Cardiogenic Shock: Monitoring Methods and

end PointsM. Maggiorini

Intensive Care UnitDepartment of Internal Medicine

University Hospital Zurich

Key elements of cardiac output

Cardiac Output (CO)

AFTERLOAD

STROKE VOLUME

CONTRACTILITY PRELOADAFTERLOAD

STROKE VOLUME HEART RATE

CAVE: Assure organ perfusion pressure !

Cardiac Function: Pressure/Volume loop

Maximal LV wall Maximal LV wall stress = LV stress = LV afterloadafterload

LV LV EndiastolicEndiastolic P.P.

DiastDiast. . AorticAortic P.P.

syst. syst. AorticAortic P.P.

activeactivediastdiast. .

relaxationrelaxation≈ DiastDiast. .

compliancecompliance

LV LV EndiastEndiast. . VolumeVolume≈≈ LV LV preloadpreload

Pressure-Volume relationship of the LV

Maximal LV Maximal LV wall stress in wall stress in

failingfailing LVLV

= = maxmax LV LV elastanceelastance

MyocMyoc. . ischemiaischemia

×in LVin LV--

compliancecompliance

LV LV EndiastolicEndiastolic P.P.

LV p

ress

ure

LV end-diastolic volume

EmaxEmax = = HighestHighest ratioratio betweenbetween LV LV endend--systolicsystolic pressurepressure and and LVLV--endend--diastolicdiastolic volumevolume

LVLV--e

ndend--

syst

olic

syst

olic

elas

tanc

eel

asta

nce

LV end-diastolicelastance

1 2 3

EEmaxmax = maximal LV = maximal LV elastanceelastance((indexindex of of contractilitycontractility))

LV end-diastolic pressure

Cardiac Contractility

LV pressure-volume histories (1, 2, 3) at different prealoads

LV end-systolic elastance (Ees) and diastoliccompliance in systolic dysfunction

Diastolic compliance

Left ventricular contractilityLV

Pre

ssur

e

LV Volume

LV E

last

ance

(Ees

)Emax

SV 1

Maximal LV elastance (Emax) = Highest ratio between LV end-systolic pressure and LV-end-diastolic volume

Loss of cardiac contractility in heart failure

Ees

SV 2

Emax

LV pressure-volumehistories at higher preload

SV1 = SV3SV1 = SV3

SV 3

Emax

LVEDP

Cardiac preload(Frank-Starling relationship)

Change in stroke volume after 200 ml fluid challenge

RV/LV end-diastolic volume

Stro

ke v

olum

e

ideal

Energy of Contraction

Degree of stretch of the myocytes during diastole

Intrinsic strength of contraction (contractility) of the myocytes for a givendegree of stretch duringdiastole

Heart failureHeart failure

Stroke Work = ∆ Pressure x Stroke Volume

Assessment of cardiac preload and contractility clinical practice

LV-enddiastolic volume (LVEDV)

Stroke volume

heart failure

normal

Optimal filling

Fluid loading

Afterloadand/or

InotropySV deficit

Global End-diastolic Volume

RA RV LA LV

EVLW

GEDV = ITTV - PTV

GEDV = CO x (MTtTDa - DStTDa)

RA RV LA LV

EVLW

RA RV LA LV

EVLW

ITTV

PTV

CO x MTtTDa

CO x DStTDa

Global end-diastolic volume

200 ml fluid challenge

Stro

ke v

olum

e best

GEDV a marker of preload

global enddiastolic volume index (GEDVI)

Cardiac output(Cardiac Index)

CI < 2.2 l/min/m2

CI 3.5-5.5 l/min/m2

~ 600 -1000 ml/m2

SV deficit

Assessment of cardiac preload and contractility clinical practice:

applied pathophysiology at the bed side

Fluid loading

Afterloadand/or

Inotropy

CI 2.9 l/min/mCI 2.9 l/min/m22

CI 1.5 l/min/m2

CI aim to cope CI aim to cope with VOwith VO22 demanddemand

Assessment of Cardiac contractility

Blood Flow / Enddiastolic Volume relationship

GEDVI (ml/m2)0 200 400 600 800 1000 1200

2.5

5.0

7.5

10.0

CI (

l/min

/m2 )

area to meet

Normal

Heart failure

• CFI = CI/GEDVI• GEF = (CI/HR)/GEDVI

0.0

2.0

4.0

6.0

8.0

10.0 CFI (1/min)

Heart failure Sepsis

P<0.001

Cardiac Funtion Index

global enddiastolic volume index (GEDVI)

Cardiac output(Cardiac Index)

CFI 2.1; GEF 8%

CFI > 3.5; GEF > 25%

~ 600 -1000 ml/m2

Deficit in contractility

Assessment of cardiac contractility by the calculation of cardiac function index (CFI) or global ejection fraction (GEF) at the bed side

Fluid loading

Dobutamine

CFI 2.9; GEF 18%CFI 2.9; GEF 18%

CFI 2.1; GEF 8%

LV p

ress

ure

LV end-diastolic volume (LVEDV)

Normal LV end-diastolicelastance

1 2 3

LV end-diastolic pressure (LVEDP)

LVLV--e

ndend--

sys t

olic

sys t

olic

elas

tanc

eel

asta

nce

Diastolic dysfunction in heart failure

LV presure-volume histories (1, 2, 3) following changes in prealoads

Decreased LV end-diastolic elastance

1a2b

3c

SV LVDP

LVEDV

In cardiac patients changes pulmonary artery occlusion (wedge) pressure reflect left ventricular elastance and not LVEDV

Cvp

/Pao

p

RV/LV end-diastolic volume RV/LV end-diastolic volume

Stro

ke v

olum

e

?

Change in stroke volume Change in venous pressure

?

Week of a correlation between PAOP and cardiac output or cardiac function index

Cardiac output Cardiac function index

Ritter et al. unpublished

Monitoring of LV elastance

Pulmonary artery occlusion (wedge) pressure in cardiac patients

Optimal Ppao is the lowest value that results in the highest cardiac output and no increase in extravascular lung water

Guided by:Systolic dysfunction

Diastolic dysfunctionLV end-distolic volume

0

10

20

30

40

50

Pres

sure

(mm

Hg)

Pra Ppa Ppao

Determinants of Cardiac Output

Cardiac Output (CO)

AFTERLOAD

STROKE VOLUME

CONTRACTILITY PRELOADAFTERLOAD

STROKE VOLUME HEART RATE

Afterload a determinant of Cardiac Output

SVR

ELASTANCE

REFLECTEDWAVE

Vascular impedance

DefinitionIs the force facing the ventricle, vascular vascular ImpedanceImpedance, which must be overcome by the ventricle to open the valve and eject blood into the artery.

Vascular impedance is best appreciated by the ratio between arterial pressure and cardiac output

Total vascular resistance SVRtot = MAP / CO

Pressure/Bloodflow relationship

Mea

nar

teria

lpre

ssur

e

β = low resistance

0

α = high resistance

Cardiac outputα β

SVR

ELASTANCE

REFLECTEDWAVE

Vascular impedance

global enddiastolic volume index (GEDVI)

Cardiac output(Cardiac Index)

CI < 2.2 l/min/m2

CI 3.5-5.5 l/min/m2

~ 600 -1000 ml/m2

SV deficit

Afterload reduction improves cardiac output:applied pathophysiology at the bed side

Fluid loading

Nitrates

CI 2.9 l/min/mCI 2.9 l/min/m22

CI 1.5 l/min/m2

CI aim to cope CI aim to cope with VOwith VO22 demanddemand

Pressure/Bloodflow relationship

MeanMean arterialarterialpressurepressure

CardiacCardiac OutputOutput

Heart rate

InotropyCFI or GEF

(> 3.5 or > 20%)

Total systemic vascular resistance

Hemodynamic management using the PiCCO monitoring system

PreloadGEDVI

(600-1000 ml/m2)

Flow = pressure / resistance

Pressure = Flow * resistanceβ = low resistance

β

α = high resistance

α

Pin

-Pou

t

00

Cardiac output

Pulmonary venous hypertension

Decreased left ventricular elastance following left ventricular systolic and diastolic dysfunction lead to pulmonary venous hypertension and in 70% of the cases to pulmonary edema

0

10

20

30

40

50

60

70

Zeit

PpaoPpao 32 mmHg32 mmHg

mPpamPpa 45 mmHg45 mmHg

PVR = mPpa - PpaoCO

Extra vascular lung water (EVLW) for the monitoring of hydrostatic pulmonary edema

ITGV

ITBV

EVLWEVLW

PVPI = EVLW / PBVPVPI = EVLW / PBVLung gas volume (ITGV)Pulmonary Vascular Permeability Index (PVPI)

GEDV

3 elements

Pulmonary venous hypertensionPulmonary Blood Volume (PBV)Pulmonary vascular permeability

PBV

PiCCO derived Extra-Vascular Lung Water

EVLW = ITTV - ITBVb

RA RV LA LV

EVLW

RA RV LA LV

EVLW

ITTVITTV

ITBVITBVbb

EVLWEVLW

RA RV LA LV

EVLW

ITTV = CO x MTtTDa

ITBVITBVbb = = GEDV * 1.25GEDV * 1.25

ITTV = intrathoracal thermovolumeITBV = ITBV = caluculatedcaluculated (b) (b) intrathoracalintrathoracalbloodvolumenbloodvolumen

EVLW = ITTV - (GEDV * 1.25)

EVLW Evolution: Changes During first 3 ICU DMean (SD) in Percent

21.9% (15)

6.3% (27)

22.4% (10)

6.2% (20)

0

5

10

15

20

25

Survivors (17 Pts) Non Survivors (9 Pts)

Perc

ent (

%)

Non cardiogenic Edema Cardiogenic Edema

p=0.04 p=0.03

EVLW Changes <10% or Maximum Value <12 ml/kg

Odds Ratio for ICU Mortality 0.07* (95% CI 0.01-0.68) *p<0.05

Changes in EVLW after ICU admission a prognostic marker

Ritter et al.SGI 2006

Transition from hydrostatic to inflammatory type of pulmonary edema

Hydrostatic Inflamm. LV failure ARDS

Acute onset +++ +++

Oxygenation

Bilateral infilt. +++ +++

Ppao (Wedge)

????

normal, = elevated, = reduced

ŅLeakÓ

Leak = PVPI

56 y. old

male

T0 T0+24h T0+48h T0+72h T0+96hHR 90 120 125 100 90MAP 70 70 70 70 72CVP 18 14 18 22 16PPA 45 40 50PAOP 24 21 24CI-PAC 1.7 2.4 1.8CI-PICCO 1.8 2.5 1.9 1.4 2.7CFI 1.6 2.2 1.9 1.7 2.9GEF 6 9 7 8 13GEDI 1037 1171 939 814 911EVLW 15 15 15 15 14PVPI 2.3 2 2.5 3 2.7Hb-aO2 97 97 96 97 95Hb-vO2 58 57 44Hb-cvO2 55 46 61lactate 3.5 1.1 1.4 3.1 1.2

Dobu 0 400 0 0 100Levo 0 0 0 0 0.2Nor 29 11 0 0 0

Balance - -850 -880 30 -2000

Limitations the PiCCO monitoring system in acute heart failure: rapid

changes in Paop can not be assessed

Kivikko et al Circ 2003, 107:81

Time (h)

Stroke volume

Time (h)

Pulmonary artery occluded pressure

Levosimendan

Placebo

Levosimendan

Placebo

RAP > PAOP

Jard

inan

d V

iellia

rd-B

aron

Cur

rOpi

nC

ritC

are

2005

, 11:

171

Limitations the PiCCO monitoring system in acute heart failure: can not

differentiate between RV and LV failure

To restore cardiac function in order to meet body oxygen requirements, hence improve oxygen supply and organs perfusion.

End points for the treatment of AHF using the PiCCO monitoring system

Hemodynamic goalsCardiac Index > 2.2 l.m-1.m2

Cardiac function index > 3.5 or GEF > 20%Mean artery pressure 55 - 75 mmHgGEDVI between 600 and 1000 ml/m2 to meet the optimal cardiac outputEVLW < 10ml/kg