Biomedical subjects
J J Marini
Publications and source records attributed to J J Marini.
PEEP in the prone position: reversing the perfusion imbalance.
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Effects of mean airway pressure and tidal excursion on lung injury induced by mechanical ventilation in an isolated perfused rabbit lung model.
OBJECTIVE: To study the relative contributions of mean airway pressure (mPaw) and tidal excursion (V(T)) to ventilator-induced lung injury under constant perfusion conditions. DESIGN: Prospective, randomized study. SETTING: Experimental animal laboratory. SUBJECTS: Fifteen sets of isolated rabbit lungs. INTERVENTIONS: Rabbit lungs were perfused (constant flow, 500 mL/min; capillary pressure, 10 mm Hg) and randomized to be ventilated at identical peak transpulmonary pressure (pressure control ventilation [30 cm H2O and frequency of 20/min]) with three different ventilatory patterns that differed from each other by either mPaw or V(T): group A (low mPaw [13.4+/-0.2 cm H2O]/large V(T) [55+/-8 mL], n = 5); group B (high mPaw [21.2+/-0.2 cm H2O]/small V(T) [18+/-1 mL], n = 5); and group C (high mPaw [21.8+/-0.5 cm H2O]/large V(T) [53+/-5 mL], n = 5). MEASUREMENTS AND MAIN RESULTS: Continuous weight gain (edema formation), change in ultrafiltration coefficient (deltaKf, vascular permeability index), and histology (lung hemorrhage) were examined. In group A, deltaKf (0.08+/-0.08 g/min/cm H2O/100 g) was less than in group B (0.28+/-0.19 g/min/cm H2O/100 g) or group C (0.41+/-0.29 g/min/cm H2O/100 g) (p = .05). Group A experienced significantly less hemorrhage (histologic score, 5.4+/-2.2) than groups B (10.3+/-2.1) and C (11.1+/-3.0) (p < .05). A similar trend was observed for weight gain. In contrast to tidal excursion, mPaw was found to be a significant factor for lung hemorrhage and increased Kf (two-way analysis of variance; p < .05). Weight gain (r2 = .54, p = .04) and lung hemorrhage (r2 = .65, p = .01) correlated with the mean pulmonary artery pressure changes that resulted from the implementation of the ventilatory strategies. The difference between the changes in mPaw and mean pulmonary artery pressure linearly predicted deltaKf (p = .005 and .05, respectively, r2 = 0.73). CONCLUSIONS: Under these experimental conditions, mPaw contributes more than tidal excursion to lung hemorrhage and permeability alterations induced by mechanical ventilation.
The American-European Consensus Conference on ARDS, part 2. Ventilatory, pharmacologic, supportive therapy, study design strategies and issues related to recovery and remodeling.
The acute respiratory distress syndrome (ARDS) continues as a contributor to the morbidity and mortality of patients in intensive care units throughout the world, imparting tremendous human and financial costs. During the last ten years there has been a decline in ARDS mortality without a clear explanation. The American-European Consensus Committee on ARDS was formed to re-evaluate the standards for the ICU care of patients with acute lung injury (ALI), with regard to ventilatory strategies, the more promising pharmacologic agents, and the definition and quantification of pathological features of ALI that require resolution. It was felt that the definition of strategies for the clinical design and coordination of studies between centers and continents was becoming increasingly important to facilitate the study of various new therapies for ARDS.
Round table conference: acute lung injury, 15th-17th March 1997 Brussels, Belgium.
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Noninvasive ventilation: an emerging supportive technique for the emergency department.
Noninvasive ventilation (NIV) is the provision of ventilatory support to a spontaneously breathing patient without endotracheal intubation. In this review, we detail concerns related to endotracheal intubation and summarize the physiologic effects and clinical application of NIV. We then address the use of NIV in 5 conditions of particular interest to the practitioner of emergency medicine: exacerbated chronic obstructive lung disease, severe asthma, patients who are not candidates for endotracheal intubation, pneumonia, and pulmonary edema.
Phasic expiratory tracheal gas insufflation: short but sweet.
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Transfusion triggers and Occam's rusty razor.
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The American-European Consensus Conference on ARDS, part 2: Ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling. Acute respiratory distress syndrome.
The acute respiratory distress syndrome (ARDS) continues as a contributor to the morbidity and mortality of patients in intensive care units throughout the world, imparting tremendous human and financial costs. During the last 10 years there has been a decline in ARDS mortality without a clear explanation. The American-European Consensus Committee on ARDS was formed to re-evaluate the standards for the ICU care of patients with acute lung injury (ALI), with regard to ventilatory strategies, the more promising pharmacologic agents, and the definition and quantification of pathologic features of ALI that require resolution. It was felt that the definition of strategies for the clinical design and coordination of studies between centers and continents was becoming increasingly important to facilitate the study of various new therapies for ARDS.
Consequences of vascular flow on lung injury induced by mechanical ventilation.
To investigate whether the magnitude of blood flow contributes to ventilator-induced lung injury, 14 sets of isolated rabbit lungs were randomized for perfusion at either 300 (Group A: n = 7) or 900 ml/ min (Group B: n = 7) while ventilated with 30 cm H2O peak static pressure. Control lungs (Group C: n = 7) were ventilated with lower peak static pressure (15 cm H2O) and perfused at 500 ml/min. Weight gain, changes in the ultrafiltration coefficient (DeltaKf) and lung static compliance (CL), and extent of hemorrhage (scored by histology) were compared. Group B had a larger decrease in CL (-13 +/- 11%) than Groups A (2 +/- 6%) and C (5 +/- 5%) (p < 0.05). Group B had more hemorrhage and gained more weight (16.2 +/- 9.5 g) than Groups A (8.7 +/- 3.4 g) and C (1.6 +/- 1.0 g) (p < 0.05 for each pairwise comparison between groups). Finally, Kf (g . min-1 . cm H2O-1 . 100 g-1) increased the most in Group B (DeltaKf = 0.26 +/- 0. 20 versus 0.17 +/- 0.10 in Group A and 0.05 +/- 0.04 in Group C; p < 0.05 for B versus C). We conclude that the intensity of lung perfusion contributes to ventilator- induced lung injury in this model.
A lung-protective approach to ventilating ARDS.
A convincing and internally consistent body of literature now suggests that the traditional high tidal volume, normoxic, normacapnic ventilation paradigm may retard healing of the acutely injured lung. A growing number of practitioners are now shifting first priority from optimizing gas exchange, oxygen delivery, or respiratory system compliance to ensuring adequate lung protection. This article reviews the basis for concern about traditional ventilatory support in ARDS and develops an approach based on current evidence and newer options for management.
Patient-ventilator interaction: a general model for nonpassive mechanical ventilation.
A general mathematical model for the dynamic behaviour of a single-compartment respiratory system in response to an arbitrary applied inspiratory airway pressure and arbitrary respiratory muscle activity is investigated. The model is used to compute explicit expressions for ventilation and pressure variables of clinical interest for clinician-selected and impedance-determined inputs. The outcome variables include tidal volume, end-expiratory pressure, minute ventilation, mean alveolar pressure, average pleural pressure, as well as the work performed by the ventilator and the respiratory muscles. It is also demonstrated that under suitable conditions, there is a flow reversal that can occur during inspiration.
Streamlining critical care: responsibilities and cost-effectiveness in intensive-care unit organization.
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Influence of prone position on the extent and distribution of lung injury in a high tidal volume oleic acid model of acute respiratory distress syndrome.
OBJECTIVE: To evaluate the influence of body position on the extent and distribution of experimental lung damage in an oleic acid canine model of acute respiratory distress syndrome, using mechanical ventilation with high tidal volumes and positive end-expiratory pressure (PEEP). DESIGN: Prospective, randomized study. SETTING: Experimental animal laboratory. SUBJECTS: Twelve anesthetized and paralyzed dogs. INTERVENTIONS: Ninety minutes after lung injury was induced by injection of oleic acid, 12 animals were randomized to be ventilated for 4 hrs, in either the supine (supine group, n = 6) or prone (prone group, n = 6) positions, using the same ventilatory pattern (F10(2) 0.6, PEEP > or = 10 cm H2O, and a tidal volume that generated a peak transpulmonary pressure of 35 cm H2O when implemented in the supine position). Regardless of randomization to position, the tidal volumes, F10(2), and PEEP were kept constant and the pulmonary artery occlusion pressure was maintained between 4 and 6 mm Hg for the duration of the study. MEASUREMENTS AND MAIN RESULTS: At the end of the protocol, the lungs were excised for gravimetric determination (wet/dry weight ratio) and histologic examination (histologic score). Changes over time in the static pressure-volume curve of the lungs (obtained in the supine position) were also used as end-point variables. At baseline, hemodynamic and respiratory variables did not differ between groups. Just before randomization to position (90 mins after oleic acid injection), both groups presented similar lung static pressure-volume curves. Pulmonary artery occlusion pressure (4.3 +/- 1.9 vs. 4.8 +/- 1.3 mm Hg [supine vs. prone group]), cardiac output (4.1 +/- 0.4 vs. 5.2 +/- 1.3 L/min [supine vs. prone group]), and venous admixture (36.7 +/- 20.7% vs. 28.3 +/- 19.4% [supine vs. prone group]) were also not significantly (p > .05) different when measured in the supine position. At the end of the experiment, lung gravimetric data in the two experimental groups were not statistically different, suggesting a similar extent of edema. Histologic abnormalities, however, were less in the prone group than in the supine group (p < .01), due primarily to marked differences in extent and severity in the dependent regions of the lungs. Static lung compliance improved over time in the prone group (34 +/- 9 to 46 +/- 19 mL/cm H2O)(p = .02), but not in the supine group (34 +/- 6 to 36 +/- 6 mL/cm H2O). CONCLUSIONS: After oleic acid-induced lung injury, animals ventilated with high tidal volume and PEEP undergo less extensive histologic change in the prone position than in the supine position. The prone position alters the distribution of histologic abnormalities.
Effect of mechanical ventilation strategy on dissemination of intratracheally instilled Escherichia coli in dogs.
OBJECTIVE: To test the effect of different mechanical ventilation strategies on dissemination of intratracheally instilled Escherichia coli in dogs and to determine the extent and distribution of lung damage. DESIGN: Prospective, randomized study. SETTING: Experimental animal laboratory. SUBJECTS: Eighteen anesthetized and paralyzed dogs. INTERVENTIONS: We studied the effect of three ventilatory strategies based on two variables: transpulmonary pressure and positive end-expiratory pressure (PEEP). Group 1 animals (n = 6) were ventilated with a PEEP of 3 cm H2O and a tidal volume of 15 mL/kg, which generated an end-inspiratory transpulmonary pressure of < or = 15 cm H2O. In group 2(n = 6), tidal volume was adjusted to generate a transpulmonary pressure of 35 cm H2O and PEEP was set to 3 cm H2O. In group 3(n = 6), tidal volume was also adjusted to yield a transpulmonary pressure of 35 cm H2O but PEEP was set to 10 cm H2O. In each group, we instilled approximately 10(8) colony-forming units of E. coli into the trachea of the dogs and ventilated them with the chosen tidal volume and PEEP for 6 hrs afterward. MEASUREMENTS AND MAIN RESULTS: We measured the pressure-volume relationship (pressure-volume curve) of the respiratory system before and 6 hrs after bacterial instillation. We obtained blood cultures before and 0.5, 1,2,3,4,5, and 6 hrs after bacterial instillation. After 6 hrs, the lungs were removed for histologic (histologic score) and gravimetric (wet-to-dry weight ratio, WW/DW) analysis. During the experiment 0, 5, and 1 dogs developed positive blood cultures in groups 1, 2, and 3, respectively. The number of dogs that developed bacteremia in group 2 was significantly greater than in the other two groups (p < .05). In group 1, pressure-volume curves demonstrated a lower inflection point which was greater than the end-inspiratory transpulmonary pressure suggesting that low transpulmonary pressure/low PEEP strategy ventilated aerated regions without expanding atelectatic areas. In group 2, pressure-volume curves demonstrated both a lower inflection point and an upper deflection point which were spanned by the tidal volume, suggesting that high transpulmonary pressure/low PEEP strategy might have caused both overdistention and cyclic closure and reopening. In group 3, pressure-volume curves demonstrated only a upper deflection point which was less than the maximal alveolar tidal pressure. At the end of the experimental protocol, group 2 manifested the most lung injury as assessed by gravimetric and histologic indices of lung injury. WW/DW of group 2(13.1 +/- 1.0 (SD); p < .05) was greater than groups 1 and 3(7.5 +/- 1.2 and 8.6 +/- 1.0, respectively). Similarly, the overall weighted histologic injury score for group 2 (1.19 +/- 0.26; p < .02) was greater than for groups 1 and 3 (0.82 +/- 0.20 and 0.88 +/- 0.22, respectively). For groups 2 and 3, the overall weighted histologic injury scores of the dependent regions were greater than the nondependent regions (p < .004). CONCLUSIONS: We conclude that the ventilatory strategy most likely to overdistend the lungs while allowing repetitive opening and closure of alveoli (group 2) facilitated bacterial translocation from the alveoli to the bloodstream and increased lung injury, as determined by histologic and gravimetric analysis. PEEP ameliorated these effects, despite lung overdistention, but increased histologic and gravimetric indices of lung injury in dependent as compared with the nondependent regions.
Theoretical interactions between ventilator settings and proximal deadspace ventilation during tracheal gas insufflation.
OBJECTIVE: To investigate the theoretical interactions between ventilator settings, tracheal gas insufflation (TGI), and alveolar ventilation. DESIGN: We derived differential equations governing compartmental volume changes in a one-compartment model of TGI-assisted ventilation and equations governing gas dilution in the airway proximal to the TGI catheter and the additional CO2 clearing ventilation arising from this dilution. This additional ventilation was called proximal ventilation. Validation was conducted in a mechanical lung analog. Model predictions for proximal ventilation were then generated over wide ranges of frequency, duty cycle, and tidal volume. RESULTS: Significant interactions were identified between ventilator settings and proximal ventilation. The persistence of end-expiratory flow from the lung decreased proximal dilution by fresh gas and thereby reduced TGI-aided proximal ventilation. Changes in end-expiratory lung flow resulting from alterations in ventilator settings were correlated inversely with proximal ventilation. CONCLUSIONS: During TGI with constant catheter flow, ventilator settings that promote end-expiratory flow of gas from the lung diminish proximal ventilation. When frequency increases, the decrease in dilution efficiency of the individual breath is partially offset by the increase in cycle number, an effect which is magnified by any concomitant decrease in inspired tidal volume. Prolongation of the duty cycle tends to decrease proximal ventilation. Increases in expiratory resistance, including those arising from the external ventilator circuit or the endotracheal tube, also impair proximal ventilation.
Evolving concepts in the ventilatory management of acute respiratory distress syndrome.
With few modifications, a high tidal volume, normoxic, normocapnic ventilation paradigm developed as the standard approach to supporting most critically ill patients. Large tidal volumes, high end-tidal (plateau) alveolar pressures, and low levels of positive end-expiratory pressure are still common in many ICUs during ventilation of acute respiratory distress syndrome (ARDS). A body of scientific literature now suggests that this traditional approach may retard healing of the injured lung. A relatively small but growing number of practitioners are shifting their first priority from optimizing oxygen exchange, oxygen delivery, or respiratory system compliance to ensuring adequate lung protection. This article reviews the basis for concern about traditional ventilatory support in ARDS and develops an approach based on current evidence and newer options for management.
Adjunctive ventilation with tracheal gas insufflation--good vibrations?
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