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  • 1
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusions Nitrite and oxygen delivery was elevated in the MODS-group in early sepsis which may be equivalent to NO-formation associated with sufficient tissue perfusion in MODS patients. The same group showed decreased values of nitrite and nitrate in late sepsis. This may correlate with an insufficient perfusion and deterioration of tissue oxygenation. Further studies are required to assess therapeutical consequences for NO-inhibitory or -supportive treatment in spesis.
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  • 2
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusions Since high CDT values were associated with an increased risk of intercurrent complications and a prolonged ICU stay it may be reasonable to use CDT as a marker to intensify research to prevent alcohol related complications.
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  • 3
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    Electronic Resource
    Springer
    Der Anaesthesist 43 (1994), S. 683-697 
    ISSN: 1432-055X
    Keywords: Schlüsselwörter: Ventilations-Perfusions-Verhältnisse – Methoden – Lungenerkrankungen ; Key words: Ventilation-perfusion ratios – Methods – Lung diseases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract. Knowledge of normal and impaired pulmonary gas exchange is essential to the anaesthesiologist. Analysis of an arterial blood sample allows evaluation of whether or not pulmonary gas exchange is normal. For this purpose comparison with the oxygenation index or the alveolar-arterial PO2 difference is helpful. Pathological changes of these variables are mainly caused by ventilation-perfusion (V˙A/Q˙) mismatch. In daily practice, venous admixture or intrapulmonary shunt can be calculated using arterial and mixed-venous blood. By analysing arterial and expired PCO2, dead-space ventilation can be determined, but extended analyses of V˙A/Q˙ distribution are not possible in daily practice. However, knowledge of the principles of typical disturbances of pulmonary gas exchange in acute and chronic lung disease allows the use of therapeutic strategies based on the pathophysiological changes.
    Notes: Zusammenfassung. Kenntnisse des normalen und des gestörten pulmonalen Gasaustauschs sind für das anästhesiologische Handeln unerläßlich. Aufgrund einer arteriellen Blutgasanalyse kann festgestellt werden, ob der Gasaustausch ungestört verläuft oder nicht. Dazu dient der Vergleich mit dem Oxygenierungsindex bzw. mit der alveolo-arteriellen O2-Partialdruckdifferenz. Pathologische Veränderungen dieser Parameter sind in überwiegendem Maße auf V˙A/Q˙-Störungen zurückzuführen. Im klinischen Alltag läßt sich über die Analyse arteriellen und gemischtvenösen Blutes die venöse Beimischung bzw. der intrapulmonale Shunt bestimmen. Die Totraumventilation kann über den arteriellen und den exspiratorischen PCO2 bestimmt werden. Aber weitergehende Analysen der V˙A/Q˙-Verteilung sind im klinischen Alltag nicht möglich. Die Kenntnis der Prinzipien der typischen Störungen des pulmonalen Gasaustauschs bei akuten und chronischen Lungenerkrankungen gestattet aber, unser therapeutisches Vorgehen sinnvoll auf die zugrundeliegenden pathophysiologischen Veränderungen auszurichten.
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  • 4
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Aneurysmatische Subarachnoidalblutung ; Zerebraler Vasospasmus ; Kalziumantagonisten ; Hypervolämische Hämodilution ; Induzierte arterielle Hypertension ; Key words Aneurysmal subarachnoid haemorrhage ; Cerebral vasospasm ; Calcium antagonists ; Hypervolaemic haemodilution ; Induced arterial hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Only 53%–58% of patients with a subarachnoid haemorrhage (SAB) following the rupture of a cerebral aneurysm survive without neurological damage. Morbidity and mortality are closely related to the delayed ischaemic neurological deficit due to cerebral vasospasm. The following review gives an account of pathophysiological mechanisms; the importance of treatment with calcium antagonists, hypervolaemic haemodilution, and induced arterial hypertension is discussed in light of the current literature. Pathophysiology. In addition to other vasoactive substances in the blood, haemoglobin, which is released from lysed erythrocytes on the 2nd to 4th day after the haemorrhage, plays an important role in inducing vasospasm. An inflammatory angiopathy ensues, with complete resolution after 6–12 weeks. The cerebral blood flow (CBF) is reduced depending on the extent of vasospasm. Irreversible infarction may follow the decrease of CBF below a critical value. Severe vasospasm causes autoregulatory disturbances and reduced responsiveness of cerebral vessels to CO2. Calcium antagonists. The calcium blocker nimodipine causes dilatation of small pial vessels with increased CBF. However, systemic vasodilation with the subsequent fall in blood pressure may limit the increase in CBF. Furthermore, it is known that nimodipine decreases intracellular calcium concentrations resulting in some protection against ischaemic cellular injury. Seven placebo-controlled clinical studies have shown that nimodipine improves the outcome of patients with severe neurological damage due to cerebral vasospasm. Hypervolaemic haemodilution. Volume expansion and haemodilution to a hematocrit of 30%–33% is suggested to improve cerebral perfusion during vasospasm. The central venous and pulmonary capillary wedge pressures should be 10–12 mm Hg and 15–18 mm Hg, respectively. But there is no evidendence of improved outcome with this measure, and pulmonary edema is a frequent side effect. However, impairment of cerebral perfusion and increased neurological damage can be demonstrated with hypovolaemia and haemoconcentration. Induced arterial hypertension. In the presence of cerebral vasospasm and resulting autoregulatory disturbances, cerebral perfusion can be increased by raising systemic arterial pressure. This measure, too, fails to improve neurological outcome. Conclusion. Treatment of cerebral vasospasm following a SAB aims to avoide any impairment of cerebral perfusion. Hypovolaemia and haemoconcentration have to be corrected. Normoventilation should be established to avoid hypocapnic vasoconstriction. Nimodipine should be administered continuously after a SAB. In view of the autoregulatory disturbances, systemic hypotension with its danger of decreased CBF must be prevented. The importance of hypervolaemic haemodilution and/or induced arterial hypertension is not clear. Despite therapeutic efforts, the number of patients who have survived a SAB without a substantial neurological deficit has not increased.
    Notes: Nach wie vor überleben lediglich 53–58% der Patienten mit einer Subarachnoidalblutung (SAB) durch Ruptur eines zerebralen Aneurysmas ohne neurologische Defizite. Eine der wichtigsten Determinanten der Morbidität und Mortalität ist die protrahiert auftretende neurologische Verschlechterung, delayed ischemic neurologic deficit (DIND), durch Vasospasmus der zerebralen Gefäße. In dieser Übersichtsarbeit werden die Pathophysiologie dargestellt und der Stellenwert der Therapie mit Kalziumantagonisten, hypervolämischer Hämodilution und induzierter arterieller Hypertonie anhand der akuten Literatur beurteilt. Dem Hämoglobin, das durch Lyse der Erythrozyten am 2.–4. Tag nach der Blutung freigesetzt wird, kommt eine besondere Bedeutung in der Pathogenese des Vasospasmus zu. In Abhängigkeit von der Ausprägung des Vasospasmus kommt es zur Reduktion des zerebralen Blutflusses (CBF). Kalziumantagonisten vom Dihydropyridintyp können die Überlebensqualität von Patienten mit schwerem neurologischen Defizit durch Vasospasmus verbessern. Ob eine induzierte Hypervolämie und eine Hämodilution bis zu einem Hämatokrit von 30–33% die zerebrale Mikrozirkulation günstig beeinflussen können, ist nicht geklärt. Aufgrund der gestörten Autoregulation der zerebralen Gefäße bei Vasospasmus kann durch Induktion einer arteriellen Hypertension die zerebrale Perfusion gesteigert werden. Eine erhoffte Verbesserung des neurologischen Folgezustands durch Erhöhen des zerebralen Perfusionsdrucks ist allerdings bis heute nicht nachgewiesen.
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  • 5
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Hypotension ; Monitoring ; Elektroenzephalogramm ; Früh akustisch evozierte Potentiale (FAEP) ; Key words Hypotension ; Monitoring ; Electroencephalogram ; Brain-stem auditory evoked potentials (BAEP)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract For surgical removal of a malignant choroid melanoma, it is necessary to reduce systolic blood pressure to around 50–60 mmHg in order to prevent choroidal haemorrhages. However, blood pressure reduction is associated with the risk of cerebral ischaemia. We report a patient with a malignant choroid melanoma in whom waves I and II of the brainstem auditory evoked potentials (BAEP) disappeared during surgery under controlled arterial hypotension and hypothermia (31.1° C). The waves could be recorded again immediately after the mean arterial pressure was increased from 48 to 77 mmHg. The oesophageal temperature had dropped by 0.3° C at this time. The 2-channel electroencephalogram (EEG) showed no irregularities during this time period. A bilateral, reversible, apparently blood-pressure-dependent loss of waves I and II during arterial hypotension despite a normal EEG has to our knowledge not been previously described in the literature. The isolated loss of waves I and II with maintenance of waves III, IV, and V is unusual. The literature contains reports of acoustic neurinoma patients in whom only wave V could be recorded. This is regarded as an indication of continued impulse conduction despite the loss of waves I to IV. Others have observed a patient with temporary and reversible loss of BAEP wave I due to vasospasm of the internal auditory artery that apparently occurred during or shortly after manipulation of the internal auditory meatus. Assuming anatomic peculiarities in the blood supply to the generators of the BAEP waves, a stenosis of the basilar artery could be considered as the cause of the bilateral reversible loss of waves I and II. Another potential source could be the induced hypothermia, but this does not seem very likely because the patient's temperature was 0.3° C lower at the return of the waves than at their loss.
    Notes: Zusammenfassung Wir berichten über einen Patienten mit einem malignen Melanom der Aderhaut, bei dem es intraoperativ unter kontrollierter Hypotension und Hypothermie (31,3° C) zum Verlust der Wellen I und II der frühen akustisch evozierten Potentiale (FAEP) kam. Nach Anhebung des mittleren arteriellen Drucks von 48 auf 77 mmHg waren die FAEP-Wellen sofort wieder ableitbar, obwohl die ösophageale Temperatur um 0,3° C abgefallen war. Das ebenfalls abgeleitete 2-Kanal-Elektroenzephalogramm (EEG) zeigte im betreffenden Zeitraum keine Auffälligkeiten. Ein beidseitiger reversibler, offensichtlich blutdruckabhängiger Ausfall der Wellen I und II während Hypotension bei gleichzeitig unauffälligem EEG ist unseres Wissens bisher in der Literatur nicht beschrieben. Der isolierte Verlust der Wellen I und II bei erhaltenen Wellen III, IV und V ist ungewöhnlich. In der Literatur sind aber Patienten mit Akustikusneurinom beschrieben, bei denen nur die Welle V abgeleitet werden konnte. Ebenso ist ein Fall mit temporärem Verlust von FAEP-Welle I beschrieben. Als Ursache wird eine lokale Minderperfusion wegen Vasospasmus während Manipulationen in Strukturen des Meatus akustikus internus diskutiert. Ausgehend von anatomisch-physiologischen Besonderheiten der Blutversorgung der Generatoren der FAEP-Wellen kann eine Stenose der Arteria basilaris als Ursache für den beidseitigen reversiblen Ausfall der Wellen I und II diskutiert werden. Der Erhalt der Wellen III bis V könnte für eine retrograde Füllung der A. basilaris aus dem Stromgebiet des Circulus Willisii sprechen. Wir interpretieren den beidseitigen Ausfall der Wellen I und II als Folge der Minderperfusion des betreffenden Hirngewebes. Die gleichzeitig bestehende Hypothermie scheidet als Ursache für den temporären Verlust der Wellen I und II aus, weil die Temperatur des Patienten beim Wiederauftreten der Wellen I und II 0,3° C niedriger war als bei ihrem Verlust.
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  • 6
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Hyperoxie ; N-Azetylzystein ; Sauerstoffverbrauch ; Gewebeoxygenierung ; Kardiale Risikopatienten ; Key words Hyperoxia ; N-acetylcysteine ; Whole-body oxygen uptake ; Tissue oxygenation ; Cardiac risk patients
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Hyperoxic ventilation, used to prevent hypoxia during potential periods of hypoventilation, has been reported to paradoxically decrease whole-body oxygen consumption (VO2). Reduction in nutritive blood flow due to oxygen radical production is one possible mechanism. We investigated whether pretreatment with the sulfhydryl group donor and O2 radical scavenger N-acetylcysteine (NAC) would preserve VO2 and other clinical indicators of tissue oxygenation in cardiac risk patients. Methods. Thirty patients, requiring hemodynamic monitoring (radial and pulmonary artery catheters) because of cardiac risk factors, were included in this randomized investigation. All patients exhibited stable clinical conditions (hemodynamics, body temperature, hemoglobin, FIO2〈0.5). Cardiac output was determined by thermodilution and VO2 by cardiovascular Fick. After baseline measurements, patients randomly received either 150 mg kg−1 NAC (n=15) or placebo (n=15) in 250 ml 5% dextrose i.v. over a period of 30 min. Measurements were repeated 30 min after starting NAC or placebo infusion, 30 min after starting hyperoxia (FIO2=1.0), and 30 min after resetting the original FIO2. Results. There were no significant differences between groups in any of the measurements before treatment and after the return to baseline FIO2 at the end of the study, respectively. NAC, but not placebo infusion, caused a slight but not significant increase in cardiac index (CI), left ventricular stroke work index (LVSWI) and a decrease in systemic vascular resistance. Significant differences between groups during hyperoxia were: VO2 (NAC: 108±38 ml min−1m−2 vs placebo: 79±22 ml min−1m−2; P≤0.05), CI (NAC: 4.6±1.0 vs placebo: 3.7±1.11 min−1m−2; P≤0.05) and LVSWI (NAC: 47±12 vs placebo: 38±9; P≤0.05). The mean decrease of VO2 was 22% in the NAC group vs 47% in the placebo group (P≤0.05) and the mean difference between groups in venoarterial carbon dioxide gradient (PvaCO2) was 14% (P≤0.05). ST segment depression (〉0.2 mV) was significantly less marked in the NAC group (NAC: −0.02±0.17 vs placebo: −0.23±0.15; P≤0.05). Conclusions. NAC helped preserve VO2, oxygen delivery, CI, LVSWI and PvaCO2 during brief hyperoxia in cardiac risk patients. Clinical signs of myocardial ischemia did not occur such as ST-depression if patients were prophylactically treated with NAC. This suggests that pretreatment with NAC could be considered to attenuate impaired tissue oxygenation and to preserve myocardial performance better in cardiac risk patients during hyperoxia.
    Notes: Zusammenfassung Hyperoxische Ventilation wird oft prophylaktisch angewandt. Dabei kommt es zu einem Abfall des globalen Sauerstoffverbrauchs (VO 2 ), bei kardialen Risikopatienten zu einer Exazerbation von myokardialen Ischämien. N-Azetylzystein (NAC) kann den VO 2 und die myokardiale Kontraktilität verbessern. Wir untersuchten, ob NAC unter Hyperoxie einen Einfluß auf klinische Parameter der Gewebeoxygenierung bei kardialen Risikopatienten hat. 30 Patienten, bei denen aufgrund ihrer kardialen Grunderkrankung ein erweitertes hämodynamisches Monitoring durchgeführt wurde, erhielten nach einer Ausgangsmessung randomisiert entweder 150 mg kg −1 NAC (n=15) oder Plazebo (n=15) i.v. über einen Zeitraum von 30 min. Die Messungen fanden 30 min nach NAC- oder Plazebogabe, 30 min nach hyperoxischer Ventilation und 30 min nach Ventilation unter der Ausgangs-F I O 2 statt. Signifikante Unterschiede fanden sich unter Hyperoxie zwischen den beiden Gruppen im Hinblick auf den VO 2 , den Herzindex und die linksventrikuläre Schlagarbeit. Der mittlere Abfall des VO 2 betrug in der NAC-Gruppe 22% und in der Plazebogruppe 47% (p≤0,05). Der venoarterielle CO 2 -Gradient lag in der NAC-Gruppe um 14% höher (p≤0,05). Die ST-Strecken-Senkung war unter NAC geringer (p≤0,05). Diese Ergebnisse könnten darauf hinweisen, daß die prophylaktische Gabe von NAC bei kardialen Risikopatienten zu einer verbesserten Gewebeoxygenierung unter Hyperoxie beitragen kann.
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  • 7
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    Electronic Resource
    Springer
    Der Anaesthesist 46 (1997), S. 984-987 
    ISSN: 1432-055X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: = die Säule”. Bei diesem in der nächsten Zeit auf den Markt kommenden Gerät der Firma Siemens handelt es sich um ein modulares, ergänzungsfähiges Anästhesie-System. Es ist mehr als nur ein Narkosebeatmungsgerät: Die Firma Siemens hat ein Narkosebeatmungsgerät in einen kompletten Anästhesiearbeitsplatz integriert. Das Monitoring umfaßt die Vitalparameter, wie beispielsweise Sättigung, Herzfrequenz und intravasale Drücke, sowie respiratorische Parameter und Gaskonzentrationen. Im folgenden wird die Funktionsweise dieses neuen Anästhesie-Systems, das dem Autor seit über einem Jahr bekannt ist und derzeit u.a. im Unfallkrankenhaus Berlin klinisch erprobt wird, näher beschrieben.
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  • 8
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    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Anaesthesia 56 (2001), S. 0 
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Point-of-care testing of coagulation parameters provides a more rapid assessment of test results compared with laboratory testing. A new coagulation monitor (GEM® PCL, Instrumentation Laboratory, Kirchheim, Germany) was evaluated. Point-of-care data for activated partial thromboplastin time and prothrombin time (expressed as the international normalised ratio) and turn-around-time were compared. Coagulation parameters were compared in the blood of 57 patients with and without heparin therapy. The point-of-care and laboratory test results showed a bias (SD) of − 0.26 (4.55) s for activated partial thromboplastin time and − 0.011 (0.150) s for prothrombin time. The average turn-around-time was 3 min for point-of-care testing vs. 52 min for laboratory testing. We conclude that the reliability of point-of-care testing is sufficient for clinical use.
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  • 9
    ISSN: 1432-1238
    Keywords: Key words Alcoholism ; Trauma ; Intensive care unit ; Complications ; Infection ; Alcohol withdrawal syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract   Objective: A chronic alcoholic group following trauma was investigated to determine whether their ICU stay was longer than that of a non-alcoholic group and whether their intercurrent complication rate was increased. Design: Prospective study. Setting: An intensive care unit. Patients: A total of 102 polytraumatized patients were transferred to the ICU after admission to the emergency room and after surgical treatment. Of these patients 69 were chronic alcoholics and 33 were allocated to the non-alcoholic group. The chronic-alcoholic group met the DSM-III-R and ICD-10 criteria for alcohol dependence or chronic alcohol abuse/harmful use. The daily ethanol intake in these patients was ≥60 g. Diagnostic indicators included an alcoholism-related questionnaire (CAGE), conventional laboratory markers and carbohydrate-deficient transferrin. Measurement and results: Major intercurrent complications such as alcohol withdrawal syndrome (AWS), pneumonia, cardiac complications and bleeding disorders were documented and defined according to internationally accepted criteria. Patients did not differ significantly between groups regarding age, TRISS and APACHE score on admission. The rate of major intercurrent complications was 196% in the chronic alcoholic vs 70% in the non-alcoholic group (P=0.0001). Because of the increased intercurrent complication rate, the ICU stay was significantly prolonged in the chronic-alcoholic group by a median period of 9 days. Conclusions: Chronic alcoholics are reported to have an increased risk of morbidity and mortality. However, to our knowledge, nothing is known about the morbidity and mortality of chronic alcoholics in intensive care units following trauma. Since chronic alcoholics in the ICU develop more major complications with a significantly prolonged ICU stay following trauma than non-alcoholics, it seems reasonable to intensify research to identify chronic alcoholics and to prevent alcohol-related complications.
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  • 10
    ISSN: 1432-1238
    Keywords: Alcoholism ; Trauma ; Intensive care unit ; Complications ; Infection ; Alcohol withdrawal syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective A chronic alcoholic group following trauma was investigated to determine whether their ICU stay was longer than that of a non-alcoholic group and whether their intercurrent complication rate was increased Design Prospective study. Setting An intensive care unit. Patients A total of 102 polytraumatized patients were transferred to the ICU after admission to the emergency room and after surgical treatment. Of these patients 69 were chronic alcoholics and 33 were allocated to the non-alcoholic group. The chronic-alcoholic group met the DSM-III-R and ICD-10 criteria for alcohol dependence or chronic alcohol abuse/harmful use. The daily ethanol intake in these patients was ≥60 g. Diagnostic indicators included an alcoholismrelated questionnaire (CAGE), conventional laboratory markers and carbohydrate-deficient transferrin. Measurement and results Major intercurrent complications such as alcohol withdrawal syndrome (AWS), pneumonia, cardiac complications and bleeding disorders were documented and defined according to internationally accepted criteria. Patients did not differ significantly between groups regarding age, TRISS and APACHE score on admission. The rate of major intercurrent complications was 196% in the chronic alcoholic vs 70% in the non-alcoholic group (P=0.0001). Because of the increased intercurrent complication rate, the ICU stay was significantly prolonged in the chronic-alcoholic group by a median period of 9 days. Conclusions Chronic alcoholics are reported to have an increased risk of morbidity and mortality. However, to our knowledge, nothing is known about the morbidity and mortality of chronic alcoholics in intensive care units following trauma. Since chronic alcoholics in the ICU develop mor major complications with a significantly prolonged ICU stay following trauma than non-alcoholics, it seems reasonable to intensify research to identify chronic alcoholics and to prevent alcohol-related complications.
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