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ISICEM 2012 in Brussels, Belgium

PULSION Abstract Book

International Symposium on Intensive Care and Emergency Medicine


Table of Contents

Perioperative hemodynamic optimization - when, why and how?

Panel members: Wolfgang Huber, Germany & Eran Segal, Israel

A closer look at goal directed algorithms, the good, the bad and the ugly

Berthold Bein, Germany

An algorithmic approach to the very high risk surgical patient

Daniel Reuter, Germany

Hemodynamic monitoring – accuracy vs. continuity

Azriel Perel, Israel

Basic vs advanced approach to hemodynamic monitoring

Panel members: Javier Belda, Spain & Julia Wendon, United Kingdom

CVP, blood pressure and urine output: Are they ever enough?

Eran Segal, Israel

How to monitor fluid therapy – a clinical case

Xavier Monnet, France

Hemodynamic monitoring during septic shock and / or ARDS

Panel members: Greg Martin, USA & Zsolt Molnar, Hungary

What are the relevant hemodynamic targets during septic shock and / or during ARDS?

Jean Louis Teboul, France

Why should I bother about the ebb and flow phases of shock?

Manu Malbrain, Belgium

PULSION Abstract Book - ISICEM Brussels 2012


The International Symposium on Intensive Care and Emergency Medicine (ISICEM), organized

annually by the department of Intensive Care and Emergency Medicine of Erasme University

Hospital, Université Libre de Bruxelle took place in Brussels from March 20 – 23, 2012.

During this meeting PULSION Medical Systems SE organized, as Platinum sponsor, three

satellite meetings regarding different aspects of hemodynamic monitoring. In this ABSTRACT

BOOK you will find the abstracts of all the presentations, that were delivered during these

meetings.

Our special thanks go to our panel members and speakers for their outstanding presentations

and contributions, making all three satellite meetings a great success, as evidenced by the

excellent feedback of more than 600 participants.

Special thanks to Harriet Adamson, Senior Clinical Resource Manager, PULSION Medical

Systems for her efforts in putting this Abstract Book together.

Patricio Lacalle Dr. Volker Humbert

CEO Head of Medical


The Abstract book is also available at www.pulsion.com for online view.

You may take the opportunity to register now for our free literature service!

We will send you current publications on “Haemodynamic Monitoring” on a monthly basis.

With each selected publication you will find a short summary and the link to PubMed.

PULSION Abstract Book - ISICEM Brussels

page 5


A closer look at goal directed algorithms:

The good, the bad and the ugly

Background

The purpose of goal directed therapy is to ensure that adequate

oxygen and energy rich substrates reach the tissues. Despite

showing such positive outcomes for the patient including reductions

in hospital length of stay, complications and mortality, to

date goal directed therapy algorithms have had only a limited

impact on daily clinical practice. The reasons for this are discussed

in this abstract.

The bad….

These days the most commonly used target for directed therapy

is to define a specific cardiac output (CO) with the main options

for increasing CO being volume loading and /or the use of catecholamines.

However, since the establishment of goal directed

therapy there have been various other parameters proposed for

directing patient care. The literature contains several examples

of algorithms that have used inappropriate goals for targeting

therapies, in particular the use of cardiac filling pressures such

as central venous pressure (CVP) and pulmonary artery occlusion

pressure (PAOP) and the use of mean arterial pressure

(MAP). These parameters have been repeatedly shown

in multiple publications

to poorly predict what the

hemodynamic response

of the patient will be to a

volume challenge which

calls into question their

suitability for inclusion in to treatment algorithms. In particular

it has been shown that there is no correlation between CO and

MAP (1), changes in CVP have been shown to not correlate

with changes in stroke volume following fluid loading (2) and

the pulmonary artery occlusion pressure has been shown to be

ineffective for predicting who is hypervolemic and who is hypovolemic

and therefore likely to respond to volume (3). Despite

this, because MAP and CVP remain standard monitoring parameters

they often appear in one or other of the treatment arms

that compare one treatment algorithm against another.

Professor Berthold Bein

Vice Chair Department of Anaesthesiology and Intensive Care Medicine

University Hospital Schleswig-Holstein, Campus Kiel, Germany

Prof. Bein has been working as an anaesthesiologist since 1989. After completing his resident training

in Munich and Hamburg he started working as a board certified anaesthesiologist and intensivist at the

Department of Anaesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein,

Campus Kiel in 2000. Currently he is the Vice Chair and Head of the Research Department. Amongst

several areas of interest his research has predominantly been dedicated to hemodynamic monitoring

and hemodynamic optimization.

The evidence is strong enough to suggest that the inclusion of

MAP, CVP or POAP into treatment algorithms as target goals

should be avoided altogether, despite their widespread and ongoing

use.

There have also been algorithms that used supranormal oxygen

delivery values (DO 2 ) (4,5), or even mixed or central venous

oxygen saturation (6) , as their treatment goals. However

in high risk patients it is of paramount important that values

should be targeted before organ failure (7), which may not be

feasible in everyday clinical practice.

The ugly….

... it has been shown that

there is no correlation between

CO and MAP. ...



Another issue with the development of a goal directed algorithm

should be its ease of use and clinical relevance. Monitoring

equipment that is difficult to set up, expensive to use, or carries

inherent side effects should be avoided. When comparing

two different treatment arms, both should be equal in terms of

time it takes to set up any monitoring equipment and costs and

risks associated with the different monitoring systems to ensure

clinical equipoise(8). For example, the pulmonary artery

catheter, the most invasive form of hemodynamic

monitoring currently available clinically has been

shown to be the most time consuming to set up.

It also carries the most risks and side effects for

the patients so for these reasons its use simply as

a cardiac output monitor in a goal directed algorithm should be

avoided.

Other algorithms have been published that use less invasive

monitoring to obtain their treatment goals (9). However, some of

these algorithms have been complex and difficult to follow, not

reflecting normal clinical routine or at least inhibiting their acceptance

into routine management. Indeed there is no evidence

that the more complicated the algorithm the better the outcome

for the patient. However, it is strongly suspected that the more

complex the algorithm the less likely it is to be accepted by nonresearch

staff and put into general clinical practice, even if has


een shown to be of benefit to the patient.

Fortunately there have been some algorithms published which

are simple and easy to follow, use well validated parameters for

their treatment goals, and largely reflect clinical routine. For example,

using the stroke volume (a component of the cardiac output)

as the treatment goal

has affected the amount

of fluids patients receive

and significantly shortened

hospital length of stay.

There have been a number

of studies that have used

the esophageal Doppler for

fluid replacement in abdominal surgery(10). Although in most

cases the results favored treatment with the Doppler, certain

aspects of the use of this technology should be considered. The

probe may be difficult to place (8) and may need to be repositioned,

particularly following cardio-pumonary bypass surgery

(11). There is also evidence to show that the more experienced

the user the better the correlation of the cardiac output measurements

with a reference method (12). In summary, measurement

tools used in a goal directed treatment algorithm will most

likely not become widely accepted if they are largely observer

dependent and if they need frequent readjustments.

The good….

In summary, in order for a goal directed treatment algorithm

to be accepted into the clinical routine it should be simple and

straightforward to use. It should be seen to be of benefit both

for patients and staff. The treatment goals should, from a physiological

standpoint, be flow based, using parameters such as

cardiac output or stroke volume (13). Because of the ongoing

trend towards less invasive monitoring, the inclusion of such

technology is also warranted here. Such technologies should

be as accurate as is possible given their less invasive nature. A

large scale multicenter trial is on its way to test the effectiveness

of the new autocalibrated ProAQT device for hemodynamic

optimization using a simple and straightforward algorithm.

References

from a physiological standpoint,

be flow based, using

parameters such as cardiac

output or stroke volume.



The treatment goals should,

PULSION Abstract Book - ISICEM Brussels 2012

page 7

1. Linton RA, Linton NW, Kelly F. Is clinical assessment of the

circulation reliable in postoperative cardiac surgical patients?

J Cardiothorac Vasc Anesth 2002; 16(1): 4-7

2. Michard F, Alaya S, Zarka V, Bahloul M, Richard C, Teboul JL.

Global end-diastolic volume as an indicator of cardiac preload in patients with

septic shock. Chest 2003; 124(5): 1900-8

3. Osman D, Ridel C, Ray P, Monnet X, Anguel N, Richard C,

Teboul JL. Cardiac filling pressures are not appropriate to predict

hemodynamic response to volume challenge*. Crit Care Med 2007;

35(1): 64-69

4. Shoemaker WC, Appel PL, Kram HB, Waxman K, Lee TS. Prospective

trial of supranormal values of survivors as therapeutic goals in

high-risk surgical patients. Chest 1988; 94(6): 1176-86

5. Perz S, Uhlig T, Kohl M, Bredle DL, Reinhart K, Bauer M,

Kortgen A. Low and „supranormal“ central venous oxygen saturation and markers

of tissue hypoxia in cardiac surgery patients: a prospective observational study.

Intensive Care Med 2011; 37(1): 52-59

6. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson

E, Tomlanovich M. Early goal-directed therapy in the treatment of severe sepsis

and septic shock.“ N Engl J Med 2001; 345(19): 1368-77

7. Kern JW and Shoemaker WC. Meta-analysis of hemodynamic optimization in

high-risk patients. Crit Care Med 2001; 30(8): 1686-92

8. Stawicki SP, Hoff WS, Cipolla J, de Quevedo R. Use of non-invasive esophageal

echo-Doppler system in the ICU: a practical experience.

J Trauma 2005; 59(2): 506-7

9. Mayer J, Boldt J, Mengistu A, Rohm KD, Suttner S. Goal-directed intraoperative

therapy based on autocalibrated arterial pressure waveform analysis reduces

hospital stay in high-risk surgical patients: a randomized, controlled trial. Crit Care

14(1): R18

10. Abbas SM and Hill AG. Systematic review of the literature for the use of

oesophageal Doppler monitor for fluid replacement in major abdominal surgery.

Anaesthesia 2008; 63(1): 44-51

11. Bein B, Worthmann F, Tonner PH, Paris A, Steinfath M, Hedderich J,

Scholz J. Comparison of esophageal Doppler, pulse contour analysis, and realtime

pulmonary artery thermodilution for the continuous measurement of cardiac

output. J Cardiothorac Vasc Anesth 2004; 18(2): 185-9

12. Lefrant JY, Bruelle P, Aya AG, Saissi G, Dauzat M, de La Coussaye JE,

Eledjam JJ. Training is required to improve the reliability of esophageal Doppler

to measure cardiac output in critically ill patients. Intensive Care Med 1998; 24(4):

347-52

13. Hamilton MA, Cecconi M, Rhodes A. A Systematic Review and Meta-Analysis

on the Use of Preemptive Hemodynamic Intervention to Improve Postoperative

Outcomes in Moderate and High-Risk Surgical Patients. Anesth Analg 2011; 112:

1392-1402


An algorithmic approach to the very

high risk surgical patient

Why use an algorithmic approach? According to its definition, an

algorithm is a set of rules that precisely defines a sequence of

operations to perform a procedure or to solve a problem. In the

perioperative setting, such an algorithmic approach can be useful

firstly to analyze, and secondly, to reduce perioperative risks

during and after very complex surgical procedures. This comprises

of a) defining the procedure associated risks, b) defining the

patient associated risks, c) outlining strategies to optimize the

preoperative status, d) defining adequate hemodynamic monitoring,

and finally e) defining an adequate hemodynamic management

regimen.

When considering procedure associated risks, the Guidelines of

the Task Force for Preoperative Cardiac Risk Assessment and

Perioperative Cardiac Management in Non-cardiac Surgery from

the European Society of


Cardiology and the European

Society of Anaesthesiology

(ESC/ESA) represents

a very helpful tool

(1). In these guidelines

surgical procedures are

stratified to low (5% risk). However,

each individual surgical and anesthesiological experience also

needs to be taken in account with such stratifications.

The patient associated risk should also be stratified preoperatively

into an algorithmic approach. The ESC/ESA guidelines

also propose a practical procedure, based on the modified Lee

criteria (2): The individual risk is stratified according to the presence

of active cardiovascular/pulmonary diseases (unstable coronary

syndrome, acute heart insufficiency, significant arrhythmias,

symptomatic valvular disease, recent myocardial infarction),

the determination of the patients’ functional capacity (quantified

Professor Daniel Reuter

Department of Anesthesiology and Intensive Care Medicine,

University Clinic Hamburg-Eppendorf, Germany

Prof Reuter completed his Medical Education at the Julius Maximilians University in

Würzburg Germany, Columbia University New York USA and finally at the Ludwig-Maximilians-University

Munich Germany. He has specialized in both Anesthesiology and

Intensive Care Medicine in Tübingen Germany, and in Munich Germany. Prof Reuter

is currently Professor of Anesthesiology and Vice Chair of the Department of Anesthesiology

in the Center of Anesthesiology and Intensive Care Medicine Hamburg-Eppendorf

University Medical Center, Germany.

The underlying rationale should

always be to have the tools to optimize

blood flow in order to ensure

an adequate circulation, leading

to adequate end-organ perfusion,

resulting in less complications

and improved outcome.kk


by the determination of metabolic equivalents), and the presence

of clinical risk factors (known coronary artery disease, heart insufficiency,

insulin dependent diabetes mellitus, cerebrovascular

diseases, and renal insufficiency). This information can then be

transferred into a treatment-matrix which defines which further

diagnostic and therapeutic steps should be taken prior to surgery

(3).

Furthermore, this information can also serve as the basis for the

definition of an appropriate hemodynamic monitoring strategy:

The complexity and invasiveness of monitoring increases based

on the quantification of patient- associated, and surgery associated

risks, as described above. The underlying ratio should

always be to have the tools to optimize blood flow in order to

ensure an adequate circulation, leading to adequate end-organ

perfusion, resulting in less complications and improved outcome.

These tools are comprised of the assessment of

cardiac output, preload and fluid responsiveness

as well as the measurement of blood pressure.

More and more technologies are becoming

available to assess these parameters with less

and less, or indeed no invasiveness – however,

in highly complex pathophysiological states, such

as in severe hemodynamic instability, shock, or

systemic inflammation, those low or non-invasive

tools will potentially fail to provide the correct

measurements – so that in these circumstances, escalation to

monitoring techniques such as transpulmonary and pulmonary

artery thermodilution are justified.

However, and most importantly, hemodynamic monitoring can

only help to improve the outcome if it is embedded into a treatment

strategy. Here the algorithmic approach, which by its very

definition clearly determines the goals of hemodynamic optimization,

is essential. The basis of all these thus far proposed

treatment algorithms is very similar: Step one is preload optimization,

which is followed by an improvement in central blood

flow (cardiac output). Optimization of perfusion pressure (blood


pressure) then comes in the second tier. The positive effects on

outcome have been demonstrated in several recent clinical trials

(4,5). However, it is very

important to point out that,

particularly in the groups

of high risk surgery patients

(e.g. cardiac surgery,

patients with underlying

cardiac diseases and septic

patients), the proposed

“optimal values” for the

parameters of preload

(global end-diastolic vo-


However, and most

importantly, hemodynamic

monitoring

can only help to improve

the outcome if

it is embedded into a

treatment strategy.


lume index obtained by transpulmonary thermodilution, enddiastolic

area index from the transesophageal echocardiography,

and others) may vary from the proposed “normal values” (6). Titration

and definition of patient-individual optimimal values may

be the choice here for optimizing hemodynamic management as

recently demonstrated in a prospective trial in 100 cardiac surgical

patients (7).

References

PULSION Abstract Book - ISICEM Brussels 2012

page 9

1. Poldermans D, Bax JJ et al. Guidelines for pre-operative cardiac risk assessment

and perioperative cardiac management in non-cardiac surgery: the Task

Force for Preoperative Cardiac Risk Assessment and Perioperative Cardiac Management

in Non-cardiac Surgery of the European Society of Cardiology (ESC)

and endorsed by the European Society of Anaesthesiology (ESA). Eur J Anaesthesiol

2010; 27(2): 92-137.

2. Lee TH, Marcantonio ER et al. Derivation and prospective validation of a

simple index for prediction of cardiac risk of major noncardiac surgery. Circulation

1999; 100(10): 1043-9.

3. Petzoldt M, Kahler J, Goetz AE, Friederich P. [Perioperative pharmacological

myocardial protection. Systematic literature-based process optimization]. Anaesthesist

2008; 57(7): 655-69

4. Goepfert MS, Reuter DA, Akyol D, Lamm P, Kilger E, Goetz AE. Goal-directed

fluid management reduces vasopressor and catecholamine use in cardiac

surgery patients. Intensive Care Med 2007; 33: 96-103

5. Hamilton MA, Cecconi M, Rhodes A. A Systematic Review and Meta-Analysis

on the Use of Preemptive Hemodynamic Intervention to Improve Postoperative

Outcomes in Moderate and High-Risk Surgical Patients. Anesth Analg 112: 1392-

1402

6. Eichhorn V, Goepfert MS, Eulenburg C, Malbrain ML, Reuter DA. Comparison

of values in critically ill patients for global end-diastolic volume and extravascular

lung water measured by transcardiopulmonary thermodilution: A metaanalysis

of the literature. Med Intensiva 2012; epub

7. Goepfert M, Richter P, von Sanersleben A et al. Does early perioperative

goal directed therapy using functional and volumetric hemodynamic parameters

improve therapy in cardiac surgery? A prospective, randomized controlled trial.

ASA 2011; BOC 12


Hemodynamic monitoring – accuracy

vs. continuity

Why is it important to measure cardiac

output (CO)?

Cardiac output (CO) is the main determinant of oxygen delivery

and may be compromised or inadequate in many disease

states. Therefore many of our therapeutic efforts are aimed at

improving low- or inadequate-flow states. And yet, physical examination

and vital signs alone often fail to reflect significant

derangements in CO. The two main reasons for monitoring

CO in clinical practice include the identification of patients who

have low (or high) CO values that are not evident clinically, and

the quantification of the response to diagnostic and therapeutic

interventions. The monitoring of CO is therefore very useful

for proper decision-making in critically ill and high-risk surgical

patients. The fact that this statement is not supported by

evidence-based medicine tells us more about the shortcomings

of EBM than those of the measurement of CO. By analogy, we

could not imagine ourselves driving a car without a speedometer,

and yet, speedometers in cars and similar devices in airplanes

have not been introduced following randomized controlled

trials. Thus it is high time to consider the CO as an additional

vital sign in critically ill and high risk surgical patients.

Are CO monitors accurate?

The introduction of uncalibrated continuous CO monitors into

clinical practice has been associated with reports that raised

questions about their accuracy in comparison with CO measured

by the pulmonary artery catheter (PAC, which is still

considered by many to

be the ‘gold standard’).

The current convention

is that any new method

for measuring CO (e.g.,

pulse contour) should

achieve an agreement

with bolus thermodilution which meets the expected 30% limits.

However, the relevance in clinical practice of these arbitrary

limits may need to be reassessed. Moreover, all of the hemo

Professor Azriel Perel

Professor and Chairman, Department of Anesthesiology and Intensive Care, Sheba Medical

Center, Tel Aviv University, Tel Aviv, Israel

Prof. Perel graduated from the Hadassah-Hebrew University Medical School, Jerusalem in 1974 and then

completed his residency in Anesthesia and Intensive Care at the same institute. From 1977 – 1979 he

received the Fulbright fellowship which he completed at the Cardiovascular Research Institute, UC San

Francisco. He also completed a Critical Care Fellowship in the University of Florida, Gainesville, from

1979-80 and was a Visiting Professor in Critical Care, at UC San Diego in 1985. Prof Perel was appointed

the Chairman, Dept Anesthesiology and Intensive Care, Sheba Medical Center, Tel Aviv in 1987. He has

served as the treasurer and member of the Executive Board, European Society of Anesthesiologists (ESA)

1998-2002. In 2004 he was a Visiting Professor at Hôpital Pitie Salpetrière, Paris. In 2005 Prof Perel was

appointed President of the Israel Society of Anesthesiologists, a position he held until 2011. Currently

(2012) Prof Perel is a Visiting Professor at the Charité University Hospital in Berlin.

The monitoring of CO is

therefore very useful for proper

decision making in critically ill and

high-risk surgical patients.



dynamic parameters that we use in our practice are either inaccurate

or are considerably influenced by many confounding

factors (e.g., blood pressure during vasoconstriction, heart rate

in a beta blocked patient, CVP or PAOP in the presence of high

PEEP, etc). Last but not least, when evaluating the role of new

CO devices in clinical care, the fundamental question is whether

the new device can replace thermodilution CO measurement

as a guide to clinical decisions.

How should we deal with the inherent inaccuracies

of our monitored parameters?

A. Maximize the information that can be

provided by real-time continuous measurements

The continuity of measurement of physiological parameters is a

powerful tool. The best and most common example is the vast

amount of information that is offered by the continuous analog

signal of the blood pressure waveform in comparison with its

digital readout. In the same way, when it comes to assessing

the response to therapeutic or diagnostic events with short time

constants, a continuous real-time CO is more useful and informative

than CO measured by intermittent bolus thermodilution,

which has a precision of ±10-20%. Examples of such therapeutic

and diagnostic events include fluid loading, passive leg raising

(PLR), and the immediate response to inotropes, to name a

few. In the field of perioperative optimization it has long been recognized

that the gold standard to monitor the response to a fluid

challenge is the continuous measurement of CO. Continuous

measurement in many other novel monitoring

devices offer this extra dimension by allowing

real-time assessment of response to therapy or

a change in patient status. The close assessment

of continuous physiological analog signals

should receive the recognition that the classic

Physical Examination has had in medicine for

decades. Such assessment should be termed Physiological Examination

and should become a part of formal medical training.


B. Beware of protocolized care.

Due to the inherent inaccuracies and confounding factors of

the parameters that we routinely monitor, one should beware

of protocols, especially those which include pre-defined physiological

end-points that should be reached in all patients. The

best examples for such a need for caution are the CVP and

ScvO 2 values that have been advocated by the Surviving Sep-

sis Guidelines. The reported

improved survival

following the adoption of

these Guidelines cannot

be viewed as justification

of the recommended initial

hemodynamic resuscitation

protocol, which,

physiologically and clinically,

may be wrong

and even dangerous for

many septic patients. In

” Continuity of measurement,

a multi-parametric approach,

and more reliable decisionmaking

strategies, are some

of the means that would allow

us to correctly use new technologies

for the benefit of our

patients.


the same manner any perioperative optimization protocol that

advocates a CI > 4.5 L/min/m 2 for all high risk patients may be

inappropriate, one reason being the insufficient accuracy of any

CO monitor.

C. Adopt a multi-parametric approach when making

a potentially critical decision.

Due to the inherent limitations of the parameters that we monitor,

one should not base a critical decision on one single parameter.

Take for example the limitations of the CO itself: The

optimal CO for an individual patient is difficult to assess; A low

CO does not tell us what to do; A ‘normal’ or even high CO does

not preclude the presence of inadequate regional

and microcirculatory flow. Therefore a perioperative

hemodynamic strategy that assumes that any

decrease in CO should be treated with fluids will be

very often wrong. Adding a functional hemodynamic

parameter like the PPV may be of great benefit

in such clinical scenarios. In the critically ill a multi-parametric

approach that includes CO, volumetric preload and extra-vascular

lung water will lead to better decisions than relying on just

one of these parameters.

PULSION Abstract Book - ISICEM Brussels

page 11

D. Adopt decision-making strategies that take into

account the uncertainty of our measurements.

The ‘gray zone’ approach that has been recently applied to

PPV for prediction of fluid responsiveness (FR) is an example

of such a strategy. Since there is a range of PPV values

(9%-13%) for which FR cannot be reliably predicted in 25% of

mechanically ventilated anesthetized patients, and in

a situation where fluid overload may be particularly

deleterious, higher-than-normal PPV values should

serve as an indication for fluid administration.

We often target and attempt to normalize abnormal

physiological variables. Such a therapeutic approach

may be hazardous because it may lead to ignoring

the underlying problem and may induce harm. This

is especially true during therapeutic conflicts. A therapeutic

conflict is a situation where each of the possible

therapeutic decisions carries some potential

harm. Therapeutic conflicts are commonly found in

critical care and present the biggest challenge for protocolized

cardiovascular management. A common example is the patient

with high lung water and low preload. In some cases the correct

answer is to optimize preload first, but in others, and especially

in those with extreme resistant hypoxemia, the answer may be

different. Such a conflict should be solved by a-priori assessment

of the possible harm that each of the respective potential

decisions may cause when found to be wrong. The decision, of

which the price of a possible mistake is lower, is most probably

the correct way to go.

In conclusion, we have to recognize that all our measurements

are a lot less informative and accurate than we may want (or

think). We have to face this challenge rather than become skep-

” “The hottest places in hell are

reserved for those who, in times

of great crisis, do nothing”.

Dante


tics, passive or even

nihilistic. Continuity of

measurement, a multiparametric

approach,

and more reliable decision-making

strategies,

are some of the means that would allow us to correctly use new

technologies for the benefit of our patients.


CVP, Blood Pressure and Urine Output:

Are they ever enough? (interactive session)

Background

When caring for critically ill patients, the question of hemodynamic

monitoring is a cardinal one. We have to assess and decide

whether the tools at our disposal are adequate for the clinical

scenario at hand. Clearly it makes sense that in the most severely

compromised patients, there is a need for information regarding

cardiovascular and pulmonary function. Unfortunately,

the situations in which these measurements can be helpful and

sometimes even mandatory and in which this information may

improve outcome, are not clearly established. In this presentation

I have attempted to look at the question of whether basic

monitoring tools are ever enough.

Question 1: ---Are blood pressure, urine output

and central venous pressure ever enough?

80

60

40

20

0

Yes, they can be enough

in many patients

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

Case Study 1

No, they are

never enough

The first example of a trauma case illustrates this point. A 25

year old male is injured by a car and brought into the Emergency

Room (ER) with chest and head injuries. In the ER the

following parameters were measured;

Blood pressure 86/50

CVP 4 cmH 0 2

Urine Output 30 ml/hr

Dr. Eran Segal, MD

Director, Department of Anesthesia, Critical Care and Pain Medicine, Assuta Medical

Centers, Israel

Dr. Segal is the director of anesthesia, Intensive Care and Pain Medicine of Assuta Medical

Centers, in Israel. Dr. Segal was trained in the Sheba Medical Center, and in Gainesville, Florida.

He is the President of the Israeli Society of Critical Care Medicine. His main interests are

advanced hemodynamic monitoring and mechanical ventilation.

I have never

needed anything else

Question 2: What is the probable diagnosis?

100

80

60

40

20

0

Septic shock

Anaphylactic

shock

Hemorrhagic

shock

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

As the audience thought, the diagnosis here is quite clear, and

in fact as reflected by the history, blood pressure, urine output

and CVP in this instance are enough.

Question 3: What should be done?

100

80

60

40

20

0

Administer

fluids

Urine

electrolytes

PA catheter

*Results (in %) of the votes of an interactive session (audience 300) during ISICEM, 2012

In this instance the CVP and blood pressure were accurate

reflectors of his hypovolemia. But we probably didn’t need them

anyway given his clinical presentation. Again, the data and the

history are enough in this case to evaluate his status and formulate

a plan.

However, things are not always so simple.

Cardiogenic

shock

PiCCO


Case Study 2

A 55 year old man is brought to the Intensive Care Unit after an

acute Myocardial Infarction. On examination he is hypotensive,

hypoxemic and has low urine output. He is intubated and mechanically

ventilated. He has clinical signs of pulmonary edema, is

normotensive on noradrenaline (131/69), heart rate 80 beats per

min, and his urine output 110ml/hour once he is put on a frusemide

(lasix) infusion. His CVP is around 3 cmH 2 0.

What is the CVP telling the treating physicians? Is he hypo- or

hyper-volemic, or is his fluid status OK?

This patient is far more complex and in his case the CVP is very

difficult to interpret. A low CVP does not really give reliable information

about the patient’s preload or cardiac function.

Ten minutes later his CVP was 10cmH 2 O.

Question 4: What improved his hemodynamics?

100

80

60

40

20

0

He received

500 ml colloids

(Haes)

He received

a bolus of

noradrenaline

We stopped

the diuretic

We changed

the way looked

at the CVP

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

In fact when the patient was checked it was discovered that the

transducer was placed incorrectly on the patient’s bed (A), level

with the patients shoulder and therefore giving an incorrect reading.

When it was re-positioned correctly at the 5th intercostal

space the CVP was actually 10 cmH 2 0(B). Indeed there is a lot

A B

PULSION Abstract Book - ISICEM Brussels 2012

page 13

of evidence in the literature regarding the variability in CVP measurements

and the potential impact that this can have on fluid

management (1,2,3,4).

Case Study 3

Here is another example: A 64 yr old woman is brought to the

Operating Room for major debulking of a peritoneal spread of a

colonic tumor. She is induced with 120mg propofol and 40mg rocuronium,

after receiving 2mg midazolam and 100 mcg fentanyl.

After induction her blood pressure decreases to 80/46 mmHg,

her CVP is 6mmHg, and a urinary catheter is inserted. The question

is what to do next? Does she need fluids to improve her

hemodynamics, should she receive a bolus of phenylephrine to

improve her vasodilation or should she receive epinephrine or

norepinephrine to increase her cardiac output that has decreased

because of the drugs given for the induction? All of these

are very common questions which anesthesiologists face on a

daily basis.

Immediately after induction a PiCCO catheter is inserted which

gave the following parameters:

Cardiac Index - CI 1.8 l/min/m 2

Global End diastolic

Volume Index – GEDI -

preload

Extravascular Lung

Water Index – EVLWI –

lung water

Stroke Volume Variation – SVV

volume responsiveness

505 ml/ m 2

3-5 l/min/m 2 *

680 – 800

ml/m 2 *

6 ml/kg ≤7 ml/kg*

18 % ≤ 10%*

* Normal Range

Given these parameters, the patient was given fluids for hypovolemia

(low CI, low GEDI and high SVV). Her CO improved

significantly.

Is it worth optimizing fluid therapy during the perioperative period?

Evidence from two meta-analysis has shown that goal

directed hemodynamic therapy reduces major gastrointestinal

complications (5), and improves overall outcome (6). We know

that we should optimize hemodynamics in the perioperative period,

and we probably need more advanced monitoring tools to

enable us to do so.


CVP, Blood Pressure and Urine Output:

Are they ever enough?

(continuation)

And finally, what about the urine output? There are multiple reasons

why a patient may be oliguric during the perioperative period.

These include hypovolemia, low flow, low blood pressure

acute kidney injury, post renal syndrome and even syndrome of

inappropriate antidiuretic hormone hypersecretion (SIADH) so

relying on urine output to indicate if the patient requires volume

or not is crude and potentially very inaccurate.

Case Study 4

A male patient is admitted to ICU following an esophagectomy.

He is hypotensive (blood pressure 100/56mmHg), CVP is 14

mmHg, he is mechanically ventilated and hypoxemic, and his

urine output remains low (40 ml/hr) despite receiving diuretics.

A PiCCO catheter is inserted which gives the following parameters:

Cardiac Index - CI 1.5 l/min/m 2 3-5 l/min/m 2 *

Global End diastolic

Volume Index – GEDI -

preload

Extravascular Lung

Water Index – EVLWI –

lung water

Stroke Volume Variation – SVV

volume responsiveness

600 ml/ m 2

680 – 800

ml/m2 *

16 ml/kg ≤7 ml/kg*

22 % ≤ 10% *

* Normal Range

Despite the very high lung water (EVLW 16) the patients was

given fluids as he had low preload (GEDI 600) and was volume

responsive (SVV 22). Over the next 12 hours, the preload

(GEDI) and CI increased, and EVLW and SVV decreased.

The CI increases as GEDI becomes higher. EVLWI decreases

despite the fluid loading.

So to summarize, maybe the more important question is not

whether CVP, blood pressure and urine output are ever enough,

the question should really be; Are they ALWAYS enough? As

can be seen in the answers to the final question – there is an almost

unanimous agreement that this is not the case, and many

complex patients require more advanced monitoring.


Question 5: Blood pressure, CVP and

Urine Output: Are they always enough?

120

100

80

60

40

20

0

I never need

more data

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

So there is almost unanimous agreement among the audience that, in fact in many cases, there

is a need for advanced monitoring.

KEY MESSAGES:

Its extremely rare that

they are not enough

Many complex

pateints require more

advanced monitoring

• Blood pressure, CVP and urine output are rough indicators

of hemodynamic status

• In some patients, the history and clinical presentation is

enough to make clinical decisions

• In more complex situations, decisions about hemodynamic

management requires more data – cardiac output,

volumetric preload and fluid responsiveness

References

PULSION Abstract Book - ISICEM Brussels 2012

page 14

1. Jain RK, Antonio BL, Bowton DL, Houle TT, MacGregor DA. Variability in

central venous pressure measurements and the potential impact on fluid management

Shock 2010; 33(3): 253-7

2. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness?:

a systematic review of the literature and the tale of seven mares.

Chest 2008; 134(1): 172-8

3. Osman D, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL.

Cardiac filling pressures are not appropriate to predict hemodynamic response to

volume challenge*. Crit Care Med 2007; 35(1): 64-69

4. Kumar A, Anel R et al. Pulmonary artery occlusion pressure and central venous

pressure fail to predict ventricular filling volume, cardiac performance, or the

response to volume infusion in normal subjects. Crit Care Med 2004; 32(3): 691-9

5. Giglio MT, Marucci M, Testini M, Brienza N. Goal-directed haemodynamic

therapy and gastrointestinal complications in major surgery: a meta-analysis of

randomized controlled trials. Br J Anaesth 200); 103(5): 637-46

6. Corcoran T, Rhodes EJ, Clarke S, Myles PS, Ho KM. Perioperative fluid

management strategies in major surgery: a stratified meta-analysis. Anesth Analg

2012; 114(3): 640-51


How to monitor fluid therapy – A clinical case

(interactive session)

Background

When monitoring fluid therapy for acute circulatory failure, there

are three questions that need to be asked: when to administer

fluids: how to ascertain if the fluid therapy is effective: and when

to stop fluids. This case study will outline the practical implications

for using available parameters available at the bedside in

order to help the treating physician through this complex predicament.

Case Study

A 52 year old woman with a history of chronic hepatis C virus

and alcoholism was admitted to the Emergency Department

with a 4 day history of myalgia and increasing dyspnea over the

last 24 hrs. She had respiratory, hemodynamic and renal failure

and was confused.

Resp rate 42 /min HR 104 beats/min pH 7.41

HCO3- 22 mmol/L Creat 180 µmol/L On 10L O 2 /min

AP 69/34/45 mmHg PaO 2 57 mmHg CRP 85 mg/L

Urea 23 mmol/L Skin mottling Temp 39°C

PaCO 2 37 mmHg Lactate 3.1 mmol/L

Over the next 30 minutes she was given 2000mL saline, norepinephrine

0.20 µg/kg/min, and was intubated and ventilated.

She was transferred to

ICU and a central venous

and an arterial line were

inserted. 30 minutes later

her observations looked

like this;

Professor Xavier Monnet

Medical ICU, Paris-Sud University Hospitals, Paris South, France

Prof. Xavier MONNET is Professor of Intensive Care at the Paris-Sud University. He works in the Medical

Intensive Care Unit of the Bicêtre Hospital (Paris-Sud University Hospitals).

Prof. Monnet completed his medical studies at the Paris-6 Medical School and he earned his medical

degree in 2000, with specialty in Cardiology and Intensive Care Medicine. Prof. Monnet also completed

a course of research and obtained his PhD in 2004 from the Paris-Sud University. Prof. Monnet’s

main fields of research investigation are acute circulatory failure and its treatment, hemodynamic

monitoring and heart-lung interactions. He has signed more than 70 articles in peer-reviewed scientific

journals and is the author of several didactic reviews and book chapters. He is regularly invited to

give lectures in international conferences.

Resp rate 22 /min PEEP 10 cmH 2 0 HR 101 beats/min

Saline 2000 mL

PaO 2 / FiO 2

160mmHg

Ceftriaxone +

levofloxacin

Vt 420mL (6mL/kg)

AP 80/35/50 mmHg Norepi 0.2 µg/kg/min

Pplat 29 cmH 2 0 PPV 6% CVP 14mmHg

Propofol 100 mg/h Lactate 2.7 mmol/L

Question 1: What would you do now?

60

50

40

30

20

10

0

I increase

the dose of

norinephrine

However, in patients with septic

shock receiving volume expansion

and/or norepinephrine, the changes in

cardiac index (CI) should be measured

directly (2).



I need to perform

an echocardiography

I need direct

measurement of

cardiac output

I am happy

with the arterial

pressure only

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

A recent hemodynamic consensus conference in 2006 recommended

that routine measurement of cardiac output (CO) for

patients with shock was not recommended unless there was

clinical evidence of ventricular failure and/or

persistent shock despite adequate fluid resuscitation

(1). However, in patients with septic

shock receiving volume expansion and/

or norepinephrine, the changes in cardiac

index (CI) should be directly measured (2).


Hence in this patient an Echocardiography was performed for

diagnosis and a PiCCO catheter inserted for her ongoing management.

HR 98 beats/min CI 2.9 L/min/m 2 CVVHF

Resp Rate 22 /min ScvO 2 70% AP 75/47/57mmHg

GEDI 720 mL/m 2 -

preload

NR 680 – 800

Rt-PCR RNA Flu

(H3N2): positive

Norepi 0.37 µg/kg/

min

PPV 7%

SSV 7%

PEEP 10mH 2 O

Saline 2000 mL Vt 420 mL (6 mL/kg)

CVP 11 mmHg

Pplat 29 cmH 2 O

PVPI 4.5 (N


How to monitor fluid therapy – A clinical case

(continuation)

Question 3: What do you do now?

60

50

40

30

20

10

0

Nothing more

Administer

fluids first

Increase

the dose of

norepinephrine

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

Because of the high EVLWI it was decided to


increase the dose of norepinephrine rather than

give fluids to increase the arterial pressure. The

lung water and permeability were monitored

closely over the coming hours. Knowing when

to stop giving fluids, as stated before, is very important. A high

cumulative fluid balance is an independent predictor of intensive

care mortality (4). Excessive fluid administration is deleterious

in septic shock patients (5).

Question 4: Which statement seems appropriate

at this stage?

60

50

40

30

20

10

0

One can rely

on PAOP for

assessing the

risk of fluid

administration

One can rely

on tlung water

for assessing

the risk of fluid

administration

The value of

PAOP is a

predictor of

mortality in such

a patients

The value of

lung water is

a predictor of

mortality in

such a patient

Re-estimate the

lung water and

premeability

in the coming

hours

The measurement of lung water is reliably estimated by transpulmonary

thermodilution, it can be relied upon for assessing

the risk of fluid administration and a high lung water is a predictor

of mortality. Fluids should be stopped when there is lack of

fluid responsiveness as indicated by the PPV / SVV (if appropriate),

PLR or EEO, but also when the relationship between

lung water and the pressure in the capillaries increases with

volume expansion to the point where the fluid goes extravascularly

instead of staying intravascularly.

Lung water estimation by transpulmonary thermodilution is reliable

and is an independent predictor of mortality in ARDS patients.

This depends on the permeability of the lungs where (for example,

in sepsis), increased permeability means that it takes

less volume to increase the pressure in

the capillaries and therefore increase

the lung water to harmful levels. On the


other hand, the pulmonary artery occlusion

pressure (PAOP) physiologically

cannot estimate the risk of fluid infusion in cases of ARDS.

Knowing when to stop

giving fluids, as stated

before, is very important.

Transpulmonary

thermodilution

reliably estimates

lung water

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

EVLW from the PiCCO has been independently validated

against the gravimetry method in humans (6). In addition EVLW

and the pulmonary vascular permeability index have been

shown to be independent prognostic factors for patients with

ARDS or Acute Lung Injury (ALI) demonstrating that lung water

measured by TPTD has real physiological significance for

the patient (Jozwiak et al. submitted 2012). Therefore in most

instances the presence of high lung water may well signify that

fluid administration should maybe cease or be given more judiciously.

It has also been shown that using EVLW to guide your

treatment may also result in lower cumulative fluid balance,

less days on the ventilator and less days in ICU (7).

PVPI is calculated from advanced analysis of the thermodilution

curve when lung water is divided by pulmonary blood volume.

It has been shown to discriminate between raised lung water

caused by sepsis or raised lung water caused by hydrostatic

factors. Values above 3 usually mean the raised lung water is a

result of increased permeability caused by sepsis (8).

With the increase in norepinephrine to 0.55µg/kg/min the patients

arterial pressures improved (91/40/57 to 110/50/70), CI

increased from 2.9 – 3.4L/min/m 2 and PLR fell to CI+10%.


KEY MESSAGES:

• Cardiac output needs to be directly measured in complex

patients receiving vasopressors

• Real time measurement of cardiac output is required for

predicting fluid responsiveness when PPV / SVV cannot

be used

• Lung water estimation by transpulmonary thermodilution

is reliable and is an independent predictor of mortality in

ARDS patients

• Lung water and lung permeability are useful in the decision

making process for avoiding fluid overload in cases of

ARDS

When to administer fluid?

spont. breath,

arrhythmias, ARDS?

no yes

PPV, SVV

PLR

EEO

+

PLR

EEO

Is fluid threapy effective?

↑ preload

↑ cardiac index

Acute circulatory failure

References

PULSION Abstract Book - ISICEM Brussels 2012

page 19

1. Antonelli M, Levy M et al. Hemodynamic monitoring in shock and implications

for management : International Consensus Conference, Paris, France, 27-28 April

2006. Intensive Care Med 2007; 33(4): 575-90.2

2. Monnet X, Jabot J, Maizel J, Richard C, Teboul JL. Norepinephrine increases

cardiac preload and reduces preload dependency assessed by passive leg raising

in septic shock patients (R3). Crit Care Med 2011; 39(4): 689-94

3. Monnet X, Osman D, Ridel C, Lamia B, Richard C, Teboul JL. Predicting

volume responsiveness by using the end-expiratory occlusion in mechanically ventilated

intensive care unit patients. Crit Care Med 2009; 37(3): 951-6

4. Vincent JL, Sakr Y et al. Sepsis in European intensive care units: results of the

SOAP study. Crit Care Med 2006; 34(2): 344-53.

5. Boyd JH, Forbes J, Nakada TA, Walley KR, Russell JA. Fluid resuscitation

in septic shock: a positive fluid balance and elevated central venous pressure are

associated with increased mortality. Crit Care Med 2011; 39(2): 259-65

6. Tagami T, Kushimoto S et al. Validation of extravascular lung water measurement

by single transpulmonary thermodilution: human autopsy study. Crit Care

2010; 14(5): R162

7. Mitchell JP, Schuller D, Calandrino FS, Schuster DP. Improved outcome

based on fluid management in critically ill patients requiring pulmonary artery catheterization.

Am Rev Respir Dis 1992; 145(5): 990-8

8. Monnet X, Anguel N, Osman D, Hamzaoui O, Richard C, Teboul JL. Assessing

pulmonary permeability by transpulmonary thermodilution allows differentiation

of hydrostatic pulmonary edema from ALI/ARDS. Intensive Care Med 2007;

33(3): 448-53.

When to stop fluid?

lack of fluid responsiveness

as indicated by PPV/SVV

high lung water

high lung permeability


What are the relevant hemodynamic targets

during septic shock and or during ARDS?

(interactive session)

Case Study

A 62 year old woman is admitted to ICU in a coma related to

drug induced self poisoning. This is complicated by aspiration

pneumonia and moderate renal failure. She has a previous history

of COPD (Chronic Obstructive Pulmonary Disease), and

severe hypertension. A culture of her tracheal secretions reveals

evidence of Staph aureus, so she was commenced on

amoxicillin–clavulanic acid combination. She was intubated

and ventilated.

Her blood pressure then dropped from 90/63/50 to 65/43/32

mmHg, with a blood lactate of 3.5 mm/L, and PaO / FiO ratio

2 2

of 280. She was given a rapid infusion of one liter of normal

saline, and a norepinephrine (NE) infusion was started at 0.3

µg/Kg/min.

Post Infusion hemodynamics

ABP 74/55/45 mmHg

Urine flow Low

PaO 2 /FiO 2 ratio 210

Lactate 4 mmol/L

Echocardiography showed a left ventricular ejection fraction

(LVEF) of 60%, no left ventricular dilatation and moderate right

ventricular dilatation. An arterial catheter and central venous

catheter were inserted - ScvO 2 70%, CVP 10 mmHg and PPV

20%.

Professor Jean Louis Teboul

Medical ICU, Bicetre Hospital, University Paris South, France

Prof Teboul is a Professor of Therapeutics and Critical Care Medicine, at the University Paris-

South in France. He works clinically at the medical intensive care unit of the Bicetre University

Hospital near Paris. His main research interests are in heart-lung interactions, cardiovascular

performance, regional blood flow assessment, tissue oygenation, invasive and noninvasive hemodynamic

monitoring, and assessment of volume status. Prof Teboul has published around

130 original papers and 100 book chapters, almost all of them in the field of hemodynamics. He

has given 230 invited lectures in international congresses and 150 invited lectures in French

congresses.

Question 1: How much can we rely on the CVP

value in this patient (10mmHg)?

80

70

60

50

40

30

20

10

0

It suggests a

normal right ventricular

preload

It suggests a

high right ventricular

preload

Right ventricular

preload can

still be low

It suggests fluid

unresponsiveness

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

Central venous pressure is commonly cited as one of the goals

for resuscitation. The Surviving Sepsis Guidelines(1) give a

range of 8-12mmHg for initial resuscitation (first 6 hours) quoting

the Rivers study as its main source (2). This study however,

used the same range in both treatment arms and so therefore

did not test this parameter for its sensitivity as a resuscitation

goal. The CVP is not a simple measurement. It is affected by

many confounding factors including PEEP, the fact that it must

be measured at the end of expiration, and even whether the

transducer has been placed at the anatomical zero level. In fact

the CVP has been repeatedly shown in the literature to not assess

right ventricular preload appropriately, and it is not able to

predict fluid responsiveness (3, 4).

The CVP should not be used to make clinical decisions regarding

fluid management.


Question 2: Which level of MAP is it best to target?

80

60

40

20

0

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

The Surviving Sepsis Guidelines cite a MAP of greater

≥ 65mmHg. The source of this was again the Rivers study where

again this was used in both treatment arms. In fact there is

evidence that the target MAP is more complicated than this. For

example, a history of hypertension affects the point at which an

increase in MAP will lead to an increase in organ blood flow

because of auto-regulatory factors (5). There is also evidence

in septic patients that incre-


asing arterial blood pressure

does not improve microcirculatory

blood flow (6). All septic

patients are not identical, and

it is unrealistic to expect that the optimal arterial pressure will

be identical in all patients – One size does not fit all! Therefore,

MAP must be targeted after individualised assessment.

Question 3: What do you think about the ScvO2 value in this patient (72%)?

80

60

40

20

0

55 mmHg 65 mmHg 75 mmHg

It sugests a

normal tisuue

oxagention status

The CVP should not be used

to make clinical decisions

regarding fluid management.

It suggests an error since

it is impossible to have

both shock and an ScvO 2

of > 70%

It suggests

some impairment

in oxygen

extraction

*Results (in %) of the votes of an interactive session (audience 300) during ISICEM, 2012

In the Rivers study the ScvO 2 was initially low (49%), suggesting

a normal oxygen extraction capacity. However, actually this

situation is uncommon in cases of severe sepsis where ScvO 2

is usually normal or even high (7-10).

PULSION Abstract Book - ISICEM Brussels 2012

page 21

Question 4: What is your attitude in

terms of hemodynamic therapy?

80

70

60

50

40

30

20

10

0

Infuse

IV fluids

again

Add

dopamine

Increase

norepinephrine

Add

doputamine

Add

steroids

Nothing

more

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

The pulse pressure variation (PPV) is 20%. As this patient is

not breathing spontaneously, has no arrhythmi-

as, normal tidal volume (9mL/kg), and normal

lung compliance, the PPV can be used as an


indicator of fluid responsiveness so she was given

one liter of saline and her hemodynamic and

renal function improved. The NE infusion was stopped on day

2, however on day 3 she developed ARDS (Acute Respiratory

Distress Syndrome), her P/F ratio decreased from 280 (day 1)

to 120 (day 3). Protective lung ventilation was started with a

tidal volume of 6mL/kg and PEEP 12 cmH O. On days 2 to 4

2

there was no other organ

dysfunction.


What are the relevant hemodynamic targets

during septic shock and or during ARDS?

(continuation)

On day 7 following a change in her central venous catheter she

had a sudden onset of severe circulatory failure.

AP 60/40/30 mmHg PPV 9% ScvO 2 72%

Fever 40°C HR 140 CVP 7 mmHg

FiO2 .5 WBC 60.3 10 9 /L CRP 394 mg/L

PaO 2 57 mmHg Hb 9.3 g/dL Fibrinogen 8.5

PaCO 73 mmHg 2 Plat count 447 109 /L Troponin 4

pH 6.89 Creatinine 169µmol/L

Chest X ray –

unchanged

HCO3 10 mmol/L ASAT 2341 U/L

Adbom Echo –

normal

Lactate 15 mmol/L ALAT 357 U/L

TTE LVEF 50%, no

LV dilatation

She was given a rapid infu-


sion of 1 liter saline, and NE

EVLW is a safety was recommenced in doses

parameter for use up to 3 µg/kg/min. Renal dia-

during fluid therapy ” k

lysis was started. Her ABP

improved (85/54/39 mmHg),

heart rate decreased (128),

PPV and CVP basically

stayed the same and ScvO increased to 76%.

2

PiCCO monitoring was established to assess volume responsiveness

using passive leg raising (PLR) shown to be more accurate

than PPV in cases of low tidal volume, and to obtain a measure

of the extravascular lung water (EVLW). The usefulness

of PLR to assess fluid responsiveness has been increasingly

reported in the literature, because unlike a fluid challenge, no

fluid is infused and its effects

are reversible and

transient. In particular

the PLR-induced increase

in pulse contour cardiac

output (PCCO) as

provided by the PiCCO,


is a good predictor of fluid responsiveness. EVLW is a safety

parameter for use during fluid therapy. An EVLW of 16 mL/kg

indexed to predicted body weight in patients with ARDS has

been shown to be highly sensitive and specific for predicting

severity of illness and survival (11).

Hemodynamic Parameters PiCCO Parameters

HR 128/min CI 3.85 L/min/m 2

AP 85/54/39 mmHg GEDVI 657 mL/m2 (normal range 680-800)

CVP 8 mmHg EVLWI 25 mL/kg

(normal range < 10)

ScvO 2 76% PVPI 6.3 (normal range < 3)

PPV 8% PLR-induced increased in

PCCO 18%

GEDVI global end-diastolic volume index

Question 5: What would you do now?

30

25

20

15

10

5

0

Nothing else

IV fluids first

then re-assess

NE first then

re-assess

Both IV fluids

and NE and

re-assess

Dobutamine first

then re-assess

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

From the PiCCO parameters it is clear the patient has severe

pulmonary edema (EVLW 25), very high lung capillary permeability

(PVPI 6.3), but is also volume responsive. This is a therapeutic

conflict as the patient needs fluid but already has severe

pulmonary edema.

All septic patients are not identical, and it is un-

realistic to expect that the optimal arterial pressure will

be identical in all patients – One size does not fit all!

Therefore, MAP must be targeted after individualised

assessment.


Given this patient‘s

clinical picture (the

low diastolic pressure

of 39 mmHg),

a vasopressor was

used rather than fluid

loading. NE was increased to 5 µg/kg/min to achieve a MAP

>75mmHg. Activated Protein C was started 10 hours after the

hemodynamic collapse. The only positive microbiological finding

was a blood culture that showed staphylococcus coagulase

negative.


KEY MESSAGES:

• Patients care needs to be individualized. The MAP needs

to be titrated to the patients specific clinical situation.

• Care must be taken with misleading parameters such as

the CVP.

• In addition to the ScvO 2 , use other relevant indices such

as dynamic indices of fluid responsiveness (PVV, PLR).

EVLW and metabolic variables (e.g. lactate clearance,

PCO 2 gap) provide useful information, particularly in the

presence of therapeutic conflicts.

References

PULSION Abstract Book - ISICEM Brussels 2012

page 23

1. Dellinger RP, Levy MM et al., Surviving Sepsis Campaign: International guidelines

for management of severe sepsis and septic shock: 2008. Intensive Care

Med 2008; 34(1): 17-60

2. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson

E, Tomlanovich M. Early goal-directed therapy in the treatment of severe sepsis

and septic shock. N Engl J Med 2001; 345(19): 1368-77

3. Osman D, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL. Cardiac

filling pressures are not appropriate to predict hemodynamic response to volume

challenge. Crit Care Med 2007; 35(1): 64-69

4. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness?:

a systematic review of the literature and the tale of seven mares.

Chest 2008; 134(1): 172-8

5. Strandgaard S, Olesen J, Skinhoj E, Lassen NA. Autoregulation of brain circulation

in severe arterial hypertension. Br Med J 1997; 1(5852): 507-10

6. Dubin A, Pozo MO et al. Increasing arterial blood pressure with norepinephrine

does not improve microcirculatory blood flow: a prospective study Crit Care 2009;

13(3): R92

7. Shapiro NI, Howell MD et al. Implementation and outcomes of the Multiple

Urgent Sepsis Therapies (MUST) protocol. Crit Care Med 2006; 34(4): 1025-32

8. Pope JV, Jones AE, Gaieski DF, Arnold RC, Trzeciak S, Shapiro NI. Multicenter

study of central venous oxygen saturation (ScvO(2)) as a predictor of mortality

in patients with sepsis. Ann Emerg Med 2010; 55(1): 40-46 e1

9. van Beest PA, Hofstra JJ, Schultz MJ, Boerma EC, Spronk PE, Kuiper MA.

The incidence of low venous oxygen saturation on admission in the ICU: a multicenter

observational study in the Netherlands Crit Care 2008; 12(2): R33

10. Jansen TC, van Bommel J, Schoonderbeek J, Sleeswijk Visse, SJ, van der

Klooster JM, Lima AP, Willemsen SP, Bakker J. Early Lactate-Guided Therapy

in ICU Patients: A Multicenter, Open-Label, Randomized, Controlled Trial. Am J

Respir Crit Care Med 2010; 182: 752-61

11. Phillips CR, Chesnutt MS, Smith SM. Extravascular lung water in sepsisassociated

acute respiratory distress syndrome: Indexing with predicted body

weight improves correlation with severity of illness and survival. Crit Care Med

2008; 36(1): 69-73


Why should I bother about the ebb and flow

phases of shock? (interactive session)

What are risks of fluid overload?

When considering fluids administration it is important to know

when to start giving fluids (what are the benefits of giving fluids),

when to stop giving fluids (what are the risks of ongoing

fluid administration), when to start removing fluids (what are the

benefits of fluid removal), and when to stop fluid removal (what

are the risks of removing too much fluid). The literature shows

that a negative fluid balance increases survival in patients with

septic shock (1). Patients managed with a conservative fluid

strategy also seem to have improved lung function, shorter duration

of mechanical ventilation and intensive care stay without

increasing non-pulmonary organ failure (2). However, any measurement

in the ICU will only be of use as long as it is accurate

and reproducible, and no measurement has ever improved survival

- only a good protocol can do this. Patients who are in the

ebb or flow phase of shock have different clinical presentations

and therefore different monitoring needs.

Case Study

A 26 year old male is admitted to intensive care with general

seizures, syncope, non palpable blood pressure, and a history

of ventricular tachycardia whilst in the Emergency Room. He

was known to have been deprived of oxygen at birth, and consequently

suffered a CVA with left hemiparesis and epilepsy

(managed with topamax, lamictal and tegretol). Because of his

cognitive deficits, he normally attends a special day care. For

the last 9 years he had been diagnosed with idiopathic cardiomyopathy

with a left ventricular ejection fraction (LVEF) of

52% (treated with coversyl). Overnight he was initially stable

hemodynamically with no further seizures. However his need

for supplemental oxygen increased and after failing a trial of

non-invasive ventilation, he was intubated and ventilated. He

then became hemodynamically unstable. A transthoracic cardiac

ultrasound was performed with the results listed below together

with the ventilator settings.

Dr. Manu Malbrain, MD, PhD

ICU and HC Burn Unit Director, ZNA STER, Antwerp Belgium

Dr. Manu Malbrain is the manager-director of the Intensive Care (30 beds) and High Care Burn Unit (7

beds) of the ZNA „ZiekenhuisNetwerk Antwerpen“, Campus Stuivenberg/St-Erasmus in Antwerp. He

is actively involved in the European Society of Intensive Care Medicine (ESICM), where he chairs the

Working Group on Abdominal Problems (WGAP, within the POIC section) and has studied the effects

of raised intra-abdominal pressure for the last 15 years. He is the founding President and Treasurer

of the World Society on Abdominal Compartment Syndrome (WSACS, www.wsacs.org). He is author

and co-author of many peer reviewed articles, reviews, book chapters and even a whole book on

Abdominal Compartment Syndrome.

MAP 59 mmHg CI 3.5 L/min/m 2 PaO 2 / FiO 2 ratio 74

CVP 16 mmHg LVEDP 25 mmHg IPAP 30 cmH O 2

LVEF 30% PEEP 10 cmH O 2

Lactate 2.8 mmol/L LVEDAI 16.2 cm 2 FiO 2 100%

Question 1: What is your treatment of choice?

80

60

40

20

0

Norepinephrine

Dobutamine Fluid Bolus Diuretics Other

*Results (in %) of the votes of an interactive session (audience 300) during ISICEM, 2012

Based on the cardiac ultrasound findings physicians were reluctant

to fill the patient with fluids. The FiO 2 was increased to

100% and the PEEP was set according to the low flow PV loop

(as can be automatically constructed with the Draeger Evita XL

ventilator). During the PV loop, that also acts as a recruitment

maneuver, his systolic blood pressure decreased to 40mmHg

during the recruitment, so norepinephrine was started and

swiftly increased to 0.4µg/kg/min. Dobutamine was also started

at 4µg/kg/min. Saturation remained poor at 88% so he was

switched to high frequency pressure ventilation (HFPV) using

the VDR4. A PiCCO catheter was also inserted. The hemodynamic

and respiratory parameters are listed below.

CI 3.5 L/min.m2 (Normal range 3.0 –

5.0)

Heart rate 119 bpm

PPV 19% (Normal range


His response to a passive leg raising maneuver was positive

(15% increase in CI) showing he was volume responsive despite

the fact that he had such bad pulmonary edema (EVLWI 38).

Question 2: What is your treatment of choice now

given the PiCCO parameters?

35

30

25

20

15

10

5

0

Norepine

phrine

Dobutamine Fluid Bolus Diuretics Other

*Results of the votes of an interactive session (audience 300) during ISICEM, 2012

Again physicians were reluctant to fill the patient. This patient

had relatively normal preload according to the volumetric preload

indicator as obtained by the PiCCO (GEDVI 757) but high

preload according to the barometric preload indicator (CVP 16

mmHg). The Surviving Sepsis Campaign Guidelines (SSCG)

(3) originally recommended that patients be resuscitated to a

CVP range of 8-12mmHg. However, using pressures to measure

preload has been found to be inaccurate time and time again,

particularly in patients ventilated with intermittent positive pressure

ventilation (IPPV), (auto) PEEP, post cardiac surgery, obese

patients and those with intra-abdominal hypertension or abdominal

compartment syndrome. Using a CVP threshold may

lead to over- but also under-resuscitation.

In this case study the patient was given small volume resuscitation

with hyperhaes (Fresenius Kabi) at a dose of 4ml/kg given

as a bolus over 10-15 minutes and 1000ml of balanced colloids

(volulyte), following the transthoracic cardiac ultrasound.

He remained on a dobutamine infusion

(9µg/kg/min) and norepinephrine

(0.4µg/kg/min). The following day his

CI increased to 5.71 L/min/m2 , GEDVI

increased to 900 ml/m2 ”

and EVLWI

had decreased to 14 ml/kg PBW. Despite the filling, his CVP

decreased from 16 to 6 mmHg.

PULSION Abstract Book - ISICEM Brussels 2012

page 25

This is an example of a therapeutic dilemma. Although the patient

had evidence of severe pulmonary edema (EVLWI 38) the

decision was made to give fluids because the PPV was high

and the PLR test was positive. The GEDVI was relatively low

in relation to the GEF (4) despite the increased CVP and left

ventricular end diastolic area (from the ultrasound). Cardiac ultrasound

also showed that his inferior vena cava collapsibility

index (IVCCI) was almost 50%.

It was really important to know where this patient was on his

Frank Starling curve. Evidence shows that when the global enddiastolic

volume and the right ventricular end-diastolic volume

are corrected for the ejection fraction they correlate more closely

(4) especially when compared to change in CVP or Pulmonary

Capillary Wedge Pressure (PCWP).

Question 3: What is the premature hump that

appeared on the transpulmonary thermo-

dilution curve?

0

Cross Talk

phenomenon

*Results of the votes of an interactive session (audience 300) during ISICEM, 2012

The premature hump is evidence of a right to left shunt where an

opening (foramen ovale) appears bet-

ween the right and left atria. Because

the patient was extremely hypovolemic,

the combination of positive pres-


sure ventilation with high PEEP led to

increased pulmonary vascular resistance,

pulmonary hypertension and a propagation of West zone

1 conditions to zone 2 and 3.

It is essential to give the right

fluid at the right time, and to use

the correct monitor correctly.

45

40

35

30

25

20

15

10

5

Right to left

shunt

Bolus

mixing

Wrong / flase

measurement

I dont

know


Why should I bother about the ebb and flow

phases of shock?

(continuation)

By late afternoon of day 2, the patient had a urine output of only

350 mls over the last 12 hours despite a positive cumulative

fluid balance of 4 litres. He was still on dobutamine 5µg/kg/min,

and norepinephrine 0.2µg/kg/min. Other parameters are listed

below;

MAP 79 mmHg CI 5.4 L/min/m 2 P/F ratio 205

CVP 8 mmHg GEF 23 % IPAP 34 cmH 2 O

PPV 6 % GEDVI 1080 ml/m 2 PEEP 11 cmH 2 O

Lactate 1.6 to 2.6

mmol/L

EVLWI 18 ml/kg

PBW

FiO 2 increased from

45 – 65%

Question 4: What is your treatment of choice now?

80

60

40

20

0

Norepinephrine

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

Finally the physicians now fully understand the clinical situation

of this patient - that after the initial Ebb phase of


shock he had not entered the flow phase spontaneously.

His PEEP was increased to 18 cmH O, 2

along with hypertonic albumin 20%, and he was

given an infusion of lasix (frusemide, 60mg/hr for

2 hours then 10 mg / hr). This treatment was recently

suggested as PAL (PEEP/ALBUMIN /LASIX). By day 3

his observations looked like this, when he required less albumin

20% and less lasix.

EVLWI 15 ml/kg

PBW

Dobutamine Fluid Bolus Diuretics Other

P/F ratio 266

Dobutamine 3µg/

kg/min

PVPI 1.9 IPAP 34 PEEP 18 Norepinephrine

0.11µg/kg/min

Things continued to fluctuate for the patient over the next few

days but with two more episodes of lasix infusions eventually

his EVLWI came down to 8 ml/kg PBW on day eight. The patient

was extubated on day 10 and left the ICU after 2 weeks.

Question 5: What is your opinion on a positive

cumulative fluid balance in septic shock?

It is just of

cosmetic

concern

It is a biomarker

of severity

of illness

It is harmful and

an independent

predictor for

morbitiy and

mortality

Fluid balance

must be positive

for the successful

resuscitation

of shock

*Results (in%) of the votes of an interactive session (audience 300) during ISICEM, 2012

In fact there is strong evidence to support conservative late fluid

management in patients with septic shock, once the initial

resuscitation is completed (5). Hospital mortality was reduced

in those patients who initially received adequate fluid resuscitation

followed by conservative post resuscitation fluid management

(defined as having 2 consecutive negative daily fluid balances

within the first 7 days of ICU stay). In a meta-analysis of

40 studies that included 23,625 patients, mean cumulative fluid

balance after

1 week was

much lower

in survivors


than in nonsurvivors:

3110 ml vs 7738 ml (manuscript under preparation).

Hospital mortality was reduced in those

patients who initially received adequate

fluid resuscitation followed by conservative

post resuscitation fluid management

I dont care

Patients don’t die from anasarca (extreme edema), they die

from multi-organ failure, however organs need varying amounts

of fluids to function. For example, the lungs prefer to be dry

but the liver cannot function if it is too dry. However when there

is clinical evidence of capillary leak with peripheral edema

then there will also be end-organ edema resulting in end-organ

dysfunction, potentially leading to multiple organ dysfunction

syndrome.

There are three phases or ‘hits’ a body takes when exposed to

an inflammatory insult which includes trauma, infection, burn,

sepsis or bleeding.


First HIT – Acute

Inflammatory

Insult leading to systemic

inflammatory

response, microcirculatory

dysfunction,

and distributive

shock (hypotension,

hypovolemia, oliguria,

myocardial depression,

interstitial

edema formation,

tissue hypoxia, increasing

lactate levels)

Fluids are life saving

for early adequate

goal directed therapy.

Fluid balance should

be positive

Monitoring;

SVV, PPV, APP

(MAP-IAP), PLR,

TEO

Second HIT –

Ischemic Reperfusion

leading to MODS

Organ dysfunction

could be acute lung

injury, acute bowel

injury, acute kidney

injury, liver failure

and central nervous

system failure

Fluids should be used

as a biomarker. Late

conservative fluid

strategy with zero

fluid balance required

Monitoring;

EVLWI, PVPI, Intra

Abdominal Pressure

Third HIT if initial

treatment unresolved

Because of globally

increased permeability

syndrome edema

occurs in the lung,

gut, kidneys, peripheries

and brain with

potentially devastating

results

Fluids are toxic at

the stage with the

goal being late goal

directed fluid removal

and a negative fluid

balance

Monitoring;

ICG PDR, ScvO 2

MODS Multi organ dysfunction, APP abdominal perfusion pressure, PLR passive leg raising,

TEO transesophageal echo, SVV stroke volume variation, PPV pulse pressure variation, EVL-

WI extra vascular lung water index, PVPI pulmonary vascular permeability index, ICG PDR

indocyanine green plasma disappearance rate, ScvO2 mixed central venous oxygen saturation

Fluid Overload: An integrated approach

Recent evidence has shown that the use of PAL treatment,

combining PEEP with hypertonic albumin and diuretics to initiate

the flow phase of shock decreased EVLWI, intraabdominal

pressure and daily and cumulative fluid balance, duration

of mechanical ventilation and increased P/F ratio and survival

in 57 patients with acute lung injury compared to 57 matched

controls (6). PAL works as follows: PEEP moves fluids from the

alveoli into the interstitium, thereby increasing interstitial hydrostatic

pressure and decreasing interstitial oncotic pressure

and moving the interstitial fluids towards the capillaries. The

hyperoncotic albumin 20% increases the intravascular oncotic

pressure thereby removing fluids from the interstitium into the

capillaries and finally the frusemide (Lasix) helps remove fluid

from the patient.

KEY MESSAGES:

It is important to know:

PULSION Abstract Book - ISICEM Brussels 2012

page 27

• When to start giving fluids (low GEF/GEDVI, high PPV

and positive PLR, increased lactate)

• When to stop giving fluids (high GEF/GEDVI, low PPV,

negative PLR, normalized lactate)

• When to start removing fluids (high EVLWI, high PVPI,

raised IAP, low APP, positive fluid balance)

• When to stop fluid removal (low ICG-PDR, low APP, low

ScvO 2 , neutral fluid balance)

However these are moving targets with moving goals (early

adequate goal directed therapy, late conservative fluid management

and late goal directed fluid removal). One must also always

bear in mind that unnecessary fluid loading may be harmful.

If the patient doesn’t need fluids, don’t give them!

It is essential to give the right fluid at the right time, and to use

the correct monitor correctly.

References

1. Alsous F, Khamiees M, DeGirolamo A, Amoateng-Adjepong Y, Manthous

CA. Negative fluid balance predicts survival in patients with septic shock: a retrospective

pilot study. Chest 2000; 117: 1749-54

2. Wiedemann HP,Wheeler AP, Bernard GR, Thompson BT, Hayden D, de-

Boisblanc B, Connors AFJr, Hite RD, Harabin AL. Comparison of two fluidmanagement

strategies in acute lung injury.N Engl J Med 2006; 354(24): 2564-75

3. Dellinger RP, Levy MM et al. Surviving Sepsis Campaign: International guidelines

for management of severe sepsis and septic shock: 2008 Intensive Care

Med 2008; 34(1): 17-60

4. Malbrain ML, De Potter TJ, Dits H, Reuter DA. Global and right ventricular

end-diastolic volumes correlate better with preload after correction for ejection

fraction. Acta Anaesthesiol Scand 54(5): 622-31

5. Murphy CV, Schramm GE, Doherty JA, Reichley RM, Gajic O, Afessa B,

Micek S, T, Kollef MH. The importance of fluid management in acute lung injury

secondary to septic shock. Chest 2009; 136(1): 102-9

6. Cordemans C, De laet I, Van Regenmortel N, Schoonheydt K,Dits H, Martin

G, Huber W, Malbrain M. Aiming for negative fluid balance in patients with acute

lung injury and increased intra-abdominal pressure: A pilot study looking at the

effects of PAL-treatment. Ann Int Care 2012, 2(Suppl 1), In Press


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Tel. +49-(0)89-45 99 14-0 • Fax +49-(0)89-45 99 14-18

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MPI7006EN_R00 07/2012

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