Based on our observations, elastance-derived transpulmonary pressure can be considered to be an adequate surrogate of the release-derived transpulmonary pressure, while the release-derived and directly measured end-expiratory transpulmonary pressure are not related.

Background Mechanical chest compression (CC) is currently suggested to deliver sustained high‐quality CC in a moving ambulance. This study compared the hemodynamic support provided by a mechanical piston device or manual CC during ambulance transport in a porcine model of cardiopulmonary resuscitation. Methods and Results In a simulated urban ambulance transport, 16 pigs in cardiac arrest were randomized to 18 minutes of mechanical CC with the LUCAS (n=8) or manual CC (n=8). ECG, arterial and right atrial pressure, together with end‐tidal CO 2 and transthoracic impedance curve were continuously recorded. Arterial lactate was assessed during cardiopulmonary resuscitation and after resuscitation. During the initial 3 minutes of cardiopulmonary resuscitation, the ambulance was stationary, while then proceeded along a predefined itinerary. When the ambulance was stationary, CC‐generated hemodynamics were equivalent in the 2 groups. However, during ambulance transport, arterial and coronary perfusion pressure, and end‐tidal CO 2 were significantly higher with mechanical CC compared with manual CC (coronary perfusion pressure: 43±4 versus 18±4 mmHg; end‐tidal CO 2 : 31±2 versus 19±2 mmHg, P <0.01 at 18 minutes). During cardiopulmonary resuscitation, arterial lactate was lower with mechanical CC compared with manual CC (6.6±0.4 versus 8.2±0.5 mmol/L, P <0.01). During transport, mechanical CC showed greater constancy compared with the manual CC, as represented by a higher CC fraction and a lower transthoracic impedance curve variability ( P <0.01). All animals in the mechanical CC group and 6 (75%) in the manual one were successfully resuscitated. Conclusions This model adds evidence in favor of the use of mechanical devices to provide ongoing high‐quality CC and tissue perfusion during ambulance transport.

Longer no-flow durations caused greater postresuscitation myocardial and neurological dysfunction and reduced survival. An untreated CA of 12-13 min may be an optimal choice for a clinically relevant model.

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Aim of the study: To evaluate in an established porcine post cardiac arrest model the effect of a mild hypercapnic ventilatory strategy on outcome. Methods: The left anterior descending coronary artery was occluded in 14 pigs and ventricular fibrillation induced and left untreated for 12 min. Cardiopulmonary resuscitation was performed for 5 min prior to defibrillation. After resuscitation, pigs were assigned to either normocapnic (end-tidal carbon dioxide (EtCO 2) target: 35-40 mmHg) or hypercapnic ventilation (EtCO 2 45-50 mmHg). Hemodynamics was invasively measured and EtCO 2 was monitored with an infrared capnometer. Blood gas analysis, serum neuron-specific enolase (NSE) and high sensitive cardiac troponin T (hs-cTnT) were assessed. Survival and functional recovery were evaluated up to 96 h. Results: Twelve pigs were successfully resuscitated and eight survived up to 96 h, with animals in the hypercapnic group showing trend towards a longer survival. EtCO 2 and arterial partial pressure of CO 2 were higher in the hypercapnic group compared to the normocapnic one (p < 0.01), during the 4-hour intervention. Hypercapnia was associated with higher mean arterial pressure compared to normocapnia (p < 0.05). No significant differences were observed in hs-cTnT and in NSE between groups, although the values tended to be lower in the hypercapnic one. Neuronal degeneration was lesser in the frontal cortex of hypercapnic animals compared to the normocapnic ones (p < 0.05). Neurological recovery was equivalent in the two groups.

Autonomic control of blood pressure (BP) and heart rate (HR) is crucial during bleeding and hemorrhagic shock (HS) to compensate for hypotension and hypoxia. Previous works have observed that at the point of hemodynamic decompensation a marked suppression of BP and HR variability occurs, leading to irreversible shock. We hypothesized that recovery of the autonomic control may be decisive for effective resuscitation, along with restoration of mean BP. We computed cardiovascular indexes of baroreflex sensitivity and BP and HR variability by analyzing hemodynamic recordings collected from five pigs during a protocol of severe hemorrhage and resuscitation; three pigs were sham-treated controls. Moreover, we assessed the effects of severe hemorrhage on heart functionality by integrating the hemodynamic findings with measures of plasma high-sensitivity cardiac troponin T and metabolite concentrations in left ventricular (LV) tissue. Resuscitation was performed with fluids and norepinephrine and then by reinfusion of shed blood. After first resuscitation, mean BP reached the target value, but cardiovascular indexes were not fully restored, hinting at a partial recovery of the autonomic mechanisms. Moreover, cardiac troponins were still elevated, suggesting a persistent myocardial sufferance. After blood reinfusion all the indexes returned to baseline. In the harvested heart, LV metabolic profile confirmed the acute stress condition sensed by the cardiomyocytes. Variability indexes and baroreflex trends can be valuable tools to evaluate the severity of HS, and they may represent a more useful end point for resuscitation in combination with standard measures such as mean values and biological measures.NEW & NOTEWORTHY Autonomic control of blood pressure was highly impaired during hemorrhagic shock, and it was not completely recovered after resuscitation despite global restoration of mean pressures. Moreover, a persistent myocardial sufferance emerged from measured cardiac troponin T and metabolite concentrations of left ventricular tissue. We highlight the importance of combining global mean values and biological markers with measures of variability and autonomic control for a better characterization of the effectiveness of the resuscitation strategy.

Introduction: Critically ill children in the pediatric intensive care unit (PICU) are at high risk for developing nutritional deficiencies and undernutrition is known to be a risk factor for morbidity and mortality. Malnutrition represents a continuous spectrum ranging from marginal nutrient status to severe metabolic and functional alterations and this in turn, affects clinical outcome. Objectives: The aim of the study was to assess nutritional status of critically ill children admitted to the PICU and its association to clinical outcomes. Methods: Critically ill children age 6 months to 18 years were prospectively enrolled on PICU admission. Nutritional status was assessed by weight for age (WFA: underweight), weight for height (WFH: wasting), height for age (HFA: stunting) z-scores and mid upper arm circumference (MUAC: wasting) according to the WHO. (1,2) Malnutrition was defined as mild, moderate, and severe if z-scores were > −1, > − 2, and > −3, respectively. Hospital and PICU length of stay (LOS), duration of mechanical ventilation (MV), and risk of mortality (ROM) by the Pediatric Index of Mortality 2 (PIM2) were obtained. Sensitivity and specificity of the MUAC to identify children with wasting (WFH) were calculated. Results: Two hundred and fifty children (136 males), aged 81 months (23-167; median (25-75 th IQR)), were prospectively included in the study. The hospital LOS was 8 (4-16) days; PICU LOS: 2 (1-4) days; duration of MV, 0 (0-1.5) days;

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