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  • 1
    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.
    Type of Medium: Electronic Resource
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  • 2
    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.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 21 (1995), S. 235-237 
    ISSN: 1432-1238
    Keywords: Hypokalemia ; Potassium shift ; Catecholamine release ; Head trauma ; Beta-2-stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A sudden decrease of serum potassium below 2.5 mmol/l carries the risk of dangerous arrhythmias and requires immediate replacement therapy [6]. We refer to a patient with a brain stem compression after head injury, who developed a profound hypokalemia (K+=1.2 mmol/l) with life-threatening arrhythmias, probably due to a catecholamine induced intracellular potassium shift (beta-2-stimulation). Only by aggressive potassium replacement up to 80 mmol/h (610 mmol/16h) could potassium levels be increased and cardiac arrhythmias terminated. Although replacement therapy was stopped when the serum K+-level increased to 2.4 mmol/l, 3.5 h later the patient became hyperkalemic (8.1 mmol/l). This was probably due to a secondary shift of potassium from intra-to extracellular space. In patients with severe head trauma and the potential risk of excessive catecholamine release special attention must be paid to changes in potassium balance.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1238
    Keywords: Key words Septic shock ; Sepsis ; Oxygen delivery ; Oxygen consumption ; Splanchnic blood flow ; Splanchnic oxygen delivery ; Splanchnic oxygen consumption ; Dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Objective: To assess the effects of low-dose dopamine on splanchnic blood flow and splanchnic oxygen uptake in patients with septic shock. Design: Prospective, controlled trial. Setting: University hospital intensive care unit Patients: 11 patients with septic shock, diagnosed according the criteria of the 1992 American College of Chest Physicians/Society of Critical Care Medicine consensus conference, who required treatment with norepinephrine. Measurements and main results: Systemic and splanchnic hemodynamics and oxygen transport were measured before and during addition of low-dose dopamine (3 μg/kg per min). Low-dose dopamine had a marked effect on total body hemodynamics and oxygen transport. The fractional splanchnic flow at baseline ranged from 0.15 to 0.57. In 7 patients with a fractional splanchnic flow less than 0.30, low-dose dopamine increased splanchnic flow and splanchnic oxygen delivery and oxygen consumption. In 4 patients with a fractional splanchnic flow above 0.30, low-dose dopamine did not appear to change splanchnic blood flow. Conclusion: Low-dose dopamine has a potential beneficial effect on splanchnic blood flow and oxygen consumption in patients with septic shock, provided the fractional splanchnic flow is not already high before treatment.
    Type of Medium: Electronic Resource
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  • 5
    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.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 22 (1996), S. 615-616 
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1238
    Keywords: Key words Septic shock ; Sepsis ; Splanchnic blood flow ; Splanchnic oxygen delivery ; Splanchnic oxygen consumption ; Norepinephrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To assess global and splanchnic blood flow and oxygen transport in patients with sepsis with and without norepinephrine treatment. Design: Prospective, clinical study. Setting: University hospital intensive care unit. Patients: A convenience sample of 15 septic shock patients treated with norepinephrine and 13 patients with severe sepsis who did not receive norepinephrine. Measurements and main results: There were no differences between the two groups in global haemodynamics and oxygen transport. Splanchnic blood flow and oxygen delivery (splanchnic DO2 303±43ml/min per m2) and consumption (splanchnic VO2 100±13 ml/min per m2) were much higher in the septic shock group compared with the severe sepsis group (splanchnic DO2 175±19ml/min per m2, splanchnic VO2 61±6ml/min per m2). Gastric mucosal pH was subnormal in both groups (septic shock 7.29±0.02, severe sepsis 7.25±0.02) with no significant difference. No significant differences between groups were detected in lactate values. Conclusion: These data confirm a redistribution of blood flow to the splanchnic region in sepsis that is even more pronounced in patients with septic shock requiring norepinephrine. However, subnormal gastric mucosal pH suggested inadequate oxygenation in parts of the splanchnic region due to factors other than splanchnic hypoperfusion. Progress in this area will depend on techniques that address not only total splanchnic blood flow, but also inter-organ flow distribution, intra-organ distribution, and other microcirculatory or metabolic malfunctions.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1238
    Keywords: Septic shock ; Sepsis ; Splanchnic blood flow ; Splanchnic oxygen delivery ; Splanchnic oxygen consumption ; Norepinephrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To assess global and splanchnic blood flow and oxygen transport in patients with sepsis with and without norepinephrine treatment. Design Prospective, clinical study. Setting University hospital intensive care unit. Patients A convenience sample of 15 septic shock patients treated with norepinephrine and 13 patients with severe sepsis who did not receive norepinephrine. Measurements and main results There were no differences between the two groups in global haemodynamics and oxygen transport. Splanchnic blood flow and oxygen delivery (splanchnic DO2 303±43 ml/min per m2) and consumption (splanchnic VO2 100±13 ml/min per m2) were much higher in the septic shock group compared with the severe sepsis group (splanchnic DO2 175±19 ml/min per m2, splanchnic VO2 61±6 ml/min per m2). Gastric mucosal pH was subnormal in both groups (septic shock 7.29±0.02, severe sepsis 7.25±0.02) with no significant difference. No significant differences between groups were detected in lactate values. Conclusion These data confirm a redistribution of blood flow to the splanchnic region in sepsis that is even more pronounced in patients with septic shock requiring norepinephrine. However, subnormal gastric mucosal pH suggested inadequate oxygenation in part of the splanchnic region due to factors other than splanchnic hypoperfusion. Progress in this area will depend on techniques that address not only total splanchnic blood flow, but also inter-organ flow distribution, intra-organ distribution, and other microcirculatory or metabolic malfunctions.
    Type of Medium: Electronic Resource
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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.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 16 (1990), S. S149 
    ISSN: 1432-1238
    Keywords: Oxygen delivery ; Critically ill patients ; Septic shock
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Standard hemodynamic support in septic shock is to increase pulmonary capillary wedge pressure to above 15 mmHg by volume replacement and to give inotropic support if the mean arterial pressure (MAP) is not adequate. In an attempt to decrease mortality in critically ill patients, oxygen delivery (DO2) was increased by switching inotropic support from dobutamine alone or in combination with norepinephrine to dopamine alone, or by adding dopexamine, prostacyclin, or hypertonic saline to the treatment. DO2 increased significantly in all patients, but the increase in DO2 was accompanied by only a 10% increase in oxygen consumption (VO2). The increase in VO2 was similar in survivors and nonsurvivors and in patients with and without septic shock. The results indicate that if adequate volume and inotropic support is provided for critically ill patients, the detectable oxygen debt is small and has little effect on patient outcome. When DO2 is adequate, factors other than a tissue oxygen deficit seem to determine patient outcome.
    Type of Medium: Electronic Resource
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