Hemodynamic Monitoring in Critically Ill Patients

Hemodynamic
Monitoring :
The Simple Logic
Dita Aditianingsih MD
Friday, November 7, 14
Objectives
• Assessment of shock and tissue
hypoperfusion in the clinical settings
• Determine the appropriate hemodynamic
monitoring for diagnosis and assessment
• Interpret advanced haemodynamic data
appropriately for diagnosis and therapy in
the major types of circulatory dysfunction
Introduction
• Hemodynamic instability associated with signs of
inadequate organ or tissue perfusion, whatever
the cause, is called circulatory shock
• Patients who survive the initial phase of shock
may then develop the multiple organ dysfunction
syndrome (MODS), which is a major cause of late
death in the intensive care unit (ICU) due to
hemodynamic instability, reduced organ perfusion
and alterations in tissue microcirculation resulting
in tissue hypoxia
First hit
Severe response
Initial tissue
MODS
injury
Second hit
Persistent hemodynamic Reduced organ

instability perfusion
Tissue microcirculation Secondary

alterations infections
MODS
Exaggerated response
Resolution
First hit
Severe response
Initial tissue
MODS
injury
Second hit


MODS
Resolution
First hit
Severe response
Initial tissue
MODS
injury
Second hit


MODS
Resolution
First hit
Severe response
Initial tissue
MODS
injury
Second hit


MODS
Resolution
First hit
Severe response
Initial tissue
MODS
injury
Second hit


MODS
Resolution
First hit
Severe response
Initial tissue
MODS
injury
Second hit


MODS
Resolution
Hemodynamic monitoring approaches
• Initial steps:
• Clinical assessment
• Basic monitoring and assessment of global perfusion
• Preload monitoring and fluid responsiveness
• Advanced monitoring measures:
• Cardiac output monitoring
• Assessment of cardiac contractility
• Assessment of tissue perfusion
Clinical assesment
• The fastest and least invasive
• Thirst, tachypnoea, tachycardia, confusion, altered
skin perfusion (cold extremities, poor peripheral
pulses, impaired capillary refill) and oliguria can be
signs of hypoperfusion
• Ischemic chest pain is indicating an imbalance
between myocardial oxygen supply and demand
• Bradycardia or tachycardia may be an underlying
cause of low cardiac output
Basic monitoring and
assessment of global
perfusion
• All critically ill patients should have
electrocardiographic (ECG), arterial blood pressure
(AP), pulse oximetry (SpO ) monitoring, preload,
2
Cardiac Output, and baseline serum lactate as an

assessment of global perfusion
Hemodynamic Monitoring in Critically
Illness (Shock)
• Macrocirculation :
• Basic monitoring : electrocardiographic (ECG), arterial blood pressure

(AP), pulse oximetry (SpO2), end-tidal CO2
• Advance monitoring :
• Preload and fluid responsiveness
• Static measure of preload : CVP
• Dynamic measures of preload : predicting fluid responsiveness
• Volumetric parameters : Extravascular lung water (EVLW)
• Cardiac output monitoring
• Microcirculation :
• Global and regional
Balance Goal Directed
Goal of Resuscitation
Therapy
needs end-point O2 delivery Approach
“Upstream” endpoints
Hemodynamic Parameter:
of resuscitation Preload (CVP, PCWP) DO2 Parameter:
Macrodynamic Afterload (MAP, SVR)
Contractility (SV)
PaO2
Hemoglobin
Heart Rate (BPM)
Monitoring Stroke Index (HR/SBP)

Coronary Perfusion Pressure
Cardiac Output
Microcirculation
Microdynamic
PslCO2
Monitoring SvO2
CELL (a-v)CO2
“Downstream” marker of Lactate
the effectiveness of
resuscitation Base Mediators
Deficit pHi
Therapy
Contractility (SV)
PaO2
Hemoglobin
Heart Rate (BPM)

Cardiac Output
Microcirculation
Microdynamic
PslCO2
Monitoring SvO2
CELL (a-v)CO2
Deficit pHi
Therapy
Contractility (SV)
PaO2
Hemoglobin
Heart Rate (BPM)

Cardiac Output
Microcirculation
Microdynamic
PslCO2
Monitoring SvO2
CELL (a-v)CO2
Deficit pHi
Therapy
Contractility (SV)
PaO2
Hemoglobin
Heart Rate (BPM)

Cardiac Output
Microcirculation
Microdynamic
PslCO2
Monitoring SvO2
CELL (a-v)CO2
Deficit pHi
Factors that affecting the haemodynamic conditions
Intravascular volume
Myocardial
contraction and
heart rate
Myocardial
contraction and
heart rate
Myocardial
contraction and
heart rate
Vasoactivity
ECG monitoring
• Cardiac output = Stroke volume x Heart rate
• Heart rate is an important determinant of cardiac output.
• Tachyarrhythmias are the most common finding in hypoperfusion states
Blood pressure monitoring
• Arterial blood pressure (AP) is a cornerstone of
haemodynamic assessment, it is an approximation of organ
perfusion pressure,
• Mean arterial pressure (MAP) is the parameter measured

during shock
• DP = Diastolic Pressure MAP = [(2DP+SP)] / 3

• SP = Systolic Pressure
• It can be measured non-invasively with a cuff placed around

a limb and attached to a sphygmomanometer or an
oscillometric device, or invasively using an indwelling
catheter in an artery
Mean Arterial Pressure and Autoregulation
MAP
• Within the autoregulatory range of blood pressure for a tissue or organ, perfusion can
be held relatively constant, and when outside this range, autoregulation fails and
perfusion becomes a function of mean arterial pressure.
• There is no “normal” MAP, it is relative to each patient and exists when organs are
adequately perfused
• For example: patients with chronic hypertension may need higher MAPs
Manual Blood Pressure Monitoring
• Manual blood pressure cuffs are the

standard method to assess
perfusion pressure or Mean Arterial
Pressure
• There are problems with using manual
blood pressure cuffs:
• It takes time to perform and is labor
intensive
• During shock, MAP assessments are needed
every few minutes and sometimes every
minute when patients are unstable
Automated Blood Pressure Monitoring
• Automated BP cuffs, a computer activates,

controls, and records the MAP
• The advantages of automated cuffs are:
• It is a non-invasive monitor and calculates the
MAP
• It is easy to apply to and perform on patients
• It automatically produces multiple pressure
readings
• The disadvantages of automated cuffs are:
• It overestimates the MAP in low-flow states
• Results can be inaccurate if cuff is improperly
applied
• Ambient noise makes measurement inaccurate
• It is not provide continuous measurements
Invasive Blood Pressure
• Invasive arterial lines are catheters
placed in arteries to directly
measure the MAP
• The advantages of an arterial line
are:
• It provides continuous blood
pressure measurements
• It provides immediate access to
arterial blood for lab draws and
measures the partial pressure of
oxygen
• It allows for hemodynamic
assessments, such as pulse
pressure variation; to be
discussed later.
Arterial pressure tracing
The systolic pressure variation (SPV) is the

difference between the maximum and the
minimum systolic blood pressures during one
ventilatory cycle (A). The SPV is the sum of the
ΔDown (B) and the ΔUp (C).
Perel A, Pizov R, Cotev S: Systolic blood pressure variation is a sensitive indicator of hypovolemia in ventilated dogs subjected to graded hemorrhage. Anesthesiology 1987;67:498
Indications for invasive
arterial pressure monitoring
• Unstable blood pressure or anticipation of unstable
blood pressure (hypo/hypertension)
• Use of rapidly acting vasoactive drugs; vasodilators,
vasopressors, inotropes
• Frequent sampling of arterial blood.
• Presence of an intra-aortic balloon pump
• Patients with unreliable, or difficult to obtain, non-
invasive BP
Contraindications to invasive
arterial pressure monitoring
• Anticipation of thrombolytic therapy
• Severe peripheral vascular disease preventing
catheter insertion
• Vascular anomalies – AV fistula, local
aneurysm, local haematoma, Raynaud’s disease
• Lack of collateral blood flow distally (e.g.
radial artery previously used for coronary
artery bypass surgery) →Allen test
• The disadvantages of an arterial line are:

• It requires an invasive catheter
• It may be uncomfortable and painful
• It must be placed under sterile conditions and may be time
consuming to place
• Several complication may occur
• The potential complications of

arterial lines include:
• Thrombosis of artery
• Distal ischemia of extremity
• Local bleeding and hematoma
• Local and systemic infections
Allen Test
• Potential insertion sites:
• Radial artery (most common)
• Femoral artery
• Axillary artery
• Dorsalis pedis artery
• The artery can be identified with:
• Palpation method
• Ultrasound for localization and guidance during placement
Diagnosing shock using Blood
Pressure
• Shock is hypotension
• Systolic pressure less than 90 mmHg
• Mean Arterial Pressure less than 70 mmHg
• Arterial pressure decrease more than 40 mmHg from baseline
• Mean Arterial Pressure
• Should be used to titrate vasoactive infusions and other
resuscitative therapies in shock.
• Results: Patients with nonhypotensive shock were more likely to have an
anterior wall myocardial infarction (71% versus 53%, P = 0.03). Both
groups of patients had similar rates of treatment with thrombolytic
therapy, angioplasty, and bypass surgery.
• Patients with nonhypotensive shock had an in-hospital mortality rate of

43% as compared with a rate of 66% among patients who had classic
cardiogenic shock with hypotension (P = 0.001).
• Mortality among 76 patients who presented with a systolic blood

pressure <90 mm Hg but no hypoperfusion was 26%.
• Conclusions: Even in the presence of normal blood pressure, clinical signs

of peripheral hypoperfusion, which may be subtle, are associated with a
substantial risk of in-hospital death following acute myocardial infarction.
Compensatory mechanism
Percentage blood loss 30% 50%

• Arterial blood pressure = Cardiac output x Systemic vascular resistance
• When stroke volume falls, MAP can be maintained by increasing heart rate or systemic
vascular resistance
• Tissue hypoperfusion may exist in the presence of reduced, normal or elevated blood pressure
Effect blood volume loss on CVP, blood presure and heart rate

vascular resistance
CVP

vascular resistance
Blood pressure
CVP

vascular resistance
Heart rate
Blood pressure
CVP

vascular resistance
Compensatory mechanisms Heart rate
Blood pressure
CVP

vascular resistance
Case
• A 70-year-old male presented with an exacerbation of COPD.

Non-invasive AP measured in the right arm was 70/40 mmHg.
Invasively-measured AP (same side) recorded similar pressure.
• A central venous catheter was inserted and noradrenaline

(norepinephrine) infusion commenced. A nursing shift change
occurred and noninvasive AP was measured from the left arm;
recorded at 160/80 mmHg. The patient was weaned off the
noradrenaline infusion.
• He had right subclavian artery stenosis secondary to peripheral

vascular disease.
• Routinely measure AP in both arms on admission to the ICU,

especially if there is discordance between clinical assessment
and AP. If there is a difference consider peripheral vascular
disease, aortic dissection or congenital heart disease
Continuous SpO2
monitoring
• It enables almost immediate detection of even a

small reduction in arterial oxygen saturation, which
is an integral part of oxygen delivery.
• However, based on the sigmoid shape of the
dissociation curve there is a time delay of the
detection of acute oxygenation failure, SpO should
2
be maintained 92%-95% in most critically ill patients.

• The SpO2 signal is often inaccurate in the presence
of altered skin perfusion. The inability to measure
SpO is an indicator of abnormal peripheral perfusion
2
End-tidal CO2
• Patient exhaled CO2, normal range is 35-45 mmHg
• Capnography refers to the graphic waveform displayedbshowing the

levels of CO2 during the various phase of respiration
End-tidal CO2
• An ETCO2 waveform corresponding to administered

ventilations is considered to be a definitive sign of a
proper ETT placement
• A low level of ETCO2 may indicate low cardiac output,

and sudden decrease in ETCO2 is earlier signal of
decrease blood pressure before the blood pressure
monitoring
• CPR a sudden increasing ETCO2 >20 mmHg is a strong

indicator of effective compression and a sign of ROSC
(regained pulse)
• Persistent ETCO2 <20 mmHg is a sign of poor perfusion

and poor outcome
End-tidal CO2
C.L. Hunter et al. American Journal of Emergency Medicine 32 (2014)

160–165
End-tidal CO2
C.L. Hunter et al. American Journal of Emergency Medicine 32 (2014) 160–165
Optimizing the
Cardiac Output
How oxygen is delivered to tissues
Oxygen Delivery
Cardiac Output - Index (CO-I) x Arterial Oxygen Content - Index
(CaO2-I)
Cardiac Output - Index (CO-I)

Arterial Oxygen Content (CaO
Stroke Volume - Index (SV-I) x Heart
(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)
Stroke Volume SV-I Heart Rate Hemoglobin SaO2 PaO2
Preload Afterload Contractility ELWI, PVPI
GEDI, CVP, SVRI, PVRI EF, Tapse

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Oxygen Delivery
(CaO2-I)

(1.38 x Hb X SaO2) + (PaO2 x 0.0031)
Rate (HR)

PAOP CPI
SVV/PPV/
PVI
PLR, EEO,
Mini Fluid
test
Relative effects of changes in PaO2, haemoglobin (Hb),
and cardiac output (Qt) on oxygen delivery (DO2)
Increasing CO is
the most efficient to
increase DO2
Leach RM, Treacher DF. The pulmonary physician in critical care: Oxygen delivery and consumption in the critically ill. Thorax 2002;57:170–177
Cardiac Output monitoring is
important in critically ill patients
SYSTEMIC VASCULAR RESISTANCE
• SWAN GAN
• ECHO
CONTRACTILITY • PICCO
• CO Cardiac
SVR
• ECHO
• PICCO
Contractility Output
• LIDCO
PRELOAD
• CVP
Preload • WEDGE
• JUGULAR PRESSURE
• SWAN GAN
• ECHO
• CO Cardiac
SVR
• ECHO
• PICCO
• LIDCO
PRELOAD
• CVP
Preload • WEDGE
• SWAN GAN
• ECHO
• CO Cardiac
SVR
• ECHO
• PICCO
• LIDCO
PRELOAD
• CVP
Preload • WEDGE
Optimizing Cardiac Output is the Key

Preload and fluid
responsiveness
• In the present of hypotension, an important

step is the assessment of preload and fluid
responsiveness
• Preload is defined as the volume present at
the end of diastole before contraction of
the ventricle has started and as end-
diastolic stretch wall tension
Right
Atrium
Right
Atrium
Right
Atrium
Right
ventricle
Right
Atrium
Right
ventricle
Pulmonal artery
Right
Atrium
Right
ventricle
Pulmonal artery
Right
Atrium
Right
ventricle
Lung
Pulmonal artery
Right
Atrium
Right
ventricle
Lung
Pulmonal artery
Pulmonal
vein
Right
Atrium
Right
ventricle
Lung
Pulmonal artery
Pulmonal
vein
Right
Atrium
Right
ventricle
Lung
Pulmonal artery
Left atrium Pulmonal
vein
Right
Atrium
Right
ventricle
Lung
Pulmonal artery
vein
Right
Atrium
Right
ventricle
Lung
Pulmonal artery
vein
Right
Atrium Left
ventricle
Right
ventricle
Lung
Pulmonal artery
vein
Right
Atrium Left
ventricle
Right
ventricle
Lung
rt a
o A
Pulmonal artery
vein
Right
Atrium Left
ventricle
Right
ventricle
Lung
rt a
o A
Pulmonal artery
vein
Right
Atrium Left
ventricle
Right
ventricle
Lung
rt a
o A
Pulmonal artery
vein
Right
Atrium Left
ventricle
Right
ventricle
Lung
rt a
o A
Pulmonal artery
vein
Right Systemic
Atrium Left
ventricle Vascular
Resistance =
Afterload
Right
ventricle
Stroke Volume x HR = CO
Lung
rt a
o A
Pulmonal artery
vein
Right Systemic
Atrium Left
ventricle Vascular
Resistance =
Afterload
Right
ventricle
organ
RVEDV ➡ LVEDV ➡ PRELOAD ➡ SV (Stroke Volume) ➡CO
Preload and fluid responsiveness
• Preload may be separated into right ventricular (RV) and left ventricular
(LV) preload.
• As static measures jugular venous pressure (JVP) and CVP are used as
surrogate estimates of RV preload and Pulmonary Artery Occlusion
Pressure (PAOP using pulmonary artery catheter) is used as a surrogate
estimate of LV preload
• Dynamic measures such as SVV-PPV are more accurate than static

measurements for assessing fluid responsiveness in mechanically
ventilated patients to assess will the cardiac output increase with fluid
administration
• The principle behind dynamic measures is that swings in intrathoracic

pressure, imposed by mechanical ventilation, affect venous return and as
a consequence cardiac output
Frank-Starling Curve and Preload-Fluid Responsiveness
Stroke
Volume
Preload
Stroke
Volume
Every increasing preload by volume loading or Passive Leg raising
Preload
Will increase the stroke volume
Stroke
Volume
Preload
Stroke
Volume
Preload
Stroke
Volume
Preload-dependence =
Fluid Responsive
Increase in preload results in stroke volume increase
Preload
rt
pa
Stroke p
ee
Volume
St
Fluid Responsive
Preload
Preload-Independence =
Fluid Unresponsive
rt
pa
Increase in preload results in minimal change in
stroke volume and will leads to lung edema/
Stroke p overloads
ee
Volume
St
Fluid Responsive
Preload
p a rt
F lat
Fluid Unresponsive
rt
pa
stroke volume and will leads to lung edema/
Stroke p overloads
ee
Volume
St
Fluid Responsive
Preload
Static and Dynamic Measure of Preload
Preload
Static Dynamic
Pressure Volume Continue

CVP (central GEDV (Global end- PPV (pulse pressure
venous pressure) diastolic volume) variation) using PiCCO,
using CV catheter using transpulmonary LiDCO Mostcare
PAOP (pulmonary thermodilution SVV (stroke volume
artery occlusion tehnique with PiCCO, variation)
pressure) using PA Volume View using PiCCO, LiDCO,
catheter LVEDV (Left Flotrac/Vigileo,
ventricular end- Mostcare, Oesophageal
diastolic volume) Doppler Echo-doppler
using
echocardiography Intermittent
ELWI (extravascular IVC (inferior vena cava)
lung water) using colapsibility/
PiCCO, Volume View, distensibility index
LiDCO using ultrasound
Preload
Static Dynamic

using
Preload
Static Dynamic

using
Preload
Static Dynamic

using
Preload
Static Dynamic

using
Static measures of preload: Central venous pressure
CVC position in
superior • Central venous pressure (CVP) is
vena cavae considered a method of assessing right
atrial pressure (RAP) directly by placing
a catheter in the superior vena cava
• Traditionally, CVP has been used to

guide fluid management, but it is a poor
predictor of fluid responsiveness and
may not accurately reflect preload: due
to the changes in venous tone,
intrathoracic pressures, LV and RV
compliance, and geometry that occur in
critically ill patients
• There is a poor relationship between the CVP and RV end-diastolic volume
• CVP is at best to guide preload with greater emphasis on dynamic values (monitoring
trends in CVP over time) rather than single measurements
Static measures of preload: Central venous pressure
CVC position in
superior • Central venous pressure (CVP) is
vena cavae considered a method of assessing right
atrial pressure (RAP) directly by placing
a catheter in the superior vena cava
• Traditionally, CVP has been used to

guide fluid management, but it is a poor
predictor of fluid responsiveness and
may not accurately reflect preload: due
to the changes in venous tone,
intrathoracic pressures, LV and RV
compliance, and geometry that occur in
critically ill patients
• There is a poor relationship between the CVP and RV end-diastolic volume
• CVP is at best to guide preload with greater emphasis on dynamic values (monitoring
trends in CVP over time) rather than single measurements
Central venous catheter
• Indications for insertion of central venous • Relative contraindications to insertion

catheter of a central venous catheter:
• Measurement of central venous pressure • Severe coagulopathy or anticipation

of need for thrombolysis
• Infusion of vasoactive drugs, hyperosmolar
fluids (parenteral nutrition), antibiotics
(vancomycin)
• Obvious infection of overlying skin
• Thrombosis of superior vena cava

• Inability to obtain peripheral intravenous or subclavian vein.
access
• Transvenous pacing.
Distal Tip:
Largest lumen so used for
blood admisnistration


(vancomycin)

access
Distal Tip:
Medial Exit Opening:

Safest location so used for
TPN


(vancomycin)

access
Distal Tip:

TPN
Proximal Exit Opening:
Least contamination from other
infusing solutions so used for
withdrawing blood samples


(vancomycin)

access
Central venous catheter All lumen can be used for
administration of IV
Distal Tip: solutions and medication.

TPN
Proximal Exit Opening:
Least contamination from other
infusing solutions so used for
withdrawing blood samples


(vancomycin)

access
Morphology trace of CVP
The classic ‘a, c, v’ pattern may
not always be obvious
a wave= atrial contraction

c wave= right ventricular contraction
v wave= passive atrial filling
Giant V wave: this occurs with severe

tricuspid regurgitation, due to
retrograde blood flow into the right
atrium during ventricular systole
Fluid Challange Using CVP
Guided by CVP (cmH2O) PAOP (mmHg) Infusion
Start <8 <10 200 ml/10 mnt
<12 <14 100 ml/10 mnt
12 14 50 ml/mnt
During infusion ↑>5 ↑>7 Stop
After 10 min 2 3 Continue
2>↑ = 5 3>↑=7 Wait 10 min
↑>5 ↑>7 Stop
After waiting 10 min Still ↑>2 Still ↑>3 Stop
↑ =2 ↑ =3 Repeat
10 cm H20 = 7.3 mm Hg. CVP, central venous pressure; PAOP, pulmonary artery occlusion pressure
Observe response to fluid therapy, a marked rise in CVP with fluid challenge indicates a failing
ventricle (e.g. volume overload, right ventricular failure, cor pulmonale, congestive cardiac failure,
cardiac tamponade, tension pneumothorax)
Other interventions may rise CVP value such as vasopressor dose change or altering patient position
Weil MH, Henning RJ: New concepts in the diagnosis and fluid treatment of circulatory shock. Anesth Analg 1979;S8:124
Fluid Challange Using CVP
Guided by CVP (cmH2O) PAOP (mmHg) Infusion
Start <8 <10 200 ml/10 mnt
<12 <14 100 ml/10 mnt
12 14 50 ml/mnt
During infusion ↑>5 ↑>7 Stop
After 10 min 2 3 Continue
2>↑ = 5 3>↑=7 Wait 10 min
↑>5 ↑>7 Stop
After waiting 10 min Still ↑>2 Still ↑>3 Stop
↑ =2 ↑ =3 Repeat
10 cm H20 = 7.3 mm Hg. CVP, central venous pressure; PAOP, pulmonary artery occlusion pressure
Observe response to fluid therapy, a marked rise in CVP with fluid challenge indicates a failing
ventricle (e.g. volume overload, right ventricular failure, cor pulmonale, congestive cardiac failure,
cardiac tamponade, tension pneumothorax)
Other interventions may rise CVP value such as vasopressor dose change or altering patient position
Weil MH, Henning RJ: New concepts in the diagnosis and fluid treatment of circulatory shock. Anesth Analg 1979;S8:124
Systemic venoconstriction
Obstruction of
the great veins
Obstruction of
the great veins
Obstruction of
the great veins
Obstruction of
the great veins
Decrease
right
ventricular
compliance
Obstruction of
the great veins
Decrease
right
ventricular
compliance
Obstruction of
the great veins
Decrease
right
ventricular
compliance
Obstruction of
the great veins
Decrease
right
ventricular
compliance
Tricuspid regurgitation
Obstruction of
the great veins
Decrease
right
ventricular
compliance
Obstruction of
the great veins
Decrease
right
ventricular
compliance
Obstruction of
the great veins
Mechanical
ventilation
Decrease
right
ventricular
compliance
Pulmonary Arterial Catheter (Swan-Ganz Catheter
was introduced in 1970
Dr. William Ganz, a cardiologist,

1919-2009
The first time of Cardiac

Output was meassured using
Pulmonary
Thermodilution
technique
Pulmonary arterial catheter
http://www.lcs.mgh.harvard.edu/projects/pacath.html
http://www.thoracic.org
ventricular ectopic beat Dicrotic notch
http://www.lcs.mgh.harvard.edu/projects/pacath.html
http://www.thoracic.org
Position of the PAC
• A chest radiograph should be taken to confirm the position of the PAC (without any loops) and to rule out a pneumothorax. The catheter tip should
not extend beyond the pulmonary hilum as in the first chest X-ray (CXR 1) below. In CXR 2, the PAC was considered to be too distal and was
withdrawn a few centimetres even though a PAP waveform was transduced
• West’s lung zones are a theoretical concept based on the fact that gravity influences blood flow within the lungs; pulmonary blood flow and vascular
pressures increase progressively down the lung
• Zone 1
• In a supine patient this is directly underneath the anterior sternum. In an erect patient Zone 1 corresponds to the lung apex. In this zone, alveolar
pressure exceeds pulmonary artery and pulmonary venous pressure. Thus, a catheter wedged in this location would record alveolar pressure instead
of reflecting left atrial pressure as the pulmonary veins would be completely collapsed.
• Zone 2
• It lies directly underneath Zone 1. In this zone, alveolar pressure exceeds pulmonary artery diastolic pressure and pulmonary venous pressure. A
catheter wedged in this position would record alveolar pressure, again because pulmonary veins would be collapsed
Position of the PAC
• Zone 3
• This is the most dependent portion of the lung in the supine or erect position. The pulmonary artery systolic and diastolic pressures
and pulmonary venous pressures are always greater than alveolar pressures in this zone. The pulmonary vessels do not collapse and a
catheter wedged in this position accurately measures PAOP.
• a checklist for verifying position of PAC in Zone 3.
• PAD >PAOP, catheter tip location below the level of the left atrium on a portable lateral chest X-ray, A and V waves visible within trace
(cardiac ripple), change in PAOP less than half the change in PEEP during a PEEP trial.
• Shock of all types
• Assessment of cardiovascular function and

response to therapy
• Assessment of pulmonary status
• Assessment of fluid requirement
• Perioperative monitoring
PAC can generate large numbers of haemodynamic variables
• Central venous pressure (CVP) and Pulmonary arterial occlusion pressure (PAOP)
• Cardiac output / cardiac index (CO / CI) and Oxygen delivery / uptake (DO2 / VO2)
• Stroke volume (SV)
• R ventricle ejection fraction/ end diastolic volume (RVEF / RVEDV)
• Systemic vascular resistance index (SVRI) and Pulmonary vascular resistance index
(PVRI)
• Sampling site for SvO2
Area under curve is
inversely proportion
to rate of blood flow
in PA ( = CO)
Static Indexes Of Preload Using
(Filling Pressure)
(Filling Pressure)
(Filling Pressure)
Hypovolemia
• Low CVP/PAOP
• Low CI
• High SVRI
Consider fluid
challenge
(Filling Pressure)
Hypovolemia Cardiogenic
• Low CVP/PAOP • High CVP/PAOP
• Low CI • Low CI
• High SVRI • High SVRI
Consider fluid Consider

challenge inotopic / IABP
(Filling Pressure)
Hypovolemia Cardiogenic Vasogenic

• Low CVP/PAOP • High CVP/PAOP • Low CVP/PAOP
• Low CI • Low CI • High CI
• High SVRI • High SVRI • Low SVRI
Consider fluid Consider Consider

challenge inotopic / IABP vasopressor
• Disadvantages
• Costly
• Invasive
• Multiple complications (eg arrhythmia, catheter

looping, balloon rupture, PA injury, pulmonary
infarction etc)
• Mortality not reduced and can be even higher
Crit Care Med 2003;31: 2734-2741

JAMA 1996;276 889-897
CVP PAOP
Role of the Filling Presures
from CVP / PCWP
1. The filling pressures CVP and PCWP do not

give an adequate assessment of cardiac
preload.
2. The PCWP is, in this regard, not superior to
CVP
3. Pressure is not volume, Right is not Left

(ARDS Network, N Engl J Med 2006;354:2564-75).

Potential CAUSES FOR ERROR IN
FILLING PRESSURE MEASUREMENT
Reliability Of Central Venous Pressure to
Assess Blood Volume in Critically Ill Patients
Low Blood Volume

High CVP
High Blood Volume

Low CVP
1500 simultaneous measurements of blood volume and CVP in 188 ICU patients
Correlation CVP - Blood volume r=0.27, Correlation ∆ CVP - Blood volume r2=0.01
Shippy CR and Shoemaker WC - Crit Care Med 1984
Cardiac filling pressure are not appropriate to
predict hemodynamic response to volume loading
Design: Retrospective study.; Setting: A 24-bed medical intensive care unit.
Patients:: All consecutive 96 mechanically ventilated septic.
Patients monitored with PAC who underwent a volume challenge between 2001 and 2004.
Responders = Increase in Cardiac Index of 15%
Osman D et al. Crit Care Med - 2007

Cardiac filling pressure are not appropriate to
predict hemodynamic response to volume loading
Design: Retrospective study.; Setting: A 24-bed medical intensive care unit.
Patients:: All consecutive 96 mechanically ventilated septic.
Patients monitored with PAC who underwent a volume challenge between 2001 and 2004.
Responders = Increase in Cardiac Index of 15%
Osman D et al. Crit Care Med - 2007

WHAT IS THERMODILUTION?
Transpulmonary thermodilution measurement simply requires the
central venous injection of a cold (< 8°C) or room-tempered (<
24°C) saline bolus…
CV Bolus
Injection
Lungs
Right Left Heart
Heart
PiCCO Catheter
e.g. in femoral artery
(thermosensor)
Sites of injection and temperature
measurement : PAC vs piCCO
Pulmonary Thermodilution (Pulmonary artery catheter PAC)
Single measurement of CO:
• The intermittent thermodilution technique. use

bolus of saline at room temperature is injected
into the right atrium via a port in the PAC and
mixes with body temperature blood in the
circulation.
• The change in temperature of blood in the

pulmonary artery is measured using a
thermistor at the tip of the PAC. and the
temperature drop over time is used to
calculate CO.
Continuous CO:
• A thermal filament that warms blood in the superior vena cava (SVC), and the change in blood
temperature at the PAC tip is measured and provides a continuous measurement of CO
• The displayed value represents an average of values over the previous 60–120 seconds, rather than a
‘beat-to-beat’ or ‘minute-to-minute’ measurement, and has a STAT mode that allows inspection of the
thermodilution curve.
Transpulmonary Thermodilution
1. Central venous line (CV)
2. Thermodilution catheter with lumen for CV

arterial pressure measurement
Axillary (A)
Brachial (B)
Femoral (F)
Radial (R), long catheter
A
3. Arterial pressure transducer B
Single measurement of CO:
• Ice cold fluid is injected into the central line and R

the change in temperature measured
downstream to calculate CO., and are referred
to as ‘transpulmonary’. F
• This single measurement is used to calibrate

the device and is recommended on set-up,
every eight hours and in periods of
haemodynamic instability or after adjustment
of vasopressor infusion rates.
Continuous CO: is derived by analysing the arterial

pressure waveform
DETERMINATION OF CARDIAC OUTPUT USING
THE STEWART HAMILTON EQUATION
After central venous injection of the indicator, the thermistor in the tip of the arterial
catheter measures the downstream temperature changes
The cardiac output is calculated by analysis of the thermodilution curve using a

modified Stewart-Hamilton algorithm:
-Tb Injection
DETERMINATION OF CARDIAC OUTPUT
USING THE STEWART HAMILTON EQUATION
-Tb Injection
t
Tb
injection
recirculation
ln Tb
e -1
time of injection
At DSt
MTt t
mean transit time down slope time
Thermodilution Curve
LiDCO
The change in concentration of

indicator over time produces an
indicator dilution curve
The temperature–time curves for

the PAC and PiCCO/VolumeView
will look slightly different because
of the different sites where the
change in temperature is
measured
(pulmonary artery for PAC;
femoral artery for PiCCO/
VolumeView)
Volumetric Parameters Measured by Thermodilution
ITBV ELWI GEDV
Global End Diastolic Volume (GEDV) is the volume of blood

contained in the 4 chambers of the heart
Intrathoracic Blood Volume (ITBV) is the volume of the 4 chambers of

the heart + the blood volume in the pulmonary vessels.
Extravascular Lung Water (EVLW) is the amount of water content in the

lungs. It allows bedside quantification of the degree of pulmonary edema.









Static Volumetric Parameters as
Preload-Fluid Responsiveness
Stroke p a rt Normal
F lat
Volume hearts
rt
Fluid Unresponsive
pa
p stroke volume and will leads to lung edema/

ee
overloads
St
Failing
hearts
Fluid Responsive
Increase in preload results in stroke
volume increase
ITBV GEDV ELWI Preload

Normal values of
volumetric parameters
Continuous CO and Dynamic Parameters measurement :
arterial pressure waveform
PiCCO analyses the systolic portion

of the arterial waveform.
LiDCO analyses the waveform with
what is called pulse power analysis.
Flotrac/Vigileo analyses the
waveform 100 times/second over 20
seconds, capturing 2000 data points
for analysis
Dynamic measures of preload: predicting fluid responsiveness
Dynamic preload measures are based on the ‘normal’ physiological effects of
positive pressure ventilation on the right and left sides of the heart
PPV SVV IVC
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
preload︎ LV stroke
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
Pleural ➡︎ RV blood ➡︎ LV ➡︎ LV stroke
pulmonary
pressure ︎ stroke preload︎ volume
transit time
volume
➡︎ RV preload︎
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
PP-SV max
Pulse pressure/
Stroke volume
MAXIMUM at the
end of inspiration
LV
volume︎
Transpulmonary
pressure ︎
➡LV
afterload︎
︎ RV
afterload︎
pulmonary
transit time
volume
Reduced RV
filling
PP-SV min
Empty
Pulse pressure/
Pulmonary
Stroke volume
Venous System
MINIMUM at the end
of expiration
Stroke Volume Variation (SVV)
In mechanically ventilated patients without arrhythmia,
1. SVV reflects the sensitivity of the heart to the cyclic changes in cardiac preload induced by
mechanical ventilation
2. SVV can predict whether stroke volume will increase with volume expansion
Mechanical
Breath
Inspiration Expiration
Arterial Wave
Mechanical
Breath
SVMax
Arterial Wave
Mechanical
Breath
SVV = (SV max – SV min) / SV mean

SVMax
SVMin
Arterial Wave
Mechanical
Breath
Interpretation of Stroke Volume Variation
SVV > 10-13%
SVV < 10-13%
Large SVV
SVV > 10-13%
Hypovolemia, need volume loading
SVV < 10-13%
Large SVV
SVV > 10-13%
Hypovolemia, need volume loading
Low SVV
SVV < 10-13%
Normovolemia, no more fluid, need

vasoactive
Pulse Pressure Variation
1. PPV reflects the sensitivity of the heart to the cyclic changes in cardiac preload induced
by mechanical ventilation
2. PPV can predict whether stroke volume will increase with volume expansion
120 PPmax - PPmin

Arterial Pressure
mmHg PPmax ∆PP =

(PPmax + PPmin)/2
PPmin
60
mmHg time
2 sec
Michard F, et al. Am J Respir Crit Care Med. 2000;162(1):134-138.
120 PPmax - PPmin

Arterial Pressure
mmHg PPmax ∆PP =

(PPmax + PPmin)/2
PPmin
60
mmHg time
2 sec
120 PPmax - PPmin

Arterial Pressure
mmHg PPmax ∆PP =

(PPmax + PPmin)/2
PPmin
Arterial Wave
60
mmHg time
2 sec
120 PPmax - PPmin

Arterial Pressure
mmHg PPmax ∆PP =

(PPmax + PPmin)/2
Mechanical
Breath
PPmin
Arterial Wave
60
mmHg time
2 sec
PPV > 10-13%
PPV < 10-13%
Large PPV
PPV > 10-13%
Hypovolemia, need volume

loading
Low PPV
PPV < 10-13%
Normovolemia, no more fluid,

need vasoactive
Dynamic Parameters as
Stroke
Volume
SVV/PPV
8%
SVV/PPV
13%
Preload
Stroke
Volume
SVV/PPV
8%
SVV/PPV
13%
Preload
Stroke
Volume
SVV/PPV
8%
SVV/PPV
13%
Preload
Stroke
Volume Normal hearts
SVV/PPV
8%
SVV/PPV
13%
Preload
Stroke
SVV/PPV
8%
SVV/PPV
13% Preload-dependence =
Fluid Responsive
Increase in preload by fluid loading
results in stroke volume increase
Preload
Stroke
SVV/PPV
8%
rt
pa
p
ee
St
SVV/PPV
Fluid Responsive
Preload
Stroke
SVV/PPV
8% Preload-Independence =
rt Fluid Unresponsive
Increase in preload results in minimal
pa
change in stroke volume and will leads to
lung edema/overloads, need vasoactives
p
ee
St
SVV/PPV
Fluid Responsive
Preload
Stroke
p a rt
Volume F lat Normal hearts
SVV/PPV
pa
p
ee
St
SVV/PPV
Fluid Responsive
Preload
Stroke
p a rt
SVV/PPV Failing hearts
pa
p
ee
St
SVV/PPV
Fluid Responsive
Preload
Stroke
p a rt
pa
p
ee
St
SVV/PPV
Fluid Responsive
Preload
Stroke
p a rt
pa
p
ee
St
SVV/PPV
Fluid Responsive
Preload
Interpretation of Stroke Volume Variation -
Normal heart
Stroke Volume
SVV/PPV Line of reference
10-13%
Preload LVEDV (mL)
Normal heart
Stroke Volume
10-13%
PPV-SVV
25 %
Preload LVEDV (mL)
Normal heart
Stroke Volume
10-13%
15 %
PPV-SVV
25 %
Preload LVEDV (mL)
Normal heart
Stroke Volume
9%
10-13%
15 %
PPV-SVV
25 %
Preload LVEDV (mL)
Normal heart
Stroke Volume
PPV-SVV
PPV-SVV 5%
9%
SVV/PPV Line of reference Preload-Independence =
10-13% Fluid Unresponsive
PPV-SVV change in stroke volume and will leads to
15 % lung edema/overloads, need vasoactives
PPV-SVV Preload-dependence =
Fluid Responsive
25 % Increase in preload by fluid loading
Preload LVEDV (mL)
Assessment of Fluid Responsiveness by
ICV diameter with ultrasound
• IVC diameter index variation is an intermittent

measurement and help assessment of volume by central
venous pressure
• In spontaneous breathing patient = IVC colapsibility index
• In controlled ventilation patient = IVC distensibility index
IVC colapsibility index > 50% = fluid unresponsive, normovolume-overload

IVC colapsibility index < 50% = fluid responsive, hipovolume- fluid loading
IVC distensibility index > 18-20% = fluid unresponsive, normovolume-overload

IVC distensibility index < 18-20% = fluid responsive, hipovolume- fluid loading
• IVC collapsible index = (IVCd exp – IVCd insp)/ IVCd exp
• 0% is overloaded, 100% is volume depleted
• 2.04 - 1.51/2.04 = 25%. (Volume overloaded)
• IVC distensibility index = (IVCd ins – IVCd exp)/ IVCd insp

• 0% is volume depleted 100% overload
• 2.04 - 1.51/2.04 = 25%. (Volume overloaded)
Inferior Vena Cava Collapse
• Ultrasound measure of iIVC and eIVC
• N = 30 septic ICU patients Correlation P-value

with eIVC
CVP 0.56 0.001
EVLW 0.59 0.001
EVLW index 0.63 0.001
ITBV 0.51 0.004
ITBV index 0.35 0.05
ITTV 0.68 0.001
PaO2/FiO2 0.47 0.008
EVLW = Extravascular lung water

ITBV = Intrathoracic blood volume
ITTV = Intrathoracic thermal volume
Schefold JC, et al. J Emerg Med. 2010;38(5):632-637.
Cardiac func+on curve demonstra+ng the eﬀect of
varia%ons of preload, contrac%lity, and a3erload on
cardiac performance.
PRELOAD
Echocardiography and Doppler technology
to measure Cardiac Output
• Cardiac output CO can be measured by 2D

echocardiography and Doppler technology, using
either a transthoracic (TTE) or transoesophageal
(TOE) technique
• Stroke volume is calculated using Doppler to

measure the velocity time integral (VTi) flow and
diameter are usually obtained at the level of the
left ventricular outflow tract (LVOT), and then
used to calculate CO.
Transthoracic Echo measures
LVOT diameter in Parasternal
Long Axis View
Transthoracic Echo measures VTi

of LVOT in Apical 5 Chamber View
SV = D2 * 0.785 * VTI
Stroke Volume
Cardiac Output
to measure Contractility - Ejection Friction
to measure Contractility - Ejection Friction
Transthoracic echo
• Advantages
– Fast to perform
– Non invasive
– Can assess valvular structure and myocardial function
– No added equipment needed
• Disadvantages
– Difficult to get good view (esp whose on ventilator /
obese)
– Cannot provide continuous monitoring
Transesophageal echo
• CO assessment by Simpson or doppler flow
technique as mentioned before
• Better view and more accurate than TTE
• Time consuming and require a high level of
operator skills and knowledge
Esophageal aortic doppler US
• Doppler assessment of decending
aortic flow
• CO determinate by measuring aortic
blood flow Velocity Time Integral
(VTI) and aortic Cross Sectional
Decending aorta Area (CSA) decending aorta
• Assuming a constant partition
between caudal and cephalic blood
supply areas
• CSA obtain either from nomograms
or by M-mode US
• Probe is smaller than that for TEE
• Correlate well with CO measured
by thermodilution
Crit Care Med 1998 Dec;26(12):2066-72
Normovolemia
Crit Care Med 1998 Dec;26(12):2066-72
• Advantages
– Easy placement, minimal training needed (~ 12 cases)
– provide continuous, real-time monitoring
– Low incidence of iatrogenic complications
– Minimal infective risk
• Disadvantages
– High cost
– Poor tolerance at awake patient, so for those intubated
– Probe displacement can occur during prolonged monitoring and
patient’s turning
– High interobserver variability when measuring changes in SV in
response to fluid challenges
Pulse contour analysis for
Continuous Cardiac Output Measurement
• Arterial pressure waveform determinate by interaction of stroke volume and SVR
P [mm Hg]
t [s]
⌠ P(t) dP
CCO = cal • HR •⌡ ( SVR + C(p) • dt ) dt
Systole
Area of Compliance Shape of

Patient-specific calibration Heart
pressure pressure
factor (determined with rate
curve curve
thermodilution)
Hemodynamic monitoring per se has
no favourable impact on outcome,
but the interventions based on
hemodynamic data will impact the
outcome
Goal of Balance Goal
Directed
Resuscitation Therapy
O2 delivery
needs end-point Approach
of resuscitation Hemodynamic Parameter:
Preload (CVP, PCWP) DO2 Parameter:
Afterload (MAP, SVR)
Macrodynamic Contractility (SV)

Heart Rate (BPM)
PaO2
Hemoglobin

Cardiac Output
Microcirculation
Microdynamic
Monitoring
PslCO2
SvO2
“Downstream” marker CELL (a-v)CO2

Lactate
of the effectiveness of
Deficit pHi
Directed
O2 delivery

Heart Rate (BPM)
PaO2
Hemoglobin

Cardiac Output
Microcirculation
Microdynamic
Monitoring
PslCO2
SvO2

Lactate
Deficit pHi
Directed
O2 delivery

Heart Rate (BPM)
PaO2
Hemoglobin

Cardiac Output
Microcirculation
Microdynamic
Monitoring
PslCO2
SvO2

Lactate
Deficit pHi
Assessment of adequate
tissue perfussion
tissue perfussion
Clinical
Parameter
tissue perfussion
Clinical Global
Parameter Parameter
tissue perfussion
Global Regional /Organ

Clinical Specific
Parameter Parameter Parameter
tissue perfussion

Clinical Specific
tissue perfussion

Clinical Specific
Mental status
Temperature
Capillary refill
Urine output
Mottling
score
tissue perfussion

Clinical Specific
Mental status
Temperature
Capillary refill
Urine output
Mottling
score
tissue perfussion

Clinical Specific
Mental status
Temperature
Capillary refill
Urine output
Mottling
score
tissue perfussion

Clinical Specific
Mental status
Temperature Hemodynamic :
Capillary refill Cardiac Ouput: SV,
Urine output HR
Mottling Preload: CVP,PCWP,
score GEDI, SVV
Contractility : CFI
Afterload : MAP, SVR
tissue perfussion

Clinical Specific
Mental status
Urine output HR
score GEDI, SVV
Contractility : CFI
Macrocirculation
tissue perfussion

Clinical Specific
Mental status
Urine output HR
score GEDI, SVV
Contractility : CFI
Macrocirculation
tissue perfussion

Clinical Specific
Mental status
Urine output HR
score GEDI, SVV
Contractility : CFI
Macrocirculation
tissue perfussion

Clinical Specific
Mental status
Cardiac Ouput: SV, DO2-VO2
Capillary refill
HR SvO2-ScVO2
Urine output
Preload: CVP,PCWP, Serum Lactate
Mottling
GEDI, SVV A-V pCO2 gap
score
Contractility : CFI Base Deficit
Macrocirculation
tissue perfussion

Clinical Specific
Mental status
Capillary refill
HR SvO2-ScVO2
Urine output
Mottling
score
Macrocirculation
tissue perfussion

Clinical Specific
Mental status
Capillary refill
HR SvO2-ScVO2
Urine output
Mottling
score
Macrocirculation
tissue perfussion

Clinical Specific
Mental status Gastric

Temperature Hemodynamic : tonometry
Capillary refill Sublingual
HR SvO2-ScVO2
Urine output capnometry
Mottling Near-infrared
score Spectroscopy
Macrocirculation
tissue perfussion

Clinical Specific
Mental status Gastric

Temperature Hemodynamic : tonometry
Capillary refill Sublingual
HR SvO2-ScVO2
Urine output capnometry
Mottling Near-infrared
score Spectroscopy
Macrocirculation Microcirculation
The Microcirculation :
The Clinical Challanges
A clinical case
• 45 yo male with severe HAP admitted for respiratory failure, and 3

hours later the patient developed circulatory failure
• PaO2 65 on VC 480 ml/RR 28/Peep 12/FiO2 0.8

• AP 105/50 (65), HR 123, CVP 9 mmHg
• CI 4.6 L/min.m2, EF 65%, ScvO2 74%, Lactate 4.9 mmol/L
• On NE 1.3ug/kg/min, dobu 5 ug/kg/min and 5 L post fluid loading,
still oligouria
• Hb 11 gr/dl, Platelet 65.000/mm2, APTT 53 sec

High CI, elevated ScvO2 but organ dysfunction ??
• Why is there signs of altered tissue
perfusion even though the cardiac output
is high and blood pressure is corrected ?
✤ Hypothesis 1 : microcirculatory perfusion is

altered
✤ Hypothesis 2 : cells cannot handle O2
The Concept of Oxygen Delivery
• The amount of oxygen available to the cell is determined by :
• Central factors are related to the adequacy of

cardiorespiratory function (cardiac index and PaO2) and
hemoglobin concentration
• Peripheral factors are related to the redistribution of

cardiac output to the various organs and to regulation of
the microcirculation :
• by the autonomic control of vascular tone local

microvascular responses
• the degree of affinity of the hemoglobin for oxygen
Vincent JL, De Backer D. Intensiv Care Med 2004

Oxygen debt, Base Deficit and
Lactate level
Base Deficit (meq/L)

O2 debt Volume (ml)
Lactate (mmol/L)
Time from start hemorrhage (min)
Siegel JH, Fabian M, Smith JA, Kingston EP, Steele KA, Wells MR: Oxygen debt criteria
quantify the effectiveness of early partial resuscitation after hypovolemic hemorrhagic shock.
J Trauma 54:862Y880, 2003
Lactate level
Hemorrhage

O2 debt Volume (ml)
Lactate (mmol/L)
J Trauma 54:862Y880, 2003
Lactate level
Partial
Resuscitation
Hemorrhage

O2 debt Volume (ml)
Lactate (mmol/L)
J Trauma 54:862Y880, 2003
Lactate level
Partial
Resuscitation
Hemorrhage
2 hours delay

O2 debt Volume (ml)
Lactate (mmol/L)
J Trauma 54:862Y880, 2003
Lactate level
Partial
Resuscitation
Hemorrhage
2 hours delay
O2 Debt

O2 debt Volume (ml)
Lactate (mmol/L)
J Trauma 54:862Y880, 2003
Lactate level
Partial
Resuscitation
Hemorrhage
2 hours delay
O2 Debt

O2 debt Volume (ml)
Lactate (mmol/L)
Lactate
J Trauma 54:862Y880, 2003
Lactate level
Partial
Resuscitation
Hemorrhage
2 hours delay
Base Deficit
O2 Debt

O2 debt Volume (ml)
Lactate (mmol/L)
Lactate
J Trauma 54:862Y880, 2003
Lactate level
Partial Full
Resuscitation Resuscitation
Hemorrhage
2 hours delay
Base Deficit
O2 Debt

O2 debt Volume (ml)
Lactate (mmol/L)
Lactate
J Trauma 54:862Y880, 2003
Lactate level
Partial Full
Resuscitation Resuscitation
Hemorrhage
2 hours delay
Base Deficit
O2 Debt

O2 debt Volume (ml)
Lactate (mmol/L)
O2 Debt
Lactate
J Trauma 54:862Y880, 2003
Oxygen debt and
recovery
bleeding for 60 min bleeding for 60 min

→ LR resuscitation → LR resuscitation
Survivorship Relative to DO2
Shoemaker WC et al. Crit Care Med 13: 85-92, 1985
450 ml/min/m2 is
enough
Survivorship Relative to DO2 Supranormal Value
Volume loading & Inotropes
450 ml/min/m2 is
enough
the survivors are able to
generate a higher cardiac output,
whereas patients with severe
cardiorespiratory compromise
may not be able to generate a
high cardiac output and have a
higher risk of death
Survivorship Relative to DO2 Supranormal Value

Volume loading & Inotropes
450 ml/min/m2 is
enough
the critically ill patients with
severe cardiorespiratory
compromise may not be able to
generate a high cardiac output,
already have MODs, and have a
higher risk of death
Gattinoni L et al. NEJM 1995

One should not discount the
value of a good physical
examination, despite of all the
interest lab values, non
invasive or invasive
monitoring device to
determine the adequacy of
tissue perfusion
Skin mottling to predict mortality in septic shock
• In the early stages of

septic shock, the skin
may be flushed, warm
and vasodilated while in
the later stages, the
extremities may become
cold and hypoperfused
• Mottling usually begins

at the knees, and can be
quantified to a mottling
score (scored 0-5, with a
higher score correlating
with increased mortality)
• High doses of
vasopressors can make
skin mottling more
Score 0= no mottling
severe Score 1= small area of mottling,
localised to centre of knee
Score 2= modest mottling area that
does not extend beyond superior
border of kneecap
Score 3= mild mottling area that does
not extend beyond the mid- thigh
Score 4= severe mottling area, not
going beyond the groin fold
Ait-Oufella H, Lemoinne S, Boelle PY, Galbois A, Baudel JL, Lemant J, et al.
Score 5= extremely severe mottling
Mottling score predicts survival in septic shock. Intensive Care Med 2011; 37(5): 801–807. area, extending beyond groin fold
Mottling score predicts
survival in septic shock
Ait-Outfella et al. Intensive Care Med 2011
Cardiac Index / O2ER relationship
increase
lactate
Cardiac index/oxygen extraction

ratio (O2ER) diagram during a
normal
lactate short-term dobutamine infusion
indicating (VO2)/(DO2)
dependency
VO2
If VO2 remains stable and is

VO2 independent of DO2, data points
on the diagram move parallel to
the VO2 isopleths; if there is VO2/
DO2 dependency, data points will
cross VO2 isopleths
The Regional Approach
• Unfortunately, global DO2 and VO2 may not be sensitive enough to be clinically
relevant and may fail to detect regional perfusion abnormalities
• The splanchnic circulation regional measurements have shown the VO2/DO2

dependency phenomenon in the hepatosplanchnic circulation in some patients
and others did not
Regional oxygen consumption (VO2)/

oxygen delivery (DO2) relationship in the
splanchnic circulation in patients with
severe sepsis no differences in clinical or
biochemical parameters
Group I: patients with gradient between

mixed venous and hepatic venous oxygen
saturation lower than or equal to 10%
Group II: patients with gradient between
mixed venous and hepatic venous oxygen
saturation higher than 10%
VO2M and DO2M refer to mesenteric VO2 and DO2
De Backer D, Vincent JL, et al. Does hepatosplanchnic VO2/DO2 dependency exist in critically ill patients. Am J Respir Crit Care Med 1988
Gastric Tonometry
Two explanations
↓ Perfusion ↓ Perfusion
↓ DO2 ↓ DO2
↑ anaerobic met ↓ CO2 washout
↑ lactate- + ↑CO2
gastric CO2 (g-CO2) ↑

hemodilution
group
hemodilution
hemodilution group
group
Curr Opin Crit Care 2008

Friday, November 7, 14 hemodilution
The oxygen supply to the renal tissue is becoming
critical already in an early stage of ANH (acute
normovolemic hemodilution) due to the
combination of increased V̇O2ren, decreased DO2ren,
and intrarenal O2 shunt
Curr Opin Crit Care 2008
Human
Microcirculation
Microvascular
alteration in sepsis
Normal Gut Sepsis Gut

OPS 5xp OPS 5xp
Decrease capillary density in
experimental sepsis
(hamster skinfold)
Hoffman, et al. CCM 2004
Microvascular
alteration in sepsis
• Decrease capillary density
• Heterogeneity of perfusion
• Absence or intermitten flow in capillaries
✤ Different models (LPS, CLP, live bacteria)

✤ Various experimental models
✤ Various organ (skin, gut, liver, lung, kidney...)
Heterogeneity of capillary
perfusion in sepsis
Pig cholangitis
Verdant, et al. CCM 2009
Sinusoidal Blood Flow in
Endotoxin Shock
Intermittent vs absent
of flow
VO2
mlO2/sec
Intermittent
No Flow
Goldmann et al. AJP 2006
Microcirculatory
alterations in sepsis
Vascular Density (n/mm) Persentage of perfused large vessels %
De Backer et al. AJCR CM 2002
Microcirculatory
alterations in sepsis
Persentage of perfused small vessels %
The
Consequences...
Control LPS
Cardiomyocytes Rat
Bateman et al. AJP 2007
Influence of intercapillary distance on the effects
of hypoxia, anaemia, and low flow on the oxygen
delivery-consumption relationship
O2 transport at microcirculatory level by diffusion more than by convection
Could you detect the altered
microcirculation using clinical
assessment, hemodynamic measurement
or biomarker ?
Global macro-microcirculation
parameters
De Backer et al. AJCR CM 2002
No correlation between
global and regional
De Backer et al. CCM 2006
Microcirculation alteration in
septic patient when resuscitation
goals already achieved
• 220 patient were observed within 24

hours of the onset of severe sepsis
• Resuscitation goals were achieved :

• MAP ≥ 65 mmhg
• CVP 8- 12 or 12-15 mmhg
• SvO2 > 65% or ScvO2 > 70%
De Backer et al. CCM 2009
Microcirculatory
alterations are more
severe in non-survivors
Evolution of microcirculatory
alteration in septic shock
patients
49 patients during period of shock Sakr et al. CCM 2004

Microcirculatory Flow Index :
altered red cell blood flow in
microcirculation
33 patients with septic shock
- 1st SDF evaluation within 3 hrs after EGDT initiation

- 2nd SDF evaluation 3 to 6 hrs after EGDT initiation
- SOFA changes between 0 and 24 hrs
Trzeciak et al. ICM 2008
Factors associated with ICU
outcome (multivariate analysis)
220 patients/ICU survival 47% (n=104)
De Backer et al. ATS 2009
How to monitor the
microcirculation ?
The technique used to evaluate the
microcirculation can evaluate heterogeneity of
the blood flow/pO2 at the microcirculatory level
Evaluation of the Microcirculation
Arteriole
Microcirculation Mitochondrion
- NIRS - Redox state
- MRS
- LDF (laser doppler) O2
- Microvideoscopy
(OPS SDF)
Capillary
Direct visualization :
-LDF
- OPS
Extracellular space - SDF
- tPO2 Indirect visualization :
- Microdialysis - NIRS
- CO2 tonometry O2 - PslCO2, PgCO2
- Microdialysis
(PslCO2, PgO2)
Venule
Arteriole
- MRS
- Microvideoscopy
(OPS SDF)
Capillary
-LDF
- OPS
- Microdialysis
(PslCO2, PgO2)
Venule
Arteriole
- MRS
- Microvideoscopy
(OPS SDF)
Capillary
-LDF
- OPS
- Microdialysis
(PslCO2, PgO2)
Venule
Arteriole
- MRS
- Microvideoscopy
(OPS SDF)
Capillary
-LDF
- OPS
- Microdialysis
(PslCO2, PgO2)
Venule
Arteriole
- MRS
- Microvideoscopy
(OPS SDF)
Capillary
-LDF
- OPS
- Microdialysis
(PslCO2, PgO2)
Venule
Anatomy
•a The sublingual area is one of the easiest to access areas in

human mucosal surfaces. Sublin¬gual microcirculation has been
considered as a surrogate measure for splanchnic blood flow,
mainly because 1) the tongue and relat¬ed areas share a
common embryogenic ori¬gin with the gut and 2) the close
correlation between sublingual capnometry and gastric
tonometry
Laser Doppler Flowmetry
only light reflected from
a tiny part of tissue confocal
• Laser Doppler flowmetry is a non-invasive

method of measuring microcirculatory
blood flow in tissue
• The technique is based on measuring the

Doppler shift induced by moving red blood
cells to the illuminating coherent light, and orthogonal light
the output often gives flux, velocity and
concentration of the moving blood cells
(sampling volume 1mm3)
Direct Microvideoscopy
• Investigate the microvascular blood flow in
human is difficult
• Direct microvideoscopy was limited to the

nailfold area that very sensitive to
vasoconstriction
Orthogonal Polarization Spectral (OPS)
imaging
OPS validated in low hematocrit
Harris P, et al. AJP 2002
Sidestream Dark Field imaging
SDF
imaging consists of a light
guide surrounded by green
light–emitting diodes (530 nm)
whose light penetrates the
tissue and illuminates the
microcirculation
SDF : Pulse light (530 nm), less blurring
for moving objects
Goedhart P, et al. Optics 2007
• OPS and SDF imaging techniques allow the
investigation of the microvascular circulation in
tissue covered by a thin epithelial layer :
• sublingual mucosa
• nailfold, eyelids
• ileostomy, colostomy
• rectal mucosa
• vaginal mucosa
• Practical Issues :
• How to perform image acquisition ?
• How to analyze the images ?
• Automatic assessment not yet ready
• Semi quantitative scoring
• Evaluate vessel density
• Evaluate perfusion heterogeneity (inside and

among areas)
De Backer et al. Crit Care 2007
• Hypoperfusion and increased flow heterogeneity
(rather than the expected hyperdynamic flow pattern)
are the main characteristics of the sublingual
microcirculation in patients with established septic
shock and cardiogenic shock
OPS and SDF limitations
• Movements
• Secretions
• Cooperation, need for sedation
• Hypoxemia in non intubated
patient
• Offline analysis
pO2 and O2 saturation measurement
✤ NIRS
✤ Reflectant Spectroscopy (EMPHO/O2C)
Clarck electrodes in abdominal
muscle
25 patients high risk surgery
Janghi et al. ICM 2009
NIRS : Near-infrared resonance
spectroscopy
Different
wavelengths to
characterize Hb and
HbO2, depend on
whether these
chromophobes
are oxygen bound
spectroscopy
• NIRS is a noninvasive optical technique based on passage of

infrared light (680-800 nm) through biologic tissues limited
to small vessels ( < 1 mm diameter) only
• Three molecules known to affect near-infrared light

absorption : hemoglobin, myoglobin, and mitochondrial
cytochrome oxidase (COX)
• NIRS predominantly assesses microvascular tissue oxygen

saturation (StO2 ) is calculated from the fractions of local
oxyhemoglobin and deoxyhemoglobin saturation, reflects
local supply-demand balance and arteriovenous shunting
spectroscopy
• StO2 reflect changes in flow and/or

metabolism, a proportional change may leave
StO2 unaltered
• This may explain why absolute values fell

outside the normal range in severely
cardiogenic shocked, shocked trauma
patients and in septic shock only when
oxygen delivery fell markedly
sensitive in hemorrhagic shock
Very sensitive in cardiogenic shock
Not sensitive in early sepsis
Sensitive in septic shock with low flow
Glycocalyx Alteration
• As endothelial gatekeeper
• Limit access of certain molecules to the endothelial

cell
• Influences blood cell-vesssel wall interaction
• Shield adhesion molecules
• As mechanotransducer
• Exposed to shear stress produce nitric oxide

(NO), which is an important determinant of
vascular tone
Glycocheck
The results confirmed previous semiquantitative evaluations
showing decreased perfusion and increased flow heterogeneity
as the main features in the septic microcirculation.
These derangements were more severe in nonsurvivors,

observed a hypodynamic rather than a hyperdynamic
microcirculatory pattern.
Crit Care Med 2012; 40:1443–1448
Crit Care Med 2012; 40:1443–1448
Crit Care Med 2012; 40:1443–1448
Crit Care Med 2012; 40:1443–1448
• Microcirculatory alterations are
stronger predictors of outcome than
global hemodynamic variables.
(Crit Care Med 2013;41:791–799)
(Crit Care Med 2013;41:791–799)
(Crit Care Med 2013;41:791–799)
(Crit Care Med 2013;41:791–799)
• The sublingual microcirculation is impaired for
at least 72 hours despite restoration of the
macrovascular circulation after surgical and/or
radiological hemostasis in traumatic
hemorrhagic shock patients, and correlates to
outcome
Crit Care Med 2014; 42:1433–1441
Crit Care Med 2014; 42:1433–1441
Microvascular alterations were
significantly higher in high SOFA
patients compared to low SOFA
patients, despite no differences in
the global hemodynamics
Crit Care Med 2014; 42:1433–1441
Microcirculation Keypoints
• Microcirculatory perfusion is one of the key determinant of

tissue perfusion
• In shock patients, marked microcirculatory impairment can

be observed despite normal or optimized systemic
hemodynamics
• Microcirculatory is under control of different mechanisms

than macrohemodynamics
• Hemodynamic optimization should comprise Individualized

Goal-Directed Resuscitation of macrocirculation in parallel
to optimize the microcirculation perfusion
Question & Discussion
Oxygen Content (CO2)
sejumlah oksigen yang berada di dalam darah, baik arteri maupun vena
(1,38 x Hgb x SO2) + (0,0031 x PO2)
1,38 adalah jumlah O2 yang didapat dengan 1 gram hemoglobin

CaO2 =(1,38 x Hgb x SaO2) + (0,0031 x PaO2)
Normal 20,1 ml/dl
CvO2 = (1,38 x Hgb x SvO2) + (0,0031 x PvO2)
Normal 15,5 ml/dl
Oxygen Delivery
DO2 = CO x CO2 x 10

• Arterial oxygen delivery (DO2) = CO x CaO2 x 10
5 L/min x 20,1 mL/dL x 10 = 1005 mL/min
• Venous oxygen return (DvO2) = CO x CvO2 x 10

5 L/min x 15,5 mL/dL x 10 = 775 mL/min
Oxygen Consump0on
Oxygen Delivery
Cardiac Output - Index (CO-I) x
Syok hypovolemic, hemorrhagic
early sepsis, cardiogenic shock
pain and agitation, increase WOB,
shivering, seizure
Serum lactate level
• The normal value is approximately 1 mmol/L (0.7-2.0)
measured in venous or arterial blood (in the absence
of a tourniquet)
• Elevated serum lactate levels associates with with
circulatory failure, anaerobic metabolism and the
presence of tissue hypoxia, may represent poor tissue
perfusion in critically ill patients
• Increased serum lactate levels at admission to ICU and
a failure to normalise levels during treatment have been
associated with increased morbidity and mortality.
Factors that may contribute to hyperlactatemia:
• Increased production of lactate:
• tissue hypoxia
• Increased aerobic glycolysis (B2 agonies, adrenaline)
• Inhibition of pyruvate dehydrogenase (in sepsis)
• Methanol/ethylene glycol/propofol toxicity

• Thiamine deficiency
• Decreased clearance of lactate: liver dysfunction or failure (50% of lactate clearance,
cardiopulmonary bypass (minor reduction in clearance)
• Exogenous sources of lactate:
• Lactate buffered solutions used in continuous veno-venous haemodiafiltration

(CVVHDF)
• Medications (metformin, nucleosidic reverse transcriptase inhibitors, long-term linezolid
use, intravenous lorazepam, valproic acid
• Haematologic malignancies.

Hemodynamic Monitoring in Critically Ill Patients

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Hemodynamic Monitoring in Critically Ill Patients

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Hemodynamic

Persistent hemodynamic Reduced organ

Tissue microcirculation Secondary

Persistent hemodynamic Reduced organ

Tissue microcirculation Secondary

Persistent hemodynamic Reduced organ

Tissue microcirculation Secondary

Persistent hemodynamic Reduced organ

Tissue microcirculation Secondary

Persistent hemodynamic Reduced organ

Tissue microcirculation Secondary

Persistent hemodynamic Reduced organ

Tissue microcirculation Secondary

Cardiac Output, and baseline serum lactate as an

• Basic monitoring : electrocardiographic (ECG), arterial blood pressure

• Preload and fluid responsiveness

• Static measure of preload : CVP

• Dynamic measures of preload : predicting fluid responsiveness

• Volumetric parameters : Extravascular lung water (EVLW)

• Cardiac output monitoring

• Global and regional

Monitoring Stroke Index (HR/SBP)

Monitoring Stroke Index (HR/SBP)

Monitoring Stroke Index (HR/SBP)

Monitoring Stroke Index (HR/SBP)

• Cardiac output = Stroke volume x Heart rate

• Heart rate is an important determinant of cardiac output.

• Tachyarrhythmias are the most common finding in hypoperfusion states

• Mean arterial pressure (MAP) is the parameter measured

• DP = Diastolic Pressure MAP = [(2DP+SP)] / 3

• It can be measured non-invasively with a cuff placed around

• Manual blood pressure cuffs are the

• Automated BP cuffs, a computer activates,

The systolic pressure variation (SPV) is the

• The disadvantages of an arterial line are:

• The potential complications of

• Patients with nonhypotensive shock had an in-hospital mortality rate of

• Mortality among 76 patients who presented with a systolic blood

• Conclusions: Even in the presence of normal blood pressure, clinical signs

Percentage blood loss 30% 50%

Percentage blood loss 30% 50%

Percentage blood loss 30% 50%

Percentage blood loss 30% 50%

Percentage blood loss 30% 50%

Compensatory mechanisms Heart rate

Percentage blood loss 30% 50%

• A 70-year-old male presented with an exacerbation of COPD.

• A central venous catheter was inserted and noradrenaline

• He had right subclavian artery stenosis secondary to peripheral

• Routinely measure AP in both arms on admission to the ICU,

• It enables almost immediate detection of even a

be maintained 92%-95% in most critically ill patients.

• Capnography refers to the graphic waveform displayedbshowing the

• An ETCO2 waveform corresponding to administered

• A low level of ETCO2 may indicate low cardiac output,

• CPR a sudden increasing ETCO2 >20 mmHg is a strong

• Persistent ETCO2 <20 mmHg is a sign of poor perfusion

C.L. Hunter et al. American Journal of Emergency Medicine 32 (2014)

C.L. Hunter et al. American Journal of Emergency Medicine 32 (2014) 160–165

Cardiac Output - Index (CO-I)

Stroke Volume SV-I Heart Rate Hemoglobin SaO2 PaO2

Preload Afterload Contractility ELWI, PVPI

GEDI, CVP, SVRI, PVRI EF, Tapse