Hemodynamics - paradigm shifts

Echocardiography Primer

for Intensivists

Bucharest 2014

But first…

A Glimpse of Hemodynamics

“New” conceptual approach?

Currently, BF and vT can be effectively assessed at the bedside Quantitative measures of capillary leak (vB) would be useful in guiding fluid therapy The objective measures for vC are cumbersome Bedside measures of vC are not yet available

REDUCTIONIST DIDACTICISM

How close are we of anything?

SVR - centered view

Critical closing pressure - centered view

Dynamic tone assess-

ment

Radioiodinated albumin

- DAXOR

Hb – dilution technique

MSFP–centered approach

ECHOCARDIOGRAPHY

PICCO

VIGILEO

SWAN

Biomarker panel

Radioiodinated albumin - DAXOR

EVLWi/PVPI - PICCO

NIRS

OPS/SDF SL tonometry

NADH fluorescence

Delayed fluorescence

mitoPO2

Miscellaneous

Paradigms have been shifting for some

time now…

SHIFTING THE PARADIGM -flow centered era-


α

β


TONE SDF

OPS


“EFFECTS OF PERFUSION PRESSURE ON TISSUE PERFUSION IN SEPTIS SHOCK”


The effects of dobutamine on microcirculatory alterations in patients

with septic shock are independent of its systemic effects


NITROGLYCERIN ?

μVESSELS TONE


FLOW

SHIFTING THE PARADIGM -μvessels centered era-

RECRUIT THE μCIRCULATION AND KEEP IT OPEN

“Run the circulation at the lowest possible pressures?” -flow centered ideas-

Monitoring the right vessels

μvessels

FLOW

MAP TONE

MAP

μvessels

FLOW

The Break-up

Open up the μcirculation and keep it open -resuscitation-

De-stress the distressed heart -contextual innuendo-

SIADH

CRITICALLY ILL CM

IMMUNO SUPR.

POST CA SYNDROME

SIRS/ALI ARDS CATECHOL

ADM.

PHEOCHR.

CSW/RSW RENAL STUNNING

SAH

HYPER CATAB.

SEPSIS

TBI

Takotsubo -like CM

DISTRESS

TL

R

RAAS

PAMP/DAMP

SU

RG

E

βblockers

Alpha7n

AChR

HMGCoA

HOLISTIC APPROACH

SIADH

CRITICALLY ILL CMP

IMMUNO SUPR.

POST CA SYNDROME

SIRS/ALI ARDS CATECHOL

ADM.

PHEOCHR.

CSW/RSW RENAL STUNNING

SAH

HYPER CATAB.

SEPSIS

TBI

Stunning

Band contraction

Uncoupling of biological oscillators

Reversibility potential

Hysteresis

HRV “fingerprint”

Tone related paradigms

How should one quantify tone state? How is tone related to ΔMAP responsiveness? Is tone a prognostic factor?

I = V / R (Ohm’s law)

Q = (P1- P2) / R

CO = (MAP - PRA) / SVR

SVR -mathematical counterfeit-

α

ctgα =(MAP-Pc)/Q Pc=critical closing pressure ctgα = Ra

Why a critical closing pressure? -intuitive image-

What if it exists a critical closing pressure? -intuitive image-

Raynaud Arteriovenous

malformation

Measuring CCP

ctgα = (MAP-Pc)/Q Pc = critical closing pressure ctgα = Ra

α

On the edge of waterfalls

Is there any purpose in waterfalls?

Organ specific PCC reflecting organ

specific vascular control

Vital organ perfusion is more efficiently

maintained

Arterial flow stability during short

lasting Pcv changes

A Pcc-Pmsf gradient means transient

heart/brain flow during stop-flow

conditions

Rsys vs Ra

Ra=0.52•Rsys-0.55

Pearson correlation 0.945

If it were that easy!

Naeije’s pressure/flow diagram -CCP in pulmonary vessels-

PcPpa

PlaPpaPVRaPVR

Inflow

pressure

Outflow

pressure

Pla Pc

Ppa PVR = (Ppa – Pla) / Q ->A PVRa = (Ppa – Pc) / Q ->B

A: Pla>Pc B: Pc>Pla

1►2: no change

1►3: VD

A

B’

B

PVR=tgα

1►2: VC 1►3: no change

A

B

PVR when Pla>Pc

PVR as seen through PVR = (Ppa – Pla) / Q

Q or Ppa

PVR

PVR when Pla<Pc

Ppa

Pla

Pc

P’c

α

α PVRa=tgα

PVR→∞

1

2

3

PVR→∞

PVR→tgα

PVR→tgα tgα

cb

cx

bxaPVR

x→∞=>PVR=PVRa=tgα

x→Pc=>(x-c)→0=> =>PVR→∞ Q

Naeije’s tone diagram -solving Versprille’s conundrum-

C

VASOCONSTRICTION

VASODILATATION

Q

Ppa

PVRa=0

Pla

Ppa-Pc=PVR→•Q

Pc

0

http://elib.fk.uwks.ac.id/asset/archieve/e-book/FISIOLOGI - FAAL - PHISIOLOGY - PATHOFISIOLOGY/Applied Physiology in Intensive Care Medicine \(Pinsky\).pdf

http://www.sassit.co.za/Journals/Physiology/Respiratory/pulmonary vascular resistance a meaningless variable.pdf

Magder’s view -didacticism with a taste of mathematical compromise-

Should the flow begin to go down, then Pv will go upwards (in this picture it appears to stand still). This Pv’s rise will dampen the resistance’s (SVR’s) rise but it will not abrogate it (Pv’s rise is less than Part’s fall due to Cart<Cven). So… SVR will appear as rising with falling flow. Should you consider Pcrit as the outflow pressure, only then you shall grasp the real picture: the tone stands still.

MAP’s preload dependence

MAP’s preload dependence -ventriculo-arterial coupling diagram-

Ees=tgα=Pes/(EDV-SV-Vo)

Ea=tgβ=Pes/SV

Pes=a•(Ved-Vo) unde

a=1/(1/Ea+1/Ees)

High baseline Ea, Ees(ESPVR)

Diastolic dysfunction(EDPVR)

High sympathetic overdrive/panic

Great redistribution potential

Active inflammation capable of

modulating Ea,EDPVR

Little to no involvement of Ees

ΔEes=0

keyw

ord

s


PPV SVV

PPV/SVV=

Eadyn

0.89

Eadyn echivaleaza cu tonus vasomotor.


Pentru Eadyn>0.89 cresterile tensionale pentru

acelasi SVV sunt mai pronuntate si denota un tonus

vasomotor mai accentuat.

Tone and prognosis -cardiogenic shock focus-

T

O

N

E

F

O

C

U

S

Weaning failure-another paradigm shift

Weaning failure

Redistribution Lusitropism Inotropism

Weaning failure

Redistribution

Why does pulmonary venous pressure rise after

onset of LV dysfunction: a theoretical analysis

Gelm→n’s two comp→rtment model

The decrease in intrathoracic pressure favours redistribution

Weaning failure

Lusitropism

Myocardial ischemia

► WOB

► tachycardia

► hypoxemia

RV dilation: RV/LV interdependence

► increase in venous return

► increase in PVR

LV afterload induced fall in relaxation

r→te filling pressure hypoxemi→, panic, sympathetic surge, myocardial

ischemia

Weaning failure

Inotropism

Effect of intrathoracic pressure on left ventricular performance, Buda NEJM 1979

Left ventricular function during weaning of patients with chronic Obstructive pulmonary disease, Richard ICM 1994

LUSITROPISM

-shift in focus-

Right ventricular protective ventilation -echo era-

Fluid responsiveness -echo era-

• Is the patient unaffected by serious valvular disease?

• Is the patient unaffected by right ventricle dysfunction or severe left ventricle dysfunction?

• 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?

• How is the patient’s IAP ?

• Have you established that the patient’s heart

rate/respiratory rate ratio is > 3.6? • Which treshhold will you use for your binary

decision?

• Have you established your patient’s compliance in order to standardize the VE?

2%

F

L

U

I

D

R

E

S

P

O

N

S

I

V

E

N

E

S

S

Welcome

to

the echo era !

Oct 2014

Hemodynamics - paradigm shifts

Health & Medicine

Transcript of Hemodynamics - paradigm shifts