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 drugs
regulation of body temperature
immunologic and blood coagulation function
evacuation 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
SV
SV
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 Absorption
Lungs
Oxygen Transportation
Blood
Oxygen Delivery
Tissues
Oxygen Utilisation
Cells / 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 Output
Hb: Hemoglobin
SaO2: Arterial Oxygen Saturation
SvO2: Mixed Venous Oxygen Saturation
DO2: Oxygen Delivery
VO2: Oxygen Consumption
SaO2CO
Hb

18
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 Output
Hb: Hemoglobin
SvO2: Mixed Venous Oxygen Saturation
DO2: Oxygen Delivery
VO2: 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
CaO2: Arterial Oxygen Content

20
Ventilation
• Transfusion
• Ventilation
CO: Cardiac Output
Hb: Hemoglobin

21
Volume
Catecholamines
• 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 Absorption
Lungs
Oxygen Transport
Blood
Oxygen Delivery
Tissues
Oxygen Utilization
Cells / Mitochondria
Supply
SaO2 CO, Hb

23
Monitoring the CO, SaO2 and Hb is essential!
Oxygen Absorption
Lungs
Oxygen Delivery
Tissues
Oxygen Utilization
Oxygen Transport
Blood
Supply
Assessment of Oxygen Delivery
CO, HbSaO2

24
SvO2
SaO2 CO, Hb
Monitoring the CO, SaO2 and Hb is essential!
VO2 = CO x Hb x 1.34 x (SaO2 – SvO2)
Oxygen Utilization
Oxygen Absorption
Lungs
Oxygen Transport
Blood
Oxygen Delivery
Tissues
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!
Oxygen Utilization
Oxygen Absorption
Lungs
Oxygen Transport
Blood
Oxygen Delivery
Tissues
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 Oxygenation
SaO2
Hemoglobine
Hb
Preload
GEDI; SVV
Afterload
SVRI; MAP
Contractility
CFI
Pulmonary
Edema
ELWI
Volume? Vasopressors? Inotropics? Blood transfusion?
Global oxygenation
ScvO2
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!
Oxygen Utilization
Oxygen Absorption
Lungs
Oxygen Transport
Blood
Oxygen Delivery
Tissues
Supply
Consumption
The central venous oxygen saturation ScvO2

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 = 29
r = 0.866
ScvO2 = 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
60
50
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 therapy
Rivers E et al. New Engl J Med 2001;345:1368-77
O2-Insufflation and Sedation
Intubation + Ventilation
Central Venous Catheter
Invasive 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 mmHg
Vasopressors
Blood transfusion to
Hematocrit 30%
Monitoring the S(c)vO2 – Clinical relevance
< 70%
Goal achieved?
yes
ScVO2
Hospital 60 days
Lethality

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
SV
SV
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 heart
Right 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

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

48
Role of Volumetric Preload Parameters GEDV / ITBV
Preload
Filling Pressures
CVP / PCWP
Volume
Responsiveness
SVV / PPV
Volumetric
Preload parameters
GEDV / ITBV
48

49
Total volume of blood in all 4 heart chambers
Left heart
Right Heart
Pulmonary
Circulation
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 heart
Right heart
Pulmonary
Circulation
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
Volume Responsiveness
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
Preload
V
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

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).
61

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
CI
CFI =
GEDI
Contractility – Thermodilution parameters

64
V
SV
SV
CI
Preload
High Contractility
Normal
Contractility
Target AreaVolume Responders Volume Overload
Low
Contractility
V
V
SV
V
V
V
SV
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
4xSV
GEF =
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 the
cardiovascular situation
• is an important parameter for controlling volume and catecholamine
therapies
(MAP – CVP) x 80
SVR =
CO
Afterload
SVR = Systemic Vascular Resistance
MAP = Mean Arterial Pressure
CVP = Central Venous Pressure
CO = Cardiac Output
80 = 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)
0
50 350

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 = 0.1
p > 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/kg
EVLWI = 14 ml/kg
EVLWI = 19 ml/kg
Extravascular lung
water index
ELWI
normal range:
3 – 7 ml/kg
Pulmonary edema
Normalrange

77
ELWI (ml/kg)
> 21
n = 54
14 - 21
n = 100
7 - 14
n = 174
< 7
n = 45
Mortality(%)
10
0
0
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 Group
22 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)
EVLW
PVPI =
PBV
Differentiating Lung Edema

80
PVPI = Pulmonary Vascular Permeability Index
Differentiating Lung Edema
Cardiogenic Lung Oedema
Increased hydrostatic pressure
with normal permeability
Permeability Lung Oedema
Normal 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 triangle
Optimization
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 Oxygenation
SaO2
Hemoglobine
Hb
Preload
GEDI; SVV
Afterload
SVRI; MAP
Contractility
CFI
Pulmonary
Edema
ELWI
Volume? Vasopressors? Inotropics? Blood transfusion?
Global oxygenation
ScvO2
Oxygen delivery Oxygen consumption

Physiology of hemodynamics & PiCCO parameters in detail

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