Publication: Efecto de la administración de un preparado probiótico sobre las alteraciones hemodinámicas de pacientes con cirrosis y ascitis
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2017-08-21
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Universidad Complutense de Madrid
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Abstract
El desarrollo del síndrome de hipertensión portal en la historia natural de la cirrosis hepática es el principal determinante de la evolución de la enfermedad desde un estado de cirrosis compensada a un estado de cirrosis descompensada, siendo responsable de las complicaciones clínicas más importantes asociadas a la cirrosis: desarrollo de varices esófago-gástricas y hemorragia secundaria, ascitis, peritonitis bacteriana espontánea (PBE), encefalopatía hepática, síndrome hepatorrenal, síndrome hepatopulmonar o hipertensión portopulomonar. En la evolución del síndrome de hipertensión portal se desarrolla un síndrome de circulación hiperdinámica caracterizado por alteraciones a nivel de la hemodinámica sistémica (disminución de las resistencias vasculares sistémicas, hipotensión arterial y aumento del gasto cardiaco). Este síndrome de circulación hiperdinámica está implicado, igualmente, en algunas de las manifestaciones clínicas más importantes de la cirrosis descompensada, como la ascitis o el síndrome hepatorrenal. Tanto el síndrome de hipertensión portal como las alteraciones hemodinámicas sistémicas son fácilmente medibles y reproducibles mediante la realización de un estudio hemodinámico, método diagnóstico totalmente introducido en la práctica clínica habitual, que permite la medición tanto del gradiente de presión venosa hepática (GPVH, que refleja el incremento de presión portal) como de parámetros hemodinámicos sistémicos (resistencias vasculares sistémicas (RVS), gasto cardiaco (GC) y tensión arterial media (TAM))...
The development of portal hypertension syndrome is the main determinant of the progression from a state of compensated cirrhosis to a state of decompensated cirrhosis, in the natural history of chronic liver disease. Portal hypertension is responsible for the major clinical complications associated with cirrhosis, namely, the development of gastroesophageal varices and secondary hemorrhage, ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome and portopulmonary hypertension. The evolution of portal hypertension is frequently associated with the development of hyperdynamic circulation, which is characterized by systemic hemodynamic alterations that include decreases of blood pressure and systemic vascular resistance, and an increased of cardiac output. This hyperdynamic circulation further contributes to clinical manifestations of decompensated cirrhosis such as ascites or hepatorenal syndrome. Both portal hypertension syndrome and the systemic hemodynamic alterations can be easily and reproducibly measured by performing a hepatic hemodynamic study, a diagnostic technique that can be fully incorporated into routine clinical practice. The hepatic hemodynamic study allows the measurement of hepatic venous pressure gradient (HVPG, an estimation of portal pressure) and of systemic hemodynamic parameters (systemic vascular resistance (SVR), cardiac output (CO) and mean arterial pressure (MAP)). Bacterial translocation is a fundamental pathophysiological event for the development of bacterial infections in patients with liver cirrhosis. In addition, bacterial translocation (both viable bacteria and non-viable bacterial products) induces a state of chronic inflammation that contributes to the worsening of the hyperdynamic circulatory state and to the perpetuation of bacterial translocation in patients with liver cirrhosis...
The development of portal hypertension syndrome is the main determinant of the progression from a state of compensated cirrhosis to a state of decompensated cirrhosis, in the natural history of chronic liver disease. Portal hypertension is responsible for the major clinical complications associated with cirrhosis, namely, the development of gastroesophageal varices and secondary hemorrhage, ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome and portopulmonary hypertension. The evolution of portal hypertension is frequently associated with the development of hyperdynamic circulation, which is characterized by systemic hemodynamic alterations that include decreases of blood pressure and systemic vascular resistance, and an increased of cardiac output. This hyperdynamic circulation further contributes to clinical manifestations of decompensated cirrhosis such as ascites or hepatorenal syndrome. Both portal hypertension syndrome and the systemic hemodynamic alterations can be easily and reproducibly measured by performing a hepatic hemodynamic study, a diagnostic technique that can be fully incorporated into routine clinical practice. The hepatic hemodynamic study allows the measurement of hepatic venous pressure gradient (HVPG, an estimation of portal pressure) and of systemic hemodynamic parameters (systemic vascular resistance (SVR), cardiac output (CO) and mean arterial pressure (MAP)). Bacterial translocation is a fundamental pathophysiological event for the development of bacterial infections in patients with liver cirrhosis. In addition, bacterial translocation (both viable bacteria and non-viable bacterial products) induces a state of chronic inflammation that contributes to the worsening of the hyperdynamic circulatory state and to the perpetuation of bacterial translocation in patients with liver cirrhosis...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Medicina, Departamento de Medicina, leída el 27-01-2016