physiology of hemodynamics & picco parameters in detail

Physiology of hemodynamics & PiCCO parameters in detail

2

Goal of intensive care medicine

Ensuring adequate organ and tissue oxygenation is the main goal in intensive care

medicine:

O2 to the tissues!

Physiology of hemodynamics

3

The circulation

heart = the pump

lung = saturation of the blood with oxygen in exchange with carbon dioxid

tissues and organs = sites where the oxygen is transported to by the circulating blood

arterial vessels = transport blood from the lung to the organs, contain oxygen-rich blood

venous vessels = transport blood from the organs to the lungs, contain oxygen-depleted blood


4

Principal task of the circulation:supply organs with oxygen-rich blood and nutrition!

others: transport of hormones and drugsregulation of body temperatureimmunologic and blood coagulation functionevacuation of body waste matters

The circulation is determined by pressure (blood pressure) and

flow (cardiac output)

großer Kreislauf

kleiner Kreislauf

capillaries of the lung

pulmonary circulation

pulmonary artery pulmonary

vein

left heart

right heart

body circulation

capillaries of the body (smallest blood vessels)

The circulation


5

Cardiac output

Cardiac Output (CO) is an important parameter for the assessment of the circulatory situation is defined as the amount of blood ejected by the heart within 1 minute is the calculation basis for most PiCCO parameters

The CO is determined by several factors:

amount of blood which fills the chambers of the heart (preload)

resistance against which the heart has to eject the blood (afterload)

heart rate (chronotropy)

power of the heart muscle (contractility)


6

Systolic (110 - 120 mmHg)

Diastolic (70 - 80 mmHg)

Cardiac Cycle

normal heart rate: 60-90 bpm

Arterial blood pressure and heart rate


7

The Heart as a Pump

Blood returns to into the Right Atrium (RA)

passes through the Tricuspid valve and into the Right

Ventricle (RV)

then through the Pulmonary valve into the Pulmonary Artery

(PA) and to the Lungs

Blood returns from the lungs into the Left Atrium (LA) via the

Pulmonary Veins

then down through the Mitral Valve into the Left Ventricle (LV)

Blood is ejected from the Left ventricle through the Aortic Valve

and into the Aorta

RA

RV

PA

LA

LV

Aorta


8

Cardiac Output

Preload Contractility Afterload Chronotropy

Determinants of Cardiac Output

8

Amount of blood inside the heart

Resistance against which the heart has to pump

Efficacy of the heart muscle

Number of heart beats per minute


9

Cardiac Output

Preload Contractility Afterload Chronotropy

Frank-Starling-Mechanism

Influence of preload and contractility on cardiac output

9


10

SV

Preload

V

V

V

SV

SVSV

Normal contractility

Preload, CO and Frank-Starling-Mechanism

Target AreaVolume Responsive Volume Overloaded

10


11

V

V

SV

SV

SV

Preload

Poor contractility

Normal contractility


11



12

V

V

SV

SV

SV

Preload

High contractility

Normal Contractility


Poor contractility

12



13

Summary and Key Points

• The goal of volume management is the optimization of cardiac output • An increase in preload leads to an increase in cardiac output, within certain

limits. This is explained through the Frank-Starling-Mechanism.

• The measurement of cardiac output does not show where the patient is located on the Frank-Starling curve.

• For optimization of the CO you must have a valid preload measurement.

13


14

Goal of intensive care medicine

Ensuring adequate organ and tissue oxygenation is the main goal in intensive care

medicine:

O2 to the tissues!


15

Processes contributing to cellular oxygen supply

Aim: Optimal Tissue Oxygenation

Pulmonary Gas exchange Macrocirculation Microcirculation Cell function

Direct Control Indirect

Oxygen AbsorptionLungs

Oxygen TransportationBlood

Oxygen DeliveryTissues

Oxygen UtilisationCells / Microchondria

Volume Catecholamines

Oxygen carriers Ventilation


17

Central role of the mixed venous oxygen saturation

Determination of Oxygen Delivery and Consumption

Delivery DO2: DO2 = CO x Hb x 1,34 x SaO2

CO: Cardiac OutputHb: HemoglobinSaO2: Arterial Oxygen SaturationSvO2: Mixed Venous Oxygen SaturationDO2: Oxygen DeliveryVO2: Oxygen Consumption

SaO2CO

Hb


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SaO2

S(c)vO2

Consumption VO2: VO2 = CO x Hb x 1,34 x (SaO2 - SvO2)Delivery DO2: DO2 = CO x Hb x 1,34 x SaO2

CO

Hb

Mixed Venous Saturation SvO2

SvO2

CO: Cardiac OutputHb: HemoglobinSaO2: Arterial Oxygen SaturationSvO2: Mixed Venous Oxygen SaturationDO2: Oxygen DeliveryVO2: Oxygen Consumption

Central role of the mixed venous oxygen saturation

Determination of Oxygen Delivery and Consumption


19

Oxygen delivery and its influencing factors

DO2 = Hb x 1,34 x SaO2 x CO

Transfusion

• Transfusion CO: Cardiac Output

Hb: Haemoglobin

SaO2: Arterial Oxygen Saturation

CaO2: Arterial Oxygen Content


20


Ventilation

• Transfusion• Ventilation

CO: Cardiac Output

Hb: Hemoglobin





21


VolumeCatecholamines

• Transfusion• Ventilation• Volume• Catecholamines

CO: Cardiac Output

Hb: Hemoglobin





22

Assessment of Oxygen Delivery

CO: Cardiac Output; Hb: Hemoglobin; SaO2: Arterial Oxygen Saturation

DO2 = CO x Hb x 1.34 x SaO2


Oxygen TransportBlood


Oxygen UtilizationCells / Mitochondria

Supply

SaO2 CO, Hb


23

Monitoring the CO, SaO2 and Hb is essential!






Supply

Assessment of Oxygen Delivery

CO, HbSaO2


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SvO2

SaO2 CO, HbMonitoring the CO, SaO2 and Hb is essential!

VO2 = CO x Hb x 1.34 x (SaO2 – SvO2)






Supply

Consumption

Assessment of Oxygen Delivery and Consumption


25

SvO2

SaO2 CO, Hb

Monitoring CO, SaO2 and Hb is essential

Monitoring the CO, SaO2 and Hb does not give information re O2-consumption!






Supply

Consumption

Assessment of Oxygen Delivery and Consumption


26

Summary and Key Points

• The purpose of the circulation is cellular oxygenation

• For an optimal oxygen supply at the cellular level the macro and micro-circulation have to be balanced along with pulmonary gas exchange

• Next to CO, Hb and SaO2 is SvO2 which plays a central role in the assessment of

oxygen supply and consumption.

• No single parameter provides enough information for a full assessment of oxygen supply at the tissues.


27

PiCCO2 - get the complete picture!

Cardiac output Arterial oxygen content

Stroke volume Heart rate OxygenationSaO2

HemoglobineHb

PreloadGEDI; SVV

AfterloadSVRI; MAP

ContractilityCFI

Pulmonary Edema

ELWI

Volume? Vasopressors? Inotropics? Blood transfusion?

Global oxygenationScvO2

Oxygen delivery Oxygen consumption

28

SvO2

SaO2 CO, Hb

Monitoring CO, SaO2 and Hb is essential

Monitoring the CO, SaO2 and Hb does not give information re O2-consumption!






Supply

Consumption

The central venous oxygen saturation ScvO2

PiCCO parameters in detail

29

Lungs

Pulmonary artery

Aorta

SvO2

(via pulmonary artery catheter)

ScvO2

(via central venous line)

V. cava sup.

V. cava inf.

Standard-CVC + CeVOX

(ScvO2)

PAC with optic fibre

(SvO2)

Mixed venous (SvO2) versus central venous (ScvO2) oxygen saturation

Site of measurement


30

Reinhart K et al: Intensive Care Med 60, 1572-1578, 2004; Ladakis C et al: Respiration 68, 279-285, 2000

n = 29r = 0.866ScvO2 = 0.616 x SvO2 + 35.35

ScvO2

SvO2

r = 0.945

30

50

70

90

70 9050

SvO2 (%)

65

70

85

70 90

90

30 6040 80

80

ScvO2 (%)

40

60

80

806040

75

6050

Monitoring the central venous oxygen saturation

The ScvO2 correlates well with the SvO2!


33

Detecting tissue hypoxia with S(c)vO2

What is “Shock”?

„Shock“ is defined as a state in which the oxgen supply cannot cover the demand, hence leading to tissue hypoxia.

Consequently, monitoring and treatment of shock states involves monitoring of oxygen supply/demand balance!

The diagnosis of „shock“ is not related to any given blood pressure, heart rate, Hb or other parameter of standard monitoring!


34

S(c)vO2 is the only clinically available parameter for assessment of oxygen consumption and is highly sensitive to tissue hypoxia!

Detecting tissue hypoxia with S(c)vO2


35

Early goal-directed therapyRivers E et al. New Engl J Med 2001;345:1368-77

O2-Insufflation and SedationIntubation + Ventilation

Central Venous CatheterInvasive Blood Pressure Monitoring

CVP

MAP

ScVO2

Cardiovascular Stabilisation

Volume therapy

8-12 mmHg

< 8 mmHg

65 mmHg

Inotropes

>70%70%

< 70%

no Therapy maintenance,regular reviews

< 65 mmHgVasopressors

Blood transfusion to Hematocrit 30%

Monitoring the S(c)vO2 – Clinical relevance

< 70%

Goal achieved?yes

ScVO2


Hospital 60 days

Leth

ality

36

Significance of ScvO2 for therapy guidance

36



37

Early monitoring of ScvO2 is crucial for rational and effective

hemodynamic management!

37



38

Tissue Hypoxia despite „normal“ or high ScvO2?

?Microcirculation disturbances in SIRS / Sepsis

Monitoring the S(c)vO2 – Limitations

S. Schaudig, 2003

38

SxO2 in %


39

Early recognition of disturbances in global tissue oxygenation

Detection of shock of any origin

ScvO2 – very fast responding parameter to hemodynamic changes (often much quicker than heart rate or blood pressure)

valid and easy to obtain via less invasive CVC line

Decreased mortality proven by normalizing ScvO2 (Rivers study)

Control of clinical course / therapy success of hemodynamic management

Summary and key points – S(c)vO2

CeVOX sales training

40


V

V

V

SV

SVSV

In order to optimize the CO you must know what the preload is!


40

Preload

SV

Importance of preload measurement

41

Methods for measuring preload

traditional method: filling pressures (CVP, PCWP)

via central venous line (CVC) or pulmonary artery catheter (PAC)

RA

RV

PA

LA

LV

AortaCVC

PAC

inherent problem: conclusion from pressures on volume!


42

modern method: direct measurement of the filling volumes (GEDV, ITBV)

via PiCCO-system

Left heartRight heart

Pulmonary Circulation

Lungs

Body Circulation



43

latest concept: volume responsiveness (SVV, PPV)

via PiCCO-system

Prediction whether the heart will respond to fluid administration with an increase in cardiac output

SV

PreloadV

SV

V

SV



44

Preload

Filling Pressures

CVP / PCWP

Volumetric Preload Parameters, Volume Responsiveness and Filling Pressures

Volume Responsiveness

SVV / PPV

Volumetric

Preload parameters

GEDV / ITBV

44


45

Kumar et al., Crit Care Med 2004;32: 691-699

Correlation between central venous pressure CVP and stroke volume

Role of Filling Pressures CVP / PCWP

45


46

Kumar et al., Crit Care Med 2004;32: 691-699

Correlation between pulmonary capillary wedge pressure PCWP with stroke volume

46

Role of Filling Pressures CVP / PCWPPiCCO parameters in detail

47

The filling pressures CVP and PCWP do not give an adequate assessment of cardiac preload. The PCWP is, in this regard, not superior to CVP (ARDS Network, N Engl J Med 2006;354:2564-75).

Pressure is not volume!

Influencing Factors:-Ventricular compliance-Position of catheters (PAC)-Mechanical Ventilation-Intra-abdominal hypertension

47

Role of Filling Pressures CVP / PCWPPiCCO parameters in detail

48

Role of Volumetric Preload Parameters GEDV / ITBV

Preload

Filling Pressures

CVP / PCWP


SVV / PPV

Volumetric Preload parameters

GEDV / ITBV

48


49

Total volume of blood in all 4 heart chambers

Left heartRight Heart


Lungs

Body Circulation

GEDV = Global Enddiastolic Volume

49



50

Michard et al., Chest 2003;124(5):1900-1908

50



GEDV shows good correlation with the stroke volume

51

ITBV = Intrathoracic Blood Volume

Total volume of blood in all 4 heart chambers plus the pulmonary blood volume

Left heartRight heart


Lungs

Body Circulation

ITBV =GEDV + PBV

51



52

Sakka et al, Intensive Care Med 2000; 26: 180-187

52

ITBVTD (ml)

ITBV = 1.25 * GEDV – 28.4 [ml]

GEDV vs. ITBV in 57 Intensive Care Patients

0

1000

2000

3000

0 1000 2000 3000 GEDV (ml)

ITBV is normally 1.25 times the GEDV



53

The static volumetric preload parameters GEDV and ITBV

• Are superior to filling pressures for assessing cardiac preload (Comment DSG/DIVI S2-Guidelines)

• In contrast to filling pressures are not falsified by other

pressures (Ventilation, intra-abdominal pressure)

53



54

Role of the Dynamic Volume Responsiveness Parameters SVV / PPV

Preload

Filling Pressures

CVP / PCWP


SVV / PPV

Volumetric Preload parameters

GEDV / ITBV

54


55

Intrathoracic pressure

Venous return to left and right ventricle

Left ventricular preload

Left ventricular stroke volume

Systolic Arterial Blood Pressure

Intrathoracic pressure

„Squeezing “ of the pulmonary blood

Left ventricular preload

Left ventricular stroke volume

Systolic Arterial Blood Pressure

PPPPmaxmax PPPPminmin

PPPPmaxmax

PPPPminmin

Inspiration

From Reuter et al., Anästhesist 2003;52: 1005-1013

Physiology of the Dynamic Parameters of Volume Responsiveness

Expiration Inspiration Expiration

Early Inspiration Late Inspiration

55

Fluctuations in blood pressure during the respiration cycle


56

SV

PreloadV

SV

V

SV

Mechanical Ventilation

Fluctuations in Stroke Volume

Intrathoracic Pressure fluctuations

Changes in intrathoracic blood volume Preload changes

Fluctuations in Stroke Volume throughout the respiratory cycle

Physiology of the Dynamic Parameters of Volume Responsiveness


57

SVSVmaxmax

SVSVminmin

SVSVmeanmean

Role of the Dynamic Parameters of Volume Responsiveness SVV / PPV

SVV = Stroke Volume Variation

• Is the variation in stroke volume over the respiratory cycle • Correlates well with the reaction of the hearts ejection volume during preload

enhancement (Volume Responsiveness)

57


-

cant change to mean

59

PPV = Pulse Pressure Variation

• Is the variation in pulse pressure amplitude over the respiration cycle • Correlates equally well as SVV for volume responsiveness

PPPPmaxmax

PPPPmeanmean

PPPPminmin

59



60

The Dynamic Preload Parameters SVV and PPV

- are good predictors of a potential increase in CO to volume administration

- are only valid with patients who are fully ventilated and who have no cardiac arrhythmias

60



61

Summary and Key Points - preload

• The volumetric parameters GEDV / ITBV are superior for measuring cardiac preload than CVP/PCWP.

• The dynamic volume responsiveness parameters SVV and PPV can predict whether CO will respond to volume administration.

• GEDV and ITBV show what the actual volume status is, whilst SVV and PPV reflect the volume responsiveness of the heart.

• For optimal control of volume therapy it is recommended to monitor simultaneously both the static preload parameters and the dynamic parameters of volume

responsiveness (F. Michard, Intensive Care Med 2003;29: 1396).

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62

Contractility is the degree of muscular power of the heart

Contractility parameters displayed by the PiCCO-Technology:

CFI = Cardiac Function Index

GEF = Global Ejection Fraction

dPmx = maximum rate of the increase in pressure

Contractility

kg


63

• is the CI divided by global enddiastolic volume index


CICFI =

GEDI


Contractility – Thermodilution parameters

64

V

SV

SV

CI

Preload

High Contractility

NormalContractility

Target AreaVolume Responders Volume Overload

LowContractility

VV

SV

V

V

VSV

SV

SV


is a parameter of both left and right ventricular contractility

has been validated successfully against echocardiographic measurement of contractility

mirrors the fraction of the preload volume which is ejected by the heart in one minute



65

• is calculated as 4 times the stroke volume divided by the global enddiastolic volume


4xSVGEF =

GEDV



66


is –like the CFI- a parameter of both left and right ventricular contractility

has been validated successfully against echocardiographic measurement of contractility

mirrors the fraction of the preload volume which is ejected by the heart during one beat



67

• maximum of pressure increase in the aorta (P/tmax)

• excellent correlation to the maximum pressure increase speed in the left ventricle

dPmx = maximum rate of the increase in arterial pressure


Contractility – Pulse contour parameter

68

• is calculated as the difference between MAP and CVP divided by CO

• as an afterload parameter it presents a further determinant of thecardiovascular situation

• is an important parameter for controlling volume and catecholamine therapies

(MAP – CVP) x 80SVR =

CO

Afterload

SVR = Systemic Vascular Resistance

MAP = Mean Arterial PressureCVP = Central Venous PressureCO = Cardiac Output80 = Correction Factor for Units


69

Afterload

SVR = Systemic Vascular Resistance


Flow (CO) =

Vasoconstriction: Flow (CO)

Vasodilation: Flow (CO)Pressure Resistance

Pressure the heart has to overcome to eject blood

If pressure is unchanged, cardiac output decreases when afterload increases

70

• The contractility parameters CFI and GEF are important parameters for assessing the global systolic function and supporting the early diagnosis of myocardial insufficiency

• dPmx from the pulse contour analysis gives specific information on the left ventricular contractility

• The Systemic Vascular Resistance SVR calculated from blood pressure and cardiac output provides an additional determinant of the cardiovascular

situation, and is an important parameter for controlling volume and catecholamine therapies

Summary and Key Points – contractility and afterload


71

Extravascular water content of the lung tissue

Pulmonary circulation

Left Heart

Right Heart

Lungs

The Extravascular Lung Water EVLW

EVLW = Extravascular Lung Water

Body circulation

71


72

The Extravascular Lung Water is the difference between the intrathoracic thermal volume and the intrathoracic blood volume.

It represents the amount of water in the lungs outside the blood vessels

Calculation of Extravascular Lung Water (EVLW)


ITTV

– ITBV

= EVLW

74

Böck, Lewis, In: Practical Applications of Fiberoptics in Critical Care Monitoring,Springer Verlag Berlin - Heidelberg - NewYork 1990, pp 129-139

High Extravascular Lung Water is not necessarily identified by blood gas analysis

EVLW as a quantifier of lung edema

PaO2 /FiO2

10

20

550

30

150 2500 450

ELWI (ml/kg)

050 350


75

40

Halperin et al, 1985, Chest 88: 649


Also, Chest X-ray is not able to quantify lung edema and is for a lot of patients difficult to judge, especially in critically ill patients in supine position.

r = 0.1p > 0.05

0

20

80

15-10-15 10

60

radiographic score

-80

-60

-40

-20 ELWI


76

EVLWI = 7 ml/kg

EVLWI = 8 ml/kgEVLWI = 14 ml/kg

EVLWI = 19 ml/kg

Extravascular lung water index

ELWInormal range:

3 – 7 ml/kg

Pulmonary ed

ema Normal range



77

ELWI (ml/kg)

> 21 n = 54

14 - 21 n = 100

7 - 14 n = 174

< 7 n = 45

Mortality(%)

10

00

n = 373*p = 0.002

20

30

40

50

60

70

80

Sturm, In: Practical Applications of Fiberoptics in Critical Care Monitoring, Springer Verlag Berlin - Heidelberg - NewYork 1990, pp 129-139

Relevance of EVLW Assessment

High Extravascular Lung Water is a predictor for mortality in intensive care patients

ELWI (ml/kg) 4 - 6

30

0

Mortality (%)

20

n = 81

40

50

60

70

80

6 - 8 8 - 10 10 - 12 12 - 16 16 - 20 > 20

90

100

Sakka et al , Chest 2002


78

Intensive Care days

Mitchell et al, Am Rev Resp Dis 145: 990-998, 1992

Volume management aimed at EVLW reduction can significantly reduce time on ventilation and ICU stay, when compared to PCWP oriented therapy

Ventilation Days

PAC Group

n = 101* p ≤ 0,05

PAC GroupEVLW Group EVLW Group22 days 15 days9 days 7 days

* p ≤ 0,05

Relevance of EVLW Assessment


79


PVPI = Pulmonary Vascular Permeability Index

• is the ratio of Extravascular Lung Water to Pulmonary Blood Volume

• is a measure of the permeability of the lung vessels and as such can classify the type of lung edema (hydrostatic vs. permeability caused)

EVLWPVPI =

PBV

Differentiating Lung Edema

80


PVPI = Pulmonary Vascular Permeability Index

Differentiating Lung Edema

Cardiogenic Lung OedemaIncreased hydrostatic pressure with normal permeability

Permeability Lung OedemaNormal hydrostatic pressure with increased permeability

Alveolus wallAlveolus wall

Capillary Capillary

PVPI normal (1-3) PVPI raised (>3)

81

Summary and key points - EVLW and PVPI

- is useful to differentiate and quantify lung edema

- for this purpose it is a unique parameter available at the bedside

- functions as a warning parameter for fluid overload

- is indexed to “predicted body weight” instead of actual body weight, allowing even better diagnosis

The Extravascular Lung Water EVLW

81


The Pulmonary Vascular Permeability Index PVPI- can differentiate between a hydrostatic and a permeability caused lung edema

82

PULSION monitoring philosophy: the hemodynamic triangle

The

hemodynamic triangleOptimization

of preload

Optimization of stroke volume

PiCCO allows the establishment of an adequate cardiac output through optimization of volume status whilst avoiding lung edema

Avoidance of lung edema


83

PiCCO2 - get the complete picture!

Cardiac output Arterial oxygen content

Stroke volume Heart rate OxygenationSaO2

HemoglobineHb

PreloadGEDI; SVV

AfterloadSVRI; MAP

ContractilityCFI

Pulmonary Edema

ELWI

Volume? Vasopressors? Inotropics? Blood transfusion?

Global oxygenationScvO2

Oxygen delivery Oxygen consumption

physiology of hemodynamics & picco parameters in detail

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