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Search Results: 1 - 10 of 1981 matches for " Davide Chiumello "
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Estimation of dead space fraction can be simplified in the acute respiratory distress syndrome
Davide Chiumello, Elisabetta Gallazzi
Critical Care , 2010, DOI: 10.1186/cc9237
Abstract: In the previous issue of Critical Care, Siddiki and colleagues [1] presented the dead space fraction data collected at admission and on day 3 from two acute lung injury/acute respiratory distress syndrome (ALI/ARDS) databases (109 patients in the Mayo Clinic and 1,896 patients in the ARDS Network). The hospital mortality increased in direct proportion to an increase in the dead space fraction. For every 0.05 increment of the dead space fraction, the odds ratios for hospital mortality were 1.07 at day 1 and 1.12 at day 3. Thus, at first sight, the results of Siddiki and colleagues represent merely a repetition of previous studies [2-4]. However, their study added a novel element in that the dead space fraction was computed more simply than in the previous studies [2-4] and, unlike in those studies, without monitoring of the expired carbon dioxide (CO2). So that the current results may be better understood, a short summary of the theoretical aspects of the dead space computation is presented.ALI and ARDS are characterized by a non-cardiogenic pulmonary edema with significant impairment of gas exchange. The increases in the right-to-left intrapulmonary shunt and in low ventilation-to-perfusion ratio lead to hypoxemia, whereas the increase in pulmonary dead space reduces CO2 removal [5,6]. The increase in pulmonary dead space is due mainly to alterations in the distribution of pulmonary blood flow originating from vascular obstruction and to regional overdistension of ventilated alveoli induced by the application of positive end-expiratory pressure (PEEP) and sometimes by the reduction in cardiac output [7-9].Nuckton and colleagues [10] found that in patients with ARDS the pulmonary dead fraction measured at admission was significantly higher in the non- survivors than in the survivors (0.63 ± 0.09 versus 0.54 ± 0.09); for every increase of 0.05 in the dead space fraction, the odds ratio of death increased by 45%. Subsequent studies showed that the dead space fraction,
Bench-to-bedside review: Chest wall elastance in acute lung injury/acute respiratory distress syndrome patients
Luciano Gattinoni, Davide Chiumello, Eleondra Carlesso, Franco Valenza
Critical Care , 2004, DOI: 10.1186/cc2854
Abstract: The respiratory system includes the lung and the chest wall, in series, and the overall mechanical behavior depends on the mechanical characteristics of its components and their interactions [1]. The common increase in the elastance (decrease in compliance) of the whole respiratory system in acute lung injury (ALI) and in acute respiratory distress syndrome (ARDS) has traditionally been attributed to the lung component. It has long been reported, however, that the chest wall elastance was also altered in many cases [2-5]. Recently, mainly due to the increased concern for the abdominal pressure, more attention has been paid to the chest wall mechanics in critically ill patients [6,7]. The problems of the mechanical impairment of the chest wall and its consequences are now widely recognized. The present review will focus on the dimension of these problems and their consequences in the critically ill patient.When partitioning the respiratory mechanics into its lung and chest wall components, it is convenient to refer to elastance instead of compliance. The total elastance of the respiratory system is the pressure required to inflate it 1 l above its resting position. This is, the applied airway pressure is spent in part to inflate the lung and in part to inflate the chest wall. The chest wall comprises the anterior and posterior thoracic cage walls and the diaphragm, which is the 'abdominal component'. Indeed, in static conditions, when the airway resistance is nil:Paw = Pl + Ppl (1)andEtot = El + Ecw (2)where Paw is the (static) airway pressure, Pl is the transpulmonary pressure, Ppl is the pleural pressure, Etot is the total respiratory system elastance, El is the lung elastance, and Ecw is the chest wall elastance.On the basis of these classical equations it is easy to grasp the mechanical interaction between the lung and the chest wall. First, however, it is important to recall that the concept of 'transmission' of alveolar pressure to the thoracic cavity is mislea
Correction: Nitrogen washout/washin, helium dilution and computed tomography in the assessment of end expiratory lung volume
Davide Chiumello, Massimo Cressoni, Monica Chierichetti, Federica Tallarini, Marco Botticelli, Virna Berto, Cristina Mietto, Luciano Gattinoni
Critical Care , 2009, DOI: 10.1186/cc7743
Abstract: The legend for Figure 5, 'Comparison of end expiratory lung volume (EELV) measured by the helium dilution technique and the nitrogen washout/washin method', was incorrect and should read as follows:Comparison of end expiratory lung volume (EELV) measured by the helium dilution technique and the nitrogen washout/washin method. (a) The EELV measured by the helium dilution as a function of the EELV measured by nitrogen washout/washin method (EELV helium dilution = -111.85 + 0.89 × EELV GE, r2 = 0.82, p < 0.00001). (b) The Bland-Altman plot of the EELV measured with the nitrogen washout/washin technique and the EELV measured with the helium dilution method. The x-axis shows the mean of the two measurements and the y-axis shows the difference between the EELV measured by then helium dilution method and the nitrogen washout/washin method (average difference -229 ± 164 ml, limits of agreement -558 – 100 ml).The values in graph (a) of Figures 1, 4 and 5 had been plotted onto the incorrect axis.The panels in Figure 3 had been switched. Graph (a) should be the linear regression plot and graph (b) should be the Bland-Altman plot.
Nitrogen washout/washin, helium dilution and computed tomography in the assessment of end expiratory lung volume
Davide Chiumello, Massimo Cressoni, Monica Chierichetti, Federica Tallarini, Marco Botticelli, Virna Berto, Cristina Mietto, Luciano Gattinoni
Critical Care , 2008, DOI: 10.1186/cc7139
Abstract: Patients admitted to the general intensive care unit of Ospedale Maggiore Policlinico Mangiagalli Regina Elena requiring ventilatory support and, for clinical reasons, thoracic CT scanning were enrolled in this study. We performed two EELV measurements with the modified nitrogen washout/washin technique (increasing and decreasing inspired oxygen fraction (FiO2) by 10%), one EELV measurement with the helium dilution technique and a CT scan. All measurements were taken at 5 cmH2O airway pressure. Each CT scan slice was manually delineated and gas volume was computed with custom-made software.Thirty patients were enrolled (age = 66 +/- 10 years, body mass index = 26 +/- 18 Kg/m2, male/female ratio = 21/9, partial arterial pressure of carbon dioxide (PaO2)/FiO2 = 190 +/- 71). The EELV measured with the modified nitrogen washout/washin technique showed a very good correlation (r2 = 0.89) with the data computed from the CT with a bias of 94 +/- 143 ml (15 +/- 18%, p = 0.001), within the limits of accuracy declared by the manufacturer (20%). The bias was shown to be highly reproducible, either decreasing or increasing the FiO2 being 117+/-170 and 70+/-160 ml (p = 0.27), respectively. The EELV measured with the helium dilution method showed a good correlation with the CT scan data (r2 = 0.91) with a negative bias of 136 +/- 133 ml, and appeared to be more correct at low lung volumes.The EELV measurement with the helium dilution technique (at low volumes) and modified nitrogen washout/washin technique (at all lung volumes) correlates well with CT scanning and may be easily used in clinical practice.Current Controlled Trials NCT00405002.The damage induced by mechanical ventilation in cases of acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) can be termed barotrauma [1], volotrauma [2,3], atelectrauma [4,5] or biotrauma [5,6] depending on the emphasis given to the pathogenic mechanism. They are all caused by the unphysiological stress and strain applied to
Chest wall mechanics during pressure support ventilation
Andrea Aliverti, Eleonora Carlesso, Raffaele Dellacà, Paolo Pelosi, Davide Chiumello, Antonio Pedotti, Luciano Gattinoni
Critical Care , 2006, DOI: 10.1186/cc4867
Abstract: In nine patients four different levels of PSV (5, 10, 15 and 25 cmH2O) were randomly applied with the same level of positive end-expiratory pressure (10 cmH2O). Flow, airway opening, and oesophageal and gastric pressures were measured, and volume variations for the entire chest wall, the ribcage and abdominal compartments were recorded by opto-electronic plethysmography. The pressure and the work generated by the diaphragm, rib cage and abdominal muscles were determined using dynamic pressure-volume loops in the various phases of each respiratory cycle: pre-triggering, post-triggering with the patient's effort combining with the action of the ventilator, pressurization and expiration. The complete breathing pattern was measured and correlated with chest wall kinematics and dynamics.At the various levels of pressure support applied, minute ventilation was constant, with large variations in breathing frequency/ tidal volume ratio. At pressure support levels below 15 cmH2O the following increased: the pressure developed by the inspiratory muscles, the contribution of the rib cage compartment to the total tidal volume, the phase shift between rib cage and abdominal compartments, the post-inspiratory action of the inspiratory rib cage muscles, and the expiratory muscle activity.During PSV, the ventilatory pattern is very different at different levels of pressure support; in patients with acute lung injury pressure support greater than 10 cmH2O permits homogeneous recruitment of respiratory muscles, with resulting synchronous thoraco-abdominal expansion.In intensive care pressure support ventilation (PSV), a form of assisted mechanical ventilation, is among the modes most commonly employed to decrease the patient's work of breathing without neuromuscular blockade [1]. It is known that for optimal unloading of the respiratory muscles, the ventilator should cycle in synchrony with the activity of the patient's respiratory rhythm. Patient-ventilator asynchrony frequently occ
Effect of a heated humidifier during continuous positive airway pressure delivered by a helmet
Davide Chiumello, Monica Chierichetti, Federica Tallarini, Paola Cozzi, Massimo Cressoni, Federico Polli, Riccardo Colombo, Antonio Castelli, Luciano Gattinoni
Critical Care , 2008, DOI: 10.1186/cc6875
Abstract: Nine patients with acute respiratory failure (arterial oxygen tension/fractional inspired oxygen ratio 209 ± 52 mmHg) and 10 healthy individuals were subjected to CPAP. The CPAP was delivered either through a mechanical ventilator or by continuous low (40 l/min) or high flow (80 l/min). Humidity was measured inside the helmet using a capacitive hygrometer. The level of patient comfort was evaluated using a continuous scale.In patients with acute respiratory failure, the heated humidifier significantly increased the absolute humidity from 18.4 ± 5.5 mgH2O/l to 34.1 ± 2.8 mgH2O/l during ventilator CPAP, from 11.4 ± 4.8 mgH2O/l to 33.9 ± 1.9 mgH2O/l during continuous low-flow CPAP, and from 6.4 ± 1.8 mgH2O/l to 24.2 ± 5.4 mgH2O/l during continuous high-flow CPAP. Without the heated humidifier, the absolute humidity was significantly higher with ventilator CPAP than with continuous low-flow and high-flow CPAP. The level of comfort was similar for all the three modes of ventilation and with or without the heated humidifier. The findings in healthy individuals were similar to those in the patients with acute respiratory failure.The fresh gas flowing through the helmet with continuous flow CPAP systems limited the possibility to increase the humidity. We suggest that a heated humidifier should be employed with continuous flow CPAP systems.During normal spontaneous breathing, ambient air – apart from being filtered for particles and micro-organisms by the nose and upper airways – is heated to body temperature and humidified, so that it is saturated by the time it reaches the alveoli [1]. Consequently, when the upper airways are bypassed (as in a patient with an endotracheal tube) medical gases, which are drier than ambient air [2], must be heated and humidified by heated humidifiers or heat-moisture exchangers [1] in order to avoid bronchial inflammation, cell damage, impairment of mucociliary clearance and loss of pulmonary function [3-6].During noninvasive positive pressu
Effects of thoraco-pelvic supports during prone position in patients with acute lung injury/acute respiratory distress syndrome: a physiological study
Davide Chiumello, Massimo Cressoni, Milena Racagni, Laura Landi, Gianluigi Li Bassi, Federico Polli, Eleonora Carlesso, Luciano Gattinoni
Critical Care , 2006, DOI: 10.1186/cc4933
Abstract: We studied 11 patients with ALI/ARDS, sedated and paralyzed, mechanically ventilated in volume control ventilation. Prone positioning with or without thoraco-pelvic supports was applied in a random sequence and maintained for a 1-hour period without changing the ventilation setting. In four healthy subjects the pressures between the body and the contact surface were measured with and without thoraco-pelvic supports. Oxygenation variables (arterial and central venous), physiologic dead space, end-expiratory lung volume (helium dilution technique) and respiratory mechanics (partitioned between lung and chest wall) were measured after 60 minutes in each condition.With thoraco-pelvic supports, the contact pressures almost doubled in comparison with those measured without supports (19.1 ± 15.2 versus 10.8 ± 7.0 cmH2O, p ≤ 0.05; means ± SD). The oxygenation-related variables were not different in the prone position, with or without thoraco-pelvic supports; neither were the CO2-related variables. The lung volumes were similar in the prone position with and without thoraco-pelvic supports. The use of thoraco-pelvic supports, however, did lead to a significant decrease in chest wall compliance from 158.1 ± 77.8 to 102.5 ± 38.0 ml/cmH2O and a significantly increased pleural pressure from 4.3 ± 1.9 to 6.1 ± 1.8 cmH2O, in comparison with the prone position without supports. Moreover, when thoraco-pelvic supports were added, heart rate increased significantly from 82.1 ± 17.9 to 86.7 ± 16.7 beats/minute and stroke volume index decreased significantly from 37.8 ± 6.8 to 34.9 ± 5.4 ml/m2. The increase in pleural pressure change was associated with a significant increase in heart rate (p = 0.0003) and decrease in stroke volume index (p = 0.0241).The application of thoraco-pelvic supports decreases chest wall compliance, increases pleural pressure and slightly deteriorates hemodynamics without any advantage in gas exchange. Consequently, we stopped their use in clinical practice.Pro
The effect of different volumes and temperatures of saline on the bladder pressure measurement in critically ill patients
Davide Chiumello, Federica Tallarini, Monica Chierichetti, Federico Polli, Gianluigi Li Bassi, Giuliana Motta, Serena Azzari, Cristian Carsenzola, Luciano Gattinoni
Critical Care , 2007, DOI: 10.1186/cc6080
Abstract: Thirteen mechanically ventilated critically ill patients (11 male; body mass index 25.5 ± 4.6 kg/m2; arterial oxygen tension/fractional inspired oxygen ratio 225 ± 48 mmHg) were enrolled. Bladder pressure was measured using volumes of saline from 50 to 200 ml at body temperature (35 to 37°C) and room temperature (18 to 20°C).Bladder pressure was no different between 50 ml and 100 ml saline (9.5 ± 3.7 mmHg and 13.7 ± 5.6 mmHg), but it significantly increased with 150 and 200 ml (21.1 ± 10.4 mmHg and 27.1 ± 15.5 mmHg). Infusion of saline at room temperature caused a significantly greater bladder pressure compared with saline at body temperature. The lowest difference between bladder and gastric pressure was obtained with a volume of 50 ml.The bladder acts as a passive structure, transmitting intra-abdominal pressure only with saline volumes between 50 ml and 100 ml. Infusion of a saline at room temperature caused a higher bladder pressure, probably because of contraction of the detrusor bladder muscle.Intra-abdominal pressure (IAP) is the pressure generated inside the abdominal cavity and depends on the degree of flexibility of the diaphragm and abdominal wall, and on the density of its contents [1]. Intra-abdominal hypertension (IAH), defined as an abnormal increase in IAP, can be common in critically ill patients, being present in 18% to 81% of the patients depending on the cut-off level used [2-8].Several clinical conditions such as accumulation of blood, ascites, retroperitoneal haematoma, bowel oedema, necrotizing pancreatitis, massive fluid resuscitation, packing after control laparotomy and closure of a swollen noncompliant abdominal wall may induce IAH [3,9]. IAH has adverse effects on several organs, causing reductions in cardiac output [10], deterioration in gas exchange [11-13] and decreases in splachnic-renal perfusion [14-16]. In surgical [17], trauma [2] and medical [6] critically patients, the IAH was an independent predictor factor of hospital mortalit
Clinical review: Humidifiers during non-invasive ventilation - key topics and practical implications
Antonio M Esquinas Rodriguez, Raffaele Scala, Arie Soroksky, Ahmed BaHammam, Alan de Klerk, Arschang Valipour, Davide Chiumello, Claude Martin, Anne E Holland
Critical Care , 2012, DOI: 10.1186/cc10534
Abstract: The human airway has an important role in heating and humidifying inspired gas, and recovering heat and moisture from expired gas. The amount of water vapor in a gas mixture can be measured as absolute humidity (AH) or relative humidity (RH) in relation to the temperature. AH is the total water present in the gas (mg H2O/L) and RH is the amount of water present expressed as the percentage of maximum carrying capacity at a given temperature [1]. The human airway must provide gas at core temperature and 100% RH at the alveolar surface in order to optimize gas exchange and protect lung tissue [2].Non-invasive ventilation (NIV) is a mechanical ventilation modality that does not utilize an invasive artificial airway (endotracheal tube or tracheostomy tube) [3]. NIV is usually delivered through a nasal or oro-nasal mask so the inspired gas passes through the upper airway where it is conditioned. Like during spontaneous breathing, patients under NIV require adequate humidification and heating of the inspired air (that is, gas conditioning) [3]. NIV delivers inspired air at high flow rates, which may overwhelm the usual airway humidification mechanisms. Inadequate gas conditioning has been associated with anatomical and functional deterioration of nasal mucosa (ciliary activity, mucus secretion, local blood flow, nasal resistance). In addition, there are also negative effects on tolerance to NIV when a patient breathes inadequately humidified air [1,3-5] (Table 1).Metaplastic changes and keratinization of the nasal epithelium and submucosa have been reported in patients on home-NIV when the level of humidification was inadequate for long periods [5]. These histopathological findings were confirmed by our recent survey, which found similar structural changes of the nasal mucosa in four patients with acute respiratory failure treated for 7 days with NIV without a humidification system added (unpublished data; Figure 1). This suggests that changes in the nasal mucosa occur rel
In vitro and in vivo evaluation of a new active heat moisture exchanger
Davide Chiumello, Paolo Pelosi, Gilbert Park, Andrea Candiani, Nicola Bottino, Ezio Storelli, Paolo Severgnini, Dunia D'Onofrio, Luciano Gattinoni, Massimo Chiaranda
Critical Care , 2004, DOI: 10.1186/cc2904
Abstract: We tested the efficiency by measuring the temperature and absolute humidity (AH) in vitro using a test lung ventilated at three levels of minute ventilation (5, 10 and 15 l/min) and at two tidal volumes (0.5 and 1 l), and in vivo in 42 patients with acute lung injury (arterial oxygen tension/fractional inspired oxygen ratio 283 ± 72 mmHg). We also evaluated the efficiency in vivo after 12 hours.In vitro, passive Performer and Hygrobac had higher airway temperature and AH (29.2 ± 0.7°C and 29.2 ± 0.5°C, [P < 0.05]; AH: 28.9 ± 1.6 mgH2O/l and 28.1 ± 0.8 mgH2O/l, [P < 0.05]) than did Hygroster (airway temperature: 28.1 ± 0.3°C [P < 0.05]; AH: 27 ± 1.2 mgH2O/l [P < 0.05]). Both devices suffered a loss of efficiency at the highest minute ventilation and tidal volume, and at the lowest minute ventilation. Active Performer had higher airway temperature and AH (31.9 ± 0.3°C and 34.3 ± 0.6 mgH2O/l; [P < 0.05]) than did Hygrobac and Hygroster, and was not influenced by minute ventilation or tidal volume. In vivo, the efficiency of passive Performer was similar to that of Hygrobac but better than Hygroster, whereas Active Performer was better than both. The active Performer exhibited good efficiency when used for up to 12 hours in vivo.This study showed that active Performer may provide adequate conditioning of inspired gases, both as a passive and as an active device.During normal breathing the upper airways condition inspired gases (i.e. with respect to heat and humidity) in order to prevent drying of the mucosal membranes and other structures [1]. However, during invasive mechanical ventilation, when the upper airways are bypassed with an endotracheal tube or tracheostomy, the inspired medical gases – if not conditioned – are heated and humidified by the lower airways with a large loss of heat and moisture from the respiratory mucosa [2]. Conditioning of medical gases by the lower airways causes severe damage to the respiratory epithelium [3], alterations in respiratory fun
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