ABSTRACT
Metabolic activity can be down-regulated throughout the reduction of mitochondrial population. Lowering O2 demand in cardiogenic, hemorrhagic and septic shock is here examined through clinical observations and trials. A decrease in the availability of O will be followed by reductions in mitochondrial population and, therefore, in a decrease in O2 demand. This response may lessen or prevent the acquisition of an O2 debt; until now, cornerstone in the pathophysiology of shock. The cost of this adaptation is less energy production, and the resulting energy deficit has been linked to multiple organ failure (MOF), a complication of acute inflammatory processes and shock. MOF is better tolerated than anaerobic metabolism and is potentially reversible if the triggering causes are reversed and the energy level is re-established through mitochondrial biogenesis.Decoupling of mitochondrial oxidative phosphorylation occurs in both experimental models and in clinical septic shock. In critical patients this phenomenon may be detected by an inordinate increase in VO2 in response to a therapeutically increased DO. This hipermetabolic stage can be mistakenly interpreted as the repayment phase of an O2 debt.
Subject(s)
Shock/metabolism , Critical Illness , Energy Metabolism/physiology , Humans , Mitochondria/physiology , Multiple Organ Failure/metabolism , Myocardial Infarction/complications , Oxygen Consumption , Shock/physiopathology , Shock, Cardiogenic/metabolism , Shock, Cardiogenic/physiopathology , Shock, Hemorrhagic/metabolism , Shock, Hemorrhagic/physiopathology , Shock, Septic/metabolism , Shock, Septic/physiopathologyABSTRACT
La actividad metabólica puede modificarse mediante la regulación de la población mitocondrial en distintas enfermedades críticas. A través de observaciones y ensayos clínicos examinamos esta adaptación metabólica en el shock cardiogénico, hemorrágico y séptico. La caída de la disponibilidad de O2 (DO2) llevaría a una reducción de la población mitocondrial y consecuentemente a una disminución del consumo de O2 (VO2). Esta secuencia permite atenuar y aun evitar la adquisición de una deuda de O2, considerada hasta hoy base fundamental de la fisiopatología del shock. El costo de esta adaptación mitocondrial es menor energía disponible y el déficit energético resultante ha sido relacionado con la falla orgánica múltiple (FOM), importante complicación de diversos procesos inflamatorios agudos y estados de shock. La FOM es mejor tolerada que el metabolismo anaeróbico y es potencialmente reversible si se revierten las causas desencadenantes y se reestablece el nivel energético por medio de la biogénesis mitocondrial.El desacople de la fosforilación oxidativa mitocondrial ocurre tanto en diversos modelos experimentales de shock como así también en el shock séptico en el hombre. Esta alteración mitocondrial puede ser detectada por un aumento desmesurado del VO2 en respuesta al incremento terapéutico de la DO2. Este aumento de la actividad metabólica puede ser equívocamente interpretado como la fase de repago de una deuda de O2.
Metabolic activity can be down-regulated throughout the reduction of mitochondrial population. Lowering O2 demand in cardiogenic, hemorrhagic and septic shock is here examined through clinical observations and trials. A decrease in the availability of O2 will be followed by reductions in mitochondrial population and, therefore, in a decrease in O2 demand. This response may lessen or prevent the acquisition of an O2 debt; until now, cornerstone in the pathophysiology of shock. The cost of this adaptation is less energy production, and the resulting energy deficit has been linked to multiple organ failure (MOF), a complication of acute inflammatory processes and shock. MOF is better tolerated than anaerobic metabolism and is potentially reversible if the triggering causes are reversed and the energy level is re-established through mitochondrial biogenesis.Decoupling of mitochondrial oxidative phosphorylation occurs in both experimental models and in clinical septic shock. In critical patients this phenomenon may be detected by an inordinate increase in VO2 in response to a therapeutically increased DO2. This hipermetabolic stage can be mistakenly interpreted as the repayment phase of an O2 debt.
Subject(s)
Humans , Shock/metabolism , Critical Illness , Energy Metabolism/physiology , Mitochondria/physiology , Multiple Organ Failure/metabolism , Myocardial Infarction/complications , Oxygen Consumption , Shock, Cardiogenic/metabolism , Shock, Cardiogenic/physiopathology , Shock, Hemorrhagic/metabolism , Shock, Hemorrhagic/physiopathology , Shock, Septic/metabolism , Shock, Septic/physiopathology , Shock/physiopathologySubject(s)
Oxygen Consumption/physiology , Resuscitation/methods , Shock, Hemorrhagic/therapy , Female , Fluid Therapy/methods , Humans , Hypoxia/pathology , Hypoxia/therapy , Middle Aged , Multiple Organ Failure/pathology , Multiple Organ Failure/therapy , Shock, Hemorrhagic/pathology , Wounds and Injuries/pathology , Wounds and Injuries/therapyABSTRACT
The high mortality rate of cardiogenic shock in acute myocardial infarction (AMI) implies that debate over the correct haemodynamic management is still unresolved. The purpose of this review is to re-evaluate the reciprocal relationships between oxygen-related variables and response to treatment in a large number of patients with AMI. A MEDLINE search of reports published between 1970 and 2008 was performed. Twelve clinical reports including 453 patients with AMI and 989 sets of oxygen delivery and oxygen consumption expressed in ml min⻹ m⻲ and oxygen extraction ratio were selected. While processing this data, we found an early down-regulation in oxygen demand linked to a decrease in oxygen supply. This mechanism is also supported in some studies by a critically low oxygen uptake that was not associated with lactic acidosis.
Subject(s)
Myocardial Infarction/metabolism , Myocardium/metabolism , Oxygen Consumption , Oxygen/metabolism , Shock, Cardiogenic/etiology , Adaptation, Physiological , Aged , Aged, 80 and over , Hemodynamics , Humans , Middle Aged , Myocardial Infarction/complications , Myocardial Infarction/physiopathology , Myocardial Infarction/therapy , Oxygen Inhalation Therapy , Shock, Cardiogenic/metabolism , Shock, Cardiogenic/physiopathology , Shock, Cardiogenic/therapyABSTRACT
The acute respiratory distress syndrome (ARDS) represents 7.7% of the intensive care population, and is associated with great morbidity and mortality (58%). Frequently, the mortality can be attributed to more than one cause. Refractory hypoxemia is uncommon (15%) and most of the patients also have multiple organic dysfunction, sepsis or septic shock. Although there are many publications concerning series of cases and clinical trials using steroids as a part of the treatment of ARDS, this issue remains controversial. In this article the role of steroids in the ARDS is evaluated by analysis of the available literature. We conclude that steroids are useful in a subgroup of patients with unresolving ARDS, after ruling out an active infection or after treatment with antibiotics.
Subject(s)
Respiratory Distress Syndrome/drug therapy , Steroids/therapeutic use , Humans , Respiratory Distress Syndrome/mortalityABSTRACT
En Argentina, el síndrome de distrés respiratorio agudo (SDRA) representa el 7.7% de las admisiones en terapia intensiva y está asociado con una alta morbilidad y mortalidad (58%). Con frecuencia la muerte puede ser atribuida a más de una causa. La hipoxemia refractaria es una causa de muerte poco frecuente (15%) y en muchos casos puede coexistir con disfunción multiorgánica, sepsis o shock séptico. La utilidad de los esteroides como parte del tratamiento es aún motivo de debate a pesar de las múltiples series de casos y estudios clínicos publicados. En el artículo se evalúa la utilidad de los esteroides en el SDRA a través de la revisión de la bibliografía disponible. Se concluye que los esteroides estarían indicados en un pequeño subgrupo de pacientes con SDRA no resuelto o tardío, después de descartar o controlar una infección activa.
Subject(s)
Humans , Respiratory Distress Syndrome/drug therapy , Steroids/therapeutic use , Respiratory Distress Syndrome/mortalityABSTRACT
En Argentina, el síndrome de distrés respiratorio agudo (SDRA) representa el 7.7% de las admisiones en terapia intensiva y está asociado con una alta morbilidad y mortalidad (58%). Con frecuencia la muerte puede ser atribuida a más de una causa. La hipoxemia refractaria es una causa de muerte poco frecuente (15%) y en muchos casos puede coexistir con disfunción multiorgánica, sepsis o shock séptico. La utilidad de los esteroides como parte del tratamiento es aún motivo de debate a pesar de las múltiples series de casos y estudios clínicos publicados. En el artículo se evalúa la utilidad de los esteroides en el SDRA a través de la revisión de la bibliografía disponible. Se concluye que los esteroides estarían indicados en un pequeño subgrupo de pacientes con SDRA no resuelto o tardío, después de descartar o controlar una infección activa.(AU)
Subject(s)
Humans , Respiratory Distress Syndrome/drug therapy , Steroids/therapeutic use , Respiratory Distress Syndrome/mortalityABSTRACT
The acute respiratory distress syndrome (ARDS) represents 7.7
of the intensive care population, and is associated with great morbidity and mortality (58
). Frequently, the mortality can be attributed to more than one cause. Refractory hypoxemia is uncommon (15
) and most of the patients also have multiple organic dysfunction, sepsis or septic shock. Although there are many publications concerning series of cases and clinical trials using steroids as a part of the treatment of ARDS, this issue remains controversial. In this article the role of steroids in the ARDS is evaluated by analysis of the available literature. We conclude that steroids are useful in a subgroup of patients with unresolving ARDS, after ruling out an active infection or after treatment with antibiotics.
