[Biopathology of idiopathic pulmonary arterial hypertension]. / Biopatología de la hipertensión arterial pulmonar idiopática.

In recent years, several important outcomes have allowed increasing our understanding in the biopathology of idiopathic pulmonary arterial hypertension. Although the triggering event remains unknown, some of the adjacent mechanisms of disease had been identified. Pharmacological manipulation of such mechanisms, due to advances in the biopathology, has produced some clear clinical benefits, related to the survival of these patients. However, little exploration has been done on other pathways such as apoptosis or gene manipulation, which may be of great interest both for scientific and clinical research.

Potentially-toxic and essential elements profile of AH1N1 patients in Mexico City.

During spring of 2009, a new influenza virus AH1N1 spread in the world causing acute respiratory illness and death, resulting in the first influenza pandemic since 1968. Blood levels of potentially-toxic and essential elements of 40 pneumonia and confirmed AH1N1 were evaluated against two different groups of controls, both not infected with the pandemic strain. Significant concentrations of potentially-toxic elements (lead, mercury, cadmium, chromium, arsenic) along with deficiency of selenium or increased Zn/Cu ratios characterized AH1N1 cases under study when evaluated versus controlled cases. Deficiency of selenium is progressively observed from controls I (influenza like illness) through controls II (pneumonia) and finally pneumonia-AH1N1 infected patients. Cases with blood Se levels greater than the recommended for an optimal cut-off to activate glutathione peroxidase (12.5 µg/dL) recovered from illness and survived. Evaluation of this essential element in critical pneumonia patients at the National Institutes is under evaluation as a clinical trial.

Biopatología de la hipertensión arterial pulmonar idiopática / Biopathology of idiopathic pulmonary arterial hypertension

In recent years, several important outcomes have allowed increasing our understanding in the biopathology of idiopathic pulmonary arterial hypertension. Although the triggering event remains unknown, some of the adjacent mechanisms of disease had been identified. Pharmacological manipulation of such mechanisms, due to advances in the biopathology, has produced some clear clinical benefits, related to the survival of these patients. However, little exploration has been done on other pathways such as apoptosis or gene manipulation, which may be of great interest both for scientific and clinical research.

Trabajo respiratorio (WOB). Fundamento fisiológico e importancia clínica / Work of breathing (WOB). physiological principle and clinical importance

El aparato respiratorio consiste básicamente de dos partes: un órgano de intercambio gaseoso (los pulmones) y una bomba que ventila los pulmones. La falla en el intercambio gaseoso debida a enfermedades pulmonares causa hipoxemia, mientras que la falla de la bomba (que también produce hipoxemia) lleva a la hipoventilación. Cuando los músculos respiratorios son incapaces de generar la fuerza suficiente para que provean una ventilación adecuada, se presenta la falla respiratoria y el trabajo respiratorio (WOB) debe ser parcial o totalmente asumido por el ventilador mecánico. En el curso de la falla respiratoria aguda la mayor parte del WOB corresponde al ventilador y esto permite que los músculos respiratorios descansen. Considerando que la actividad de los músculos respiratorios puede dificultar descontinuar la ventilación mecánica es esencial optimiraz el esfuerzo respiratorio del paciente. Por otra parte se ha considerado que el WOB es uno de los factores predictivos para el retiro del ventilador, particularmente en pacientes con ventilación mecánica prolongada; el WOB permite también el uso fisiológico y racional del descanso (parcial o total) de los músculos ventilatorios