Ventilación pulmonar/Lung ventilation

Disfunción pulmonar postoperatoria y ventilación mecánica en cirugía cardiaca Postoperative pulmonary dysfunction and mechanical ventilation in cardiac surgery. Badenes R, Lozano A, Belda FJ. Crit Care Res Pract. 2015;2015:420513. doi: 10.1155/2015/420513. Epub 2015 Feb 3. Abstract Postoperative pulmonary dysfunction (PPD) is a frequent and significant complication after cardiac surgery. It contributes to morbidity and mortality and increases hospitalization stay and its associated costs. Its pathogenesis is not clear but it seems to be related to the development of a systemic inflammatory response with a subsequent pulmonary inflammation. Many factors have been described to contribute to this inflammatory response, including surgical procedure with sternotomy incision, effects of general anesthesia, topical cooling, and extracorporeal circulation (ECC) and mechanical ventilation (VM). Protective ventilation strategies can reduce the incidence of atelectasis (which still remains one of the principal causes of PDD) and pulmonary infections in surgical patients. In this way, the open lung approach (OLA), a protective ventilation strategy, has demonstrated attenuating the inflammatory response and improving gas exchange parameters and postoperative pulmonary functions with a better residual functional capacity (FRC) when compared with a conventional ventilatory strategy. Additionally, maintaining low frequency ventilation during ECC was shown to decrease the incidence of PDD after cardiac surgery, preserving lung function. PDF   Avances recientes en ventilación mecánica en pacientes sin ARDS Recent advances in mechanical ventilation in patients without acute respiratory distress syndrome. Serpa Neto A1, Filho RR2, Rocha LL2, Schultz MJ3. F1000Prime Rep. 2014 Dec 1;6:115. doi: 10.12703/P6-115. eCollection 2014. Abstract While being an essential part of general anesthesia for surgery and at times even a life-saving intervention in critically ill patients, mechanical ventilation has a strong potential to cause harm. Certain ventilation strategies could prevent, at least to some extent, the injury caused by this intervention. One essential element of so-called 'lung-protective' ventilation is the use of lower tidal volumes. It is uncertain whether higher levels of positive end-expiratory pressures have lung-protective properties as well. There are indications that too high oxygen fractions of inspired air, or too high blood oxygen targets, are harmful. Circumstantial evidence further suggests that spontaneous modes of ventilation are to be preferred over controlled ventilation to prevent harm to respiratory muscle. Finally, the use of restrictive sedation strategies in critically ill patients indirectly prevents ventilation-induced injury, as daily spontaneous awakening and breathing trials and bolus instead of continuous sedation are associated with shorter duration of ventilation and shorten the exposure to the injurious effects of ventilation. PDF Daño pulmonary hiperóxico agudo Hyperoxic acute lung injury. Kallet RH, Matthay MA. Respir Care. 2013 Jan;58(1):123-41. doi: 10.4187/respcare.01963. Abstract Prolonged breathing of very high F(IO(2)) (F(IO(2)) ≥ 0.9) uniformly causes severe hyperoxic acute lung injury (HALI) and, without a reduction of F(IO(2)), is usually fatal. The severity of HALI is directly proportional to P(O(2)) (particularly above 450 mm Hg, or an F(IO(2)) of 0.6) and exposure duration. Hyperoxia produces extraordinary amounts of reactive O(2) species that overwhelms natural anti-oxidant defenses and destroys cellular structures through several pathways. Genetic predisposition has been shown to play an important role in HALI among animals, and some genetics-based epidemiologic research suggests that this may be true for humans as well. Clinically, the risk of HALI likely occurs when F(IO(2)) exceeds 0.7, and may become problematic when F(IO(2)) exceeds 0.8 for an extended period of time. Both high-stretch mechanical ventilation and hyperoxia potentiate lung injury and may promote pulmonary infection. During the 1960s, confusion regarding the incidence and relevance of HALI largely reflected such issues as the primitive control of F(IO(2)), the absence of PEEP, and the fact that at the time both ALI and ventilator-induced lung injury were unknown. The advent of PEEP and precise control over F(IO(2)), as well as lung-protective ventilation, and other adjunctive therapies for severe hypoxemia, has greatly reduced the risk of HALI for the vast majority of patients requiring mechanical ventilation in the 21st century. However, a subset of patients with very severe ARDS requiring hyperoxic therapy is at substantial risk for developing HALI, therefore justifying the use of such adjunctive therapies. PDF

Anestesiología y Medicina del Dolor 52 664 6848905 vwhizar@anestesia-dolor.org anestesia-dolor.org Copyright © 2015

Hierro en falla cardiaca/Iron in heart failure

¿Es la corrección de deficiencia de hierro algo nuevo en el manejo de la insuficiencia cardiaca? Is Correction of Iron Deficiency a New Addition to the Treatment of the Heart Failure? Silverberg DS, Wexler D, Schwartz D Int J Mol Sci. 2015 Jun 18;16(6):14056-74. doi: 10.3390/ijms160614056. Abstract Anemia is present in about 40% of heart failure (HF) patients. Iron deficiency (ID) is present in about 60% of the patients with anemia (about 24% of all HF patients) and in about 40% of patients without anemia (about 24% of all HF patients). Thus ID is present in about half the patients with HF. The ID in HF is associated with reduced iron stores in the bone marrow and the heart. ID is an independent risk factor for severity and worsening of the HF. Correction of ID with intravenous (IV) iron usually corrects both the anemia and the ID. Currently used IV iron preparations are very safe and effective in treating the ID in HF whereas little information is available on the effectiveness of oral iron. In HF IV iron correction of ID is associated with improvement in functional status, exercise capacity, quality of life and, in some studies, improvement in rate of hospitalization for HF, cardiac structure and function, and renal function. Large long-term adequately-controlled intervention studies are needed to clarify the effect of IV iron in HF. Several heart associations suggest that ID should be routinely sought for in all HF patients and corrected if present. In this paper we present our approach to diagnosis and treatment of iron deficiency in heart failure. KEYWORDS: anemia; erythropoietin; heart failure; intravenous iron; iron; iron deficiency; renal failure PDF

Anestesiología y Medicina del Dolor 52 664 6848905 vwhizar@anestesia-dolor.org anestesia-dolor.org Copyright © 2015

Hemoglobina, transfusión y cirugía cardiaca/Hemoglobin, transfusion and cardiac surgery

Optimización de la hemoglobina y estrategias de transfusión en pacientes programados para cirugía cardiaca Hemoglobin optimization and transfusion strategies in patients undergoing cardiac surgery. Najafi M, Faraoni D. World J Cardiol. 2015 Jul 26;7(7):377-82. doi: 10.4330/wjc.v7.i7.377. Abstract Although red blood cells (RBCs) transfusion is sometimes associated with adverse reactions, anemia could also lead to increased morbidity and mortality in high-risk patients. For these reasons, the definition of perioperative strategies that aims to detect and treat preoperative anemia, prevent excessive blood loss, and define "optimal" transfusion algorithms is crucial. Although the treatment with preoperative iron and erythropoietin has been recommended in some specific conditions, several controversies exist regarding the benefit-to-risk balance associated with these treatments. Further studies are needed to better define the indications, dosage, and route of administration for preoperative iron with or without erythropoietin supplementation. Although restrictive transfusion strategies in patients undergoing cardiac surgery have been shown to effectively reduce the incidence and the amount of RBCs transfusion without increase in side effects, some high-risk patients (e.g., symptomatic acute coronary syndrome) could benefit from higher hemoglobin concentrations. Despite all efforts made last decade, a significant amount of work remains to be done to improve hemoglobin optimization and transfusion strategies in patients undergoing cardiac surgery. KEYWORDS: Anemia; Blood transfusion; Cardiac surgery; Risk factor; Transfusion threshold PDF

Anestesiología y Medicina del Dolor 52 664 6848905 vwhizar@anestesia-dolor.org anestesia-dolor.org Copyright © 2015

Eritrocitos suicida/Suicidal erythrocyte

Disparadores, inhibidores, mecanismos, y la importancia de la eriptosis: la muerte de eritrocitos suicida. Triggers, inhibitors, mechanisms, and significance of eryptosis: the suicidal erythrocyte death. Lang E, Lang F. Department of Physiology, University of Tübingen, Gmelinstrasse 5, 72076 Tübingen, Germany. Biomed Res Int. 2015;2015:513518. doi: 10.1155/2015/513518. Epub 2015 Mar 4 Abstract Suicidal erythrocyte death or eryptosis is characterized by erythrocyte shrinkage, cell membrane blebbing, and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include Ca(2+) entry, ceramide formation, stimulation of caspases, calpain activation, energy depletion, oxidative stress, and dysregulation of several kinases. Eryptosis is triggered by a wide variety of xenobiotics. It is inhibited by several xenobiotics and endogenous molecules including NO and erythropoietin. The susceptibility of erythrocytes to eryptosis increases with erythrocyte age. Phosphatidylserine exposing erythrocytes adhere to the vascular wall by binding to endothelial CXC-Motiv-Chemokin-16/Scavenger-receptor for phosphatidylserine and oxidized low density lipoprotein (CXCL16). Phosphatidylserine exposing erythrocytes are further engulfed by phagocytosing cells and are thus rapidly cleared from circulating blood. Eryptosis eliminates infected or defective erythrocytes thus counteracting parasitemia in malaria and preventing detrimental hemolysis of defective cells. Excessive eryptosis, however, may lead to anemia and may interfere with microcirculation. Enhanced eryptosis contributes to the pathophysiology of several clinical disorders including metabolic syndrome and diabetes, malignancy, cardiac and renal insufficiency, hemolytic uremic syndrome, sepsis, mycoplasma infection, malaria, iron deficiency, sickle cell anemia, thalassemia, glucose 6-phosphate dehydrogenase deficiency, and Wilson's disease. Facilitating or inhibiting eryptosis may be a therapeutic option in those disorders. PDF

Anestesiología y Medicina del Dolor 52 664 6848905 vwhizar@anestesia-dolor.org anestesia-dolor.org Copyright © 2015

Niño con Intestino Corto, como abordarlo

Estimado Ciberpediatra te invito al Seminario de Pediatría, Cirugía Pediátrica y Lactancia Materna. El día 16 Septiembre 2015 las 21hrs (Centro, México DF, Guadalajara y Lima Perú) a la Conferencia: “Niño con Intestino Corto, como abordarlo” por el “Dr. Jose Luis Martínez Orozco”, Gastroenterologo Pediatra de la Cd. de Fresno Ca. La sesión inicia puntualmente las 21 hrs.
Para entrar a la Sala de Conferencia:
1.- hacer click en la siguiente liga, o cópiala y escríbela en tu buscador http://connectpro60196372.adobeconnect.com/intestino_corto/
2.- “Entra como Invitado” Escribes tu nombre y apellido en el espacio en blanco
3.- Hacer click en el espacio que dice “Entrar en la Sala”
5.- A disfrutar la conferencia
6.- Recomendamos que dejes tu Nombre Completo, Correo electrónico y que participes.

Henrys



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