Biomedical subjects

Eleonora Carlesso

Publications and source records attributed to Eleonora Carlesso.

8 recordsLinked to original sources

PubMed2005

How to ventilate patients with acute lung injury and acute respiratory distress syndrome.

PURPOSE OF REVIEW: The purpose of this paper is to review the mechanisms of ventilator-induced lung injury as a basis for providing the less damaging mechanical ventilation in patients with acute respiratory failure. RECENT FINDINGS: In normal lungs, high tidal volume causes an immediate gene upregulation and downregulation. Although the importance of alveolar inflammatory reaction is well known, recent findings suggest the potential role of airway distension in causing ventilator-induced lung injury. The initial activation has been shown to occur in the airways, accounting for the damages induced by high peak flow. The healthier lung regions are more exposed to the injury, since they may be subjected to strain. Challenge with endotoxin enhances in a synergistic manner the pulmonary inflammation induced by mechanical ventilation. However, mechanical strain and endotoxin seem to trigger lung inflammation through two different pathways. Despite convincing experimental and clinical evidences of lung injury, the clinical implementation of low tidal volume ventilation is still limited and has not yet become part of standard clinical practice. Setting positive end-expiratory pressure remains an open problem because the ALVEOLI study did not provide any exhaustive answers, likely because of methodologic problems and, unphysiologic design. SUMMARY: Gentle lung ventilation must be standard practice. Because stress and strain are the triggers of ventilator-induced lung injury, their clinical equivalents should be measured (transpulmonary pressure and the ratio between tidal volume and end-expiratory lung volume). For a rational application of positive end-expiratory pressure, the potential for recruitment in any single patient should be estimated.

Animals↗

PubMed2005

Prone position delays the progression of ventilator-induced lung injury in rats: does lung strain distribution play a role?

OBJECTIVE: To investigate if prone position delays the progression of experimental ventilator-induced lung injury, possibly due to a more homogeneous distribution of strain within lung parenchyma. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory of a university hospital. SUBJECTS: Thirty-five Sprague Dawley male rats (weight 257 +/- 45 g). INTERVENTIONS: Mechanical ventilation in either supine or prone position and computed tomography scan analysis. MEASUREMENTS: : Animals were ventilated in supine (n = 15) or prone (n = 15) position until a similar ventilator-induced lung injury was reached. To do so, experiments were interrupted when respiratory system elastance was 150% of baseline. Ventilator-induced lung injury was assessed as lung wet-to-dry ratio and histology. Time to reach lung injury was considered as a main outcome measure. In five additional animals, computed tomography scans (GE Light Speed QX/I, thickness 1.25 mm, interval 0.6 mm, 100 MA, 100 Kv) were randomly taken at end-expiration and end-inspiration in both positions, and quantitative analysis was performed. Data are shown as mean +/- sd. MEASUREMENTS AND MAIN RESULTS: Similar ventilator-induced lung injury was reached (respiratory system elastance, wet-to-dry ratio, and histology). The time taken to achieve the target ventilator-induced lung injury was longer with prone position (73 +/- 37 mins vs. 112 +/- 42, supine vs. prone, p = .011). Computed tomography scan analysis performed before lung injury revealed that at end-expiration, the lung was wider in prone position (p = .004) and somewhat shorter (p = .09), despite similar lung volumes (p = .455). Lung density along the vertical axis increased significantly only in supine position (p = .002). Lung strain was greater in supine as opposed to prone position (width strain, 7.8 +/- 1.8% vs. 5.6 +/- 0.9, supine vs. prone, p = .029). CONCLUSIONS: Prone position delays the progression of ventilator-induced lung injury. Computed tomography scan analysis suggests that a more homogeneous distribution of strain may be implicated in the protective role of prone position against ventilator-induced lung injury.

Animals↗

PubMed2004

Acute respiratory distress syndrome, the critical care paradigm: what we learned and what we forgot.

In the last several years, we definitely learned that the acute respiratory distress syndrome lung is small, nonhomogeneous, and that mechanical ventilation in this baby lung may cause physical damage as well as inflammatory reaction. The clinical benefit of the gentle lung treatment, based on a decrease of global/regional stress and strain into the lung, has been finally proved. However, we forgot the importance of lung perfusion and its distribution in this syndrome and, besides a low tidal volume, we still do not know how to handle the other variables of mechanical ventilation. Measurements of variables as transpulmonary pressure and end expiratory lung volume, for a rational setting of mechanical ventilation, should be introduced in routine clinical practice.

Humans↗

PubMed2003

An increase of abdominal pressure increases pulmonary edema in oleic acid-induced lung injury.

Increased abdominal pressure is common in intensive care unit patients. To investigate its impact on respiration and hemodynamics we applied intraabdominal pressure (aIAP) of 0 and 20 cm H(2)O (pneumoperitoneum) in seven pigs. The whole-lung computed tomography scan and a complete set of respiratory and hemodynamics variables were recorded both in healthy lung and after oleic acid (OA) injury. In healthy lung, aIAP 20 cm H(2)O significantly lowered the gas content, leaving the tissue content unchanged. In OA-injured lung at aIAP 0 cm H(2)O, the gas content significantly decreased compared with healthy lung. The excess tissue mass (edema) amounted to 30 +/- 24% of the original tissue weight (455 +/- 80 g). The edema was primarily distributed in the base regions and was not gravity dependent. Heart volume, central venous, pulmonary artery, wedge, and systemic arterial pressures significantly increased. At aIAP 20 cm H(2)O in OA-injured lung, the central venous and pulmonary artery pressures further increased. The gas content further decreased, and the excess tissue mass rose up to 103 +/- 37% (tissue weight 905 +/- 134 g), with homogeneous distribution along the cephalocaudal and sternovertebral axis. We conclude that in OA-injured lung, the increase of IAP increases the amount of edema.

Abdomen↗

PubMed2003

Intra-abdominal pressure may be decreased non-invasively by continuous negative extra-abdominal pressure (NEXAP).

OBJECTIVE: To investigate the possibility of artificially decreasing intra-abdominal pressure (IAP) by applying continuous negative pressure around the abdomen. MATERIAL AND METHODS: We investigated the effects of negative extra-abdominal pressure (NEXAP) on IAP and central venous pressure (CVP) in 30 patients admitted to our intensive care unit (age 57+/-17 years, BMI 26.1+/-4.0 kg/m2, SAPS II 41.8+/-17.0). Patients with severe hemodynamic instability and/or those admitted following a laparotomy were not studied. Measurements included bladder pressure as an estimate of IAP, CVP, invasive mean arterial pressure (MAP) and heart rate (HR). In five patients extensive hemodynamic measurements were also taken using a Swan-Ganz catheter. Following measurements at baseline (Basal), NEXAP (Life Care - Nev 100, Respironics) was applied on the abdomen, in random order, at a pressure equal to IAP (NEXAP0), 5 cmH(2)O (NEXAP-5) or 10 cmH(2)O (NEXAP-10) more negative than NEXAP0. RESULTS: Basal IAP ranged from 4 to 22 mmHg. NEXAP decreased IAP from 8.7+/-4.3 mmHg to 6+/-4.2 (Basal vs NEXAP0 p<0.001). There was a further decrease of IAP when more negative pressure was applied: 4.3+/-3.2 mmHg, 3.8+/-3.7 mmHg (NEXAP-5 and NEXAP-10 vs NEXAP0, respectively, p<0.001). Similarly, CVP decreased from 9.3+/-3.4 mmHg to 7.5+/-3.8 (Basal vs NEXAP-10, p<0.001). The lower the IAP when NEXAP was applied, the lower the CVP (r2=0.778, p<0.001, multiple linear regression). When measured, cardiac output did not significantly change with NEXAP. CONCLUSIONS: Negative extra-abdominal pressure may be applied in critically ill patients to decrease intra-abdominal pressure non-invasively.

Abdomen↗

PubMed2003

Noninvasive positive pressure ventilation delivered by helmet vs. standard face mask.

OBJECTIVE: This bench and human study compared large and small helmets with face mask (FM) for delivery of noninvasive positive pressure ventilation. DESIGN: A lung simulator was employed, and the human study involved six healthy subjects. We evaluated a continuous high-flow (CPAPHF), low flow (CPAPLF), ventilator (CPAPVENT) CPAP, and pressure support ventilation (PSV 10 and 20 cmH2O). In the human study we used CPAPHF, CPAPVENT, and PSV 5 cmH2O. PEEP was 5 cmH2O. MEASUREMENTS: In the bench study during CPAP we measured the negative airway pressure time product (areaCPAP), i.e., the area of airway pressure (Paw) under PEEP and during PSV the pressure airway time product (areaPSV), i.e., the area of Paw from onset to end of inspiratory flow. In the human study we measured the breathing pattern and work of breathing (WOB). RESULTS: In the bench study during CPAPLF the helmets had a lower areaCPAP than the FM, while during CPAPHF the three interfaces had similar areaCPAP. Using CPAPVENT and PSV the FM reduced areaCPAP and increased areaPSV compared to helmets. At 20 cmH2O of PSV using helmets areaPSV was similar to that obtained at 10 cmH2O of PSV using the FM. In human study using CPAPHF and CPAPVENT the tree interfaces had similar effects on breathing pattern and WOB, while using PSV the FM reduced WOB more than helmets. CONCLUSIONS: During CPAPLF helmets were more efficient than FM, while during CPAPHF the three interfaces were comparable. Using CPAPVENT and PSV, FM was more efficient than helmets

Equipment Design↗

PubMed2003

Physiologic rationale for ventilator setting in acute lung injury/acute respiratory distress syndrome patients.

OBJECTIVES: To review the physiologic approach to setting mechanical ventilation in acute lung injury/acute respiratory distress syndrome. DATA SOURCES: MEDLINE search from 1979 to the present. DATA SELECTION: Personal selection of some articles we believe relevant for understanding acute lung injury/acute respiratory distress syndrome physiopathology and its physiologic management. DATA SUMMARY: Knowing the underlying pathology is key to estimating the potential for recruitment. The potential for recruitment is rather low when the consolidation of pulmonary units exceeds collapse, as in diffuse pneumonia. In contrast, when pulmonary unit collapse exceeds consolidation, as in acute lung injury/acute respiratory distress syndrome from extrapulmonary origin, the potential for recruitment may be high. To exploit the potential for recruitment, a transpulmonary pressure greater than the opening pressure must be applied to the lung. To do so, chest wall elastance must be measured or estimated. To avoid collapse after recruitment, a positive end-expiratory pressure greater than the compressive forces operating on the lung and an alveolar ventilation sufficient to prevent absorption atelectasis must be provided. Indeed, avoidance of stretch (low airway plateau pressure) and prevention of cyclic collapse and reopening (adequate positive end-expiratory pressure and alveolar ventilation) are the physiologic cornerstones of mechanical ventilation in acute lung injury/acute respiratory distress syndrome. When considering all the randomized clinical trials reported so far, it is tempting to speculate that transpulmonary pressure and stresses, rather than tidal volume per se, are the key factors that may have an impact on mortality. CONCLUSIONS: The majority of physiologic, experimental, and clinical trial data converge on one simple concept: treat the lung gently.

Humans↗

PubMed2003

Decrease in PaCO2 with prone position is predictive of improved outcome in acute respiratory distress syndrome.

OBJECTIVE: To determine whether gas exchange improvement in response to the prone position is associated with an improved outcome in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). DESIGN: Retrospective analysis of patients in the pronation arm of a controlled randomized trial on prone positioning and patients enrolled in a previous pilot study of the prone position. SETTING: Twenty-eight Italian and two Swiss intensive care units. PATIENTS: We studied 225 patients meeting the criteria for ALI or ARDS. INTERVENTIONS: Patients were in prone position for 10 days for 6 hrs/day if they met ALI/ARDS criteria when assessed each morning. Respiratory variables were recorded before and after 6 hrs of pronation with unchanged ventilatory settings. MEASUREMENTS AND MAIN RESULTS: We measured arterial blood gas alterations to the first pronation and the 28-day mortality rate. The independent risk factors for death in the general population were the Pao2/Fio2 ratio (odds ratio, 0.992; confidence interval, 0.986-0.998), the minute ventilation/Paco2 ratio (odds ratio, 1.003; confidence interval, 1.000-1.006), and the concentration of plasma creatinine (odds ratio, 1.385; confidence interval, 1.116-1.720). Pao2 responders (defined as the patients who increased their Pao2/Fio2 by > or =20 mm Hg, 150 patients, mean increase of 100.6 +/- 61.6 mm Hg [13.4 +/- 8.2 kPa]) had an outcome similar to the nonresponders (59 patients, mean decrease -6.3 +/- 23.7 mm Hg [-0.8 +/- 3.2 kPa]; mortality rate 44% and 46%, respectively; relative risk, 1.04; confidence interval, 0.74-1.45, p =.65). The Paco2 responders (defined as patients whose Paco2 decreased by > or =1 mm Hg, 94 patients, mean decrease -6.0 +/- 6 mm Hg [-0.8 +/- 0.8 kPa]) had an improved survival when compared with nonresponders (115 patients, mean increase 6 +/- 6 mm Hg [0.8 +/- 0.8 kPa]; mortality rate 35.1% and 52.2%, respectively; relative risk, 1.48; confidence interval, 1.07-2.05, p =.01). CONCLUSION: ALI/ARDS patients who respond to prone positioning with reduction of their Paco2 show an increased survival at 28 days. Improved efficiency of alveolar ventilation (decreased physiologic deadspace ratio) is an important marker of patients who will survive acute respiratory failure.

Aged↗