Empirical evidence for safety of mechanical ventilation during simulated cardiopulmonary resuscitation on a physical model.

BACKGROUND: Cardiac arrest is a critical event requiring adequate and timely response in order to increase a patient's chance of survival. In patients mechanically ventilated with advanced airways, cardiopulmonary resuscitation (CPR) maneuver may be simplified by keeping the ventilator on. This work assessed the response of an intensive care mechanical ventilator to CPR using a patient manikin ventilated in three conventional modes. METHODS: Volume-controlled (VCV), pressure-controlled (PCV) and pressure regulated volume-controlled (PRVC) ventilation were applied in a thorax physical model, with or without chest compressions. The mechanical ventilator was set with inspiratory time of 1.0 s, ventilation rate of 10 breaths/min, positive end-expiratory pressure of 0 cmH2O, FiO2 of 1.0, target tidal volume of 600 mL and trigger level of -20 cmH2O. Airway opening pressure and ventilatory flow signals were continuously recorded. RESULTS: Chest compression resulted in increased airway peak pressure in all ventilation modes (p < 0.001), especially with VCV (137% in VCV, 83% in PCV, 80% in PRVC). However, these pressures were limited to levels similar to release valves in manual resuscitators (~60 cmH2O). In pressure-controlled modes tidal/min volumes decreased (PRVC = 11%, p = 0.027 and PCV = 12%, p < 0.001), while still within the variability observed during bag-valve-mask ventilation. During VCV, variation in tidal/min volumes were not significant (p = 0.140). Respiratory rate did not change with chest compression. CONCLUSIONS: Volume and pressure ventilation modes responded differently to chest compressions. Yet, variation in delivered volume and the measured peak pressures were within the reported for the standard bag-valve-mask system.

Individualised positive end-expiratory pressure guided by electrical impedance tomography for robot-assisted laparoscopic radical prostatectomy: a prospective, randomised controlled clinical trial.

BACKGROUND: Robot-assisted laparoscopic radical prostatectomy requires general anaesthesia, extreme Trendelenburg positioning and capnoperitoneum. Together these promote impaired pulmonary gas exchange caused by atelectasis and may contribute to postoperative pulmonary complications. In morbidly obese patients, a recruitment manoeuvre (RM) followed by individualised PEEP improves intraoperative oxygenation and end-expiratory lung volume (EELV). We hypothesised that individualised PEEP with initial RM similarly improves intraoperative oxygenation and EELV in non-obese individuals undergoing robot-assisted prostatectomy. METHODS: Forty males (age, 49-76 yr; BMI <30 kg m-2) undergoing prostatectomy received volume-controlled ventilation (tidal volume 8 ml kg-1 predicted body weight). Participants were randomised to either (1) RM followed by individualised PEEP (RM/PEEPIND) optimised using electrical impedance tomography or (2) no RM with 5 cm H2O PEEP. The primary outcome was the ratio of arterial oxygen partial pressure to fractional inspired oxygen (Pao2/Fio2) before the last RM before extubation. Secondary outcomes included regional ventilation distribution and EELV which were measured before, during, and after anaesthesia. The cardiovascular effects of RM/PEEPIND were also assessed. RESULTS: In 20 males randomised to RM/PEEPIND, the median PEEPIND was 14 cm H2O [inter-quartile range, 8-20]. The Pao2/Fio2 was 10.0 kPa higher with RM/PEEPIND before extubation (95% confidence interval [CI], 2.6-17.3 kPa; P=0.001). RM/PEEPIND increased end-expiratory lung volume by 1.49 L (95% CI, 1.09-1.89 L; P<0.001). RM/PEEPIND also improved the regional ventilation of dependent lung regions. Vasopressor and fluid therapy was similar between groups, although 13 patients randomised to RM/PEEPIND required pharmacological therapy for bradycardia. CONCLUSION: In non-obese males, an individualised ventilation strategy improved intraoperative oxygenation, which was associated with higher end-expiratory lung volumes during robot-assisted laparoscopic prostatectomy. CLINICAL TRIAL REGISTRATION: DRKS00004199 (German clinical trials registry).

The role of sphingolipid metabolism disruption on lipopolysaccharide-induced lung injury in mice.

AIM: This study assessed pulmonary outcomes generated by inhibiting key enzymes of sphingolipid metabolism pathways related to ceramide synthesis in a murine model of lung injury induced by lipopolysaccharide (LPS). METHODS: C57BL/6 male adult mice received LPS intratracheally and the expressions of acid sphingomyelinase (ASM), neutral sphingomyelinase (NSM), serine palmitoyl transferase (SPT) and dihydroceramide synthase (DS) were assessed at 2, 4, 6, 12 and 24 h after LPS instillation in lung homogenate (n = 30). The pharmacological inhibition of ASM, NSM, SPT and DS were assayed in other mice groups by three different doses of desipramine, GW4869, myriocin and fumonisin, respectively (n = 90). Their most effective doses were administered intraperitoneally 1 or 2 h before LPS to different animal groups (n = 120). Mice underwent determination of pulmonary mechanics, lung histopathological aspects and apoptosis. RESULTS: The expression levels of the enzymes reached their peak at 2-4 h after LPS administration. ASM inhibition attenuated alveolar collapse and GW4869 decreased lung elastance, proinflammatory cytokines' levels and was more effective to improve alveolar collapse than desipramine. On the other hand, SPT blockage aggravated lung lesion and no effects it was observed with fumonisin. Moreover, simultaneous administration of inhibitors (desipramine + GW4869, myriocin + fumonisin and all inhibitors together) resulted in no changes. CONCLUSION: Blockage of sphingomyelinases and the de novo pathways improved and aggravated lung injury, respectively, putatively suggesting specific targets to therapeutic strategies in LPS-induced lung injury.