Guytonian approach to shock - mean systemic filling pressure centered

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


Elastance=tg =ΔP/ΔV

Compliance=1/tg =ΔV/ΔP=V2-V1

=Vt-Vo=Vs/P

Capacitance=Vt/P


COMPLIANCE vs CAPACITANCE

σ

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


STARLING RESISTOR

VENOUS RETURN ON GRAPHS

Starling Resistor

Thoracic- Abdominal interface Pabd>Ppl

Pleuro-vascular interface – PPVent.


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↑


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


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


CO

/ V

R

0

VASOPRESSORS

α α

1

2

3

1

2

Modified from

Jacobsohn 2013


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


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


CO

/ V

R

0

1

2

3

1

2

4

3


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


CO

/ V

R

0

1

2

3

1

2

3

4


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


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


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


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


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

../../../medicina/drager/evita_trainer_large/start.exe

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

Guytonian approach to shock - mean systemic filling pressure centered

Health & Medicine

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