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    Pulsion 548790 Strong Trading Buy (Seite 281)

    eröffnet am 26.11.03 07:50:03 von
    neuester Beitrag 26.10.23 12:16:59 von
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    ISIN: DE0005487904 · WKN: 548790 · Symbol: PUS
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     Ja Nein
      Avatar
      schrieb am 20.01.04 14:52:54
      Beitrag Nr. 47 ()
      @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!
      Avatar
      schrieb am 20.01.04 12:13:19
      Beitrag Nr. 46 ()
      pulsion stößt langsam wieder auf interesse...
      Avatar
      schrieb am 20.01.04 10:42:35
      Beitrag Nr. 45 ()
      katel,

      schau dir das geschäftsmodell genauer an...
      dann stellst du andere fragen und bekommst antworten.
      Avatar
      schrieb am 19.01.04 23:10:16
      Beitrag Nr. 44 ()
      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
      Avatar
      schrieb am 19.01.04 22:01:47
      Beitrag Nr. 43 ()
      @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
      :cool: FS :cool:

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      Die Aktie mit dem “Jesus-Vibe”!mehr zur Aktie »
      Avatar
      schrieb am 19.01.04 19:03:45
      Beitrag Nr. 42 ()
      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
      Avatar
      schrieb am 19.01.04 18:38:49
      Beitrag Nr. 41 ()
      Alles weniger erfreulich, offenbar ist weiter Konsolidierung angesagt. Ich hoffe, dass wenigstens die Unterstützung bei 2,40 hält.......
      Avatar
      schrieb am 19.01.04 17:30:57
      Beitrag Nr. 40 ()
      Jetzt wirds brenzlig.

      Avatar
      schrieb am 16.01.04 10:19:04
      Beitrag Nr. 39 ()
      #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
      Avatar
      schrieb am 16.01.04 10:07:05
      Beitrag Nr. 38 ()
      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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