt/P
Modified from Jacobsohn 2013
COMPLIANCE vs CAPACITANCE
σ
Gelman’s
Gelman’s
Gelman’s
VENOUS RESISTANCE
RV = 8ηl / πr4
RV is influenced by the size of the venous
circulation venous circ. time constant is
determined by vascular volume / flux ( L∙min∙L-1 =
min ) - ( = C∙R)
Vasopressors could redistribute blood from one
teritory to another from slow la fast RV si
VR
Modified from Jacobsohn 2013
STARLING RESISTOR
VENOUS RETURN ON GRAPHS
Starling Resistor
Thoracic- Abdominal interface Pabd>Ppl
Pleuro-vascular interface – PPVent.
Modified from Jacobsohn 2013
VENOUS RETURN ON GRAPHS
α
tg α = slope
VASCULAR FUNCTION CURVES IN A BUNDLE
α α α
Pms↑
Rv↓
Normal
Rv↑
Pms↓
RIGHT ATRIAL PRESSURE
VE
NO
US
RE
TU
RN
FRANK STARLING CURVE
0
inotropism ↓ afterload↑
RIGHT ATRIAL PRESSURE
CA
RD
IAC
OU
TP
UT
DIDACTICISM WITH A TASTE OF MATHEMATICAL COMPROMISE
O X
Y Y
X O
O
Y
X
CO
RA
P
iva
sc
Pms
CO
RAP tm
CO
RAP ?
Pms
Right shift in case of increasing Pextramural
but with constant inotropism. RIGHT
TREATMENTS AND THEIR HEMODYNAMIC CONSEQUENCES
A
B
C
↑ Pms
↓ Rv
D
normal
↑Vt,↑Vs
α α
RIGHT ATRIAL PRESSURE
CO
/ V
R
BLOOD vs CRISTALOID / COLOID
0
1
2
1
2
3
Modified from
Jacobsohn 2013
normal
↑Rv+↑Pms(↑Vs)
↑Rv
A
C
B
D
RIGHT ATRIAL PRESSURE
CO
/ V
R
0
VASOPRESSORS
α α
1
2
3
1
2
Modified from
Jacobsohn 2013
RIGHT ATRIAL PRESSURE
CO
/ V
R
0
↓Rv
↓Rv+↓Pms
↓Vs
normal
A
C B
D
α α
INODILATORS
1
2
1
2
3
Modified from
Jacobsohn 2013
normal
↑Rv+↑Pms (↑Vs)
↑Rv
B
A
C
D
INOVASOPRESSORS
0 RIGHT ATRIAL PRESSURE
CO
/ V
R
α α
1
2
3
2
1
Modified from Jacobsohn 2013
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
A
B
C
D
E
↓Rv
normal
fluid shift
↓Pms (↓Vt)
α α α
RIGHT ATRIAL PRESSURE
CO
/ V
R
0
1
2
3
1
2
4
3
Modified from Jacobsohn 2013
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 )
Pms↑ through fluid shift+adm.
Rv↓and Pms ↓(Dtx/Mil) + fluid shift+adm.
normal
A
B
C
D
E
α α
RIGHT ATRIAL PRESSURE
CO
/ V
R
0
1
2
3
1
2
3
4
Modified from Jacobsohn 2013
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
RIGHT ATRIAL PRESSURE
CO
/ V
R
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
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
normal
plateau shift
plateau shift
Rv↑
Plateau shift Rv↑ Pms↑(fluid,SS)
afterload ↑
A
A1
B
C
D
E
F
0 RIGHT ATRIAL PRESSURE
CO
/ V
R
SHIFT PLATEAU
Ppl
α α
1
2
3
4
1
2
3
4
Modified from Jacobsohn 2013
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
Rv↑ Pms↑ (fluid,SS)
normal
Rv↑
Rv↑ Pms↓ dehydration
Rig
ht s
hift
SHIFT PLATEAU
Rig
ht s
hift +
+
A
B
E
C
D
F
0 Ppl+ Ppl++ RIGHT ATRIAL PRESSURE
CO
/ V
R
α α α
1
2
4
3
4
2
3
1
Modified from Jacobsohn 2013
1959
CvCa
VPms
CvCa
VPms
C
CaRaRv
PD
Heart
Lung
Rv
Ra
Cv
Ca
Ra Rv
Cv Ca
Pa
Pra
CvCa
VvVaPms
CvCa
PvCvPaCaPms
Pv
DRvRAPPv
DRaPvPa
CvCa
)DRvRAP(Cv)DRaPv(CaPms
RAPCvCa
)DRvRAP(Cv)DRaPv(CaRAPPms
CvCa
DRaCaDRvCv)RAPPv(CaRAPPms
CvCa
DRaCaDRvCvDRvCaRAPPms
C
RaCaCRvDRAPPms
C
CaRaRv
PD
1959
C
CaRaRv
PD
Cv
Ra,Ca
Rv
VR ml/min
%∙initial value 100 50 150
1993
LV RV
Rv
Rc
Rc
Ca
Ra
Cv
Rv
Cv Ca
Ra
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
Gelman’s again favouring Tyberg
Gelman’s…
UNICORNS IN ICU
VOLEMIA
Fluid responsiveness is function of system performance.
Volemia is just a (VOLUME) state. Volemia is linked to TBW.
SVV IVCI
SVCI
PLR
PEPV
PPV
ΔABF
ΔVpeak
SPV
RSVT
Hold Exp
Searching for performance (fluid responsiveness) in statics…
Or reductionism at its absolute funniest.
REDV
LEDV
GEDV
ITBV
LVEDP PVC PAOP
REDA
LEDA
P R
E S S U R E
V
O L U M E
DYNAMIC STATIC
VOLEMIA
DAXOR -volume/static-
Albumin I 131
Vx
Vy
Cx
dCx/dt
t
Rad
iois
oto
pe
Blo
od
vo
lum
e
Injecting Measuring
Regression to time 0
tgα
+
_ _
+
Mixing
DAXOR
BV PV RBCV CLI
Guytonian view on volemia -pressure/dynamic-
functional-active-effective (Parkin) -RVR and Cv/Ca dependent-
‘anatomical’-passive (Pinsky)
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
AMERICAN MSFP
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
AUSTRALIAN MSFP -modified demonstration-
QRPP ava
QRRAPP vv
)CC(PCPCP vamsvvaa
Flux equations
Volume equation
a
v
C
Cx
1:24x
COcMAP04,0RAP96,0Pmsa SVRRR
25:1R
R
av
a
v
2.1,3.0c
)CC(PC)RAPQR(CRAPQRR vamsvvava
)CC(P)CC(RAPQRCCQ)RR( vamsvavvava
RAPC
RC)RR(CQP
tot
vvvaams
RAPx1
xR)RR(QP
vVams
RAP1x
xRQ
1x
SVRQP
vms
)1x
11(RAP
1x
MAP
1x
xRQP
vms
AUSTRALIAN MSFP
COactcMAPact04,0RAPact96,0Pmsa
1x
xRc
v
25
1
R
R
a
v24
C
Cx
a
v
SVRst038.0SVRst26
196.0
2625
SVR24c
AUSTRALIAN MSFP
SVRst st
st
CO
MAP
99.05.4CI
MAPst = 94.17+0.19γ•age
CIst=4.5•(0.99age-15)=COst/BSA
BSA=0.007184•(height0.725)•(weight0.425)
BSACI
MAP038.0SVR038.0c
st
stst
Parkin’s EH
HEART PERFORMANCE
STATE
ARTERIAL TONE STATE
VOLUME STATE
Circulatory dynamic variables
Blood volume
Unstressed volume
Stressed volume
Compliance
Venous resistance
Chronotropy
Dromotropy
Inotropy
Lusitropy
SVR
Volume state Tone state Performance state
MAP-RAP=Pms•Eh•SVR/RVR
MSFP
MCFP
There ain’t no time for summertime blues
Fluid unresponsiveness-you do not want to go there
Microcirculation Microcirculation
N
VD
VC VP↑
N
AP↓ P
mmHg P mmHg
A V A V
Bakker’s case
In a world of PPV or SVV…
is there any room left for
basic physiology?
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?
Trending MSFP and Eh in PPV’s world