Biomedical subjects

Pietro Caironi

Publications and source records attributed to Pietro Caironi.

7 recordsLinked to original sources

PubMed2005

5-Lipoxygenase deficiency prevents respiratory failure during ventilator-induced lung injury.

RATIONALE: Mechanical ventilation with high VT (HVT) progressively leads to lung injury and decreased efficiency of gas exchange. Hypoxic pulmonary vasoconstriction (HPV) directs blood flow to well-ventilated lung regions, preserving systemic oxygenation during pulmonary injury. Recent experimental studies have revealed an important role for leukotriene (LT) biosynthesis by 5-lipoxygenase (5LO) in the impairment of HPV by endotoxin. OBJECTIVES: To investigate whether or not impairment of HPV contributes to the hypoxemia associated with HVT and to evaluate the role of LTs in ventilator-induced lung injury. METHODS: We studied wild-type and 5LO-deficient mice ventilated for up to 10 hours with low VT (LVT) or HVT. RESULTS: In wild-type mice, HVT, but not LVT, increased pulmonary vascular permeability and edema formation, impaired systemic oxygenation, and reduced survival. HPV, as reflected by the increase in left pulmonary vascular resistance induced by left mainstem bronchus occlusion, was markedly impaired in animals ventilated with HVT. HVT ventilation increased bronchoalveolar lavage levels of LTs and neutrophils. In 5LO-deficient mice, the HVT-induced increase of pulmonary vascular permeability and worsening of respiratory mechanics were markedly attenuated, systemic oxygenation was preserved, and survival increased. Moreover, in 5LO-deficient mice, HVT ventilation did not impair the ability of left mainstem bronchus occlusion to increase left pulmonary vascular resistance. Administration of MK886, a 5LO-activity inhibitor, or MK571, a selective cysteinyl-LT(1) receptor antagonist, largely prevented ventilator-induced lung injury. CONCLUSIONS: These results indicate that LTs play a central role in the lung injury and impaired oxygenation induced by HVT ventilation.

Animals↗

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

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

Continuous positive airway pressure delivered with a "helmet": effects on carbon dioxide rebreathing.

OBJECTIVE: The "helmet" has been used as a novel interface to deliver noninvasive ventilation without applying direct pressure on the face. However, due to its large volume, the helmet may predispose to CO2 rebreathing. We hypothesized that breathing with the helmet is similar to breathing in a semiclosed environment, and therefore the PCO2 inside the helmet is primarily a function of the subject's CO2 production and the flow of fresh gas through the helmet. DESIGN: Human volunteer study. SETTING: Laboratory in a university teaching hospital. SUBJECTS: Eight healthy volunteers. INTERVENTIONS: We delivered continuous positive airway pressure (CPAP) with the helmet under a variety of ventilatory conditions in a lung model and in volunteers. MEASUREMENTS AND MAIN RESULTS: Gas flow and CO2 concentration at the airway were measured continuously. End-tidal PCO2, CO2 production, and ventilatory variables were subsequently computed. We found that a) when CPAP was delivered with a ventilator, the inspired CO2 of the volunteers was high (12.4 +/- 3.2 torr [1.7 +/- 0.4 kPa]); b) when CPAP was delivered with a continuous high flow system, inspired CO2 of the volunteers was low (2.5 +/- 1.2 torr [0.3 +/- 0.2 kPa]); and c) the inspired CO2 calculated mathematically for a semiclosed system model of CO2 rebreathing was highly correlated with the values measured in a lung model (r = .97, slope = 0.92, intercept = -1.17, p < .001) and in the volunteers (r = .94, slope = 0.96, intercept = 0.90, p < .001). CONCLUSIONS: a) The helmet predisposes to CO2 rebreathing and should not be used to deliver CPAP with a ventilator; b) continuous high flow minimizes CO2 rebreathing during CPAP with the helmet; and c) minute ventilation and Pco2 should be monitored during CPAP with the helmet.

Adult↗

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

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↗

PubMed2002

Sigh in supine and prone position during acute respiratory distress syndrome.

Interventions aimed at recruiting the lung of patients with acute respiratory distress syndrome (ARDS) are not uniformly effective. Because the prone position increases homogeneity of inflation of the lung, we reasoned that it might enhance its potential for recruitment. We ventilated 10 patients with early ARDS (PaO2/FIO2, 121 +/- 46 mm Hg; positive end-expiratory pressure, 14 +/- 3 cm H2O) in supine and prone, with and without the addition of three consecutive "sighs" per minute to recruit the lung. Inspired oxygen fraction, positive end-expiratory pressure, and minute ventilation were kept constant. Sighs increased PaO2 in both supine and prone (p < 0.01). The highest values of PaO2 (192 +/- 41 mm Hg) and end-expiratory lung volume (1840 +/- 790 ml) occurred with the addition of sighs in prone and remained significantly elevated 1 hour after discontinuation of the sighs. The increase in PaO2 associated with the sighs, both in supine and prone, correlated linearly with the respective increase of end-expiratory lung volume (r = 0.82, p < 0.001). We conclude that adding a recruitment maneuver such as cyclical sighs during ventilation in the prone position may provide optimal lung recruitment in the early stage of ARDS.

Aged↗