Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05516.x
M Hayes
Total body oxygen consumption 0702) is a measure of global aerobic metabolism and it has been suggested that an inability to consume oxygen is the best early predictor of organ failure1. V02 is however, dependent on metabolic demands, which may vary widely in critically ill patients and there has therefore been considerable interest in using the relationship between oxygen delivery (DO21 and V02 as a means of evaluating the adequacy of tissue oxygenation. A number of studies have demonstrated that in apparently stable critically ill patients, in contrast to normal physiology, V02 increases when DO2 is augmented and falls in response to reductions in D022,3. Characteristically this phenomenon, termed supply dependency, is associated with increased oxygen demand, a diminished ability of the tissues to alter oxygen extraction in response to a change in DO2 and the presence of raised lactate levels. The demonstration of supply dependency has been regarded as indi4 rect evidence of occult tissue oxygen debt and associated with a high mortality. In contrast, in some recent studies although an oxygen flux test was not specifically performed, the ability to increase VO2 when DO2 was enhanced was associated with survival, whereas in those in whom V02 was unresponsive to increases in DO2 had persistently elevated lactate concentrations and an extremely poor prognosis5.6. Studies investigating the relationship between DO2 and V02 are complicated by many factors including; mathematical coupling7; the spontaneous fluduations in V02 and DO2 in apparently stable critically ill patients8; and the effect of catecholamines on oxidative metabolism which can lead to increases in V029. Recent work has even suggested that the critical level of oxygen delivery is much lower than that previously reported in normal humans and perhaps surprisingly is not altered by sepsislO. The uncertainty surrounding supply dependency and the knowledge that the critical level of oxygen delivery may not be altered by sepsis undermines the basis for goal directed therapy in critically ill patients. It is now clear that outcome of this group of patients is worsened when aggressive treatment with inotropes is directed towards attaining supranormal levels of both oxygen delivery and consumption. It is also understood that it is the ability to attain a hypermetabolic state with elevated levels of cardiac index, D02, and V02 that is associated with a good outcome. Administration of very small doses of endotoxin to normal human volunteers produces a significant increase in both DO2 and VO2l1. Patients with uncomplicated sepsis have a greater capacity to extract oxygen (and consequently a higher V02) despite a lower cardiac index and DO2 than more severely ill patients with sepsis syndrome12. Hypermetabolism therefore appears to be an important component of a successful host response particularly in sepsis. In rats made septic by caecal ligation and puncture, those who survived remained hypermet
{"title":"Therapeutic aspects of oxygen utilisation.","authors":"M Hayes","doi":"10.1111/j.1399-6576.1997.tb05516.x","DOIUrl":"https://doi.org/10.1111/j.1399-6576.1997.tb05516.x","url":null,"abstract":"Total body oxygen consumption 0702) is a measure of global aerobic metabolism and it has been suggested that an inability to consume oxygen is the best early predictor of organ failure1. V02 is however, dependent on metabolic demands, which may vary widely in critically ill patients and there has therefore been considerable interest in using the relationship between oxygen delivery (DO21 and V02 as a means of evaluating the adequacy of tissue oxygenation. A number of studies have demonstrated that in apparently stable critically ill patients, in contrast to normal physiology, V02 increases when DO2 is augmented and falls in response to reductions in D022,3. Characteristically this phenomenon, termed supply dependency, is associated with increased oxygen demand, a diminished ability of the tissues to alter oxygen extraction in response to a change in DO2 and the presence of raised lactate levels. The demonstration of supply dependency has been regarded as indi4 rect evidence of occult tissue oxygen debt and associated with a high mortality. In contrast, in some recent studies although an oxygen flux test was not specifically performed, the ability to increase VO2 when DO2 was enhanced was associated with survival, whereas in those in whom V02 was unresponsive to increases in DO2 had persistently elevated lactate concentrations and an extremely poor prognosis5.6. Studies investigating the relationship between DO2 and V02 are complicated by many factors including; mathematical coupling7; the spontaneous fluduations in V02 and DO2 in apparently stable critically ill patients8; and the effect of catecholamines on oxidative metabolism which can lead to increases in V029. Recent work has even suggested that the critical level of oxygen delivery is much lower than that previously reported in normal humans and perhaps surprisingly is not altered by sepsislO. The uncertainty surrounding supply dependency and the knowledge that the critical level of oxygen delivery may not be altered by sepsis undermines the basis for goal directed therapy in critically ill patients. It is now clear that outcome of this group of patients is worsened when aggressive treatment with inotropes is directed towards attaining supranormal levels of both oxygen delivery and consumption. It is also understood that it is the ability to attain a hypermetabolic state with elevated levels of cardiac index, D02, and V02 that is associated with a good outcome. Administration of very small doses of endotoxin to normal human volunteers produces a significant increase in both DO2 and VO2l1. Patients with uncomplicated sepsis have a greater capacity to extract oxygen (and consequently a higher V02) despite a lower cardiac index and DO2 than more severely ill patients with sepsis syndrome12. Hypermetabolism therefore appears to be an important component of a successful host response particularly in sepsis. In rats made septic by caecal ligation and puncture, those who survived remained hypermet","PeriodicalId":75373,"journal":{"name":"Acta anaesthesiologica Scandinavica. Supplementum","volume":"110 ","pages":"99-100"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-6576.1997.tb05516.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20192814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05518.x
D Bevan
{"title":"Reversal of neuromuscular block: the case FOR reversal.","authors":"D Bevan","doi":"10.1111/j.1399-6576.1997.tb05518.x","DOIUrl":"https://doi.org/10.1111/j.1399-6576.1997.tb05518.x","url":null,"abstract":"","PeriodicalId":75373,"journal":{"name":"Acta anaesthesiologica Scandinavica. Supplementum","volume":"110 ","pages":"102"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-6576.1997.tb05518.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20192816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05524.x
U Lendahl
The transgenic technique allows specific genetic alterations to be made in all cells of an animal and this has greatly improved our understanding of how the embryonic and adult central nervous system (CNS) develop. The CNS originates from the neuroectoderm in the neural plate on the dorsal side of the embryo and after closure of the neural tube the cells of the neuroepithelium, i.e. the CNS stem cells, transiently proliferate to generate neurons and glial cells. Here we review our attempts to gain insights into the control of CNS development. We have identified a gene, nestin, which is predominantly expressed in embryonic and adult CNS stem cells. In addition to its normal expression in the CNS stem cells, nestin is reexpressed in CNS tumors and in the adult spinal cord and brain after CNS injury. By using the lacZ reporter gene assay in transgenic mice, we have identified regulatory regions (enhancer) in the nestin gene required for expression in embryonic CNS stem cells and in the adult spinal cord after injury. In a second project, we have cloned and characterized the Notch gene family (the Notch 1, 2 and 3 genes) in mouse and man. These genes encode trans-membrane receptors, which appear to be key regulatory molecules for proliferation and differentiation both in the developing CNS and in other tissues. Expression of an activated form of the Notch 3 receptor from the nestin promoter in transgenic mice leads to a lethal, exencephaly-like phenotype in the embryo, probably as a result of excess proliferation of the CNS stem cells. The recent finding that the Notch 3 gene is the genetic cause for familial stroke is discussed in the context of current models for Notch function.
{"title":"Transgenic analysis of central nervous system development and regeneration.","authors":"U Lendahl","doi":"10.1111/j.1399-6576.1997.tb05524.x","DOIUrl":"https://doi.org/10.1111/j.1399-6576.1997.tb05524.x","url":null,"abstract":"<p><p>The transgenic technique allows specific genetic alterations to be made in all cells of an animal and this has greatly improved our understanding of how the embryonic and adult central nervous system (CNS) develop. The CNS originates from the neuroectoderm in the neural plate on the dorsal side of the embryo and after closure of the neural tube the cells of the neuroepithelium, i.e. the CNS stem cells, transiently proliferate to generate neurons and glial cells. Here we review our attempts to gain insights into the control of CNS development. We have identified a gene, nestin, which is predominantly expressed in embryonic and adult CNS stem cells. In addition to its normal expression in the CNS stem cells, nestin is reexpressed in CNS tumors and in the adult spinal cord and brain after CNS injury. By using the lacZ reporter gene assay in transgenic mice, we have identified regulatory regions (enhancer) in the nestin gene required for expression in embryonic CNS stem cells and in the adult spinal cord after injury. In a second project, we have cloned and characterized the Notch gene family (the Notch 1, 2 and 3 genes) in mouse and man. These genes encode trans-membrane receptors, which appear to be key regulatory molecules for proliferation and differentiation both in the developing CNS and in other tissues. Expression of an activated form of the Notch 3 receptor from the nestin promoter in transgenic mice leads to a lethal, exencephaly-like phenotype in the embryo, probably as a result of excess proliferation of the CNS stem cells. The recent finding that the Notch 3 gene is the genetic cause for familial stroke is discussed in the context of current models for Notch function.</p>","PeriodicalId":75373,"journal":{"name":"Acta anaesthesiologica Scandinavica. Supplementum","volume":"110 ","pages":"116-8"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-6576.1997.tb05524.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20192823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05527.x
U Ungerstedt
Microdialysis is a technique for sampling the chemistry of essentially all organs and tissues of the body. It was conceived of in the early 70th by Delgado's group in the USA and our group in Sweden. The idea was to implant an "artificial blood capillary" in the tissue, perfuse it with a physiological solution, recover molecules that diffuse over the membrane, and analyse the dialysate. The technique is now universally accepted for investigations of the brain and peripheral organs in animals and more than 4000 papers are published using the technique in essentially every organ of the body. The first implantation of microdialysis catheters in human subcutaneous and brain tissue were made ten years ago at the Karolinska institute in order to follow tissue metabolism. The lack of available instruments slowed the development of the technique. However, two years ago suitable catheters, a portable microdialysis pump and a bedside analyser became available. Today more than 200 papers are published on human investigations mainly in the field of diabetes, adipous tissue metabolism, neuro intensive and neonatal care. The microdialysis catheter is a flexible concentric catheter covered with a 10-30 mm dialysis membrane distally. An inlet tube connects to a small portable pump and the outlet tube to a microvial holder. There is one catheter intended for implantation into subcutaneous tissue or resting muscle and another for implantation into the brain. In the clinical situation the microvial is usually changed every 1W min and the sample analysed in the bedside analyser and then often brought to the laboratory for a more extensive analysis of various analytes. The usefulness of microdialysis rests on two features of the technique: 1) It samples the chemistry in individual tissues and organs as opposed from blood samples and 2) It allows very frequent sampling without any removal of blood or tissue from the body. In the first case microdialysis represent a new and unique possibility to follow tissue metabolism, for example during hypoxia or ischemia as well as the local concentration of drugs and other exogenuous substances. In the second case it is a well tolerated technique for monitoring, for example, a diabetes patient in order to adjust insulin treatment or a neonate where frequent blood sampling is a severe problem. There is a strong interest for applying microdialysis in various clinical situations: In vascular and plastic surgery for monitoring preand postsurgical tissue metabolism. In intensive care for monitoring metabolism after multi trauma and sepsis. In neurointensive care for monitoring brain trauma and hemorrhage. In neonates for minimizing blood samp ling and during and between hemodialysis treatments for monitoring tissue urea. The analytes of immediate interest for bedside monitoring are glucose, lactate, pyruvate, glycerol, glutamate and urea. The lactate/pyruvate ratio is of particular interest for distinguishing hypermetabolism from hypo
{"title":"Microdialysis--a new technique for monitoring local tissue events in the clinic.","authors":"U Ungerstedt","doi":"10.1111/j.1399-6576.1997.tb05527.x","DOIUrl":"https://doi.org/10.1111/j.1399-6576.1997.tb05527.x","url":null,"abstract":"Microdialysis is a technique for sampling the chemistry of essentially all organs and tissues of the body. It was conceived of in the early 70th by Delgado's group in the USA and our group in Sweden. The idea was to implant an \"artificial blood capillary\" in the tissue, perfuse it with a physiological solution, recover molecules that diffuse over the membrane, and analyse the dialysate. The technique is now universally accepted for investigations of the brain and peripheral organs in animals and more than 4000 papers are published using the technique in essentially every organ of the body. The first implantation of microdialysis catheters in human subcutaneous and brain tissue were made ten years ago at the Karolinska institute in order to follow tissue metabolism. The lack of available instruments slowed the development of the technique. However, two years ago suitable catheters, a portable microdialysis pump and a bedside analyser became available. Today more than 200 papers are published on human investigations mainly in the field of diabetes, adipous tissue metabolism, neuro intensive and neonatal care. The microdialysis catheter is a flexible concentric catheter covered with a 10-30 mm dialysis membrane distally. An inlet tube connects to a small portable pump and the outlet tube to a microvial holder. There is one catheter intended for implantation into subcutaneous tissue or resting muscle and another for implantation into the brain. In the clinical situation the microvial is usually changed every 1W min and the sample analysed in the bedside analyser and then often brought to the laboratory for a more extensive analysis of various analytes. The usefulness of microdialysis rests on two features of the technique: 1) It samples the chemistry in individual tissues and organs as opposed from blood samples and 2) It allows very frequent sampling without any removal of blood or tissue from the body. In the first case microdialysis represent a new and unique possibility to follow tissue metabolism, for example during hypoxia or ischemia as well as the local concentration of drugs and other exogenuous substances. In the second case it is a well tolerated technique for monitoring, for example, a diabetes patient in order to adjust insulin treatment or a neonate where frequent blood sampling is a severe problem. There is a strong interest for applying microdialysis in various clinical situations: In vascular and plastic surgery for monitoring preand postsurgical tissue metabolism. In intensive care for monitoring metabolism after multi trauma and sepsis. In neurointensive care for monitoring brain trauma and hemorrhage. In neonates for minimizing blood samp ling and during and between hemodialysis treatments for monitoring tissue urea. The analytes of immediate interest for bedside monitoring are glucose, lactate, pyruvate, glycerol, glutamate and urea. The lactate/pyruvate ratio is of particular interest for distinguishing hypermetabolism from hypo","PeriodicalId":75373,"journal":{"name":"Acta anaesthesiologica Scandinavica. Supplementum","volume":"110 ","pages":"123"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-6576.1997.tb05527.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20192825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05493.x
P O Grände, B Asgeirsson, C Nordström
An actively raised cerebral perfusion pressure by vasopressors is nowadays often advocated during therapy of a post traumatic brain oedema to improve oxygenation of the brain. In this paper we argue that the arterial pressure not uncritically can be raised as the subsequent increase in hydrostatic capillary pressure may favour transcapillary filtration if the blood-brain barrier is opened for solutes. Further, the use of vasoconstrictor drugs to increase the perfusion pressure may in fact impair oxygenation to the penumbra zones around brain contusions but also to other tissues of the body, like the intestinal mucosa and the kidney. An alternative therapeutical concept which both ensures an adequate oxygenation of the brain and controls the intracranial pressure (ICP) is given. In short, it implies active antistress and sedative treatment, adequate fluid therapy with blood and colloids to normal haemoglobine and albumin values, artificial ventilation to normal PaCO2 and PaO2, and this in combination with antihypertensive and catecholamine reducing treatment with alpha 2-agonist and beta 1-antagonist.
{"title":"Aspects on the cerebral perfusion pressure during therapy of a traumatic head injury.","authors":"P O Grände, B Asgeirsson, C Nordström","doi":"10.1111/j.1399-6576.1997.tb05493.x","DOIUrl":"https://doi.org/10.1111/j.1399-6576.1997.tb05493.x","url":null,"abstract":"<p><p>An actively raised cerebral perfusion pressure by vasopressors is nowadays often advocated during therapy of a post traumatic brain oedema to improve oxygenation of the brain. In this paper we argue that the arterial pressure not uncritically can be raised as the subsequent increase in hydrostatic capillary pressure may favour transcapillary filtration if the blood-brain barrier is opened for solutes. Further, the use of vasoconstrictor drugs to increase the perfusion pressure may in fact impair oxygenation to the penumbra zones around brain contusions but also to other tissues of the body, like the intestinal mucosa and the kidney. An alternative therapeutical concept which both ensures an adequate oxygenation of the brain and controls the intracranial pressure (ICP) is given. In short, it implies active antistress and sedative treatment, adequate fluid therapy with blood and colloids to normal haemoglobine and albumin values, artificial ventilation to normal PaCO2 and PaO2, and this in combination with antihypertensive and catecholamine reducing treatment with alpha 2-agonist and beta 1-antagonist.</p>","PeriodicalId":75373,"journal":{"name":"Acta anaesthesiologica Scandinavica. Supplementum","volume":"110 ","pages":"36-40"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-6576.1997.tb05493.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20191619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05494.x
S Gelman
Arterial hypertension is the most dramatic and consistent component of the hernodynamic response to aortic cross-clamping. Most texts attribute this sign to a sudden increase in impedance to aortic flow and an increase in afterload. Increases in left ventricle endsystolic wall stress and systemic arterial pressure’ are consistent with this notion. However, Caldini, et a12 provided theoretical ground for the following speculations; clamping of the thoracic aorta increases cardiac output by diverting blood away from the longtime constant area, presumably the splanchnic vasculature. In other words, the splanchnic venous vasculature collapses when intramural venous pressure decreases; the latter results from a decrease in blood flow from the arterial to the venous vasculature with a subsequent decrease in venous capacitance, secondary to an elastic recoil. Splanchnic venous collapse, in turn, results in an increase in venous return and cardiac output. There is some experimental sup port for this theory: Occlusion of the inferior caval vein prevented increases in arterial pressure and in enddiastolic myocardial segment length, whereas occlusion of other, smaller veins modified the increases to different degrees, presumably reflecting different amounts of blood volume translocated from various veins, thereby affecting venous return, preload and the degree of arterial hypertension. The authors concluded that blood volume shift from the nonsplanchnic region maintains cardiac output during infraceliac aortic occlusion whereas during occlusion of the thoracic aorta, drainage from the splanchnic area accounts for about 70% of the increase in enddiastolic myocardial segment length.’ Cross-clamping of the thoracic aorta is associated with almost a twofold increase in blood flow through the upper part of the body,‘” and more than a three-fold increase in blood flow though the muscle proximal to the clamp’. These observations are consistent with (but do not prove) the hypothesis of blood volume redistribution. using whole-body scintigraphy with Tc“ -labeled plasma albumin we demonstrated that aortic crossclamping at the diaphragmatic level is associated with a significant increase in blood volume in the organs and tissues proximal to the level of occl~sion.~ Thus, the data presented provide evidence that blood volume shifts from the lower to the upper part of the body during aortic cross-clamping. Variation in the blood volume status of splanchnic vascular tone, resulting from differences in fluid load, depth of anesthesia, pharmacodynamics of an anesthetic, and other factors might affect the degree and pattern of blood volume redistribution. For example, during infrasplanchnic aortic occlusion, the blood volume redistributed from the vasculature below the occlusion might travel to the heart, increasing preload and inducing central hypervolemia, or it might travel to the compliant splanchnic venous vasculature. The distribution of volume between the heart and t
{"title":"Pathophysiology of aortic cross-clamping.","authors":"S Gelman","doi":"10.1111/j.1399-6576.1997.tb05494.x","DOIUrl":"https://doi.org/10.1111/j.1399-6576.1997.tb05494.x","url":null,"abstract":"Arterial hypertension is the most dramatic and consistent component of the hernodynamic response to aortic cross-clamping. Most texts attribute this sign to a sudden increase in impedance to aortic flow and an increase in afterload. Increases in left ventricle endsystolic wall stress and systemic arterial pressure’ are consistent with this notion. However, Caldini, et a12 provided theoretical ground for the following speculations; clamping of the thoracic aorta increases cardiac output by diverting blood away from the longtime constant area, presumably the splanchnic vasculature. In other words, the splanchnic venous vasculature collapses when intramural venous pressure decreases; the latter results from a decrease in blood flow from the arterial to the venous vasculature with a subsequent decrease in venous capacitance, secondary to an elastic recoil. Splanchnic venous collapse, in turn, results in an increase in venous return and cardiac output. There is some experimental sup port for this theory: Occlusion of the inferior caval vein prevented increases in arterial pressure and in enddiastolic myocardial segment length, whereas occlusion of other, smaller veins modified the increases to different degrees, presumably reflecting different amounts of blood volume translocated from various veins, thereby affecting venous return, preload and the degree of arterial hypertension. The authors concluded that blood volume shift from the nonsplanchnic region maintains cardiac output during infraceliac aortic occlusion whereas during occlusion of the thoracic aorta, drainage from the splanchnic area accounts for about 70% of the increase in enddiastolic myocardial segment length.’ Cross-clamping of the thoracic aorta is associated with almost a twofold increase in blood flow through the upper part of the body,‘” and more than a three-fold increase in blood flow though the muscle proximal to the clamp’. These observations are consistent with (but do not prove) the hypothesis of blood volume redistribution. using whole-body scintigraphy with Tc“ -labeled plasma albumin we demonstrated that aortic crossclamping at the diaphragmatic level is associated with a significant increase in blood volume in the organs and tissues proximal to the level of occl~sion.~ Thus, the data presented provide evidence that blood volume shifts from the lower to the upper part of the body during aortic cross-clamping. Variation in the blood volume status of splanchnic vascular tone, resulting from differences in fluid load, depth of anesthesia, pharmacodynamics of an anesthetic, and other factors might affect the degree and pattern of blood volume redistribution. For example, during infrasplanchnic aortic occlusion, the blood volume redistributed from the vasculature below the occlusion might travel to the heart, increasing preload and inducing central hypervolemia, or it might travel to the compliant splanchnic venous vasculature. The distribution of volume between the heart and t","PeriodicalId":75373,"journal":{"name":"Acta anaesthesiologica Scandinavica. Supplementum","volume":"110 ","pages":"41-2"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-6576.1997.tb05494.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20191620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05509.x
C Wade, J Grady, G Kramer
Small volume resuscitation, using hypertonic saline/hyperoncotic colloid solutions, effectively restores blood volume and cardiovascular function after hemorrhagic shock in experimental models (I). Clinical evaluation of trauma resuscitation using 7.5% saline/6% Dextran 70 (HSD), as to over all mortality, has been inconclusive (2-9). This inconclusiveness appears to be primarily a result of limited statistical power. However, efficacy has been demonstrated in subpopulations such as patients who subsequently require surgery. What was unique about these clinical trials was they were prospective randomized controlled double-blind studies (RCTs) of trauma patients treated with HSD (2-9). Using verified data collected from previous RCTs, we prospectively designed an individual patient data meta-analysis to assess the efficacy of HSD. Metaanalysis using individual patient data from multiple studies ranks high in the hierarchy of evidence. These methods also allow for assessment of the efficacy of HSD in improving survival in subpopula tions. We utilized rigorous experimental methods, including development of and adherence to a prospectively defined protocol for data acquisition and analysis, with blinding as to treatment assignments to avoid bias to the extent possible. Our objective was to evaluate the efficacy of HSD for initial treatment of trauma versus standard-of-care (SOC) treatment. Specifically, we evaluated the efficacy of a 250 ml infusion of HSD versus an equivalent infusion of isotonic solution for initial management of traumatic hypovolemia and improvement of survival rates.
{"title":"Efficacy of hypertonic saline dextran (HSD) in patients with traumatic hypotension: meta-analysis of individual patient data.","authors":"C Wade, J Grady, G Kramer","doi":"10.1111/j.1399-6576.1997.tb05509.x","DOIUrl":"https://doi.org/10.1111/j.1399-6576.1997.tb05509.x","url":null,"abstract":"Small volume resuscitation, using hypertonic saline/hyperoncotic colloid solutions, effectively restores blood volume and cardiovascular function after hemorrhagic shock in experimental models (I). Clinical evaluation of trauma resuscitation using 7.5% saline/6% Dextran 70 (HSD), as to over all mortality, has been inconclusive (2-9). This inconclusiveness appears to be primarily a result of limited statistical power. However, efficacy has been demonstrated in subpopulations such as patients who subsequently require surgery. What was unique about these clinical trials was they were prospective randomized controlled double-blind studies (RCTs) of trauma patients treated with HSD (2-9). Using verified data collected from previous RCTs, we prospectively designed an individual patient data meta-analysis to assess the efficacy of HSD. Metaanalysis using individual patient data from multiple studies ranks high in the hierarchy of evidence. These methods also allow for assessment of the efficacy of HSD in improving survival in subpopula tions. We utilized rigorous experimental methods, including development of and adherence to a prospectively defined protocol for data acquisition and analysis, with blinding as to treatment assignments to avoid bias to the extent possible. Our objective was to evaluate the efficacy of HSD for initial treatment of trauma versus standard-of-care (SOC) treatment. Specifically, we evaluated the efficacy of a 250 ml infusion of HSD versus an equivalent infusion of isotonic solution for initial management of traumatic hypovolemia and improvement of survival rates.","PeriodicalId":75373,"journal":{"name":"Acta anaesthesiologica Scandinavica. Supplementum","volume":"110 ","pages":"77-9"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1399-6576.1997.tb05509.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20191635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-01-01DOI: 10.1111/j.1399-6576.1997.tb05513.x
J Takala
Maintenance of adequate tissue perfusion and oxygenation is one of the major goals of intensive care. Imminent or manifest acute circulatory and respiratory failure are the most common causes of emergency admission to intensive care. Tissue hypoxia due to insufficient blood flow and low arterial oxygen content is common in these patients. The presence and pathogenesis of tissue hypoxia during circulatory shock has been well documented and the importance of tissue oxygenation at this phase of intensive care is not controversial. The presence and relevance of tissue hypoxia in patients without shock is a controversial issue; whether tissue hypoxia is of any importance in patients with stabile haemodynamics remains to be confirmed. Since oxygen delivery to the tissues is the product of blood flow and arterial oxygen content, it is evident that blood flow is a major component of the overall adequacy of tissue oxygen supply. For any given blood flow, the adequacy of the flow depends on the metabolic demands of the tissues and the capability of the tissues to extract the available oxygen. At unchanged blood flow, local and regional blood flow redistribution and changes in local or regional metabolic demand have a considerable impact on the adequacy of tissue perfusion and oxygen supply 11 I. In most clinical disorders of tissue oxygenation, blood volume, cardiac output, and arterial oxygen content are of primary concern. The effects of any therapeutic interventions, such as administration of Vasoadive drugs and mechanical ventilation, will be markedly modified by the volume status of the patient. Two different scenarios of impaired tissue oxygenation due to inadequate perfusion can be distinguished [l]. In low flow states (cardiogenic and hypovolemic shock) both the whole body blood flow and the Various regional blood flows are decreased and the metabolic demands are normal. Under these conditions, various regional circulations are gradually compromised in order to maintain sufficient perfusion of the heart and the brain. In this respect, the splanchnic region has a special role, since splanchnic Vasoconstriction is the first line mechanism in the defense of blood volume and flow [21. Splanchnic vasoconstriction, once established, is maintained even after restoration of the circulating blood volume. This is the most likely explanation for the commonly observed prolonged visceral hypoperfusion after severe hypodynamic shock. The second scenario, which is especially common in sepsis and severe systemic inflammation, includes increased metabolic demand despite normal or even increased blood flow [l]. The main threat for the adequacy of tissue oxygenation here is the substantially increased oxygen demand [3,41. Also in these settings, the splanchnic region appears to have a central role, since the hypermetabolism associated with inflammation is primarily a reflection of splanchnic hypermetabolism. As the result of the regional or local hypermetabolism, spl
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