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Purpose of review Current cardiac arrest guidelines are based on a fixed, time-based defibrillation strategy. Rhythm analysis and shock delivery (if indicated) are repeated every 2 min requiring cyclical interruptions of chest compressions. This approach has several downsides, such as the need to temporarily stop cardiopulmonary resuscitation (CPR) for a variable amount of time, thus reducing myocardial perfusion and decreasing the chance of successful defibrillation. A tailored defibrillation strategy should identify treatment priority for each patient, that is chest compressions (CCS) or defibrillation, minimize CCs interruptions, speed up the delivery of early effective defibrillation and reduce the number of ineffective shocks. Recent findings Real-time ECG analysis (using adaptive filters, new algorithms robust to chest compressions artifacts and shock-advisory algorithms) is an effective strategy to correctly identify heart rhythm during CPR and reduce the hands-off time preceding a shock. Similarly, ventricular fibrillation waveform analysis, that is amplitude spectrum area (AMSA) represents a well established approach to reserve defibrillation in patients with high chance of shock success and postpone it when ventricular fibrillation termination is unlikely. Both approaches demonstrated valuable results in improving cardiac arrest outcomes in experimental and observational study. Summary Real-time ECG analysis and AMSA have the potential to predict ventricular fibrillation termination, return of spontaneous circulation and even survival, with discretely high confidence. Prospective studies are now necessary to validate these new approaches in the clinical scenario.

Perfusion pressure and chest compression quality are generally considered key determinants of brain oxygenation during cardiopulmonary resuscitation (CPR) and the impact of oxygen administration is less clear. We compared ventilation with 100% and 50% oxygen during ineffective manual chest compressions and hypothesized that 100% oxygen would improve brain oxygenation.Ventricular fibrillation (VF) was induced electrically in anaesthetized pigs and left untreated for 5 minutes, followed by randomization to ineffective manual CPR with ventilation of 50% or 100% oxygen. The first defibrillation was performed 10 minutes after induction of VF, and CPR continued with mechanical chest compressions (LUCAS2™) and defibrillation every 2 minutes until 36 minutes or return of spontaneous circulation (ROSC). Brain oxygenation was measured with near-infrared spectroscopy (rSOTwenty-eight pigs were included in the study: 14 subjects in each group. During ineffective chest compressions relative PbtOThe use of 100% compared to 50% oxygen during ineffective manual CPR improved brain oxygenation measured invasively in brain tissue, but there was no difference in rSO

Objectives. Viral bronchiolitis represents one of the main cause of hospitalization for children in developed and incoming countries. Nasal High Flow (NHF) oxygen therapy improves oxygenation and reduces respiratory drive by enhancing carbon dioxide wash-out. However, little is known about physiological effects of noninvasive helmet-Continuous Positive Airway Pressure (h-CPAP) and NHF on respiratory Work Of Breathing (WOB) in bronchiolitis. Objective of the study is to measure Esophageal Pressure Time Product*minute (PTPes*min-1) as a surrogate for WOB in acute bronchiolitis during NH at different flow rates in comparison with conventional h-CPAP. Pressure Rate Product, physiological parameters and gas exchange were considered as secondary end-points. Methods. This is a physiological randomized crossover-study comparing four 20-minute trials: oxygen therapy delivered by non-fitting mask, NHF2l/Kg, NHF3l/Kg, h-CPAP 7cmH2O. Results. Were enrolled ten children with bronchiolitis needing noninvasive respiratory support. PTPes*min-1, Respiratory Rate and Pressure Rate Product decreased progressively from h-CPAP compared to NHF3l/kg, NHF2l/kg and oxygen mask (p

Anoxic brain injuries represent the main determinant of poor outcome after cardiac arrest (CA). Large animal models have been described to investigate new treatments during CA and post-resuscitation phase, but a detailed model that includes extensive neuromonitoring is lacking.Before an electrically-induced 10-minute CA and resuscitation, 46 adult pigs underwent neurosurgery for placement of a multifunctional probe (intracranial pressure or ICP, tissue oxygen tension or PbtO42 animals underwent the CA procedure and 41 achieved the return of spontaneous circulation (ROSC). In 4 cases (8.6%) an adverse event took place during preparation, but only in two cases (4.3%) this was related to the neurosurgery. In 6 animals (13.3%) the minor complications that occurred resolved after probe repositioning.Herein we provide a detailed comprehensive neuromonitoring approach in a large animal model of CA that might help future research.

Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p p p p

Postcardiac arrest myocardial dysfunction (PCAMD) is a frequent complication faced during post-resuscitation care that adversely impacts survival and neurological outcome. Both mechanical and electrical factors contribute to the occurrence of PCAMD. Prearrest ventricular function, the cause of cardiac arrest, global ischemia, resuscitation factors, ischemia/reperfusion injury and post-resuscitation treatments contribute to the severity of PCMAD. the pathophysiology of PCAMD is complex and include myocytes energy failure, impaired contractility, cardiac edema, mitochondrial damage, activation of inflammatory pathways and the coagulation cascade, persistent ischemic injury and myocardial stiffness. Hypotension and low cardiac output with vasopressor/inotropes need are frequent after resuscitation. However, clinical, hemodynamic and laboratory signs of shock are frequently altered by cardiac arrest pathophysiology and post-resuscitation treatment, potentially being misleading and not fully reflecting the severity of postcardiac arrest syndrome. Even if validated criteria are lacking, an extensive hemodynamic evaluation is useful to define a "benign" and a "malign" form of myocardial dysfunction and circulatory shock, potentially having treatment and prognostic implications. cardiac output is frequently decreased after cardiac arrest, particularly in patients treated with target temperature management (TTM); however, it is not independently associated with outcome. sinus bradycardia during TTM seems independently associated with survival and good neurological outcome, representing a promising prognostic indicator. Higher mean arterial pressure (MAP) seems to be associated with improved survival and cerebral function after cardiac arrest; however, two recent randomized clinical trials failed to replicate these results. recommendations on hemodynamic optimization are relatively poor and are largely based on general principle of intensive care medicine. Skrifvars, MB (corresponding author), Univ Helsinki, Dept Anesthesiol Intens Care & Pain Med, Haartmaninkatu 4, Helsinki 00029, Finland. markus.skrifyars@hus.fi

Background Ventilation with the noble gas argon (Ar) has shown neuroprotective and cardioprotective properties in different in vitro and in vivo models. Hence, the neuroprotective effects of Ar were investigated in a severe, preclinically relevant porcine model of cardiac arrest. Methods and Results Cardiac arrest was ischemically induced in 36 pigs and left untreated for 12 minutes before starting cardiopulmonary resuscitation. Animals were randomized to 4‐hour post‐resuscitation ventilation with: 70% nitrogen–30% oxygen (control); 50% Ar–20% nitrogen–30% oxygen (Ar 50%); and 70% Ar–30% oxygen (Ar 70%). Hemodynamic parameters and myocardial function were monitored and serial blood samples taken. Pigs were observed up to 96 hours for survival and neurological recovery. Heart and brain were harvested for histopathology. Ten animals in each group were successfully resuscitated. Ninety‐six‐hour survival was 60%, 70%, and 90%, for the control, Ar 50%, and Ar 70% groups, respectively. In the Ar 50% and Ar 70% groups, 60% and 80%, respectively, achieved good neurological recovery, in contrast to only 30% in the control group ( P P P =0.007), after Ar compared with control treatment. A lower increase in circulating biomarkers of brain injury, together with less kynurenine pathway activation ( P P Conclusions Post‐resuscitation ventilation with Ar significantly improves neurologic recovery and ameliorates brain injury after cardiac arrest with long no‐flow duration. Benefits are greater after Ar 70% than Ar 50%.

Purpose Available animal models of acute heart failure (AHF) and their limitations are discussed herein. A novel and preclinically relevant porcine model of decompensated AHF (ADHF) is then presented. Methods Myocardial infarction (MI) was induced by occlusion of left anterior descending coronary artery in 17 male pigs (34 ± 4 kg). Two weeks later, ADHF was induced in the survived animals (n = 15) by occlusion of the circumflex coronary artery, associated with acute volume overload and increases in arterial blood pressure by vasoconstrictor infusion. After onset of ADHF, animals received 48-h iv infusion of either serelaxin (n = 9) or placebo (n = 6). The pathophysiology and progression of ADHF were described by combining evaluation of hemodynamics, echocardiography, bioimpedance, blood gasses, circulating biomarkers, and histology. Results During ADHF, animals showed reduced left ventricle (LV) ejection fraction 35%, pulmonary edema, and high pulmonary capillary wedge pressure ~ 30 mmHg (p 2 and high PCO2; and LV dysfunction, i.e., increased LV end-diastolic/systolic volumes, were observed (p p Conclusion This new model, resulting from a combination of chronic and acute MI, and volume and pressure overload, was able to reproduce all the typical clinical signs occurring during ADHF in a consistent and reproducible manner.

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 P P 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.

Aim Systemic proteolysis has been proposed as part of the complex pathologic events occurring during haemorrhagic shock (HS). Hypoperfusion may increase permeability of the gut mucosa, promoting intestinal proteases translocation into the circulation and multiorgan failure (‘autodigestion hypothesis’). 1 The interruption of this cascade of events may improve systemic perfusion and organ functions. Method The present study investigated the effects of the enteral administration of a protease inhibitor, i.e. tranexamic acid (TXA), on hemodynamics in a porcine model of controlled severe acute bleeding, fluid resuscitation and blood transfusion. Six animals underwent HS without any treatment while five animals were treated with enteral TXA. Results Baseline measurements were similar in both HS and TXA groups. Both groups showed a significant reduction in mean arterial pressure (MAP) after bleeding compared to baseline values, however at the end of the fluid resuscitation MAP was significantly higher in the TXA group (62.67±13.17 vs 92.20±22.35 mmHg, p Conclusion In this experimental model of HS the enteral administration of TXA was associated with a global improvement in hemodynamics; however, only small benefits were observed on mixed venous saturation and lactate levels. Reference . Schmid-Schonbein GW. 2008landis award lecture. Inflammation and the autodigestion hypothesis. Microcirculation 2009;16(4):289–306. Conflict of interest None Funding None

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 (EtCO2) target: 35-40 mmHg) or hypercapnic ventilation (EtCO2 45-50 mmHg). Hemodynamics was invasively measured and EtCO2 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. EtCO2 and arterial partial pressure of CO2 were higher in the hypercapnic group compared to the normocapnic one (p

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.

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Prone positioning is a life-saving treatment used in ARDS patients in order to improve oxygenation and reduce lung injury due to mechanical ventilation. The beneficial effects of this procedure are the result of complex mechanisms that cooperate in improving gas exchange and in reducing global “stress” and “strain” of the lung. Prone positioning seems to be more effective in extrapulmonary form of ARDS, where the main feature of the disease is represented by compression atelectasis in dependent lung regions caused by the gain in lung weight due to pulmonary edema. To date, it is recommended in ARDS patients that maintain a PaO2/FiO2 ratio lower than 150 mmHg even after optimization of mechanical ventilation. However, only the patients who react to prone positioning with a decrease in PaCO2 show a real benefit in terms of survival rate. The relationship between improvement in gas exchange and patient outcome still remains unclear. This is not a maneuver free of complications, and it is important to balance risks and benefits associated with the procedure. An expert team is required to safely prone the patient and to reduce the incidence of adverse effects.

The optimal method for estimating transpulmonary pressure (i.e. the fraction of the airway pressure transmitted to the lung) has not yet been established.In this study on 44 patients with acute respiratory distress syndrome (ARDS), we computed the end-inspiratory transpulmonary pressure as the change in airway and esophageal pressure from end-inspiration to atmospheric pressure (i.e. release derived) and as the product of the end-inspiratory airway pressure and the ratio of lung to respiratory system elastance (i.e. elastance derived). The end-expiratory transpulmonary pressure was estimated as the product of positive end-expiratory pressure (PEEP) minus the direct measurement of esophageal pressure and by the release method.The mean elastance- and release-derived transpulmonary pressure were 14.4 ± 3.7 and 14.4 ± 3.8 cmH₂O at 5 cmH₂O of PEEP and 21.8 ± 5.1 and 21.8 ± 4.9 cmH₂O at 15 cmH₂O of PEEP, respectively (P = 0.32, P = 0.98, respectively), indicating that these parameters were significantly related (r(2) = 0.98, P0.001 at 5 cmH₂O of PEEP; r(2) = 0.93, P0.001 at 15 cmH₂O of PEEP). The percentage error was 5.6 and 12.0 %, respectively. The mean directly measured and release-derived transpulmonary pressure were -8.0 ± 3.8 and 3.9 ± 0.9 cmH₂O at 5 cmH₂O of PEEP and -1.2 ± 3.2 and 10.6 ± 2.2 cmH₂O at 15 cmH₂O of PEEP, respectively, indicating that these parameters were not related (r(2) = 0.07, P = 0.08 at 5 cmH₂O of PEEP; r (2) = 0.10, P = 0.53 at 15 cmH₂O of PEEP).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.

Lung transplantation is associated with an inflammatory reaction known as primary graft dysfunction. This clinical syndrome occurs within the first 72 hours after transplantation and is characterized by hypoxemia (PaO2/FiO2

ARDS is characterized by edema diffuse to all lung fields. Distribution of excess tissue mass had been studied with CT scan in a few patients on a single slice, comparing with data obtained in healthy controls.

Traditionally, ARDS obese patients are ventilated with higher tidal volumes and higher PEEP due to expected increased in pleural pressure. However, data from the literature regarding the influence of body mass on lung mechanics and, particularly, on chest wall elastance are not univocal [1,2]. Failure to account for how the increase in body weight could affect the respiratory function can result in injurious mechanical ventilation and in the onset of VILI. The aim of this study was to evaluate the role of the body weight on respiratory mechanics in ARDS patients.

Intratidal opening/closing is believed to be one of the main triggers of ventilator-induced lung injury; the application of higher PEEP united with the limitation of plateau pressure at 30 cmH2O may limit this phenomenon. We aim to evaluate the intratidal opening/ closing at different PEEP levels and the amount of lung parenchyma that regains inflation going from 30 (pressure limit of tidal ventilation) to 45 cmH2O.

CT-scan quantitative analysis (qCT) represents the gold standard to assess lung aeration and recruitment in ARDS patients. Lung ultrasound (LUS) has been proposed as a bedside nonirradiating alternative to assess lung recruitability, identifying patients who may benefit from higher PEEP levels. We compared the two methods in the assessment of PEEP-induced lung aeration changes.