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Biomedical subjects

John J Marini

Publications and source records attributed to John J Marini.

At least 19 recordsLinked to original sources
PubMed2007

Time course of physiologic variables in response to ventilator-induced lung injury.

BACKGROUND: The time course of the physiological derangements that result from ventilator-induced lung injury has not been adequately described. Similarly, the regional topographies of pleural pressure and tissue edema have not been carefully mapped for this injury process. METHODS: Lung injury was induced in 9 normal pigs by ventilating for 6 hours at a transpulmonary pressure of 35 cm H(2)O, with the animals in the supine position. Eight additional normal pigs received right thoracotomy to place pleural-surface-pressure sensors prior to an identical period and intensity of injurious ventilation. Gas exchange and lung mechanics were tracked in all the animals. Cytokines (tumor necrosis factor alpha, interleukin 6, and interleukin 8) in peripheral blood were assayed at 2 hour intervals, beginning at the onset of mechanical ventilation, from all the animals. RESULTS: After a brief "induction" period, P(aO(2)) and tidal volume declined steadily in the animals that were ventilated to induce lung injury. The rate of decline was greater in the animals that received thoracotomy. The pleural pressure gradient steadily increased from ventral to dorsal. The serum cytokine levels did not evolve with developing injury, but cytokines were elevated at the onset of ventilation. Tissue edema, as assessed by the ratio of wet weight to dry weight, was greater in the thoracotomized animals than in the nonthoracotomized animals, and tissue edema tended to be greater in the caudal lung regions than in the cephalad lung regions. CONCLUSIONS: Following the induction period, the development of ventilator-induced lung injury progressed steadily and then plateaued, as assessed by quantitative physiology variables during 6 hours of ventilation at a transpulmonary pressure of 35 cm H(2)O. Greater injury developed in animals that had a coexisting potential insult (thoracotomy). Injury development was not paralleled by bloodborne inflammatory cytokines.

Animals↗
PubMed2006

Pressure-flow signatures of central-airway mucus plugging.

SETTING: Medical Intensive Care Unit of Regions Hospital, a University of Minnesota-affiliated teaching hospital. PATIENT: Mechanically ventilated woman with status asthmaticus and acute respiratory failure. INTERVENTION: Observations of airway pressure and flow tracings before and after bronchoscopic inspection and airway lavage. MAIN RESULTS: Four newly observed signs were recorded that may serve to identify occult central airway mucus plugging in the ventilated asthmatic patient.

Adrenal Cortex Hormones↗
PubMed2006

Limitations of clinical trials in acute lung injury and acute respiratory distress syndrome.

PURPOSE OF REVIEW: To review the challenges and limitations of randomized clinical trials in acute respiratory distress syndrome, with special emphasis on those pertaining to ventilatory management. RECENT FINDINGS: Superbly executed randomized trials of ventilatory strategy have garnered deserved attention from the critical care community and yet have illustrated the limitations of our current approach to clinical research in this area. Inexact definitions, incomplete mechanistic understanding of complex pathophysiology, inappropriate outcome variables, diverse therapeutic environments, lengthy data acquisition time and ethical constraints on trial design limit the applicability of randomized control trial methodology to acute respiratory distress syndrome and acute lung injury. As yet, clinical practice does not seem to have been greatly impacted by the implications of completed randomized controlled trials per se. Recent issues, both ethical and interpretive, regarding control group participants have raised troubling and theoretically important issues that are yet to be fully resolved. SUMMARY: Without tighter definitions of the condition under treatment, more specific targets for interventions to act upon, stratification that recognizes key interactive elements, and cointerventions based on better mechanistic understanding, randomized controlled trials of new drugs, ventilatory strategy, and other management approaches in acute respiratory distress syndrome are likely to remain a blunt instrument for investigation. As valuable as they are for calling important therapeutic principles to attention and for helping to suggest general guidelines for care, the limitations of randomized controlled trials for treating the individual with acute respiratory distress syndrome must be acknowledged.

Critical Care↗
PubMed2006

Intensive care and emergency medicine: progress over the past 25 years.

Over the last quarter of a century, intensive care medicine has developed into an established hospital specialty with its own unique identity and characteristics. Significant advances have occurred, mostly in a succession of small steps rather than any dramatic leap, with many being linked to advances in health care across other disciplines. In addition, many changes have resulted from the scientific identification of the detrimental effects of certain traditional practices once thought to be therapeutic. Here, in an attempt to learn from the past and offer guidance for future progress, we detail some of the key changes in various aspects of intensive care medicine including respiratory, cardiovascular, metabolic, and nutritional care, as well as sepsis, polytrauma, organization, and management.

Cardiovascular Diseases↗
PubMed2006

A proposed curvilinearity index for quantifying airflow obstruction.

BACKGROUND: Though forced expiratory volume in the first second (FEV(1)) is the primary indicator of airway obstruction, curvilinearity in the expiratory flow-volume curve is used to support the quantitative assessment of obstruction via FEV(1). Currently there is no available index to quantify a pathological contour of curvilinearity. STUDY PURPOSE: We propose a "curvature" index (k(max)) and compare FEV(1) values to the index with a sequential sample of spirometry data. METHODS: The hyperbolic function b(0)Q + b(1)Q V + b(2)V = 1 (in which Q = flow rate, V = volume, and b(0), b(1), and b(2) are estimated from the patient's flow-volume data) is fit to a fixed segment of the descending phase of the expiratory flow-volume curve. A previously developed biomechanical interpretation of this relationship associates the coefficient b(1) with the rate of airway-resistance-increase as exhaled volume increases. A global curvature index k(max)=b(1)/2(b(0)b(2)+b(1)) is defined to quantify the curvilinearity phenomenon. We used statistics software to determine the k(max) of spirometry data from 67 sequential patients, and to determine the relationship of k(max) to FEV(1). RESULTS: Individual k(max) estimates appeared to correspond well with the degree of curvilinearity observed and were related in an exponential manner to FEV(1). CONCLUSIONS: We defined a curvature index to quantify the curvilinearity phenomenon observed in the expiratory limb of flow-volume loops from patients with obstructive lung disease. This index uses data from a major segment of the flow-volume curve, and our preliminary data indicate an exponential relationship with FEV(1). This new index allows the putative association between curvilinearity and obstructive lung disease to be examined quantitatively in clinical practice and future studies.

Female↗
PubMed2004

Reluctant horses at the digital river.

Mastery of the changing bank of information needed to practice at the cutting edge will require the exploitation of emerging informatics and communication technologies. Whether their limitless promise will be embraced or forgone will depend as much on human as on technological practice.

Attitude of Health Personnel↗
PubMed2004

Effect of core body temperature on ventilator-induced lung injury.

OBJECTIVE: Ventilator-induced lung injury is a risk in patients requiring elevated ventilatory support pressures. We hypothesized that thermal stress modulates the development of ventilator-induced lung injury. DESIGN: Experimental study. SETTING: University laboratory. SUBJECTS: Anesthetized rabbits. INTERVENTIONS: Two experimental studies were designed to determine the role of temperature as a cofactor in ventilator-induced lung injury. In the first study, three groups of anesthetized rabbits were randomized to be ventilated for 2 hrs at core body temperatures of 33, 37, or 41 degrees C while ventilated with pressure control ventilation of 15/3 cm H2O (noninjurious settings-control) or 35/3 cm H2O (potentially injurious settings-experimental). To exclude effects arising from cardiac output fluctuations or from extrapulmonary organs, an isolated lung model was used for the second study, perfused at a fixed rate and studied at either 33 degrees C or 41 degrees C. MEASUREMENTS AND MAIN RESULTS: In the first study, the hyperthermic group compared with the hypothermic animals had significantly reduced mean PaO2 (-114 vs. + 14 mm Hg, p <.05), increased lung edema formation (mean wet weight/dry weight ratio of 8.1 vs. 5.7), and altered pressure-volume curves. The hyperthermic isolated, perfused lungs had an increased ultrafiltration coefficient, formed more edema, and experienced greater alveolar hemorrhage than hypothermic lungs. CONCLUSIONS: In two studies of ventilator-induced lung injury in rabbits, maintaining hyperthermia compared with hypothermia augmented the development of lung injury. Similar results from both the in vivo and isolated, perfused lung studies suggest that the observed effects were not due to cardiovascular factors or consequences of heating nonpulmonary organs.

Analysis of Variance↗
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

Effects of ventilatory pattern on experimental lung injury caused by high airway pressure.

OBJECTIVE: To determine the influence of clinician-adjustable ventilator settings on the development of ventilator-induced lung injury, as assessed by changes in gas exchange (Pao2), compliance, functional residual capacity, and wet weight to dry weight ratio. DESIGN: Randomized in vivo rabbit study. SETTING: Hospital research laboratory. SUBJECTS: Forty-four anesthetized, mechanically ventilated adult rabbits. INTERVENTIONS: Ventilation for 2 hrs with pressure control ventilation at 45 cm H2O, Fio2 = 0.6, and randomization to one of five ventilatory strategies using combinations of positive end-expiratory pressure (3 or 12 cm H2O), inspiratory time (0.45, 1.0, or 2.0 secs), and frequency (9 or 23/min). MEASUREMENTS AND MAIN RESULTS: Among the ventilator strategies applied, PEEP at 12 cm H2O (elevated positive end-expiratory pressure) and inspiratory time at 0.45 secs (reduced inspiratory time) best preserved Pao2 (p <.003) and compliance (p <.035). During injury development, two consistent changes were observed: Tidal volume increased, and airway pressure waveform was transformed by extending the time to attain target pressure. CONCLUSIONS: In this preclinical model, lung injury was attenuated by decreasing inspiratory time. As lung injury occurred, tidal volume increased and airway pressure waveform changed.

Analysis of Variance↗
PubMed2004

Mechanical ventilation in sepsis-induced acute lung injury/acute respiratory distress syndrome: an evidence-based review.

OBJECTIVE: In 2003, critical care and infectious disease experts representing 11 international organizations developed management guidelines for mechanical ventilation in sepsis-induced acute lung injury/acute respiratory distress syndrome (ARDS) that would be of practical use for the bedside clinician, under the auspices of the Surviving Sepsis Campaign, an international effort to increase awareness and improve outcome in severe sepsis. DESIGN: The process included a modified Delphi method, a consensus conference, several subsequent smaller meetings of subgroups and key individuals, teleconferences, and electronic-based discussion among subgroups and among the entire committee. METHODS: The modified Delphi methodology used for grading recommendations built on a 2001 publication sponsored by the International Sepsis Forum. We undertook a systematic review of the literature graded along five levels to create recommendation grades from A to E, with A being the highest grade. Pediatric considerations to contrast adult and pediatric management are in the article by Parker et al. on p. S591. CONCLUSION: A minimum amount of positive end-expiratory pressure should be set to prevent lung collapse at end expiration in ARDS. Setting the level of positive end-expiratory pressure may be guided by Fio2 requirement or measurement of thoracopulmonary compliance. Role of noninvasive positive-pressure ventilation in acute lung injury/ARDS is undefined. Small tidal volume ventilation and limitation of end-inspiratory plateau pressure is important in the management of ARDS and may be facilitated by permissive hypercapnia. Prone positioning should be considered in the severest of ARDS patients. The ideal fluid management strategy in ARDS is unknown. Weaning protocols should be in place that include spontaneous breathing trials and criteria for initiating such trials. The role of high-frequency oscillatory ventilation and airway pressure release ventilation in ARDS is uncertain.

Administration, Inhalation↗
PubMed2004

Transient hemodynamic effects of recruitment maneuvers in three experimental models of acute lung injury.

OBJECTIVE: Elevated lung volumes and increased pleural pressures associated with recruitment maneuvers (RM) may adversely affect pulmonary vascular resistance and cardiac filling or performance. We investigated the hemodynamic consequences of three RM techniques after inducing acute lung injury. DESIGN: Prospective, randomized, controlled experimental study. SETTING: Hospital research laboratory. SUBJECTS: Thirteen anesthetized, mechanically ventilated pigs. INTERVENTIONS: We induced three types of acute lung injury: oleic acid injury (n = 4); ventilator-induced lung injury (n = 4); and pneumonia (n = 5). All three models were designed to initiate a similar severity of oxygenation impairment. RM methods tested were sustained inflation, incremental positive end-expiratory pressure (PEEP) with a limited peak pressure, and pressure-controlled ventilation with increased PEEP and a fixed driving pressure. From a baseline PEEP of 8 cm H2O, all interventions were tested using post-RM PEEP levels of 8, 12, and 16 cm H2O. Cardiac output by thermodilution and systemic and pulmonary artery pressures were measured frequently during the RM and for 15 mins after its completion. MEASUREMENTS AND MAIN RESULTS: During the RM, cardiac output decreased to a greater extent in the pneumonia model (0.49 of baseline cardiac output) than in the oleic acid injury (0.67 of baseline) or ventilator-induced lung injury (0.79 of baseline) models. Cardiac output recovered to the baseline value by 5 mins post-RM in oleic acid injury and ventilator-induced lung injury models. However, cardiac output remained decreased 15 mins post-RM in the pneumonia model. There were no differences in hemodynamic parameters among RM methods in oleic acid injury and ventilator-induced lung injury models. In the pneumonia model, however, cardiac output decreased to a greater extent during the RM with sustained inflation (to 0.33 of baseline cardiac output) compared with pressure-controlled ventilation (to 0.68 of baseline). CONCLUSIONS: We conclude that RM transiently but profoundly depressed cardiac output in three models of acute lung injury. The results imply that a lung recruiting maneuver should be used with caution, especially when using sustained inflation in the setting of pneumonia.

Analysis of Variance↗