Pulse pressure variation (PPV) and stroke volume variation (SVV) are frequently used to assess fluid responsiveness in critically ill patients on mechanical ventilation (MV). There are many factors, in addition to preload that influence the magnitude of these cyclic variations. We sought to investigate the effect of tidal volume (VT) on PPV and SVV, and prediction of fluid responsiveness in a model of intra-abdominal hypertension (IAH). Twelve anesthetized and mechanically ventilated piglets on continuous pulse contour cardiac output monitoring. Hypovolemia was ruled out with 2 consecutive fluid boluses after instrumentation. IAH was induced by intraperitoneal instillation of colloid solution with a goal of reducing respiratory system compliance by 50 %. Subjects were classified as fluid responders if stroke volume increased >15 % after each fluid challenge. SVV and PPV were recorded with tidal volumes (VT) of 6, 12 and 18 ml/kg before IAH after IAH induction and after a fluid challenge during IAH. VT influenced PPV and SVV at baseline and during IAH, being significantly larger with higher VT. These differences were attenuated after fluid administration in both conditions. After IAH induction, there was a significant increase in SVV with the three-tested VT, but the magnitude of that change was larger with high VT: with 6 ml/kg from 3 % (3, 4) to 5 % (4, 6.25) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 11 % (8.75, 17) (p = 0.02) and 18 ml/kg from 5 % (4,7.5) to 15 % (8.75, 19.5) (p = 0.02). Similarly, PPV increased with all the tested VT after IAH induction, being this increase larger with high VT: with 6 ml/kg from 3 % (2, 4.25) to 6 % (4.75, 7) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 13.5 % (10.25, 15.5) (p = 0.02) and 18 ml/kg from 7 % (5.5, 8.5) to 24 % (13.5, 30.25) (p = 0.02). One third of subjects responded to fluid administration after IAH, but neither SVV nor PPV were able to identify the fluid responders with the tested VT. IAH induction in non-hypovolemic subjects significantly increased SVV and PPV with the three tested VT, but the magnitude of that change was higher with larger VT. This observation reveals the dependence of functional hemodynamic markers on intrathoracic as well intra-abdominal pressures, in addition to volemic status. Also, PPV and SVV were unable to predict fluid responsiveness after IAH induction. Future studies should take into consideration these findings when exploring relationships between dynamic preload indicators and fluid responsiveness during IAH.

Two hundred years have passed since the publication that revealed the clinical use of the stethoscope. Rene Theophile Hyacinthe Laennec published it in 1819. Laennec spent his childhood in the social effervescence of the French Revolution and studied medicine in Paris, where he graduated in 1804. His clinical experience at Necker Hospital peaked with the invention of the stethoscope in 1816. Three years later, he published his masterpiece De L'Auscultation Mediate, which underlined a more rational clinical-pathological approach, especially in the understanding of cardiopulmonary diseases. Undoubtedly, Laennec revolutionized medicine by perfecting the art of thoracic semiology, which allowed him to translate the sounds he heard into an image that could be visualized. In the bicentennial of the invention of such fundamental milestone in modern medicine, the purpose of this article is to go over its history.

The ability to maintain an adequate energy balance and to respond and adapt to environmental stress at the cellular level are cornerstones for the survival and evolution of organisms. Therefore, in the presence of various factors, a cellular protection response is triggered by activation of mitochondrial function-dependent signaling. However. this essential reaction for individual cell survival can be detrimental to organ function (maladaptation), transforming the close balance between the two into the pathogenetic axis of organ dysfunction and eventual recovery in septic patients. Macrocirculatory and microcirculatory disruption undoubtedly contributes to organ dysfunction in the early stage of septic shock, while intrinsic metabolic-bioenergetic failure (cytopathic hypoxia) perpetuates inadequate cellular function. Therefore, mitochondrial dysfunction is a key process in the induction of multiple organ dysfunction syndrome in the septic patient. This syndrome can be considered as a complex hypometabolic adaptive phenomenon in the face of excessive and prolonged inflammatory stimulus to achieve regulation of energy homeostasis and preservation of organ function. In the future, there should be a transition from the current consensus therapeutic options, which are limited to control of the infectious focus, hemodynamic and life support, to metabolic resuscitation based on the molecular and genetic alterations triggered by the infection.

Fever is a very common sign to observe in critically ill children during their intensive care unit stay. This should be understood as an evolutionary biological response, of normal adaptive character, from the host to the physiological stress. It is the result of a complex response to pyrogenic stimuli, resulting in the generation of cytokines and prostaglandins. The molecular mechanisms involved in the onset of fever are not yet fully specified, thus creating difficulties in the knowledge of the exact pathophysiological processes involved and, therefore, necessary to elaborate an adequate and specific therapeutic strategy. Experimental studies conclude that fever and inflammation are beneficial to the host. However, antipyretic therapy is commonly employed and human studies on the presence of fever and its treatment for the prognosis of critically ill septic patients are inconclusive. Up-to-date information on the physiology of human thermoregulation, the effect of temperature on febrile range over multiple biological processes involved in host defense, and thermoregulatory interventions in the septic patient are essential to know by the critical care physician.

Down syndrome is the most common chromosomal abnormality in newborns, with a high incidence in Chile. This condition presents unique physiological aspects that should be known, which can affect the child during their stay in an Intensive Care Unit, beyond the neonatal period This review is focused on the respiratory, cardiovascular, infectious and neurological disorders. Anesthetic management and postoperative analgesia considerations, weaning from mechanical ventilation, cervical spine instability and prognosis of the critically ill child with Down syndrome are also analyzed. The evaluation of these conditions should be performed when the patient is admitted to the intensive care unit. The purpose of this update is to update the knowledge of the diagnosis and treatment of potential complications of children with Down syndrome during their stay in the unit of critical patient.

An adequate drug dosage at treatment initiation is particularly relevant for critically ill patients. An inadequate dosage may result in therapeutic failure, potentially severe adverse events, and unnecessary health expenditures. At present, due to the higher incidence of childhood obesity, primary care physicians are more commonly faced with this population, so they need to make appropriate therapeutic decisions. Knowledge of the resulting pharmacokinetic alterations caused by increased body fat is critical. The optimal drug dosage is not completely defined and the correct body descriptor should be used, although there is no consensus on which is the most adequate one. The objective of this update is to gain insight on pharmacokinetic alterations that affect dosage in the critically ill obese pediatric patient and, specifically, those related to the drugs most commonly used in this population during their stay in the pediatric intensive care unit.