Hemodynamic resuscitation with fluids bolus and norepinephrine increases severity of lung damage in an experimental model of septic shock / La resucitación hemodinámica con bolos de fluidos y noradrenalina incrementa la severidad del daño pulmonar en un modelo experimental de shock séptico

Objective Hemodynamic resuscitation is considered a cornerstone of the initial treatment of septic shock. However, there is growing concern about its side effects. Our objective was to assess the relationship between fluid administration and norepinephrine infusion and the development of lung injury. Design Randomized in vivo study in rabbits. Setting University animal research laboratory. Patients Eighteen New Zealand rabbits. Control group (SHAM, n=6), Sepsis group with or without hemodynamic resuscitation (ETX-R, n=6; ETX-NR, n=6). Interventions Sepsis was induced by intravenous lipopolysaccharide administration and animals were followed-up for 4h. Hemodynamic resuscitation with Ringer lactate (20mL·kg−1) was administered and later norepinephrine was initiated 3h after sepsis induction. At the end, the left lung was excised. Main variables of interestAn indwelling arterial catheter and an esophageal Doppler were placed. Lung mechanics were monitored with side stream spirometry. Lung damage was analyzed by histopathological examination. Results The SHAM group did not show hemodynamic or respiratory changes. Lipopolysaccharide administration aimed an increase in cardiac output and arterial hypotension. In the ETX-NR group, animals remained hypotensive until the end of the experiment. Resuscitation with fluids and norepinephrine reversed arterial hypotension. Compared to the ETX-NR group, the remaining lung of the ETX-R group showed greater accumulation of neutrophils and reactive type-II pneumocytes, thicker alveolar wall, alveolar hemorrhage and non-aerated pulmonary areas. Lung injury score was larger in the ETX-R group. Conclusions In our experimental study, following a strategy with bolus fluids and late norepinephrine used in the early phase of endotoxic septic shock has a negative influence on the development of lung injury. (AU)

Objetivo La resucitación hemodinámica es considerada piedra angular en el tratamiento inicial del shock séptico. Sin embargo, existe creciente preocupación sobre sus efectos indeseables. Nuestro objetivo fue evaluar la relación entre la administración de fluidos e infusión de noradrenalina y el desarrollo de lesión pulmonar. Diseño Estudio aleatorizado en animales vivos. Ámbito Laboratorio universitario de investigación. Participantes Dieciocho conejos de raza New Zealand White. Grupo control (SHAM, n=6), grupo séptico con o sin resucitación hemodinámica (ETX-R, n=6; ETX-NR, n=6). Intervención La sepsis fue inducida tras administración intravenosa de lipopolisacárido, y los animales fueron seguidos durante 4h. La resucitación hemodinámica mediante suero Ringer lactato (20ml·kg-1) y posterior noradrenalina fue iniciada a las 3h de ser inducida la sepsis. Al final del estudio, el pulmón izquierdo fue extraído. Principales variables de interés Fueron empleados catéter arterial y doppler esofágico. La mecánica pulmonar fue monitorizada con sensor de flujo. El daño pulmonar fue analizado mediante examen histopatológico. Resultados El grupo control no mostró cambios hemodinámicos ni respiratorios. La administración del lipopolisacárido produjo un incremento del gasto cardíaco e hipotensión arterial. En el grupo ETX-NR, los animales permanecieron hipotensos hasta el final del estudio. La resucitación con fluidos y noradrenalina revirtió la hipotensión arterial. Comparados con el grupo ETX-NR, en el grupo ETX-R el estudio histopatológico mostró mayor acumulación de neutrófilos, así como mayor presencia de neumocitos activados tipo II, engrosamiento de la pared alveolar, hemorragia alveolar y zonas pulmonares no aireadas. La escala final de daño pulmonar fue mayor en el grupo ETX-R. Conclusiones En nuestro estudio experimental ... (AU)

Hemodynamic resuscitation with fluids bolus and norepinephrine increases severity of lung damage in an experimental model of septic shock.

OBJECTIVE: Hemodynamic resuscitation is considered a cornerstone of the initial treatment of septic shock. However, there is growing concern about its side effects. Our objective was to assess the relationship between fluid administration and norepinephrine infusion and the development of lung injury. DESIGN: Randomized in vivo study in rabbits. SETTING: University animal research laboratory. PATIENTS: Eighteen New Zealand rabbits. Control group (SHAM, n=6), Sepsis group with or without hemodynamic resuscitation (ETX-R, n=6; ETX-NR, n=6). INTERVENTIONS: Sepsis was induced by intravenous lipopolysaccharide administration and animals were followed-up for 4h. Hemodynamic resuscitation with Ringer lactate (20mL·kg-1) was administered and later norepinephrine was initiated 3h after sepsis induction. At the end, the left lung was excised. MAIN VARIABLES OF INTEREST: An indwelling arterial catheter and an esophageal Doppler were placed. Lung mechanics were monitored with side stream spirometry. Lung damage was analyzed by histopathological examination. RESULTS: The SHAM group did not show hemodynamic or respiratory changes. Lipopolysaccharide administration aimed an increase in cardiac output and arterial hypotension. In the ETX-NR group, animals remained hypotensive until the end of the experiment. Resuscitation with fluids and norepinephrine reversed arterial hypotension. Compared to the ETX-NR group, the remaining lung of the ETX-R group showed greater accumulation of neutrophils and reactive type-II pneumocytes, thicker alveolar wall, alveolar hemorrhage and non-aerated pulmonary areas. Lung injury score was larger in the ETX-R group. CONCLUSIONS: In our experimental study, following a strategy with bolus fluids and late norepinephrine used in the early phase of endotoxic septic shock has a negative influence on the development of lung injury.

Hemodynamic resuscitation with fluids bolus and norepinephrine increases severity of lung damage in an experimental model of septic shock.

OBJECTIVE: Hemodynamic resuscitation is considered a cornerstone of the initial treatment of septic shock. However, there is growing concern about its side effects. Our objective was to assess the relationship between fluid administration and norepinephrine infusion and the development of lung injury. DESIGN: Randomized in vivo study in rabbits. SETTING: University animal research laboratory. PATIENTS: Eighteen New Zealand rabbits. Control group (SHAM, n=6), Sepsis group with or without hemodynamic resuscitation (ETX-R, n=6; ETX-NR, n=6). INTERVENTIONS: Sepsis was induced by intravenous lipopolysaccharide administration and animals were followed-up for 4h. Hemodynamic resuscitation with Ringer lactate (20mL·kg-1) was administered and later norepinephrine was initiated 3h after sepsis induction. At the end, the left lung was excised. MAIN VARIABLES OF INTEREST: An indwelling arterial catheter and an esophageal Doppler were placed. Lung mechanics were monitored with side stream spirometry. Lung damage was analyzed by histopathological examination. RESULTS: The SHAM group did not show hemodynamic or respiratory changes. Lipopolysaccharide administration aimed an increase in cardiac output and arterial hypotension. In the ETX-NR group, animals remained hypotensive until the end of the experiment. Resuscitation with fluids and norepinephrine reversed arterial hypotension. Compared to the ETX-NR group, the remaining lung of the ETX-R group showed greater accumulation of neutrophils and reactive type-II pneumocytes, thicker alveolar wall, alveolar hemorrhage and non-aerated pulmonary areas. Lung injury score was larger in the ETX-R group. CONCLUSIONS: In our experimental study, following a strategy with bolus fluids and late norepinephrine used in the early phase of endotoxic septic shock has a negative influence on the development of lung injury.

Effects of arterial load variations on dynamic arterial elastance: an experimental study.

BACKGROUND.: Dynamic arterial elastance (Ea dyn ), the relationship between pulse pressure variation (PPV) and stroke volume variation (SVV), has been suggested as a functional assessment of arterial load. The aim of this study was to evaluate the impact of arterial load changes during acute pharmacological changes, fluid administration, and haemorrhage on Ea dyn . METHODS.: Eighteen anaesthetized, mechanically ventilated New Zealand rabbits were studied. Arterial load changes were induced by phenylephrine ( n =9) or nitroprusside ( n =9). Thereafter, animals received a fluid bolus (10 ml kg -1 ), followed by stepwise bleeding (blood loss: 15 ml kg -1 ). The influence of arterial load and cardiac variables on PPV, SVV, and Ea dyn was analysed using a linear mixed-effects model analysis. RESULTS.: After phenylephrine infusion, mean ( sd ) Ea dyn decreased from 0.89 (0.14) to 0.49 (0.12), P <0.001; whereas after administration of nitroprusside, Ea dyn increased from 0.80 (0.23) to 1.28 (0.21), P <0.0001. Overall, the fluid bolus decreased Ea dyn [from 0.89 (0.44) to 0.73 (0.35); P <0.01], and haemorrhage increased it [from 0.78 (0.23) to 0.95 (0.26), P =0.03]. Both PPV and SVV were associated with similar arterial factors (effective arterial elastance, arterial compliance, and resistance) and heart rate. Furthermore, PPV was also related to the acceleration and peak velocity of aortic blood flow. Both arterial and cardiac factors contributed to the evolution of Ea dyn throughout the experiment. CONCLUSIONS.: Acute modifications of arterial load induced significant changes on Ea dyn ; vasodilatation increased Ea dyn , whereas vasoconstriction decreased it. The Ea dyn was associated with both arterial load and cardiac factors, suggesting that Ea dyn should be more properly considered as a ventriculo-arterial coupling index.

Preemptive hemodynamic intervention restricting the administration of fluids attenuates lung edema progression in oleic acid-induced lung injury / La restricción preventiva en la administración de fluidos disminuye la formación del edema en la lesión pulmonar inducida por ácido oleico

OBJECTIVE: A study is made of the influence of preemptive hemodynamic intervention restricting fluid administration upon the development of oleic acid-induced lung injury. DESIGN: A randomized in vivo study in rabbits was carried out. SETTING: University research laboratory. Subjects: Sixteen anesthetized, mechanically ventilated rabbits. VARIABLES: Hemodynamic measurements obtained by transesophageal Doppler signal. Respiratory mechanics computed by a least square fitting method. Lung edema assessed by the ratio of wet weight to dry weight of the right lung. Histological examination of the left lung. INTERVENTIONS: Animals were randomly assigned to either the early protective lung strategy (EPLS) (n=8) or the early protective hemodynamic strategy (EPHS) (n=8). In both groups, lung injury was induced by the intravenous infusion of oleic acid (OA) (0.133mlkg−1h−1 for 2h). At the same time, the EPLS group received 15mlkg−1h−1 of Ringer lactate solution, while the EPHS group received 30mlkg−1h−1. Measurements were obtained at baseline and 1 and 2h after starting OA infusion. RESULTS: After 2h, the cardiac index decreased in the EPLS group (p < 0.05), whereas in the EPHS group it remained unchanged. Lung compliance decreased significantly only in the EPHS group (p < 0.05). Lung edema was greater in the EPHS group (p < 0.05). Histological damage proved similar in both groups (p = 0.4). CONCLUSIONS: In this experimental model of early lung injury, lung edema progression was attenuated by preemptively restricting the administration of fluids

OBJETIVO: Conocer cómo influye una intervención hemodinámica preventiva basada en la restricción de fluidos sobre el desarrollo de la lesión pulmonar inducida por la administración de ácido oleico. DISEÑO: Estudio aleatorizado en animales vivos. Lugar: Laboratorio universitario de investigación experimental. VARIABLES: Mecánica respiratoria (método de los mínimos cuadrados), medidas hemodinámicas (doppler esofágico), estimación del edema pulmonar (relación peso húmedo/seco del pulmón derecho) y daño histológico del pulmón izquierdo. INTERVENCIONES: Ocho animales fueron asignados a un grupo con una estrategia protectora pulmonar (EPP), y otros 8 a otro grupo con una estrategia protectora hemodinámica (EPH). En ambos grupos la lesión pulmonar se desencadenó mediante la administración intravenosa de ácido oleico (0,133mL/kg−1/h−1 durante 2h), recibiendo simultáneamente los animales del grupo EPP 15mL/kg−1/h−1 de Ringer Lactato y los del grupo EPH 30mLKg−1h−1. Se obtuvieron medidas basales, a la hora y a las 2h. RESULTADOS: Transcurridas las 2h de experimento el índice cardiaco permaneció estable en el grupo EPH, pero disminuyó en el grupo EPP (p < 0,05). Por el contrario, la distensibilidad pulmonar disminuyó significativamente solo en el grupo EPH (p < 0,05), en el cual el edema pulmonar estimado mediante la relación peso húmedo/seco del pulmón derecho fue mayor (p < 0,05). El daño histológico fue similar en ambos grupos (p = 0,4). CONCLUSIONES: En este modelo experimental de lesión pulmonar aguda en fase inicial, la formación del edema pulmonar fue atenuada por la restricción preventiva en la administración de fluidos

Preemptive hemodynamic intervention restricting the administration of fluids attenuates lung edema progression in oleic acid-induced lung injury.

OBJECTIVE: A study is made of the influence of preemptive hemodynamic intervention restricting fluid administration upon the development of oleic acid-induced lung injury. DESIGN: A randomized in vivo study in rabbits was carried out. SETTING: University research laboratory. SUBJECTS: Sixteen anesthetized, mechanically ventilated rabbits. VARIABLES: Hemodynamic measurements obtained by transesophageal Doppler signal. Respiratory mechanics computed by a least square fitting method. Lung edema assessed by the ratio of wet weight to dry weight of the right lung. Histological examination of the left lung. INTERVENTIONS: Animals were randomly assigned to either the early protective lung strategy (EPLS) (n=8) or the early protective hemodynamic strategy (EPHS) (n=8). In both groups, lung injury was induced by the intravenous infusion of oleic acid (OA) (0.133mlkg-1h-1 for 2h). At the same time, the EPLS group received 15mlkg-1h-1 of Ringer lactate solution, while the EPHS group received 30mlkg-1h-1. Measurements were obtained at baseline and 1 and 2h after starting OA infusion. RESULTS: After 2h, the cardiac index decreased in the EPLS group (p<0.05), whereas in the EPHS group it remained unchanged. Lung compliance decreased significantly only in the EPHS group (p<0.05). Lung edema was greater in the EPHS group (p<0.05). Histological damage proved similar in both groups (p=0.4). CONCLUSIONS: In this experimental model of early lung injury, lung edema progression was attenuated by preemptively restricting the administration of fluids.

Evidencia de la utilidad de la monitorización hemodinámica en el paciente crítico / Evidence on the utility of hemodynamic monitorization in the critical patient

La monitorización hemodinámica es una herramienta de indudable valor para la evaluación de los pacientes críticos. Nos permite no solo detectar y determinar el origen de la inestabilidad hemodinámica, sino también guiar la elección del tratamiento más adecuado y evaluar con posterioridad su efectividad. Sin embargo, la monitorización per se no constituye una herramienta terapéutica y su empleo, sin un objetivo claramente definido, no tiene por qué afectar a la evolución de los pacientes. Para que la monitorización hemodinámica redunde en beneficio para este debe ir necesariamente acoplada a un protocolo de tratamiento que efectivamente haya demostrado mejorar su pronóstico. En consecuencia, la utilidad de los sistemas de monitorización no debería evaluarse tan solo por la exactitud y fiabilidad de sus medidas, sino también por la capacidad de afectar favorablemente a la evolución de los pacientes. En este sentido, gran parte de los argumentos utilizados en contra del empleo de la monitorización hemodinámica tienen su origen en un uso no racionalizado de la misma y en la aplicación no dirigida a objetivos hemodinámicos concretos y de demostrado beneficio para el paciente (AU)

Hemodynamic monitoring is a tool of great value for the assessment of critically ill patients. It can not only detect and determine the source of hemodynamic instability, but also guide the choice of appropriate treatment and further evaluate its effectiveness. However, monitoring per se is not a therapeutic tool and its use in the absence of a well-defined objective, need not affect patient outcome. To improve outcome, hemodynamic monitoring necessarily must be coupled to a treatment protocol that has effectively been shown to improve outcome. Accordingly, the usefulness of monitoring systems should be evaluated not only on the basis of the accuracy and reliability of their measurements, but also on the ability to positively affect patient outcome. In this regard, many of the arguments against the use of hemodynamic monitoring are a consequence of non-protocolized use and of application not directed towards specific hemodynamic objectives of proven benefit for the patient (AU)

[Evidence on the utility of hemodynamic monitorization in the critical patient]. / Evidencia de la utilidad de la monitorización hemodinámica en el paciente crítico.

Hemodynamic monitoring is a tool of great value for the assessment of critically ill patients. It can not only detect and determine the source of hemodynamic instability, but also guide the choice of appropriate treatment and further evaluate its effectiveness. However, monitoring per se is not a therapeutic tool and its use in the absence of a well-defined objective, need not affect patient outcome. To improve outcome, hemodynamic monitoring necessarily must be coupled to a treatment protocol that has effectively been shown to improve outcome. Accordingly, the usefulness of monitoring systems should be evaluated not only on the basis of the accuracy and reliability of their measurements, but also on the ability to positively affect patient outcome. In this regard, many of the arguments against the use of hemodynamic monitoring are a consequence of non-protocolized use and of application not directed towards specific hemodynamic objectives of proven benefit for the patient.

Incidencia, características y evolución del barotrauma durante la ventilación mecánica con apertura pulmonar / Incidence, characteristics and outcome of barotrauma during open lung ventilation

Objetivo: Describir la incidencia y principales características clínicas del barotrauma durante la ventilación mecánica con apertura pulmonar. Diseño: Estudio retrospectivo, observacional, descriptivo, en 100 pacientes con insuficiencia respiratoria aguda e infiltrados pulmonares bilaterales. Intervenciones: 1) maniobra de reclutamiento pulmonar (MRP) con presión de ventilación fija e incrementos progresivos de presión positiva al final de la espiración (PEEP), seguida de decrementos escalonados hasta establecer la PEEP de apertura en el valor asociado a la máxima distensibilidad respiratoria; 2) ventilación asistida/controlada por presión ajustada para un volumen tidal de 6-8ml/kg; y 3) radiografía de tórax después de la MRP y diariamente mientras persistió la insuficiencia respiratoria. Resultados: Nueve pacientes, 7 con neumonía y 2 con trauma torácico, desarrollaron barotrauma (2 enfisema subcutáneo y 7 neumotórax), lo cual supuso una incidencia total del 9% y del 16% en aquellos pacientes con lesión pulmonar primaria. En 7 pacientes fue tan solo de un hallazgo radiológico; en los otros dos, se manifestó como un neumotórax bilateral y a tensión, cursando con hipoventilación pulmonar. Únicamente en estos dos casos se modificó la estrategia ventilatoria. No hubo diferencias en las presiones ni en los volúmenes respiratorios entre pacientes con o sin barotrauma. La mortalidad fue similar en ambos grupos. Conclusiones: El barotrauma resultó una complicación exclusiva de pacientes con lesión pulmonar primaria, en los que tuvo una incidencia elevada. En la mayoría de las ocasiones fue un hallazgo radiológico sin manifestaciones clínicas, manteniéndose la ventilación con apertura pulmonar. Su aparición no se relacionó con presiones ni volúmenes respiratorios mayores, ni se asoció a mayor mortalidad (AU)

Objective: To describe the incidence and main clinical characteristics of barotrauma during open lung ventilation (OLV). Design: A retrospective, observational, descriptive study was made of 100 patients with acute respiratory failure and bilateral pulmonary infiltrates. Interventions: 1) A lung recruitment maneuver (LRM) with fixed ventilation pressure and progressive positive end-expiratory pressure (PEEP) elevations was carried out, followed by stepwise decreases until establishing open-lung PEEP at the value associated to maximum respiratory compliance; 2) assisted/controlled pressure ventilation to achieve a tidal volume of 6-8ml/kg; and 3) chest X-rays after LRM and daily for as long as respiratory failure persisted. Results: Nine patients, 7 with pneumonia and 2 with chest trauma, developed barotrauma (2 subcutaneous emphysemas and 7 cases of pneumothorax), representing an overall incidence of 9% and 16% in patients with primary lung injury. In 7 patients barotrauma was only a radiological finding; in the other 2 patients, it manifested as bilateral and tension pneumothorax, inducing pulmonary hypoventilation without hemodynamic impairment. Only in these two cases was the ventilatory strategy modified. There were no differences in the airway pressures or volumes between patients with and without barotrauma. Mortality was similar in both groups. Conclusions: Barotrauma was an exclusive complication of patients with primary lung injury, and the incidence in this group was high. In most cases, there were only radiological findings without clinical significance that did not require the suspension of OLV. Barotrauma was neither related to high pressures and volumes nor associated with increased mortality (AU)

Cambios respiratorios y hemodinámicos durante una maniobra de reclutamiento pulmonar mediante incrementos y decrementos progresivos de PEEP / Respiratory and hemodynamic changes during lung recruitment maneuvering through progressive increases and decreases in PEEP level

Objetivo: Estudiar los cambios respiratorios y hemodinámicos durante una maniobra de reclutamiento pulmonar (MRP) mediante incrementos y decrementos progresivos de PEEP. Diseño y ámbito: Estudio retrospectivo en una UCI de 17 camas. Pacientes: Un total de 21 pacientes con insuficiencia respiratoria aguda e infiltrados pulmonares bilaterales. Intervención: MRP consistente en incrementos progresivos de PEEP (4cmH2O cada 3 minutos), con presión de ventilación fija, hasta alcanzar un valor máximo de 36cmH2O de PEEP (rama ascendente), seguida de decrementos progresivos (2cmH2O cada 3 minutos) hasta establecer la PEEP de apertura en el valor asociado a la máxima distensibilidad del sistema respiratorio (Dsr) (rama descendente). La monitorización hemodinámica se realizó de forma continua con una sonda ecodoppler esofágica. Resultados: La Dsr disminuyó gradualmente en la rama ascendente de la MRP y aumentó de forma progresiva superando el valor inicial al establecer la PEEP de apertura en la rama descendente, reduciéndose la presión de ventilación y aumentando la relación SpO2/FiO2. Los cambios hemodinámicos consistieron fundamentalmente en una disminución del gasto cardiaco y de la precarga del ventrículo izquierdo, junto con un aumento de la frecuencia y de la contractilidad cardiaca. A niveles equiparables de PEEP y presión media en vía aérea, estos cambios fueron más intensos durante la rama descendente. Conclusiones: 1) La realización de la MRP incrementó la Dsr mejorando la oxigenación y disminuyendo la presión de ventilación; 2) la principal consecuencia hemodinámica fue la disminución del gasto cardiaco y de la precarga ventricular izquierda; 3) la afectación hemodinámica desigual en ambas ramas, a niveles equiparables de PEEP y presión media en vía aérea, puso de manifiesto que, junto a la presión intratorácica, otros factores como la Dsr y la hipercapnia pudieron influir en las consecuencias hemodinámicas en este tipo de MRP (AU)

Objective: To evaluate the respiratory and hemodynamic changes during lung recruitment maneuvering (LRM) through stepwise increases and decreases in PEEP level. Design and setting: A retrospective study in a 17-bed ICU was carried out. Patients: Twenty-one patients with acute respiratory failure and bilateral pulmonary infiltration. Intervention: LRM was carried out, consisting of stepwise increases in PEEP (4cmH2O every 3minutes), with fixed ventilation pressure, until reaching a maximal value of 36cmH2O PEEP (ascending branch), followed by progressive decreases in PEEP (2cmH2O every 3minutes) until establishing the open-lung PEEP at the value associated to maximum respiratory compliance (Crs) (descending branch). Continuous hemodynamic monitoring was performed using an esophageal echodoppler probe. Results: Crs gradually decreased in the ascending branch of the LRM, and progressively increased surpassing the initial value after establish the open-lung PEEP in the descending branch, reducing the ventilation pressure and increasing the SpO2/FiO2 ratio. Hemodynamic changes primarily consisted of a fall in cardiac output and left ventricular preload, together with an increased heart rate and cardiac contractility. At comparable levels of PEEP and mean airway pressure, these changes were more pronounced during the descending branch of the LRM. Conclusions: 1) LRM increased Crs, improving oxygenation and decreasing ventilation pressure; 2) the main hemodynamic consequence was the drop in cardiac output and left ventricular preload; and 3) the unequal hemodynamic derangement in both branches, at the same level of PEEP and mean airway pressure, showed that, along with intrathoracic pressure, other factor such as Crs and hypercapnia may have influenced the hemodynamic consequences of this type of LRM (AU)

[Incidence, characteristics and outcome of barotrauma during open lung ventilation]. / Incidencia, características y evolución del barotrauma durante la ventilación mecánica con apertura pulmonar.

OBJECTIVE: To describe the incidence and main clinical characteristics of barotrauma during open lung ventilation (OLV). DESIGN: A retrospective, observational, descriptive study was made of 100 patients with acute respiratory failure and bilateral pulmonary infiltrates. INTERVENTIONS: 1) A lung recruitment maneuver (LRM) with fixed ventilation pressure and progressive positive end-expiratory pressure (PEEP) elevations was carried out, followed by stepwise decreases until establishing open-lung PEEP at the value associated to maximum respiratory compliance; 2) assisted/controlled pressure ventilation to achieve a tidal volume of 6-8 ml/kg; and 3) chest X-rays after LRM and daily for as long as respiratory failure persisted. RESULTS: Nine patients, 7 with pneumonia and 2 with chest trauma, developed barotrauma (2 subcutaneous emphysemas and 7 cases of pneumothorax), representing an overall incidence of 9% and 16% in patients with primary lung injury. In 7 patients barotrauma was only a radiological finding; in the other 2 patients, it manifested as bilateral and tension pneumothorax, inducing pulmonary hypoventilation without hemodynamic impairment. Only in these two cases was the ventilatory strategy modified. There were no differences in the airway pressures or volumes between patients with and without barotrauma. Mortality was similar in both groups. CONCLUSIONS: Barotrauma was an exclusive complication of patients with primary lung injury, and the incidence in this group was high. In most cases, there were only radiological findings without clinical significance that did not require the suspension of OLV. Barotrauma was neither related to high pressures and volumes nor associated with increased mortality.

[Respiratory and hemodynamic changes during lung recruitment maneuvering through progressive increases and decreases in PEEP level]. / Cambios respiratorios y hemodinámicos durante una maniobra de reclutamiento pulmonar mediante incrementos y decrementos progresivos de PEEP.

OBJECTIVE: To evaluate the respiratory and hemodynamic changes during lung recruitment maneuvering (LRM) through stepwise increases and decreases in PEEP level. DESIGN AND SETTING: A retrospective study in a 17-bed ICU was carried out. PATIENTS: Twenty-one patients with acute respiratory failure and bilateral pulmonary infiltration. INTERVENTION: LRM was carried out, consisting of stepwise increases in PEEP (4 cmH(2)O every 3 minutes), with fixed ventilation pressure, until reaching a maximal value of 36 cmH(2)O PEEP (ascending branch), followed by progressive decreases in PEEP (2 cmH(2)O every 3 minutes) until establishing the open-lung PEEP at the value associated to maximum respiratory compliance (Crs) (descending branch). Continuous hemodynamic monitoring was performed using an esophageal echodoppler probe. RESULTS: Crs gradually decreased in the ascending branch of the LRM, and progressively increased surpassing the initial value after establish the open-lung PEEP in the descending branch, reducing the ventilation pressure and increasing the SpO(2)/FiO(2) ratio. Hemodynamic changes primarily consisted of a fall in cardiac output and left ventricular preload, together with an increased heart rate and cardiac contractility. At comparable levels of PEEP and mean airway pressure, these changes were more pronounced during the descending branch of the LRM. CONCLUSIONS: 1) LRM increased Crs, improving oxygenation and decreasing ventilation pressure; 2) the main hemodynamic consequence was the drop in cardiac output and left ventricular preload; and 3) the unequal hemodynamic derangement in both branches, at the same level of PEEP and mean airway pressure, showed that, along with intrathoracic pressure, other factor such as Crs and hypercapnia may have influenced the hemodynamic consequences of this type of LRM.

Shock séptico / Septic shock

El shock séptico es un estado de hipoperfusión tisular en el contexto de un síndrome de respuesta inflamatoria sistémica, caracterizado clínicamente por vasodilatación excesiva y el requerimiento de agentes presores para mantener la presión de perfusión de los órganos. La típica respuesta cardiovascular hiperdinámica no está presente en todos los enfermos, por lo que su presencia o ausencia no debe usarse para el diagnóstico del shock séptico. El tratamiento exige la normalización de la volemia y la administración de agentes inotropos para normalizar el gasto cardíaco si se encuentra bajo, y aumentar la presión de perfusión de los tejidos. El tratamiento debe ser guiado por una adecuada monitorización. Es preferible el uso de técnicas que permiten valorar la precarga del ventrículo derecho, más que mediciones aisladas de presiones de llenado ventricular (que no se relacionan con la precarga ni con la respuesta del individuo a la sobrecarga de fluidos). Recientemente, se ha puesto de manifiesto que la variación de la presión de pulso está en relación con la respuesta del gasto cardíaco a una sobrecarga de fluidos y con la consiguiente mejoría en la hemodinámica, más que mediciones de presión de llenado del ventrículo derecho o izquierdo. Otras mediciones sensibles a la perfusión de los órganos, incluyendo la monitorización de la acidosis láctica y de la lactacidemia, deben también usarse para guiar la resucitación con fluidos. La precocidad del tratamiento y la rapidez con que se resuelven los signos de hipoperfusión tisular son aspectos fundamentales del manejo, puesto que están en íntima relación con el pronóstico

Septic shock is a state of tissue hypoperfusion in the context of a systemic inflammatory response syndrome, characterized clinically by excessive vasodilatation and the requirement of vasopressor agents in order to maintain the perfusion pressure of organs system. The typical hyperdynamic cardiovascular response is not present in all the patients, which means that its presence or absence should not be used for the diagnosis of septic shock. The treatment requires the normalization of volemia and the administration of inotropic agents in order to normalize the cardiac output if it is low, and to increase the perfusion pressure of tissues. The treatment should be guided by an adequate monitoring. The use of techniques that make possible to assess right ventricle preload is preferable, more than isolated measurements of ventricular filling pressures (that are not related to preload nor to the response of the patient to fluids overload). Recently, it has been shown that the variation of pulse pressure is related to the response of the cardiac output to fluid overload and to the consequent hemodynamic improvement, more than measurements of right or left ventricle filling pressures. Other measurements sensitive to the organs perfusion should be also used to guide resuscitation with fluids, including monitoring of lactic acidosis and lactacidemia. Speed of treatment and speed with which the sings of tissue hypoperfusion are resolved are fundamental components of management because are closely related to prognosis