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  • 1
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Sepsis ; SIRS ; Sauerstofftransport ; Stoffwechsel ; Splanchnikus ; Key wordsSepsis ; SIRS ; Oxygen transport ; Metabolism ; Splanchnic area
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Sepsis and SIRS are characterised by increased hepatosplanchnic blood flow and oxygen transport due to sepsis-associated hypermetabolism with enhanced oxygen uptake. Regional hypermetabolism may be linked with a mismatch of oxygen availability and demand potentially resulting in a pathological splanchnic oxygen uptake/supply dependency. Splanchnic hypermetabolism has been hypothesised to be due to increased hepatic gluconeogenesis caused by accelerated glucose precursor uptake resulting from increased release from the peripheral tissues. This increased precursor efflux is triggered by cytokines. The response of splanchnic haemodynamics and oxygen kinetics, however, to therapeutic interventions does not necessarily parallel the different metabolic pathways. Therefore, understanding of both tissue perfusion and oxygenation as well as metabolism is pivotal for evaluating the effects of different therapeutic strategies in intensive care medicine.
    Notes: Zusamenfassung Sepsis und SIRS sind charakterisiert durch gesteigerten Blutfluss und Sauerstofftransport im Hepato-Splanchnikusgebiet, hervorgerufen durch eine Steigerung der Stoffwechselanforderungen mit dem Ergebnis einer erhöhten O2-Aufnahme. In Folge des Sepsis-induzierten Hypermetabolismus kann es zu einem Missverhältnis zwischen vorhandener Sauerstoffverfügbarkeit und aktuellem Sauerstoffbedarf kommen und daraus potentiell eine pathologische Abhängigkeit zwischen Sauerstoffverfügbarkeit und -bedarf resultieren. Als Ursache für den Hypermetabolismus wird unter anderem die gesteigerte hepatische Glukoneogenese diskutiert, die als Folge einer gesteigerten Aufnahmerate von vermehrt peripher freigesetzten Glukosepräkursoren angesehen wird. Dieser gesteigerte Fluss von Glukosepräkursoren wiederum ist durch reaktiv freigesetzte Zytokine mitbedingt. Bezüglich therapeutischer Interventionen muss beachtet werden, dass Effekte auf Hämodynamik und Sauerstofftransport im Splanchnikusgebiet der entsprechenden Stoffwechselantwort angepasst sein müssen, um eine zusätzliche Imbalanz zwischen regionalen Blutfluss, Sauerstoff- und Substratfluss einerseits und den regionalen Anforderungen andererseits zu vermeiden. Deshalb ist das Verständnis sowohl der Gewebeperfusion und -oxygenierung als auch der wesentlichen Stoffwechselaktivität unerlässlich, um Behandlungskonzepte einzuordnen und bewerten zu können.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Perioperativer Myokardinfarkt ; Akut-PTCA ; Thrombolyse ; kardiogener SchockPerioperative myocardial infarction ; Acute-PTCA ; Thrombolytic therapy ; Cardiogenic shock ; Key words Perioperativer Myokardinfarkt ; Akut-PTCA ; Thrombolyse ; kardiogener SchockPerioperative myocardial infarction ; Acute-PTCA ; Thrombolytic therapy ; Cardiogenic shock
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract The mortality of perioperative myocardial infarction is still high and according to recently published data amounts to 17 to 42%. In the seventies introduction of thrombolytic therapy has led to a dramatic reduction in mortality of non-perioperative myocardial infarction. However, in the perioperative situation thrombolytic therapy remains to be problematic in most cases because of expected severe bleeding complications. In the last 4–6 years acute-PTCA has been established in the therapy of acute myocardial infarction. Up to date no data are available concerning the effect of acute-PTCA on mortality of perioperative myocardial infarction. Nevertheless it can be assumed, that acute-PTCA will lead to a considerable reduction in mortality of perioperative myocardial infarction. Therefore, in patients with significant perioperative myocardial infarction immediate coronary angiography and, if indicated, acute-PTCA should be performed. In principle, thrombolytic therapy is considered to be contraindicated in the intra- or postoperative situation. However, if coronary angiography and PTCA are not possible, thrombolysis might be taken into consideration, in particular if the expected bleeding complications are small in relation to the expected benefit of thrombolysis. Since acute-PTCA has been shown to remarkably reduce mortality in patients with cardiogenic shock after acute myocardial infarction, this group of patients should be especially considered.
    Notes: Zusammenfassung Die Letalität des perioperativen Myokardinfarkts ist auch nach neueren Untersuchungen mit 17–42% ausgesprochen hoch. Während die thrombolytische Therapie Ende der 70er Jahre zu einer drastischen Senkung der Letalität des nicht-perioperativen Myokardinfarkts geführt hat, blieb für die perioperative Situation die Thrombolyse wegen der zu erwartenden Blutungskomplikationen im allgemeinen ausgeschlossen. In den letzten Jahren hat sich neben der Thrombolyse die Akut-PTCA (Percutane Transluminale Coronare Angioplastie) in der Therapie des Myokardinfarkts etabliert. Bisher liegen keine Studien zum Einfluß der Akut-PTCA auf die Letalität des perioperativen Myokardinfarkts vor. Dennoch ist davon auszugehen, daß die Akut-PTCA zu einer erheblichen Reduktion der Letalität des perioperativen Infarkts führt. Somit sollte bei jedem Patienten mit einem größeren oder hämodynamisch beeinträchtigenden Myokardinfarkt eine sofortige Koronarangiographie und ggf. eine Akut-PTCA durchgeführt werden. Die thrombolytische Therapie ist in der intra- und postoperativen Phase im allgemeinen kontraindiziert. Sind jedoch logistisch die Voraussetzungen zur Akut-PTCA nicht gegeben und sollte ein größerer Infarkt bzw. eine bedrohliche Situation vorliegen, kann unter Abwägung des zu erwartenden Blutungsrisikos und des zu erwartenden Nutzens eine Thrombolyse in Betracht gezogen werden. Besonders bei Patienten, die infolge des Myokardinfarkts einen kardiogenen Schock entwickelt haben, hat die Akut-PTCA zu einer erheblichen Reduktion der sonst ausgesprochen hohen Krankenhausletalität geführt und läßt auch bei dem perioperativen Infarkt mit kardiogenem Schock eine deutliche Reduktion der Letalität erwarten.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Der Anaesthesist 47 (1998), S. 269-289 
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Hyperbare Oxygenation ; Intensivtherapie ; Notfallmedizin ; Tauchmedizin ; Indikationen ; Key words Hyperbaric oxygen ; Emergency medicine ; Intensive care therapy ; Diving medicine ; Indications
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Hyperbaric Oxygen (HBO) therapy is a kind of medical treatment in which a patient breathes 100% of oxygen inside a pressure chamber while the pressure of the chamber is increased to a point higher than sea level pressure. It is strongly based on clearly defined physical laws and physiological regularities. For the clinical use of HBO therapy, according to international recommendations, there are several commonly accepted indications in which HBO either is the only causative life-saving kind of treatment, or is an essential and oftenly decisive component of a comprehensive interdisciplinary intensive care therapy. Among potential adverse effects, barotrauma of the lungs and especially oxygen toxicity to the central nervous system have to be mentioned. Clinical use of HBO therefore requires special knowledge of its effects, risks, and adverse effects, a clear and distinct indication, and the ability and skills to keep complications under control by means of intensive care or emergency medical measures. The clinical use of hyperbaric oxygen with its interdisciplinary-like character of emergency medicine or intensive care therapy therefore should be an additional, most interesting field of activity for the anaesthesiologist.
    Notes: Zusammenfassung Hyperbare Oxygenation (HBO) ist eine medizinische Behandlungsform, bei der der Patient in einer Überdruckkammer Sauerstoff unter einem höheren Partialdruck atmet als dem Luftdruck auf Meereshöhe. Sie beruht streng auf klaren physikalischen Gesetzen und definierten physiologischen Gesetzmäßigkeiten. Nach internationalen Empfehlungen gibt es für die HBO-Therapie eine Reihe von allgemein anerkanntenen Indikationen, bei denen sie entweder die einzige kausal wirkende, lebensrettende Therapieform oder aber eine wesentliche, oftmals ausschlaggebende Therapiekomponente einer umfassenden, interdisziplinären Intensivtherapie darstellt. Unter den potentiellen Nebenwirkungen sind neben Barotraumen der Lunge vor allem die Möglichkeit einer zentral-nervösen Sauerstoffintoxikation besonders zu berücksichtigen. Die klinische Anwendung der HBO erfordert daher spezifische Kenntnisse ihrer Wirkungen, Nebenwirkungen und Risiken, eine gezielte und kritische Indikationsstellung sowie die Fähigkeiten und Fertigkeiten, auftretende Komplikationen mit intensiv- oder notfallmedizinischen Maßnahmen sicher zu beherrschen. Die klinische Anwendung der hyperbaren Oxygenation mit ihrem interdisziplinären, notfallmedizinischen oder intensivtherapeutischen Charakter sollte daher für den Anästhesisten ein zusätzliches, äußerst interessantes Betätigungsfeld sein können.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1238
    Keywords: Septic shock ; Nitric oxide ; Prostacyclin ; Gastric intramucosal pH ; PCO2 gap ; Splanchnic oxygenation ; Indocyanine-green extraction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objectives To compare the effects of inhaled nitric oxide and aerosolized prostacyclin (PGI2) on hemodynamics and gas exchange as well as on the indocyanine-green plasma disappearance rate and gastric intramucosal pH in patients with septic shock. Design Prospective, randomized, interventional clinical study. Setting Intensive care unit in a university hospital. Patients Sixteen patients with pulmonary hypertension and septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine and/or epinephrine to maintain mean arterial blood pressure above 65 mmHg. Methods and interventions Patients were randomly assigned to receive either nitric oxide or aerosolized prostacyclin. Nitric oxide was inhaled using a commercially available delivery system, prostacyclin was administered with a modified ultrasound nebulizer. Both nitric oxide and prostacyclin were incrementally adjusted to obtain a 15% decrease of mean pulmonary artery pressure. Hemodynamics and gas exchange as well as indocyaninegreen plasma disappearance rate and gastric intramucosal pH were determined at baseline after 90 min in steady state, after 90 min of nitric oxide inhalation or prostacyclin aerosol administration had elapsed in stable conditions, and after 90 min in stable conditions after nitric oxide or prostacyclin with-drawal. Results Both inhaled nitric oxide and aerosolized prostacyclin selectively reduced the mean pulmonary artery pressure from 35±4, 30±4 mmHg (p〈0.05) and 34±4 to 30±3 mmHg (p〈0.05) respectively; after removal of nitric oxide and prostacyclin, the mean pulmonary artery pressure returned to the baseline values. Systemic hemodynamics remained unaltered during the vasodilator treatment. While the mean PaO2 was not significantly influenced, it increased in 4/8 of the NO- and 3/8 of the PGI2 — treated patients. Neither of the drugs influenced indocyanine-green plasma disappearance rate, but prostacyclin — unlike nitric oxide — significantly increased gastric intramucosal pH (from 7.26±0.07 to 7.30±0.05,p〈0.05) which remained elevated in four of these patients after prostacyclin removal, and decreased the arterial-gastric mucosal pressure of carbon dioxide gap from 19±6 to 15±4 mmHg (p〈0.05). Conclusions Our data suggest that aerosolized prostacyclin — unlike nitric oxide — has similar beneficial effects on splanchnic perfusion and oxygenation as intravenous prostacyclin without detrimental effects on systemic hemodynamics. The different effects of prostacyclin and nitric oxide might be explained by the longer half-life of prostacyclin associated with a certain spillover into the systemic circulation.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 22 (1996), S. S22 
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion 1)Basal production in pig is comparable to human basal production[1]; 2) Endotoxin significantly increases the NO release; 3) Our technique allows to reliably estimate the excess endogenous NO production in hyperdynamic states as documented by the significant correlation between the changes in SVR and those of NO formation.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusions Low dose filgrastim in postoperative/posttraumatic patients at risk of and with sepsis may boost host defense by stimulating neutrophil function and simultaneously counteract progression of sepsis by improving an antiinflammatory cytokine response with protective effects on the endothelium.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 23 (1997), S. 1289-1289 
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1238
    Keywords: Prostacyclin ; Gastric intramucosal pH ; Splanchnic blood flow ; Splanchnic oxygenation ; Septic shock
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To investigate whether infusing prostacyclin (PGI2) in patients with septic shock improves splanchnic oxygenation as assessed by gastric intramucosal pH (pHi). Design Interventional clinical study. Setting Surgical ICU in a university hospital. Patients 16 consecutive patients with septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine to maintain arterial blood pressure. Interventions All patients received PGI2 (10 ng/kg·min) after no further increase in oxygen delivery could be obtained by volume expansion, red cell transfusion and dobutamine infusion. The results were compared with those before and after conventional resuscitation. The patients received continuous PGI2 infusion for 3–32 days. Measurements and results O2 uptake was measured directly in the respiratory gases, pHi was determined by tonometry. Baseline O2 delivery, O2 uptake and pHi were 466±122 ml/min·m2, 158±38 ml/min·m2, and 7.29±0.09, respectively. While O2 uptake remained unchanged, infusing PGI2 increased O2 delivery (from 610±140 to 682±155 ml/min·m2,p〈0.01) and pHi (from 7.32±0.09 to 7.38±0.08,p〈0.001) beyond the values obtained by conventional resuscitation. While 9 of 11 patients with final pHi〉7.35 survived, all patients with final pHi〈7.35 died (p〈0.01). Conclusions Infusing PGI2 in patients with septic shock increases pHi probably by enhancing blood flow to the splanchnic bed and thereby improves splanchnic oxygenation even when conventional resuscitation goals have been achieved.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 22 (1996), S. 1274-1275 
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion In contrast to its preserved stimulatory effect on lipolysis epinephrine failed to enhance hepatic glucose production in cirrhotic patients. Since this blunted response was not related to changes of ß-adrenoreceptors our findings suggest that epinephrine resistance in cirrhosis was due to a postreceptor defect.
    Type of Medium: Electronic Resource
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