Pulsion 548790 Strong Trading Buy (Seite 281)
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Beitrag zu dieser Diskussion schreiben
@scrollan1,
da nicht alle so klug sind wie Du, wollte ich gerne von Deinem Erfahrungsschatz bezüglich Pulsion profitieren! Hättest Du vielleicht Lust mir das Geschäftsmodell zu erklären, und mir die dann logischerweise auftretenden Fragen zu nennen?
Danke, katjuscha
PS: Das kann mir natürlich auch jemand anderes erklären!
da nicht alle so klug sind wie Du, wollte ich gerne von Deinem Erfahrungsschatz bezüglich Pulsion profitieren! Hättest Du vielleicht Lust mir das Geschäftsmodell zu erklären, und mir die dann logischerweise auftretenden Fragen zu nennen?
Danke, katjuscha
PS: Das kann mir natürlich auch jemand anderes erklären!
pulsion stößt langsam wieder auf interesse...
katel,
schau dir das geschäftsmodell genauer an...
dann stellst du andere fragen und bekommst antworten.
schau dir das geschäftsmodell genauer an...
dann stellst du andere fragen und bekommst antworten.
hallo Leute,
da Kontraindikator RicheyJames hier basht (der meist eh nur einsteigen will), habe ich mir die Aktie einmal genauer angeschaut!
Ich habe bei Ariva schon gefragt, aber keine Antwort erhalten! Deshalb frage ich mal hier!
Könnt Ihr mir sagen, wieviel Umsatz der Vertrag mit Draeger bringen könnte? genauer interessiert mich welchen Preis man pro Stückzahl man durch die Picco-Monitore erzielt, und wieviel Stückzahlen man nur durch den Deal mit Draeger voraussichtlich verkaufen kann! Schätzungen eurerseits würden mir schon reichen, da ich überhaupt keine Vorstellung habe!
katjuscha
da Kontraindikator RicheyJames hier basht (der meist eh nur einsteigen will), habe ich mir die Aktie einmal genauer angeschaut!
Ich habe bei Ariva schon gefragt, aber keine Antwort erhalten! Deshalb frage ich mal hier!
Könnt Ihr mir sagen, wieviel Umsatz der Vertrag mit Draeger bringen könnte? genauer interessiert mich welchen Preis man pro Stückzahl man durch die Picco-Monitore erzielt, und wieviel Stückzahlen man nur durch den Deal mit Draeger voraussichtlich verkaufen kann! Schätzungen eurerseits würden mir schon reichen, da ich überhaupt keine Vorstellung habe!
katjuscha
@all
Hallo zusammen, ich habe mich gerade bei WO: angemeldet, verfolge diese Thread aber schon eine Weile. Noch länger verfolge ich aber die Entwicklung von Pulsion. In den letzten Wochen habe ich mehrmals nachgekauft und Pulsion ist inzwischen zum wichtigsten Titel in meinem Depot herangewachsen. Aus diesem Grund ist es natürlich traurig das am Ende des heutigen Handelstages ein Minus zu Buche steht. Ich bin jedoch keineswegs bereit ohne eine Horrormeldung (die meines erachtens nicht kommen wird) auch nur eine dieser Aktien zu verkaufen. Ich halte es da wie Polyesterbauer, sollte der Kurs noch einmal unter 2,40 Euro fallen, dann wird nachgelegt. Es ist schon erstaunlich aber ich war mir selten so sicher das es einfach nur nach oben gehen kann wie jetzt bei Pulsion. Wer sich ein wenig mit Pulsion auskennt und weiß womit die ihr Geld verdienen wird mir sicherlich zustimmen. Allen anderen kann ich nur die Webseite http://ww.pulsion.de empfehlen, im Besonderen die Quartalsberichte.
Ob es bei Pulsion nun gerade charttechnisch gut oder schlecht aussieht ist mir eigentlich völlig egal. Die Storry stimmt und der Rest wird sich in den nächsten Monaten finden.
Gruß
FS
Hallo zusammen, ich habe mich gerade bei WO: angemeldet, verfolge diese Thread aber schon eine Weile. Noch länger verfolge ich aber die Entwicklung von Pulsion. In den letzten Wochen habe ich mehrmals nachgekauft und Pulsion ist inzwischen zum wichtigsten Titel in meinem Depot herangewachsen. Aus diesem Grund ist es natürlich traurig das am Ende des heutigen Handelstages ein Minus zu Buche steht. Ich bin jedoch keineswegs bereit ohne eine Horrormeldung (die meines erachtens nicht kommen wird) auch nur eine dieser Aktien zu verkaufen. Ich halte es da wie Polyesterbauer, sollte der Kurs noch einmal unter 2,40 Euro fallen, dann wird nachgelegt. Es ist schon erstaunlich aber ich war mir selten so sicher das es einfach nur nach oben gehen kann wie jetzt bei Pulsion. Wer sich ein wenig mit Pulsion auskennt und weiß womit die ihr Geld verdienen wird mir sicherlich zustimmen. Allen anderen kann ich nur die Webseite http://ww.pulsion.de empfehlen, im Besonderen die Quartalsberichte.
Ob es bei Pulsion nun gerade charttechnisch gut oder schlecht aussieht ist mir eigentlich völlig egal. Die Storry stimmt und der Rest wird sich in den nächsten Monaten finden.
Gruß
FS
Hallo Swiftnick,
bitter an solchen Tagen, aber doch wunderschön mit anzusehen, wie ein Ausbruch Pulsions über 2,90e verhindert werden soll. Kaum in den angesprochenen Bereich hervorgearbeitet, wird der zuvor sehr dünnbesiedelte ASK-Bereich mit 2k-Pakten im Centabstand
verteidigt. Die ASK-Wand zur Abschreckung und danach hier und da ein paar Stücke geschmissen, so dass die Aktie wieder in den Konsolidierungsbereich zwischen 2,40e und 2,80e fällt.
Denke nicht, dass wir noch einmal unter 2,40e fallen. Falls doch, wird gekauft, was das Zeug hält. Auf jeden Fall von meiner Seite aus. Von meinen ganzen Aktien im Depot kann ich mit einer Pulsion am besten schlafen.
Grüße
PoB
bitter an solchen Tagen, aber doch wunderschön mit anzusehen, wie ein Ausbruch Pulsions über 2,90e verhindert werden soll. Kaum in den angesprochenen Bereich hervorgearbeitet, wird der zuvor sehr dünnbesiedelte ASK-Bereich mit 2k-Pakten im Centabstand
verteidigt. Die ASK-Wand zur Abschreckung und danach hier und da ein paar Stücke geschmissen, so dass die Aktie wieder in den Konsolidierungsbereich zwischen 2,40e und 2,80e fällt.
Denke nicht, dass wir noch einmal unter 2,40e fallen. Falls doch, wird gekauft, was das Zeug hält. Auf jeden Fall von meiner Seite aus. Von meinen ganzen Aktien im Depot kann ich mit einer Pulsion am besten schlafen.
Grüße
PoB
Alles weniger erfreulich, offenbar ist weiter Konsolidierung angesagt. Ich hoffe, dass wenigstens die Unterstützung bei 2,40 hält.......
Jetzt wirds brenzlig.
#38
Kursbewegungen bei Miniumsätzen sind zu vernachlässigen, die nächsten Q.-Zahlen werden mit Sicherheit ordentlich ausfallen, sind allerdings höchstens für Zocker relevant, da die Pulsionstory von anderen Fakten (Vertragsabschlüsse/Marktdurchdringung) abhängig ist.
Für Hardcore-Fan´s hier noch ein paar neuere Info´s vom 9.1.04 (leider zum Großteil nur in Englisch):
Review
Cardiovascular monitoring tools: use and misuse
Bellomo R, Uchino S
Curr Opin Crit Care 9: 225 – 229, 2003
Objective: Review on current and novel hemodynamic practice in the intensive care unit.
Conclusion: Recent publications demonstrated that there is no benefit of therapy directed by the pulmonary artery
catheter (PAC). On the other hand, critically ill patients who require fluid administration and vasoactive drug therapy
typically have their central venous pressure and arterial pressure monitored. In this setting, the PiCCO Technology offers
the measurement of cardiac output, intrathoracic blood volume, and extravascular lung water at no additional risk to the
patient. Thus, the PAC may soon become obsolete. The lack of randomized studies to detect evidence of an effect on
clinical outcome is due to the fact that a study population of more than 10,000 patients would have to be included.
PULSION Comment:
Based on scientific argumentation, this review article clearly demonstrates the superiority of the PiCCO Technology over
the PAC. It also contains an excellent table on the risks associated with PAC vs PiCCO which is much in favour of the
PiCCO. In conclusion this article favours the wide-spread, deliberate use of the PiCCO Technology and gives the PAC
little chance to survive as a standard monitoring tool.
Zweck: Übersichtsartikel zur bisherigen und neuartigen Praxis der hämodynamischen Überwachung auf der
Intensivstation.
Zusammenfassung: Neuere Publikationen haben gezeigt, dass die Therapiesteuerung basierend auf dem
Pulmonalarterienkatheter (PAC) keinerlei Vorteile bringt. Andererseits wird bei kritisch kranken Patienten, bei denen ein
Volumenmanagement und eine Therapie mit vasoaktiven Substanzen notwendig ist, typischer weise auch der
zentralvenöse und arterielle Druck überwacht. In dieser Konfiguration bietet die PiCCO Technologie eine Messung von
Herzzeitvolumen, intrathorakalem Blutvolumen und extravasalem Lungenwasser ohne zusätzliches Risiko für den
Patienten. Daher wird der PAC in Kürze überflüssig werden. Das Fehlen von randomisierten Studien zum Nachweis
eines Effekts auf den Outcome liegt daran, dass dafür eine Studienpopulation von über 10.000 Patienten
eingeschlossen werden müsste.
PULSION Kommentar:
Basierend auf einer rein wissenschaftlichen Argumentation, zeigt diese Übersichtsarbeit deutlich die Überlegenheit der
PiCCO Technologie gegenüber dem PAC. Beinhaltet ist ebenfalls eine ausgezeichnete Tabelle in der die Risiken von
PAC vs. PiCCO dargestellt werden, mit überzeugenden Vorteilen von PiCCO. Insgesamt befürwortet dieser Artikel die
weit verbreitete und wohl erwogene Anwendung der PiCCO Technologie und gibt dem PAC nur geringe
Überlebenschancen als Standardmethode des Monitorings.
Cardiovascular monitoring tools: use and misuse
Rinaldo Bellomo, MD,* and Shigehiko Uchino, MD†
Purpose of review
To review important areas of current and novel hemodynamic
monitoring practice in the intensive care unit and to highlight
potential areas of physiologic and clinical use or misuse, as
well as areas of uncertainty and ongoing controversy.
Recent findings
To truly determine when hemodynamic monitoring tools are
misused would require randomized controlled evidence of a
measurable improvement in relevant clinical (as opposed to
physiologic) outcomes. Unfortunately, little evidence of this
kind exists, and that which does exist is highly controversial in
nature. Because of the limited evidence of an effect of
hemodynamic monitoring on clinical outcomes, the use and
misuse of hemodynamic monitoring tools is typically judged on
physiologic grounds (Does it improve physiology? Does it
predict physiology? Is it physiologically rational?). The relation
between physiologic gain and final clinical outcome, however,
is tenuous. Recent investigations confirm this lack of a clear
link. They also suggest that new technology that is now
emerging to less invasively measure cardiac output and
intrathoracic fluid compartments is ready for formal evaluations
of efficacy and effectiveness.
Summary
The effectiveness of hemodynamic monitoring in the intensive
care unit remains inadequately tested and unproven. New tools
are now rapidly emerging to challenge established
technologies. Formal assessment of their efficacy and
effectiveness is needed to avoid a repeat of the pulmonary
artery catheter experience.
Keywords
blood pressure, cardiac output, monitoring, outcome, pulse
contour analysis
Curr Opin Crit Care 9:225–229 © 2003 Lippincott Williams & Wilkins.
The evils of controversy are transitory, while its benefits
are permanent.
—R. Hall (1830)
Noninvasive hemodynamic monitoring (feeling and
counting the radial pulse, measuring the blood pressure
with a sphygmomanometer, visually assessing the jugular
venous pressure or the pressure in the neck veins, and so
on) appears, at first glance, to be safer than invasive hemodynamic
monitoring (use of central venous catheters,
arterial catheters, pulmonary artery catheters, transesophageal
Doppler monitoring, pulse contour analysis
with transpulmonary thermodilution). It is probably safer
in ambulatory patients, but it may not be safer when
applied to critically ill patients. In such situations, physicians
over the last 25 years have come to agree that
more invasive monitoring is ultimately safer for some
patients. Accordingly, they have created ICUs and operating
rooms with complex electronic monitoring systems
to apply such invasive hemodynamic technology as
deemed appropriate. However, no randomized controlled
trials have compared the management of acutely
ill patients using integrated clinical and laboratory assessment
(eg, Is the skin warm? Is the patient alert? Is the
patient producing urine? Is the sphygmomanometerdetermined
arterial pressure adequate? Is the blood lactate
normal? Is the serum creatinine stable?) with the
management of patients using the same noninvasive assessment
conducted with the addition of invasive hemodynamic
monitoring. Thus, we do not know for sure that
the way we practice every day in every ICU in developed
countries is beneficial to our patients. Although no such
trial will ever be conducted because of lack of equipoise,
and although consensus is strong, it is sobering to realize
how little formal validation there has been of any tools of
invasive hemodynamic monitoring in the ICU.
Efficacy of monitoring
Although we do not have direct evidence of any clinical
benefits from invasive hemodynamic monitoring, we believe
that more intensive monitoring (invasive and noninvasive)
is needed to ensure the safety of acutely ill
patients. If we did not, we would not have ICUs. Let’s
now, therefore, for a moment, take such safety for
granted (even though the insertion of intravascular catheters
is actually associated with a defined risk of infection,
pneumothorax, inadvertent arterial puncture, and
bleeding), and let’s simply ask ourselves whether advanced
monitoring is efficacious.
This question is difficult to answer because the concept
of efficacy indicates that an agent is capable of producing
Departments of *Intensive Care and †Surgery, Austin & Repatriation Medical
Center, Melbourne Victoria, Australia.
Correspondence to Rinaldo Bellomo, MD, Department of Intensive Care, Austin &
Repatriation Medical Center, Studley Rd., Heidelberg, Victoria 3084, Australia;
e-mail: rb@austin.unimelb.edu.au
Current Opinion in Critical Care 2003, 9:225–229
Abbreviations
CVP central venous pressure
PAC pulmonary artery catheter
PiCCO pulse contour cardiac output
ISSN 1070–5295 ©2003 Lippincott Williams & Wilkins
225
the desired effect. This may be obvious and easy to
define for an antihypertensive agent: the drug decreases
blood pressure compared with placebo. What should be
the measure of efficacy for a monitoring tool? A possible
answer is that it should be able to measure that which it
is designed to measure. Thus, a pulmonary artery catheter
(PAC) designed to measure the cardiac output
should be able to do so with accuracy and precision.
Using such criteria, most currently available monitoring
tools perform to an imperfect but seemingly reasonable
degree. Whether that is “good enough” remains controversial
yet practically unimportant because clinically applicable
more precise and accurate tools do not exist. If
they did, they would be used instead. More importantly,
however, such measurements cannot bring about physiologic
changes by themselves because they are not
therapeutic tools. In the field of hemodynamics, the
therapeutic tools are intravenous fluids, vasopressors,
inotropic agents, vasodilators, diuretics, and so on. Thus,
the effect of hemodynamic tools on physiology depends
on how the signals they provide are used by clinicians to
alter the use of therapeutic tools. There is ample evidence
that (1) some signals are not correctly interpreted
by physicians and (2) for a given signal, there can be
extremely variable responses, which will inevitably lead
to different physiologic outcomes and perhaps different
clinical outcomes [1].
Faced with such uncertainty and variability, many articles
have been written, debates conducted, and guidelines
issued about what kind of responses represent
physiologically correct or physiologically rational actions
given a certain signal [1]. However, although physiologically
rational behavior seems desirable, there is no evidence
that applying it makes any difference in terms of
patient outcome, that experts consistently agree on what
such “correct” approaches are, or that some of the signals
that we have used and continue to use to guide hemodynamic
management are the ones that we should be
measuring [1].
Furthermore, although there is much evidence that
nurses’ and physicians’ knowledge of the PAC is limited
[2–4], there is no evidence that clinicians who err in their
interpretation of, for example, PAC waves, would then
administer “wrong” therapies to patients, which would
result in worse clinical outcomes. Thus, establishing use
and misuse is very difficult indeed. Nonetheless, some
physiologic facts have emerged over the last 25 years that
are worth emphasizing.
Facts, not opinions
Despite the aforementioned controversies, some important
facts related to hemodynamic monitoring have been
convincingly demonstrated by many investigators
[5,6,7•,8•,9–11,12•,13,14•] in different groups of patients
as outlined in Table 1.
It should be reasonably assumed that these facts are well
known to critical care physicians, as they have been discussed,
presented, published, and disseminated over
many years. However, we do not have epidemiologic
evidence that such knowledge does exist. We also have
no evidence that clinicians who are aware of these hemodynamic
facts achieve better clinical outcomes than
physicians who are not. We would like to think so, but
we do not know. More importantly, daily observation in
any ICU would immediately indicate to any educated
observer that clinicians do not typically use any of these
hemodynamic signals in isolation. If they measure the
central venous pressure (CVP) to help them assess the
need for intravenous fluids, they use this information in
a context in which the blood pressure is known; skin
perfusion is assessed; urinary output, serum creatinine,
and blood lactate are measured; the fluid balance for the
last 24 hours or last few days is known in detail; and so
on. Thus, although the CVP, for example, is by itself a
rather inaccurate tool to predict a given cardiac output
response to intravenous fluids or to predict the right ventricular
end-diastolic volume, such deficiencies may not
matter in the clinical context. In such a situation it is the
CVP, lactate concentration, physical examination, urine
output, noninvasive echocardiographic data, serum creatinine
concentration, blood pressure, skin perfusion,
ventilator data, chest radiograph, arterial blood gases,
fluid balance, and more, all integrated with knowledge of
the patient’s illness and pre-illness status, that determine
hemodynamic management. No studies have been conducted
to test either the efficacy or the predictive value
or effectiveness of this approach. Thus, in 2003, we do
not know what the precision, accuracy, or physiologic
relevance of integrated hemodynamic monitoring (which
is what is used in ICUs in the developed world every
day) really is. This lack of knowledge is a problem. If we
Table 1. Factual observations about hemodynamic monitoring
1. The central venous pressure does not reliably predict the right
ventricular end-diastolic volume [5].
2. The pulmonary artery occlusion pressure does not reliably predict
left (or right) end-diastolic volume [5].
3. Neither the central venous pressure nor the pulmonary artery
occlusion pressure reliably predicts whether the administration of
a fluid bolus will or will not significantly increase cardiac output
[6,7•,8•].
4. The cardiac output cannot be reliably predicted by physical
examination [9].
5. Neither the central venous pressure nor the pulmonary artery
occlusion pressure reliably predicts the likelihood of developing
or having just developed pulmonary edema [10].
6. A mean arterial blood pressure within normal limits does not
reliably indicate an adequate cardiac output [9].
7. A normal value for calculated systemic oxygen delivery does not
reliably indicate adequate organ perfusion [11].
8. A normal mixed venous oxygen saturation does not reliably
indicate adequate organ perfusion [12].
9. A change in oxygen consumption in response to a change in
calculated oxygen delivery does not reliably indicate the presence
of an “oxygen debt” [13].
10. The pulmonary artery occlusion pressure is not the pressure in
the pulmonary capillaries [14•].
226 Cardiopulmonary monitoring
do not know the physiologic relevance of integrated data
from hemodynamic monitoring tools, how can we possibly
know their clinical relevance? If we know neither
physiologic nor clinical relevance, how can we establish
what is correct use and what is misuse of such tools?
We can probably say that using a single tool in isolation
is prone to a high likelihood of error, but we cannot say
much more than that. Furthermore, the meaning of such
statements is unclear. Investigators, if they so wish (and
they do seem to do so), can take a dozen single hemodynamic
signals and use each one in isolation to predict
an increment in cardiac output in response to fluid
therapy [5,6,7•,8•,9–11,12•]. They can statistically prove
that hemodynamic variable x correlates better than hemodynamic
variable y with a given increment in cardiac
output. Yet what is the clinical relevance of such information?
How many clinicians practice that way? Even if
thousands of physicians did, and even if variable x was
100% accurate in predicting a cardiac output response to
an intravenous fluid bolus, we still do not know whether
that fluid should be given in the first place. We still do
not know whether the clinical cost of 1 additional liter of
fluid in the body is worth the clinical gain of a 15%
increase in cardiac output. The cost–benefit ratio may be
low in a low cardiac output state (fluid should be given),
limited in the presence of a normal cardiac output (it
does not matter), and perhaps high in the setting of a
high cardiac output state (fluid makes things worse).
We can predict with an area under the receiver operating
characteristic curve of 1 that the blood pressure will increase
if norepinephrine is infused intravenously? This is
much better than the reported area under the receiver
operating characteristic curve for blood pressure variation’s
ability to predict an increment in cardiac output
with intravenous fluids during mechanical ventilation
[15]. Does that mean that we should therefore administer
norepinephrine? We think not. Is all of this hemodynamic
manipulation “much ado about nothing”? Is it
beneficial for the patient? Is it actually deleterious? In
modern ICUs, how often does organ failure occur because
of overt or covert hemodynamic insufficiency? Or
is organ failure immunologic in nature [16•], cytopathic
[17], or a result of mitochondrial dysfunction [18]? Does
increasing cardiac output in a septic patient simply lead
to an extra surge in cytotoxic plasma delivery to several
vital organs, thereby increasing rather than decreasing
organ injury? Until these fundamental questions have
been more clearly answered, it is impossible to define use
and misuse of hemodynamic tools.
What’s the point of measuring anything?
Based on the previous discussion, one could reasonably
conclude that (1) we have no adequate data to convincingly
show that hemodynamic monitoring tools are clinically
useful and (2) we have no data on how they are
being used in ICUs around the world. Given such observations,
perhaps we should call for a moratorium on all
invasive hemodynamic monitoring, just as some investigators
recently did for the PAC [1].
We believe that such an approach would be irrational. In
patients with shock who need vasoactive drugs, their
administration requires the presence of a central venous
catheter to avoid local tissue injury and to ensure reliable
delivery. Why not obtain continuous measurement of
CVP to add yet more data to help assess the patient’s
hemodynamic status?
If the patient needs an arterial line to help guide such
potent vasopressor drug administration in the same setting,
why not make the arterial catheter a thermistortipped
one and thus obtain continuous pulse contour
measurement of cardiac output and intermittent measurement
of intrathoracic blood volume and extravascular
lung water [8•]? Given that such data can be so easily
collected, why not do so?
At this point it is important to ask oneself how many
patients would have to be randomized to detect evidence
of an effect on clinical outcome of one kind of monitoring
versus another. Such thoughts would help clinicians
realize why we still know so little of what constitutes use
or misuse of these tools.
Trial size, if mortality rate is the primary outcome measure,
depends on the expected mortality rate of the control
group. Assuming a mortality rate of 15% in the control
group, it would take a study population of more than
10,000 patients to detect a 10% relative decrease in mortality
rate. Assuming a minimal cost of $300 per patient
recruited, this study would cost more than $3 million. If
the baseline mortality rate were 7.7%, as in the recent
largest study of the PAC in surgical patients [19•], even
with 1994 patients one would only have a 20% power of
detecting a 20% relative decrease in mortality rate. To
change the power to 90%, 14,240 patients would have to
be randomized!
What should we measure? Pressures
or volumes?
Critically ill patients who require fluid resuscitation and
vasoactive drug therapy typically have their CVP and
arterial pressure monitored. With the arrival of the PAC,
the availability of cardiac output measurement created
further goals for manipulation. Because of the perceived
need to augment cardiac output (When is a given cardiac
output ever enough?), various investigations have been
conducted to allow physicians to predict when the administration
of an intravenous bolus of fluids would increase
the cardiac output. It has become clear that static
pressure measurements are not very good at predicting
such changes and that, in fact, phasic changes in blood
pressure induced by mechanical ventilation might be the
best pressure-based measurements to use in predicting
Cardiovascular monitoring tools Bellomo and Uchino 227
such a response [15]. Should we be going back to just
measuring the blood pressure then? Probably not. We
need the cardiac output to confirm such a response and
perhaps filling pressures to help us decide when to stop.
All of this might still require a PAC, with all of its risks
[20,21]. More recently, however, technology that provides
a simple and easier alternative has been developed
and applied (pulse contour cardiac output [PiCCO] system;
Pulsion Medical Systems, Munich, Germany). Such
new technology means that any patient who needs a
central venous catheter and an arterial catheter for drug
infusion and pressure monitoring can also have three
other variables measured to help guide therapy: continuous
cardiac output, intrathoracic blood volume, and extravascular
lung water [22,23,24•,25,26]. In this setting,
the PiCCO system offers a whole new set of data at no
additional risk to the patient. Will such technology deliver
better patient outcomes? Once again, it will take a
long time to arrive at the answer given that, almost 30
years later, we still do not know whether the PAC can
deliver better patient outcomes. Nonetheless, evidence
is emerging that volume-based assessment of intravascular
filling associated with continuous cardiac output can
deliver levels of prediction of cardiac output changes that
might be superior to those obtained with older technology
[8•]. As practitioners familiar with both technologies,
we find ourselves increasingly abandoning the PAC in
favor of the PiCCO system because (1) the data on volume
and extravascular lung water seem more physiologically
and clinically relevant [24•,25,26] in defining the
variables we wish to modulate and (2) there is no additional
risk to a patient who has a central venous catheter
and needs an arterial catheter for continuous blood pressure
monitoring anyway (Table 2).Thus, the PAC may
soon become obsolete.
Testing hemodynamic monitoring tools:
science and controversy
To our knowledge, there are two important randomized
controlled trials that have attempted to address the issue
of whether hemodynamic monitoring can affect clinical
outcomes. The first study was conducted by Rivers et al.
[27•], who randomized 263 emergency department patients
with severe sepsis or septic shock to receive 6
hours of goal-directed therapy guided by a new central
venous catheter able to deliver continuous central venous
oximetric data or standard care. Patients randomized
to the intervention experienced a close to 30% decrease
in mortality rate (P = 0.009).
Sandham et al. [19•] recently completed a large trial during
which the investigators randomized 1994 American
Society of Anesthesiologists physical status III or IV patients
who were scheduled for surgery and postoperative
ICU stay. Half of the patients were randomized to receive
goal-directed therapy guided by PAC, while the
other half received standard care without the use of the
PAC [20]. Goal-directed therapy meant that, in this trial,
those patients randomized to have a PAC should receive
interventions whenever possible to achieve the following
goals in order of priority: (1) an oxygen delivery of 550 to
600 mL/min/m2, (2) a cardiac index of 3.5 to 4.5
L/min/m2; (3) a mean arterial pressure of 70 mm Hg, (4)
a pulmonary artery occlusion pressure of 18 mm Hg; (5)
a heart rate less that 120 beats per minute; and (6) a
hematocrit greater than 27%. This trial showed that more
patients in the goal-directed therapy group received inotropic
agents (P < 0.001), vasodilators (P < 0.001), antihypertensive
medication (P < 0.001), packed cells (P <
0.001), and colloid fluids (P = 0.002). The mortality rate
of control patients was 7.7% compared with 7.8% in the
PAC group. Interestingly, there was a significant increase
in the incidence of pulmonary embolism among the PAC
patients (P = 0.004). The investigators concluded that
there was “no benefit of therapy directed by PAC over
standard care in elderly, high-risk surgical patients requiring
intensive care” [19•].
Although each trial deserves detailed discussion, which
cannot be done here, the recent evidence appears to
overwhelmingly suggest that, in patients in the ICU or
operating room, either (1) using the PAC to guide
therapy is not helpful or (2) PAC monitoring might be
unhelpful but only when “wrongly” used to achieve supranormal
values of cardiac index or oxygen delivery.
Things might be different in emergency room patients,
but the study by Rivers et al. [27•] is a single-center
investigation with a higher than expected mortality rate
in the control group and huge potential for a “Hawthorne
effect” of monitoring. Thus, more information is needed
in this setting.
Table 2. Comparative advantages and disadvantages of the
pulmonary artery catheter and pulse contour cardiac
output technology
Aspect/variable PAC PiCCO
Cardiac output Yes (continuous with
special technology)
Yes (always
continuous)
PAOP Yes No
Pulmonary pressures Yes No
RAP Yes Yes
RVEDV Yes, with special
technology
No
End-diastolic
intrathoracic volume
No Yes
Extravascular lung water
index
No Yes
Risk of pneumothorax Yes No
Risk of infection +++ +
Risk of arterial puncture Yes No
Risk of pulmonary artery
rupture
Yes No
Risk of air embolus Yes No
PAC, pulmonary artery catheter; PAOP, pulmonary artery occlusion
pressure; PiCCO, pulse contour cardiac output; RAP, right atrial
pressure; RVEDV, right ventricular end-diastolic volume.
228 Cardiopulmonary monitoring
Conclusions
Much work needs to be done before we can decide how
best to use hemodynamic tools and how to avoid their
misuse. Such research is difficult and controversial in
design. The so-called experts have spent almost 15 years
trying to tell us that we should maximize oxygen delivery
in ICU or operative patients [19•]. The data now stand in
stark contrast to such claims and demonstrate a case of
past and probably present misuse. The experts are now
going to tell us how to use the PAC in acute respiratory
distress syndrome with protocols (ARDSNet:
http://hedwig.mgh.harvard.edu/ardsnet/ards05.html) that
make no physiologic sense. With the proposed acute respiratory
distress syndrome protocol, clinicians could
give patients with acute respiratory distress syndrome
randomized to so-called “fluid conservative therapy”
who have a cardiac index of 4 L/min/m2, a CVP of 14 mm
Hg, a urine output of 0.6 mL/kg/h, a fraction of inspired
oxygen of 0.65, an arterial oxygen tension of 58 mm Hg,
and develop a mean arterial pressure of 55 mm Hg (vasodilatory
shock) a bolus of 15 mL/kg of saline [sic] as
possible therapy. How is this physiologically reasonable?
In our opinion, when it comes to such expert advice, the
expression caveat emptor seems most appropriate. Thus,
the debate will continue, physiologically irrational use of
hemodynamic tools will also continue, and controversy
will flourish. Nonetheless, we look forward to the day
when trials of the PAC use this tool not to achieve supranormal
values but to maintain homeostasis, when volume-
based instead of pressure-based hemodynamic tools
are used to guide therapy and prevent both inadequate
diastolic filling and inappropriate surges in extravascular
lung water, and when, in the field of hemodynamics,
more clinical outcome-based studies become available to
help us choose the right tool and the right use for the
tool.
References and recommended reading
Papers of particular interest, published within the annual period of review,
have been highlighted as:
• Of special interest
•• Of outstanding interest
1 Pulmonary Artery Catheter Consensus Conference: consensus statement.
New Horiz 1997, 5:175–194.
2 Iberti TJ, Daily EK, Leibowitz AB, et al.: Assessment of critical care nurses’
knowledge of the pulmonary artery catheter. Crit Care Med 1994, 22:1674–
1678.
3 Iberti TJ, Fischer EP, Liebowitz AB, et al.: A multicenter study of physicians’
knowledge of the pulmonary artery catheter. JAMA 1990, 264:2928–2932.
4 Gnaegi A, Feihl F, Perret C: Intensive care physicians’ insufficient knowledge
of right heart catheterization at the bedside: time to act? Crit Care Med 1997,
25:213–220.
5 Nelson L: The new pulmonary artery catheter: continuous venous oximetry,
right ventricular ejection fraction and continuous cardiac output. New Horiz
1997, 5:251–258.
6 Diebel L, Wilson R, Tagett MG, et al.: End-diastolic volume: a better indicator
of pre-load in the critically ill. Arch Surg 1992, 127:817–822.
•
7 Pinsky MR: Functional hemodynamic monitoring. Intensive Care Med 2002,
28:386–388.
This article provides a clear explanation of the possible utility of functional dynamic
monitoring instead of static pressure monitoring in ventilated patients.
•
8 Reuter DA, Felbinger TW, Schmidt C, et al.: Stroke volume variations for
assessment of cardiac responsiveness to volume loading in mechanically
ventilated patients after cardiac surgery. Intensive Care Med 2002, 28:392–
398.
This article provides preliminary evidence that variations in continuously measured
volume signals using PiCCO technology can usefully predict the cardiac output
response to fluid therapy.
9 Eisenberg PR, Jaffe AS, Schuster DP: Clinical evaluation compared to pulmonary
artery catheterization in the hemodynamic assessment of critically ill
patients. Crit Care Med 1984, 12:549–553.
10 Levy MM: Pulmonary capillary pressure and tissue perfusion: clinical implications
during resuscitation from shock. New Horiz 1996, 4:504–518.
11 Schlichtig R, Kramer D, Pinsky MR: Flow redistribution during progressive
hemorrhage is a determinant of critical O2 delivery. J Appl Physiol 1991,
70:169–178.
•
12 Boldt J: Clinical review: hemodynamic monitoring in the intensive care unit.
Crit Care 2002, 6:52–59.
A useful brief review of new technology for hemodynamic monitoring.
13 Bellomo R, Pinsky MR: Invasive hemodynamic monitoring. In Critical Care:
Standards, Audit and Ethics. Edited by Tinker J, Browne DRG, Sibbald WJ.
New York: Oxford University Press; 1996:82–104.
•
14 Pinsky MR: Pulmonary artery occlusion pressure. Intensive Care Med 2003,
29:19–22.
An excellent review of issues related to the interpretation of pulmonary artery occlusion
pressure waves.
15 Michard F, Boussat S, Chemla D, et al.: Relation between respiratory
changes in arterial pulse pressure and fluid responsiveness in septic patients
with acute circulatory failure. Am J Respir Crit Care Med 2000, 162:134–
138.
•
16 Hotchkiss RS, Karl IE: The pathophysiology and treatment of sepsis. N Engl J
Med 2003, 348:138–150.
An excellent review of the importance of nonhemodynamic factors in sepsis.
17 Fink MP: Bench-to-bedside review: cytopathic hypoxia. Crit Care 2002,
6:491–499.
18 Adrie C, Bachelot M, Vayssier-Taussat, et al.: Mitochondrial membrane potential
and apoptosis of peripheral blood monocytes in severe human sepsis.
Am J Respir Crit Care Med 2001, 164:389–395.
•
19 Sandham JD, Hull RD, Brant RF, et al.: A randomized controlled trial of the use
of pulmonary artery catheters in high-risk surgical patients. N Engl J Med
2003, 348:5–14.
The largest randomized controlled trial of the PAC in surgical patients.
20 Boyd KD, Thomas SJ, Gold J, et al.: A prospective study of complications of
pulmonary artery catheters in 500 consecutive patients. Chest 1983,
84:245–249.
21 Connors AF Jr, Castele RJ, Farhat NZ, et al.: Complications of pulmonary
artery catheterization. A prospective autopsy study. Chest 1985, 88:567–
572.
22 Sakka SG, Ruhl CC, Pfeiffer UJ, et al.: Assessment of cardiac preload and
extravascular lung water by single transpulmonary thermodilution. Intensive
Care Med 2000, 26:180–187.
23 Holm C, Melcer B, Horbrand F, et al.: Intrathoracic blood volume as an end
point in resuscitation of the severely burned: an observational study of 24
patients. J Trauma 2000, 48:728–734.
•
24 Sakka SG, Klein M, Reinhart K, et al.: Prognostic value of extravascular lung
water in critically ill patients. Chest 2002, 122:2080–2086.
The first demonstration of the clinical relevance of the extravascular lung water
signal in ICU patients.
25 Boussat S, Jacques T, Levy B, et al.: Intravascular volume monitoring and
extravascular lung water in septic patients with pulmonary edema. Intensive
Care Med 2002, 28:712–718.
26 Goedje O, Hoeke K, Lichtwarck-Aschoff M, et al.: Continuous cardiac output
by femoral thermodilution calibrated contour analysis: comparison with pulmonary
arterial thermodilution. Crit Care Med 1999, 27:2407–2412.
•
27 Rivers E, Nguyen B, Havstad S, et al.: Early goal-directed therapy in the treatment
of severe sepsis and septic shock. N Engl J Med 2001, 345:1368–
1377.
The first randomized controlled trial of mixed venous saturation monitoring in septic
patients in the emergency department.
Cardiovascular monitoring tools Bellomo and Uchino 229
Kursbewegungen bei Miniumsätzen sind zu vernachlässigen, die nächsten Q.-Zahlen werden mit Sicherheit ordentlich ausfallen, sind allerdings höchstens für Zocker relevant, da die Pulsionstory von anderen Fakten (Vertragsabschlüsse/Marktdurchdringung) abhängig ist.
Für Hardcore-Fan´s hier noch ein paar neuere Info´s vom 9.1.04 (leider zum Großteil nur in Englisch):
Review
Cardiovascular monitoring tools: use and misuse
Bellomo R, Uchino S
Curr Opin Crit Care 9: 225 – 229, 2003
Objective: Review on current and novel hemodynamic practice in the intensive care unit.
Conclusion: Recent publications demonstrated that there is no benefit of therapy directed by the pulmonary artery
catheter (PAC). On the other hand, critically ill patients who require fluid administration and vasoactive drug therapy
typically have their central venous pressure and arterial pressure monitored. In this setting, the PiCCO Technology offers
the measurement of cardiac output, intrathoracic blood volume, and extravascular lung water at no additional risk to the
patient. Thus, the PAC may soon become obsolete. The lack of randomized studies to detect evidence of an effect on
clinical outcome is due to the fact that a study population of more than 10,000 patients would have to be included.
PULSION Comment:
Based on scientific argumentation, this review article clearly demonstrates the superiority of the PiCCO Technology over
the PAC. It also contains an excellent table on the risks associated with PAC vs PiCCO which is much in favour of the
PiCCO. In conclusion this article favours the wide-spread, deliberate use of the PiCCO Technology and gives the PAC
little chance to survive as a standard monitoring tool.
Zweck: Übersichtsartikel zur bisherigen und neuartigen Praxis der hämodynamischen Überwachung auf der
Intensivstation.
Zusammenfassung: Neuere Publikationen haben gezeigt, dass die Therapiesteuerung basierend auf dem
Pulmonalarterienkatheter (PAC) keinerlei Vorteile bringt. Andererseits wird bei kritisch kranken Patienten, bei denen ein
Volumenmanagement und eine Therapie mit vasoaktiven Substanzen notwendig ist, typischer weise auch der
zentralvenöse und arterielle Druck überwacht. In dieser Konfiguration bietet die PiCCO Technologie eine Messung von
Herzzeitvolumen, intrathorakalem Blutvolumen und extravasalem Lungenwasser ohne zusätzliches Risiko für den
Patienten. Daher wird der PAC in Kürze überflüssig werden. Das Fehlen von randomisierten Studien zum Nachweis
eines Effekts auf den Outcome liegt daran, dass dafür eine Studienpopulation von über 10.000 Patienten
eingeschlossen werden müsste.
PULSION Kommentar:
Basierend auf einer rein wissenschaftlichen Argumentation, zeigt diese Übersichtsarbeit deutlich die Überlegenheit der
PiCCO Technologie gegenüber dem PAC. Beinhaltet ist ebenfalls eine ausgezeichnete Tabelle in der die Risiken von
PAC vs. PiCCO dargestellt werden, mit überzeugenden Vorteilen von PiCCO. Insgesamt befürwortet dieser Artikel die
weit verbreitete und wohl erwogene Anwendung der PiCCO Technologie und gibt dem PAC nur geringe
Überlebenschancen als Standardmethode des Monitorings.
Cardiovascular monitoring tools: use and misuse
Rinaldo Bellomo, MD,* and Shigehiko Uchino, MD†
Purpose of review
To review important areas of current and novel hemodynamic
monitoring practice in the intensive care unit and to highlight
potential areas of physiologic and clinical use or misuse, as
well as areas of uncertainty and ongoing controversy.
Recent findings
To truly determine when hemodynamic monitoring tools are
misused would require randomized controlled evidence of a
measurable improvement in relevant clinical (as opposed to
physiologic) outcomes. Unfortunately, little evidence of this
kind exists, and that which does exist is highly controversial in
nature. Because of the limited evidence of an effect of
hemodynamic monitoring on clinical outcomes, the use and
misuse of hemodynamic monitoring tools is typically judged on
physiologic grounds (Does it improve physiology? Does it
predict physiology? Is it physiologically rational?). The relation
between physiologic gain and final clinical outcome, however,
is tenuous. Recent investigations confirm this lack of a clear
link. They also suggest that new technology that is now
emerging to less invasively measure cardiac output and
intrathoracic fluid compartments is ready for formal evaluations
of efficacy and effectiveness.
Summary
The effectiveness of hemodynamic monitoring in the intensive
care unit remains inadequately tested and unproven. New tools
are now rapidly emerging to challenge established
technologies. Formal assessment of their efficacy and
effectiveness is needed to avoid a repeat of the pulmonary
artery catheter experience.
Keywords
blood pressure, cardiac output, monitoring, outcome, pulse
contour analysis
Curr Opin Crit Care 9:225–229 © 2003 Lippincott Williams & Wilkins.
The evils of controversy are transitory, while its benefits
are permanent.
—R. Hall (1830)
Noninvasive hemodynamic monitoring (feeling and
counting the radial pulse, measuring the blood pressure
with a sphygmomanometer, visually assessing the jugular
venous pressure or the pressure in the neck veins, and so
on) appears, at first glance, to be safer than invasive hemodynamic
monitoring (use of central venous catheters,
arterial catheters, pulmonary artery catheters, transesophageal
Doppler monitoring, pulse contour analysis
with transpulmonary thermodilution). It is probably safer
in ambulatory patients, but it may not be safer when
applied to critically ill patients. In such situations, physicians
over the last 25 years have come to agree that
more invasive monitoring is ultimately safer for some
patients. Accordingly, they have created ICUs and operating
rooms with complex electronic monitoring systems
to apply such invasive hemodynamic technology as
deemed appropriate. However, no randomized controlled
trials have compared the management of acutely
ill patients using integrated clinical and laboratory assessment
(eg, Is the skin warm? Is the patient alert? Is the
patient producing urine? Is the sphygmomanometerdetermined
arterial pressure adequate? Is the blood lactate
normal? Is the serum creatinine stable?) with the
management of patients using the same noninvasive assessment
conducted with the addition of invasive hemodynamic
monitoring. Thus, we do not know for sure that
the way we practice every day in every ICU in developed
countries is beneficial to our patients. Although no such
trial will ever be conducted because of lack of equipoise,
and although consensus is strong, it is sobering to realize
how little formal validation there has been of any tools of
invasive hemodynamic monitoring in the ICU.
Efficacy of monitoring
Although we do not have direct evidence of any clinical
benefits from invasive hemodynamic monitoring, we believe
that more intensive monitoring (invasive and noninvasive)
is needed to ensure the safety of acutely ill
patients. If we did not, we would not have ICUs. Let’s
now, therefore, for a moment, take such safety for
granted (even though the insertion of intravascular catheters
is actually associated with a defined risk of infection,
pneumothorax, inadvertent arterial puncture, and
bleeding), and let’s simply ask ourselves whether advanced
monitoring is efficacious.
This question is difficult to answer because the concept
of efficacy indicates that an agent is capable of producing
Departments of *Intensive Care and †Surgery, Austin & Repatriation Medical
Center, Melbourne Victoria, Australia.
Correspondence to Rinaldo Bellomo, MD, Department of Intensive Care, Austin &
Repatriation Medical Center, Studley Rd., Heidelberg, Victoria 3084, Australia;
e-mail: rb@austin.unimelb.edu.au
Current Opinion in Critical Care 2003, 9:225–229
Abbreviations
CVP central venous pressure
PAC pulmonary artery catheter
PiCCO pulse contour cardiac output
ISSN 1070–5295 ©2003 Lippincott Williams & Wilkins
225
the desired effect. This may be obvious and easy to
define for an antihypertensive agent: the drug decreases
blood pressure compared with placebo. What should be
the measure of efficacy for a monitoring tool? A possible
answer is that it should be able to measure that which it
is designed to measure. Thus, a pulmonary artery catheter
(PAC) designed to measure the cardiac output
should be able to do so with accuracy and precision.
Using such criteria, most currently available monitoring
tools perform to an imperfect but seemingly reasonable
degree. Whether that is “good enough” remains controversial
yet practically unimportant because clinically applicable
more precise and accurate tools do not exist. If
they did, they would be used instead. More importantly,
however, such measurements cannot bring about physiologic
changes by themselves because they are not
therapeutic tools. In the field of hemodynamics, the
therapeutic tools are intravenous fluids, vasopressors,
inotropic agents, vasodilators, diuretics, and so on. Thus,
the effect of hemodynamic tools on physiology depends
on how the signals they provide are used by clinicians to
alter the use of therapeutic tools. There is ample evidence
that (1) some signals are not correctly interpreted
by physicians and (2) for a given signal, there can be
extremely variable responses, which will inevitably lead
to different physiologic outcomes and perhaps different
clinical outcomes [1].
Faced with such uncertainty and variability, many articles
have been written, debates conducted, and guidelines
issued about what kind of responses represent
physiologically correct or physiologically rational actions
given a certain signal [1]. However, although physiologically
rational behavior seems desirable, there is no evidence
that applying it makes any difference in terms of
patient outcome, that experts consistently agree on what
such “correct” approaches are, or that some of the signals
that we have used and continue to use to guide hemodynamic
management are the ones that we should be
measuring [1].
Furthermore, although there is much evidence that
nurses’ and physicians’ knowledge of the PAC is limited
[2–4], there is no evidence that clinicians who err in their
interpretation of, for example, PAC waves, would then
administer “wrong” therapies to patients, which would
result in worse clinical outcomes. Thus, establishing use
and misuse is very difficult indeed. Nonetheless, some
physiologic facts have emerged over the last 25 years that
are worth emphasizing.
Facts, not opinions
Despite the aforementioned controversies, some important
facts related to hemodynamic monitoring have been
convincingly demonstrated by many investigators
[5,6,7•,8•,9–11,12•,13,14•] in different groups of patients
as outlined in Table 1.
It should be reasonably assumed that these facts are well
known to critical care physicians, as they have been discussed,
presented, published, and disseminated over
many years. However, we do not have epidemiologic
evidence that such knowledge does exist. We also have
no evidence that clinicians who are aware of these hemodynamic
facts achieve better clinical outcomes than
physicians who are not. We would like to think so, but
we do not know. More importantly, daily observation in
any ICU would immediately indicate to any educated
observer that clinicians do not typically use any of these
hemodynamic signals in isolation. If they measure the
central venous pressure (CVP) to help them assess the
need for intravenous fluids, they use this information in
a context in which the blood pressure is known; skin
perfusion is assessed; urinary output, serum creatinine,
and blood lactate are measured; the fluid balance for the
last 24 hours or last few days is known in detail; and so
on. Thus, although the CVP, for example, is by itself a
rather inaccurate tool to predict a given cardiac output
response to intravenous fluids or to predict the right ventricular
end-diastolic volume, such deficiencies may not
matter in the clinical context. In such a situation it is the
CVP, lactate concentration, physical examination, urine
output, noninvasive echocardiographic data, serum creatinine
concentration, blood pressure, skin perfusion,
ventilator data, chest radiograph, arterial blood gases,
fluid balance, and more, all integrated with knowledge of
the patient’s illness and pre-illness status, that determine
hemodynamic management. No studies have been conducted
to test either the efficacy or the predictive value
or effectiveness of this approach. Thus, in 2003, we do
not know what the precision, accuracy, or physiologic
relevance of integrated hemodynamic monitoring (which
is what is used in ICUs in the developed world every
day) really is. This lack of knowledge is a problem. If we
Table 1. Factual observations about hemodynamic monitoring
1. The central venous pressure does not reliably predict the right
ventricular end-diastolic volume [5].
2. The pulmonary artery occlusion pressure does not reliably predict
left (or right) end-diastolic volume [5].
3. Neither the central venous pressure nor the pulmonary artery
occlusion pressure reliably predicts whether the administration of
a fluid bolus will or will not significantly increase cardiac output
[6,7•,8•].
4. The cardiac output cannot be reliably predicted by physical
examination [9].
5. Neither the central venous pressure nor the pulmonary artery
occlusion pressure reliably predicts the likelihood of developing
or having just developed pulmonary edema [10].
6. A mean arterial blood pressure within normal limits does not
reliably indicate an adequate cardiac output [9].
7. A normal value for calculated systemic oxygen delivery does not
reliably indicate adequate organ perfusion [11].
8. A normal mixed venous oxygen saturation does not reliably
indicate adequate organ perfusion [12].
9. A change in oxygen consumption in response to a change in
calculated oxygen delivery does not reliably indicate the presence
of an “oxygen debt” [13].
10. The pulmonary artery occlusion pressure is not the pressure in
the pulmonary capillaries [14•].
226 Cardiopulmonary monitoring
do not know the physiologic relevance of integrated data
from hemodynamic monitoring tools, how can we possibly
know their clinical relevance? If we know neither
physiologic nor clinical relevance, how can we establish
what is correct use and what is misuse of such tools?
We can probably say that using a single tool in isolation
is prone to a high likelihood of error, but we cannot say
much more than that. Furthermore, the meaning of such
statements is unclear. Investigators, if they so wish (and
they do seem to do so), can take a dozen single hemodynamic
signals and use each one in isolation to predict
an increment in cardiac output in response to fluid
therapy [5,6,7•,8•,9–11,12•]. They can statistically prove
that hemodynamic variable x correlates better than hemodynamic
variable y with a given increment in cardiac
output. Yet what is the clinical relevance of such information?
How many clinicians practice that way? Even if
thousands of physicians did, and even if variable x was
100% accurate in predicting a cardiac output response to
an intravenous fluid bolus, we still do not know whether
that fluid should be given in the first place. We still do
not know whether the clinical cost of 1 additional liter of
fluid in the body is worth the clinical gain of a 15%
increase in cardiac output. The cost–benefit ratio may be
low in a low cardiac output state (fluid should be given),
limited in the presence of a normal cardiac output (it
does not matter), and perhaps high in the setting of a
high cardiac output state (fluid makes things worse).
We can predict with an area under the receiver operating
characteristic curve of 1 that the blood pressure will increase
if norepinephrine is infused intravenously? This is
much better than the reported area under the receiver
operating characteristic curve for blood pressure variation’s
ability to predict an increment in cardiac output
with intravenous fluids during mechanical ventilation
[15]. Does that mean that we should therefore administer
norepinephrine? We think not. Is all of this hemodynamic
manipulation “much ado about nothing”? Is it
beneficial for the patient? Is it actually deleterious? In
modern ICUs, how often does organ failure occur because
of overt or covert hemodynamic insufficiency? Or
is organ failure immunologic in nature [16•], cytopathic
[17], or a result of mitochondrial dysfunction [18]? Does
increasing cardiac output in a septic patient simply lead
to an extra surge in cytotoxic plasma delivery to several
vital organs, thereby increasing rather than decreasing
organ injury? Until these fundamental questions have
been more clearly answered, it is impossible to define use
and misuse of hemodynamic tools.
What’s the point of measuring anything?
Based on the previous discussion, one could reasonably
conclude that (1) we have no adequate data to convincingly
show that hemodynamic monitoring tools are clinically
useful and (2) we have no data on how they are
being used in ICUs around the world. Given such observations,
perhaps we should call for a moratorium on all
invasive hemodynamic monitoring, just as some investigators
recently did for the PAC [1].
We believe that such an approach would be irrational. In
patients with shock who need vasoactive drugs, their
administration requires the presence of a central venous
catheter to avoid local tissue injury and to ensure reliable
delivery. Why not obtain continuous measurement of
CVP to add yet more data to help assess the patient’s
hemodynamic status?
If the patient needs an arterial line to help guide such
potent vasopressor drug administration in the same setting,
why not make the arterial catheter a thermistortipped
one and thus obtain continuous pulse contour
measurement of cardiac output and intermittent measurement
of intrathoracic blood volume and extravascular
lung water [8•]? Given that such data can be so easily
collected, why not do so?
At this point it is important to ask oneself how many
patients would have to be randomized to detect evidence
of an effect on clinical outcome of one kind of monitoring
versus another. Such thoughts would help clinicians
realize why we still know so little of what constitutes use
or misuse of these tools.
Trial size, if mortality rate is the primary outcome measure,
depends on the expected mortality rate of the control
group. Assuming a mortality rate of 15% in the control
group, it would take a study population of more than
10,000 patients to detect a 10% relative decrease in mortality
rate. Assuming a minimal cost of $300 per patient
recruited, this study would cost more than $3 million. If
the baseline mortality rate were 7.7%, as in the recent
largest study of the PAC in surgical patients [19•], even
with 1994 patients one would only have a 20% power of
detecting a 20% relative decrease in mortality rate. To
change the power to 90%, 14,240 patients would have to
be randomized!
What should we measure? Pressures
or volumes?
Critically ill patients who require fluid resuscitation and
vasoactive drug therapy typically have their CVP and
arterial pressure monitored. With the arrival of the PAC,
the availability of cardiac output measurement created
further goals for manipulation. Because of the perceived
need to augment cardiac output (When is a given cardiac
output ever enough?), various investigations have been
conducted to allow physicians to predict when the administration
of an intravenous bolus of fluids would increase
the cardiac output. It has become clear that static
pressure measurements are not very good at predicting
such changes and that, in fact, phasic changes in blood
pressure induced by mechanical ventilation might be the
best pressure-based measurements to use in predicting
Cardiovascular monitoring tools Bellomo and Uchino 227
such a response [15]. Should we be going back to just
measuring the blood pressure then? Probably not. We
need the cardiac output to confirm such a response and
perhaps filling pressures to help us decide when to stop.
All of this might still require a PAC, with all of its risks
[20,21]. More recently, however, technology that provides
a simple and easier alternative has been developed
and applied (pulse contour cardiac output [PiCCO] system;
Pulsion Medical Systems, Munich, Germany). Such
new technology means that any patient who needs a
central venous catheter and an arterial catheter for drug
infusion and pressure monitoring can also have three
other variables measured to help guide therapy: continuous
cardiac output, intrathoracic blood volume, and extravascular
lung water [22,23,24•,25,26]. In this setting,
the PiCCO system offers a whole new set of data at no
additional risk to the patient. Will such technology deliver
better patient outcomes? Once again, it will take a
long time to arrive at the answer given that, almost 30
years later, we still do not know whether the PAC can
deliver better patient outcomes. Nonetheless, evidence
is emerging that volume-based assessment of intravascular
filling associated with continuous cardiac output can
deliver levels of prediction of cardiac output changes that
might be superior to those obtained with older technology
[8•]. As practitioners familiar with both technologies,
we find ourselves increasingly abandoning the PAC in
favor of the PiCCO system because (1) the data on volume
and extravascular lung water seem more physiologically
and clinically relevant [24•,25,26] in defining the
variables we wish to modulate and (2) there is no additional
risk to a patient who has a central venous catheter
and needs an arterial catheter for continuous blood pressure
monitoring anyway (Table 2).Thus, the PAC may
soon become obsolete.
Testing hemodynamic monitoring tools:
science and controversy
To our knowledge, there are two important randomized
controlled trials that have attempted to address the issue
of whether hemodynamic monitoring can affect clinical
outcomes. The first study was conducted by Rivers et al.
[27•], who randomized 263 emergency department patients
with severe sepsis or septic shock to receive 6
hours of goal-directed therapy guided by a new central
venous catheter able to deliver continuous central venous
oximetric data or standard care. Patients randomized
to the intervention experienced a close to 30% decrease
in mortality rate (P = 0.009).
Sandham et al. [19•] recently completed a large trial during
which the investigators randomized 1994 American
Society of Anesthesiologists physical status III or IV patients
who were scheduled for surgery and postoperative
ICU stay. Half of the patients were randomized to receive
goal-directed therapy guided by PAC, while the
other half received standard care without the use of the
PAC [20]. Goal-directed therapy meant that, in this trial,
those patients randomized to have a PAC should receive
interventions whenever possible to achieve the following
goals in order of priority: (1) an oxygen delivery of 550 to
600 mL/min/m2, (2) a cardiac index of 3.5 to 4.5
L/min/m2; (3) a mean arterial pressure of 70 mm Hg, (4)
a pulmonary artery occlusion pressure of 18 mm Hg; (5)
a heart rate less that 120 beats per minute; and (6) a
hematocrit greater than 27%. This trial showed that more
patients in the goal-directed therapy group received inotropic
agents (P < 0.001), vasodilators (P < 0.001), antihypertensive
medication (P < 0.001), packed cells (P <
0.001), and colloid fluids (P = 0.002). The mortality rate
of control patients was 7.7% compared with 7.8% in the
PAC group. Interestingly, there was a significant increase
in the incidence of pulmonary embolism among the PAC
patients (P = 0.004). The investigators concluded that
there was “no benefit of therapy directed by PAC over
standard care in elderly, high-risk surgical patients requiring
intensive care” [19•].
Although each trial deserves detailed discussion, which
cannot be done here, the recent evidence appears to
overwhelmingly suggest that, in patients in the ICU or
operating room, either (1) using the PAC to guide
therapy is not helpful or (2) PAC monitoring might be
unhelpful but only when “wrongly” used to achieve supranormal
values of cardiac index or oxygen delivery.
Things might be different in emergency room patients,
but the study by Rivers et al. [27•] is a single-center
investigation with a higher than expected mortality rate
in the control group and huge potential for a “Hawthorne
effect” of monitoring. Thus, more information is needed
in this setting.
Table 2. Comparative advantages and disadvantages of the
pulmonary artery catheter and pulse contour cardiac
output technology
Aspect/variable PAC PiCCO
Cardiac output Yes (continuous with
special technology)
Yes (always
continuous)
PAOP Yes No
Pulmonary pressures Yes No
RAP Yes Yes
RVEDV Yes, with special
technology
No
End-diastolic
intrathoracic volume
No Yes
Extravascular lung water
index
No Yes
Risk of pneumothorax Yes No
Risk of infection +++ +
Risk of arterial puncture Yes No
Risk of pulmonary artery
rupture
Yes No
Risk of air embolus Yes No
PAC, pulmonary artery catheter; PAOP, pulmonary artery occlusion
pressure; PiCCO, pulse contour cardiac output; RAP, right atrial
pressure; RVEDV, right ventricular end-diastolic volume.
228 Cardiopulmonary monitoring
Conclusions
Much work needs to be done before we can decide how
best to use hemodynamic tools and how to avoid their
misuse. Such research is difficult and controversial in
design. The so-called experts have spent almost 15 years
trying to tell us that we should maximize oxygen delivery
in ICU or operative patients [19•]. The data now stand in
stark contrast to such claims and demonstrate a case of
past and probably present misuse. The experts are now
going to tell us how to use the PAC in acute respiratory
distress syndrome with protocols (ARDSNet:
http://hedwig.mgh.harvard.edu/ardsnet/ards05.html) that
make no physiologic sense. With the proposed acute respiratory
distress syndrome protocol, clinicians could
give patients with acute respiratory distress syndrome
randomized to so-called “fluid conservative therapy”
who have a cardiac index of 4 L/min/m2, a CVP of 14 mm
Hg, a urine output of 0.6 mL/kg/h, a fraction of inspired
oxygen of 0.65, an arterial oxygen tension of 58 mm Hg,
and develop a mean arterial pressure of 55 mm Hg (vasodilatory
shock) a bolus of 15 mL/kg of saline [sic] as
possible therapy. How is this physiologically reasonable?
In our opinion, when it comes to such expert advice, the
expression caveat emptor seems most appropriate. Thus,
the debate will continue, physiologically irrational use of
hemodynamic tools will also continue, and controversy
will flourish. Nonetheless, we look forward to the day
when trials of the PAC use this tool not to achieve supranormal
values but to maintain homeostasis, when volume-
based instead of pressure-based hemodynamic tools
are used to guide therapy and prevent both inadequate
diastolic filling and inappropriate surges in extravascular
lung water, and when, in the field of hemodynamics,
more clinical outcome-based studies become available to
help us choose the right tool and the right use for the
tool.
References and recommended reading
Papers of particular interest, published within the annual period of review,
have been highlighted as:
• Of special interest
•• Of outstanding interest
1 Pulmonary Artery Catheter Consensus Conference: consensus statement.
New Horiz 1997, 5:175–194.
2 Iberti TJ, Daily EK, Leibowitz AB, et al.: Assessment of critical care nurses’
knowledge of the pulmonary artery catheter. Crit Care Med 1994, 22:1674–
1678.
3 Iberti TJ, Fischer EP, Liebowitz AB, et al.: A multicenter study of physicians’
knowledge of the pulmonary artery catheter. JAMA 1990, 264:2928–2932.
4 Gnaegi A, Feihl F, Perret C: Intensive care physicians’ insufficient knowledge
of right heart catheterization at the bedside: time to act? Crit Care Med 1997,
25:213–220.
5 Nelson L: The new pulmonary artery catheter: continuous venous oximetry,
right ventricular ejection fraction and continuous cardiac output. New Horiz
1997, 5:251–258.
6 Diebel L, Wilson R, Tagett MG, et al.: End-diastolic volume: a better indicator
of pre-load in the critically ill. Arch Surg 1992, 127:817–822.
•
7 Pinsky MR: Functional hemodynamic monitoring. Intensive Care Med 2002,
28:386–388.
This article provides a clear explanation of the possible utility of functional dynamic
monitoring instead of static pressure monitoring in ventilated patients.
•
8 Reuter DA, Felbinger TW, Schmidt C, et al.: Stroke volume variations for
assessment of cardiac responsiveness to volume loading in mechanically
ventilated patients after cardiac surgery. Intensive Care Med 2002, 28:392–
398.
This article provides preliminary evidence that variations in continuously measured
volume signals using PiCCO technology can usefully predict the cardiac output
response to fluid therapy.
9 Eisenberg PR, Jaffe AS, Schuster DP: Clinical evaluation compared to pulmonary
artery catheterization in the hemodynamic assessment of critically ill
patients. Crit Care Med 1984, 12:549–553.
10 Levy MM: Pulmonary capillary pressure and tissue perfusion: clinical implications
during resuscitation from shock. New Horiz 1996, 4:504–518.
11 Schlichtig R, Kramer D, Pinsky MR: Flow redistribution during progressive
hemorrhage is a determinant of critical O2 delivery. J Appl Physiol 1991,
70:169–178.
•
12 Boldt J: Clinical review: hemodynamic monitoring in the intensive care unit.
Crit Care 2002, 6:52–59.
A useful brief review of new technology for hemodynamic monitoring.
13 Bellomo R, Pinsky MR: Invasive hemodynamic monitoring. In Critical Care:
Standards, Audit and Ethics. Edited by Tinker J, Browne DRG, Sibbald WJ.
New York: Oxford University Press; 1996:82–104.
•
14 Pinsky MR: Pulmonary artery occlusion pressure. Intensive Care Med 2003,
29:19–22.
An excellent review of issues related to the interpretation of pulmonary artery occlusion
pressure waves.
15 Michard F, Boussat S, Chemla D, et al.: Relation between respiratory
changes in arterial pulse pressure and fluid responsiveness in septic patients
with acute circulatory failure. Am J Respir Crit Care Med 2000, 162:134–
138.
•
16 Hotchkiss RS, Karl IE: The pathophysiology and treatment of sepsis. N Engl J
Med 2003, 348:138–150.
An excellent review of the importance of nonhemodynamic factors in sepsis.
17 Fink MP: Bench-to-bedside review: cytopathic hypoxia. Crit Care 2002,
6:491–499.
18 Adrie C, Bachelot M, Vayssier-Taussat, et al.: Mitochondrial membrane potential
and apoptosis of peripheral blood monocytes in severe human sepsis.
Am J Respir Crit Care Med 2001, 164:389–395.
•
19 Sandham JD, Hull RD, Brant RF, et al.: A randomized controlled trial of the use
of pulmonary artery catheters in high-risk surgical patients. N Engl J Med
2003, 348:5–14.
The largest randomized controlled trial of the PAC in surgical patients.
20 Boyd KD, Thomas SJ, Gold J, et al.: A prospective study of complications of
pulmonary artery catheters in 500 consecutive patients. Chest 1983,
84:245–249.
21 Connors AF Jr, Castele RJ, Farhat NZ, et al.: Complications of pulmonary
artery catheterization. A prospective autopsy study. Chest 1985, 88:567–
572.
22 Sakka SG, Ruhl CC, Pfeiffer UJ, et al.: Assessment of cardiac preload and
extravascular lung water by single transpulmonary thermodilution. Intensive
Care Med 2000, 26:180–187.
23 Holm C, Melcer B, Horbrand F, et al.: Intrathoracic blood volume as an end
point in resuscitation of the severely burned: an observational study of 24
patients. J Trauma 2000, 48:728–734.
•
24 Sakka SG, Klein M, Reinhart K, et al.: Prognostic value of extravascular lung
water in critically ill patients. Chest 2002, 122:2080–2086.
The first demonstration of the clinical relevance of the extravascular lung water
signal in ICU patients.
25 Boussat S, Jacques T, Levy B, et al.: Intravascular volume monitoring and
extravascular lung water in septic patients with pulmonary edema. Intensive
Care Med 2002, 28:712–718.
26 Goedje O, Hoeke K, Lichtwarck-Aschoff M, et al.: Continuous cardiac output
by femoral thermodilution calibrated contour analysis: comparison with pulmonary
arterial thermodilution. Crit Care Med 1999, 27:2407–2412.
•
27 Rivers E, Nguyen B, Havstad S, et al.: Early goal-directed therapy in the treatment
of severe sepsis and septic shock. N Engl J Med 2001, 345:1368–
1377.
The first randomized controlled trial of mixed venous saturation monitoring in septic
patients in the emergency department.
Cardiovascular monitoring tools Bellomo and Uchino 229
Ich vermute, dass die Zahlen für Q4/03 nicht so gut ausgefallen sind, wie erwartet. Daher geht der Kurs etwas zurück.
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