Biomedical subjects

Luciano Gattinoni

Publications and source records attributed to Luciano Gattinoni.

At least 19 recordsLinked to original sources

PubMed2005

The concept of "baby lung".

BACKGROUND: The "baby lung" concept originated as an offspring of computed tomography examinations which showed in most patients with acute lung injury/acute respiratory distress syndrome that the normally aerated tissue has the dimensions of the lung of a 5- to 6-year-old child (300-500 g aerated tissue). DISCUSSION: The respiratory system compliance is linearly related to the "baby lung" dimensions, suggesting that the acute respiratory distress syndrome lung is not "stiff" but instead small, with nearly normal intrinsic elasticity. Initially we taught that the "baby lung" is a distinct anatomical structure, in the nondependent lung regions. However, the density redistribution in prone position shows that the "baby lung" is a functional and not an anatomical concept. This provides a rational for "gentle lung treatment" and a background to explain concepts such as baro- and volutrauma. CONCLUSIONS: From a physiological perspective the "baby lung" helps to understand ventilator-induced lung injury. In this context, what appears dangerous is not the V(T)/kg ratio but instead the V(T)/"baby lung" ratio. The practical message is straightforward: the smaller the "baby lung," the greater is the potential for unsafe mechanical ventilation.

Extracorporeal Membrane Oxygenation↗

PubMed2005

Pulmonary computed tomography and adult respiratory distress syndrome.

Computed tomography has completely changed the views and interpretation of ARDS, opening a new era in our understanding of the physiological, pathological and clinical aspects of this syndrome. In this brief review we will emphasize the most relevant new knowledge achieved using CT scanning and we will briefly discuss its clinical use in ARDS patients.

Animals↗

PubMed2005

Oxygen and carbon dioxide in the cerebral circulation during progression to brain death.

BACKGROUND: The authors propose that for a moderate reduction of perfusion during progressive irreversible ischemia, oxygen extraction increases to maintain aerobic metabolism, and arteriojugular oxygen difference (AJDo2) increases. Because of reduced carbon dioxide washout, venoarterial difference in carbon dioxide tension (DPco2) increases, with no change in the DPco2/AJDo2 ratio. With further reduction of cerebral perfusion, the aerobic metabolism will begin to decrease, AJDo2 will decrease while DPco2 will continue to increase, and the ratio will increase. When brain infarction develops, the metabolism will be abated, no oxygen will be consumed, and no carbon dioxide will be produced. METHODS: The authors studied 12 patients with acute cerebral damage that evolved to brain death and collected intermittent arterial and jugular blood samples. RESULTS: Four patterns were observed: (1) AJDo2 of 4.1 +/- 0.7 vol%, DPco2 of 6.5 +/- 1.9 mmHg, and a ratio of 1.55 +/- 0.3 with cerebral perfusion pressure of 62.5 +/- 13.4 mmHg; (2) a coupled increase of AJDo2 (5.8 +/- 0.7 vol%) and DPco2 (10.1 +/- 1.0 mmHg) with no change in ratio (1.92 +/- 0.14) and cerebral perfusion pressure (57.9 +/- 5.8 mmHg); (3) AJDo2 of 4.7 +/- 0.4 vol% with an increase in DPco2 (11.8 +/- 1 mmHg) and correspondingly higher ratio (2.7 +/- 0.2); in this phase, cerebral perfusion pressure was 39.7 +/- 10.5 mmHg; (4) immediately before diagnosis of brain death (cerebral perfusion pressure, 17 +/- 10.4 mmHg), there was a decrease of AJDo2 (1.1 +/- 0.1 vol%) and of DPco2 (5.3 +/- 0.6 mmHg) with a further ratio increase (5.1 +/- 0.8). CONCLUSIONS: Until compensatory mechanisms are effective, AJDo2 and DPco2 remain coupled. However, when the brain's ability to compensate for reduced oxygen delivery is exceeded, the ratio of DPco2 to AJDo2 starts to increase.

Adult↗

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↗

PubMed2005

Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study.

OBJECTIVE: Intraabdominal hypertension is associated with significant morbidity and mortality in surgical and trauma patients. The aim of this study was to assess, in a mixed population of critically ill patients, whether intraabdominal pressure at admission was an independent predictor for mortality and to evaluate the effects of intraabdominal hypertension on organ functions. DESIGN: Multiple-center, prospective epidemiologic study. SETTING: Fourteen intensive care units in six countries. PATIENTS: A total of 265 consecutive patients admitted for >24 hrs during the 4-wk study period. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Intraabdominal pressure was measured twice daily via the bladder. Data recorded on admission were the patient demographics with Simplified Acute Physiology Score II, Acute Physiology and Chronic Health Evaluation II score, and type of admission; during intensive care stay, Sepsis-Related Organ Failure Assessment score and intraabdominal pressure were measured daily together with fluid balance. Nonsurvivors had a significantly higher mean intraabdominal pressure on admission than survivors: 11.4 +/- 4.8 vs. 9.5 +/- 4.8 mm Hg. Independent predictors for mortality were age (odds ratio, 1.04; 95% confidence interval, 1.01-1.06; p = .003), Acute Physiology and Chronic Health Evaluation II score (odds ratio, 1.1; 95% confidence interval, 1.05-1.15; p < .0001), type of intensive care unit admission (odds ratio, 2.5 medical vs. surgical; 95% confidence interval, 1.24-5.16; p = .01), and the presence of liver dysfunction (odds ratio, 2.5; 95% confidence interval, 1.06-5.8; p = .04). The occurrence of intraabdominal hypertension during the intensive care unit stay was also an independent predictor of mortality (relative risk, 1.85; 95% confidence interval, 1.12-3.06; p = .01). Patients with intraabdominal hypertension at admission had significantly higher Sepsis-Related Organ Failure Assessment scores during the intensive care unit stay than patients without intraabdominal hypertension. CONCLUSIONS: Intraabdominal hypertension on admission was associated with severe organ dysfunction during the intensive care unit stay. The mean intraabdominal pressure on admission was not an independent risk factor for mortality; however, the occurrence of intraabdominal hypertension during the intensive care unit stay was an independent outcome predictor.

APACHE↗

PubMed2005

Monitoring of pulmonary mechanics in acute respiratory distress syndrome to titrate therapy.

PURPOSE OF REVIEW: This paper reviews recent findings regarding the respiratory mechanics during acute respiratory distress syndrome as a tool for tailoring its ventilatory management. RECENT FINDINGS: The pressure-volume curve has been used for many years as a descriptor of the respiratory mechanics in patients affected by acute respiratory distress syndrome. The use of the sigmoidal equation introduced by Venegas for the analysis of the pressure-volume curve seems to be the most rigorous mathematical approach to assessing lung mechanics. Increasing attention has been focused on the deflation limb for titration of positive end-expiratory pressure. Based on physiologic reasoning, a novel parameter, the stress index, has been proposed for tailoring a safe mechanical ventilation, although its clinical impact has still to be proved. Evidence has confirmed that a variety of underlying pathologies may lead to acute respiratory distress syndrome, making unrealistic any attempt to unify the ventilatory approach. Although extensively proposed to tailor mechanical ventilation during acute respiratory distress syndrome, there is no evidence that the pressure-volume curve may be useful in setting a lung-protective strategy in the presence of different potentials for recruitment. SUMMARY: The Venegas approach should be the standard analysis of pressure-volume curves. In any patient, the potential for recruitment should be assessed, as a basis for tailoring the most effective mechanical ventilation. Further studies are needed to clarify the potential use of the pressure-volume curve to guide a lung-protective ventilatory strategy.

Humans↗

PubMed2004

Effects of continuous negative extra-abdominal pressure on cardiorespiratory function during abdominal hypertension: an experimental study.

OBJECTIVE: To investigate whether negative extra-abdominal pressure (NEXAP) improves respiratory function and induces a blood shift from the intrathoracic compartment and to assess whether these effects are influenced by abdominal pressure. DESIGN AND SETTING: Prospective, randomized, controlled trial in the animal laboratory of a university hospital. SUBJECTS: Eight sedated and paralyzed pigs (19.6+/-3.4 kg). INTERVENTIONS: Application of NEXAP (-20 cmH(2)O). MEASUREMENTS AND RESULTS: Airway, esophageal, gastric and central venous pressures were recorded simultaneously. Intrathoracic blood volume was assessed by PiCCO. The effects of NEXAP were assessed with and without abdominal hypertension by intraperitoneal insufflation of helium. NEXAP caused a lasting drop of gastric (1.97+/-2.26 mmHg) and esophageal (1.21+/-0.67 mmHg) pressures, while end-expiratory airway pressure was similar, hence transpulmonary pressure increased. Intrathoracic blood volume dropped from 358+/-47 to 314+/-47 ml. The fall was associated with a decrease in central venous pressure (R(2)=0.820). When peritoneal pressure was raised (24.7+/-5.5 mmHg), the effects were less marked. However, the difference between negative pressure around the abdomen and the pressure inside the abdomen (effective NEXAP) was correlated with the proportional changes in intrathoracic blood volume (R(2)=0.648), being greater with more negative effective NEXAP. NEXAP improved chest wall elastance during abdominal hypertension (from 0.067+/-0.023 to 0.056+/-0.021 cmH(2)O/ml). CONCLUSIONS: NEXAP increases lung volume and causes a shift of blood from the intrathoracic compartment. It needs to be tailored against abdominal pressure to be effective.

Animals↗

PubMed2004

In vitro and in vivo evaluation of a new active heat moisture exchanger.

INTRODUCTION: In order to improve the efficiency of heat moisture exchangers (HMEs), new hybrid humidifiers (active HMEs) that add water and heat to HMEs have been developed. In this study we evaluated the efficiency, both in vitro and in vivo, of a new active HME (the Performer; StarMed, Mirandola, Italy) as compared with that of existing HMEs (Hygroster and Hygrobac; Mallinckrodt, Mirandola, Italy). METHODS: 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. RESULTS: In vitro, passive Performer and Hygrobac had higher airway temperature and AH (29.2 +/- 0.7 degrees C and 29.2 +/- 0.5 degrees 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 degrees 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 degrees 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. CONCLUSION: This study showed that active Performer may provide adequate conditioning of inspired gases, both as a passive and as an active device.

Acute Disease↗

PubMed2004

Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distress syndrome patients.

The importance of chest wall elastance in characterizing acute lung injury/acute respiratory distress syndrome patients and in setting mechanical ventilation is increasingly recognized. Nearly 30% of patients admitted to a general intensive care unit have an abnormal high intra-abdominal pressure (due to ascites, bowel edema, ileus), which leads to an increase in the chest wall elastance. At a given applied airway pressure, the pleural pressure increases according to (in the static condition) the equation: pleural pressure = airway pressure x (chest wall elastance/total respiratory system elastance). Consequently, for a given applied pressure, the increase in pleural pressure implies a decrease in transpulmonary pressure (airway pressure - pleural pressure), which is the distending force of the lung, implies a decrease of the strain and of ventilator-induced lung injury, implies the need to use a higher airway pressure during the recruitment maneuvers to reach a sufficient transpulmonary opening pressure, implies hemodynamic risk due to the reductions in venous return and heart size, and implies a possible increase of lung edema, partially due to the reduced edema clearance. It is always important in the most critically ill patients to assess the intra-abdominal pressure and the chest wall elastance.

Humans↗

PubMed2004

Prevalence of intra-abdominal hypertension in critically ill patients: a multicentre epidemiological study.

OBJECTIVE: Although intra-abdominal hypertension (IAH) can cause dysfunction of several organs and raise mortality, little information is available on the incidence and risk factors for IAH in critically ill patients. This study assessed the prevalence of IAH and its risk factors in a mixed population of intensive care patients. DESIGN: A multicentre, prospective 1-day point-prevalence epidemiological study conducted in 13 ICUs of six countries. INTERVENTIONS: None. PATIENTS: Ninety-seven patients admitted for more than 24 h to one of the ICUs during the 1-day study period. METHODS: Intra-abdominal pressure (IAP) was measured four times (every 6 h) by the bladder pressure method. Data included the demographics, medical or surgical type of admission, SOFA score, etiological factors such as abdominal surgery, haemoperitoneum, abdominal infection, massive fluid resuscitation, and ileus and predisposing conditions such as hypothermia, acidosis, polytransfusion, coagulopathy, sepsis, liver dysfunction, pneumonia and bacteraemia. RESULTS: We enrolled 97 patients, mean age 64+/-15 years, 57 (59%) medical and 40 (41%) surgical admission, SOFA score of 6.5+/-4.0. Mean IAP was 9.8+/-4.7 mmHg. The prevalence of IAH (defined as IAP 12 mmHg or more) was 50.5 and 8.2% had abdominal compartment syndrome (defined as IAP 20 mmHg or more). The only risk factor significantly associated with IAH was the body mass index, while massive fluid resuscitation, renal and coagulation impairment were at limit of significance. CONCLUSION: Although we found a quite high prevalence of IAH, no risk factors were reliably associated with IAH; consequently, to get valid information about IAH, IAP needs to be measured.

Abdomen↗

PubMed2004

A complication of amiodarone infusion.

A 76-year-old man underwent an emergency laparotoray for a ruptured abdominal aortic ancurysm After a few days he presented ischemia of the left side of the colon and subsequently atrial fibrillation developed that was treated with Amiodarone. After an intravascular loading dose of 300 mg, he received a maintenance dose of 600 mg daily through a central line access. After 28 days of intravascular drug therapy, a chest X-ray showed a high attenuation homogeneous image in the right part of the mediastinum. A contrast enhanced thoracic and abdominal computed tomography scan showed: a high attenuation intravascular mass in the superior vena cava around the catheter. The catheter was substituted but the intravascular mass remained. The Amiodarone was then given by mouth. The mass spontaneously decreased its size and after three months completely disappeared Due to high iodine content, any deposition of Amiodarone can be detected by a radiological study as a high attenuation image. After reviewing all the drugs infused through the catheter, we did not find any other drugs that contain iodine or other material that could justify the chest X-ray image. We hypothesized that this intravascular mass was due to a deposition of the Amiodarone during the infusion in the central line

Administration, Oral↗

PubMed2004

Ventilatory management of acute respiratory distress syndrome: a consensus of two.

OBJECTIVE: To synthesize the emerging body of experimental, observational, and clinical trial data into a practical guideline for safe and effective ventilatory management of acute respiratory distress syndrome. DATA SOURCES: Relevant, peer-reviewed, scientific literature and personal observations from clinical practice. STUDY SELECTION: Relevant experimental studies and high-impact observational and clinical trials of acute respiratory distress syndrome management. DATA EXTRACTION: Detailed review of information contained in published scientific work. DATA SYNTHESIS: Interactive discussions between the authors that culminated in our consensus view of appropriate management. CONCLUSIONS: Prevention of ventilator-induced lung injury while accomplishing the essential life-supporting roles of mechanical ventilation is a complex undertaking that requires application of principles founded on a broad experimental and clinical database and on the results of well-executed clinical trials. At the bedside, execution of an effective lung-protective ventilation strategy remains an empirical process best guided by integrated physiology and a readiness to revise the management approach depending on the individual's response.

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

Volume of activity and occupancy rate in intensive care units. Association with mortality.

OBJECTIVE: Mortality after many procedures is lower in centers where more procedures are done. It is controversial whether this is true for intensive care units, too. We examined the relationship between the volume of activity of intensive care units (ICUs) and mortality by a measure of risk-adjusted volume of activity specific for ICUs. DESIGN: Prospective, multicenter, observational study. SETTING: Eighty-nine ICUs in 12 European countries. PATIENTS: During a 4-month study period, 12,615 patients were enrolled. INTERVENTIONS: Demographic and clinical statistics, severity at admission and a score of nursing complexity and workload were collected. RESULTS: Total volume of activity was defined as the number of patients admitted per bed per year, high-risk volume as the number of high-risk patients admitted per bed per year (selected combining of length of stay and severity of illness). A multi-step risk-adjustment process was planned. ICU volume corresponding both to overall [odds ratio (OR) 0.966] and 3,838 high-risk (OR 0.830) patients was negatively correlated with mortality. Relative mortality decreased by 3.4 and 17.0% for every five extra patients treated per bed per year in overall volume and high-risk volume, respectively. A direct relationship was found between mortality and the ICU occupancy rate (OR 1.324 and 1.351, respectively). CONCLUSIONS: Intensive care patients, whatever their level of risk, are best treated where more high-risk patients are treated. Moreover, the higher the ICU occupancy rate, the higher is the mortality.

Critical Illness↗

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↗