High positive end-expiratory pressure : only a dam against edema formation?

Introduction Healthy piglets ventilated with Tidal Volume (VT) close to inspiratory capacity (IC; maximal physiological lung inflation) always largely increase their lung weight within 24-36 hours [1], as for fluid filtration through a disrupted blood-gas barrier. We have recently noted that when a similar degree of lung inflation is mainly due to high Positive End-Expiratory Pressure (PEEP), lung weight never changes. Aim To clarify whether PEEP acts only as a dam, preventing fluid filtration through a blood-gas barrier that is invariably damaged when lungs are inflated up to their physiological limit. If that is the case, removal of PEEP will rapidly lead to lung edema formation. Methods Three healthy piglets (21\ub12 Kg) had their IC measured with lung computed tomography (CT). They were then ventilated with high PEEP (around 75% of IC) and low VT (25% of IC). After 36 hours, PEEP was removed and ventilation continued with low VT for 18 hours. Lung weight was measured at the beginning (CT) and end (balance, following autopsy) of the study. Results IC was 1023\ub1136 ml. Accordingly, animals were initially ventilated with PEEP 19\ub11 cmH2O (volume of gas 898\ub1211 ml) and VT 213\ub112 ml. Following PEEP removal, VT was 217\ub121 ml. As shown in figure, lung weight never increased. InitialFinalLung Weight ( g)200300400 Figure. Individual changes in lung weight. p = 0.13 ( Paired t-test ) Conclusion Our preliminary findings suggest that high PEEP does not merely act as a dam, as its removal is not followed by an increase in lung weight. We therefore hypothesize that ventilation with high PEEP and low VT somehow protects the blood-gas barrier. [1]: Protti et al. AJRCCM, 2011; 183(10):1354-1362

How to measure transpulmonary pressure at the bedside : comparison between two methods

Introduction Transpulmonary(PTP), and not airway (PAW), pressure is the force really acting on the lung, even during mechanical ventilation[1]. PTP can be measured at the bedside using two different methods. One (method A) requires the removal of any externally applied Positive End Expiratory Pressure (PEEP) [2], while the other one does not (method B) [3]. Aim To compare two methods for measuring PTPat the bedside in the presence of externally applied PEEP. Methods Three piglets with Acute Respiratory Distress Syndrome (ARDS) were ventilated with Tidal Volume (TV) 10 ml/Kg. In each animal PEEP was set at 5, 10 and 15 cmH2O, according to a random order. During each study period, PAW and esophageal pressure (PES) were recorded at end-expiration (PAW PEEP, PES PEEP), at end-inspiration (PAW PLAT, PES PLAT) and after lungs were allowed to deflate down to functional residual capacity (PAW ZEEP, PES ZEEP). PTP was computed as (PAW PLAT \u2013 PAW ZEEP [0 cmH2O]) \u2013 (PES PLAT \u2013 PES ZEEP) (method A) or PAW PLATx \u394PTP/\u394PAW (method B), with delta (\u394) indicating the increase in PTP or PAW associated with TV inflation. Figure. Bland & Altman plot. The X axis shows the mean of the two measurements and the Y axis the difference between PTP method A and method B

Antithrombin During Extracorporeal Membrane Oxygenation in Adults: National Survey and Retrospective Analysis

The impact of antithrombin replacement during extracorporeal membrane oxygenation (ECMO) in adults remains unclear. This work comprises a survey, showing that antithrombin is routinely supplemented in many Italian ECMO-Centers, and a retrospective analysis on 66 adults treated with veno-venous ECMO and unfractionated heparin at our Institution. Twenty-four to 72 h after the beginning of ECMO, antithrombin activity was 6470% in 47/66 subjects and activated partial thromboplastin time (aPTT) ratio was <1.5 in 20/66 subjects. Activated partial thromboplastin time ratio <1.5 was associated not with lower antithrombin activity (61 \ub1 17 vs. 63 \ub1 22%; p = 0.983) but with higher circulating level of C-reactive protein (23 \ub1 8 vs. 11 \ub1 9 mg/dl; p < 0.001). In 34 subjects who received antithrombin concentrate, antithrombin activity increased (from 54 \ub1 9 to 84 \ub1 13%; p < 0.001); the proportion of subjects with aPTT ratio 651.5 increased (from 21/34 [62%] to 31/34 [91%]; p = 0.004); heparin dosage remained constant (from 19 \ub1 7 to 19 \ub1 6 IU/kg/h; p = 0.543); and C-reactive protein decreased (from 17 \ub1 10 to 13 \ub1 9 mg/dl; p = 0.013). Among those with aPTT ratio <1.5, aPTT ratio remained <1.5 in 3 out of 13 subjects. Antithrombin is frequently supplemented during veno-venous ECMO although low antithrombin activity does not constantly impede, and antithrombin replacement does not constantly ensure, reaching the target aPTT ratio. Inflammation possibly affects the individual response to heparin

Clinical feasibility of &quot;awake-ECMO&#8221; in acute respiratory failure

Introduction: Veno-venous extracorporeal membrane oxygenation (vv-ECMO) is nowadays safer due to recent technical improvements and thus is increasingly used as a rescue therapy for acute respiratory failure. Mechanical ventilation is the standard support for patient with respiratory failure, but can itself damage the lung. Objective: To explore vv-ECMO as an alternative to conventional mechanical ventilation in acute respiratory failure, we tested feasibility of vv-ECMO in spontaneous breathing patients (\u201cawake- ECMO\u201d). Methods: We retrospectively analyzed all consecutive patients who underwent vv-ECMO support from June 2012 to January 2015. Results: A total of 48 patients with acute respiratory failure (30 acute respiratory distress syndrome - ARDS, 7 acute exacerbation of chronic obstructive pulmonary disease - AECOPD, 11 end-stage pulmonary disease bridged to lung transplantation - ESPD) were analyzed. Figure shows the number of days on ECMO and on \u201cawake-ECMO\u201d for different patients\u2019 categories. All ESPD and all out of one AECOPD patients were successfully treated while spontaneous breathing, whereas only 26% of ARDS patients could remove invasive ventilation and only during shorter time of ECMO support (p<0,001). Patients who could not undergo \u201cawake-ECMO\u201d were sicker than \u201cawake\u201d patients (SOFA 9.1\ub13.4 vs 4.5\ub11.3, p<0,001). Reasons underlying the impossibility of weaning from ventilator ARDS patients were pulmonary plasma-leakage (n=7), hemodynamic derangements (n=10), neurologic impairments (n=4), bleeding (n=7), severe respiratory distress and hypoxemia (n=8). Conclusion: vv-ECMO in awake spontaneous breathing patients is feasible as a bridge to lung transplantation and in AECOPD patients, while in sick ARDS patients we were not able to use vv- ECMO as an alternative to mechanical ventilation

Plateau airway pressure understimates end-inspiratory alveolar pressure during mechanical ventilation

Introduction: Plateau airway pressure is thought to reflect end-inspiratory alveolar pressure. If this is true, Peak Expiratory Flow (PEF) following an inspiratory pause (when plateau airway pressure is the driving force) will be equal to PEF during on-going mechanical ventilation (when end-inspiratory alveolar pressure is the driving force). Methods: Five healthy anesthetized piglets were ventilated with 24 different combinations of Tidal Volume (300, 400, 500, 600, 700 and 800 ml) and Inspiratory Flow (300, 600, 900 and 1200 ml/sec). Following 5 minutes of ventilation with each combination, PEF was measured after a 5-sec inspiratory pause (PEFstat) and during on-going mechanical ventilation (PEFdyn, Fig. 1). Results: PEF recorded after an end-inspiratory pause was significantly lower than PEF recorded during on-going ventilation (49\ub112 L/sec vs. 55\ub115 L/sec, p<0.001; paired t-test). This discrepancy increased with Tidal Volume and Inspiratory Flow (p<0.005 for both; 2-way repeated measures analysis of variance). Conclusions: PEF driven by plateau airway pressure (PEFstat) is significantly lower than PEF driven by end-inspiratory alveolar pressure (PEFdyn). Based on this finding, one can conclude that plateau airway pressure is significantly lower than end-inspiratory alveolar pressure (especially if Tidal Volume)

Hemodynamic effects of lactic acid infusion in healthy piglets

Introduction Lactic acidosis is considered detrimental for cardiovascular system. Ex vivo, it may alter the function of myocardial fibers [1] and whole heart [2]. In vivo, its association with cardiovascular impairment is less well defined [3,4]. Aim To evaluate the effects of lactic acidosis on hemodynamics of healthy piglets. Methods Ten sedated and mechanically ventilated healthy piglets were infused with lactic acid (30% solution) to induce severe lactic acidosis (lactic acid group, n=5) or with normal saline (control group, n=5), for ten hours. Arterial pH and lactate, heart rate (HR), mean arterial pressure (MAP), stroke volume (SV) and cardiac output (CO) were recorded over time. Results Compared to saline, lactic acid infusion increased arterial lactate (18\ub15 vs. 1\ub10 mmol/l, p<0.001) and decreased arterial pH (6.90\ub1 0.10 vs.7.51\ub10.08, p<0.001). None of the variables of interest significantly differed between the two groups at the beginning (data not shown) and at the end (see Table) of the study. All animals survived until the end of the study. [Control Group (n=5) Lactic acid Group (n=5) probability ]HR (bpm) 101 \ub1 17 84 \ub1 12 0.10 MAP (mmHg) 82 \ub1 17 109 \ub1 27 0.09 SV (ml) 23 \ub1 4 27 \ub1 7 0.35 CO (l/min) 2.4 \ub1 0.8 2.3 \ub1 0.8 0.84 Table. Data are expressed as mean \ub1 standard deviation; p reflects the result of t-test. Conclusions These results show that lactic acidosis, per se, does not cause major hemodynamic impairment and is well tolerated by healthy animals

Can lung weight be measured by computed tomography?

Introduction Computed Tomography (CT) may be a non-invasive tool for measuring lung weight (a surrogate of edema) in vivo [1]. Aim To compare lung weight measured with the balance with lung weight measured with CT scan. Methods Thirteen sedated and mechanically ventilated piglets (21 \ub1 3 Kg) underwent lung CT at the end of different experimental protocols and were then sacrificed. Lungs were excised and weighed on a balance. Pre-mortem CT scans were manually delineated and processed with a dedicated software (quantitative analysis). Lung weights measured with the balance (reference) were compared with those obtained with CT. Results Lung weight measured with the balance was 407 \ub1 236 g and lung weight obtained by quantitative analysis of CT scan was 509 \ub1 232 g (P < 0,001; paired t-test). Comparison between the two methods is reported in Figure. Figure. Bland & Altman plot. X axis: mean of the results obtained with the two methods. Y axis: difference between the two results (lung weight measured with the balance acted as reference method). Conclusions On average, CT overestimated lung weight (as measured with the balance) by 100 g. Since CT scan was taken before autopsy (and exsanguination) this discrepancy is likely explained by greater (and heavier) pulmonary blood content.[1] Gattinoni L., Cressoni M., Intensive Care Med, 2010; 36:1803-180

Role of tidal volume and positive end-expiratory pressure in the development of Ventilator-Induced Lung Injury

Puede afirmarse que cuando en el Mercurio Peruano y en marzo de 1829 (es decir apenas ocho años después de la declaración de la independencia nacional), Felipe Pardo y Aliaga publica la sátira en verso "El carnaval de Lima", se inicia la historia del Costumbrismo en sentido estricto en el Perú O si se prefiere tomar como referencia una obra de mayor entidad, puede sostenerse mejor que el hito inicial está dado por el estreno de Frutos de la Educación, la primera comedia del mismo Pardo (6 de ..