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David J Dries

Publications and source records attributed to David J Dries.

15 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↗
PubMed2005

Purpura fulminans due to Staphylococcus aureus.

BACKGROUND: Purpura fulminans is an acute illness commonly associated with meningococcemia or invasive streptococcal disease, and it is typically characterized by disseminated intravascular coagulation (DIC) and purpuric skin lesions. In this article, we report the first 5 cases (to our knowledge) of purpura fulminans directly associated with Staphylococcus aureus strains that produce high levels of the superantigens toxic shock syndrome toxin-1 (TSST-1), staphylococcal enterotoxin serotype B (SEB), or staphylococcal enterotoxin serotype C (SEC). METHODS: Cases were identified in the Minneapolis-St. Paul, Minnesota, metropolitan area during 2000-2004. S. aureus infection was diagnosed on the basis of culture results, and susceptibility to methicillin was determined. The ability of the isolated organisms to produce TSST-1, SEB, SEC, and Panton-Valentine leukocidin (PVL) was determined. TSST-1, SEB, and SEC levels were also quantified after in vitro growth of the organisms. RESULTS: In 3 of the 5 cases, the infecting S. aureus strain was isolated from the blood cultures. In 2 of the 5 cases, the infecting S. aureus strain was isolated only from the respiratory tract, indicating that purpura fulminans and toxic shock syndrome resulted from exotoxin and/or other host factors, rather than septicemia. One of these latter 2 patients also had necrotizing pneumonia, and the isolated S. aureus was a methicillin-resistant strain that produced both SEC and PVL. Only 2 of the 5 patients survived, and 1 of the survivors received activated protein C. CONCLUSIONS: Staphylococcal purpura fulminans may be a newly emerging illness associated with superantigen production. Medical practitioners should be aware of this illness.

Adult↗
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

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↗
PubMed2004

Intercomparison of recruitment maneuver efficacy in three models of acute lung injury.

OBJECTIVE: To compare the relative efficacy of three forms of recruitment maneuvers in diverse models of acute lung injury characterized by differing pathoanatomy. DESIGN: We compared three recruiting maneuver (RM) techniques at three levels of post-RM positive end-expiratory pressure in three distinct porcine models of acute lung injury: oleic acid injury; injury induced purely by the mechanical stress of high-tidal airway pressures; and pneumococcal pneumonia. SETTING: Laboratory in a clinical research facility. SUBJECTS: Twenty-eight anesthetized mixed-breed pigs (23.8 +/- 2.6 kg). INTERVENTIONS: The RM techniques tested were sustained inflation, extended sigh or incremental positive end-expiratory pressure, and pressure-controlled ventilation. PRIMARY MEASUREMENTS: Oxygenation and end-expiratory lung volume. MAIN RESULTS: The post-RM positive end-expiratory pressure level was the major determinant of post-maneuver PaO2, independent of the RM technique. The pressure-controlled ventilation RM caused a lasting increase of PaO2 in the ventilator-induced lung injury model, but in oleic acid injury and pneumococcal pneumonia, there were no sustained oxygenation differences for any RM technique (sustained inflation, incremental positive end-expiratory pressure, or pressure-controlled ventilation) that differed from raising positive end-expiratory pressure without RM. CONCLUSIONS: Recruitment by pressure-controlled ventilation is equivalent or superior to sustained inflation, with the same peak pressure in all tested models of acute lung injury, despite its lower mean airway pressure and reduced risk for hemodynamic compromise. Although RM may improve PaO2 in certain injury settings when traditional tidal volumes are used, sustained improvement depends on the post-RM positive end-expiratory pressure value.

Analysis of Variance↗
PubMed2004

Protocol-driven ventilator weaning reduces use of mechanical ventilation, rate of early reintubation, and ventilator-associated pneumonia.

BACKGROUND: Mechanical ventilation is the defining event of intensive care unit management. To reduce use, a literature-based protocol was introduced to facilitate weaning. The effect of protocol-driven ventilator weaning on ventilator use, ventilator-associated pneumonia (VAP), and intensive care unit (ICU) length of stay (LOS) is described in a survey of 2 years' activity in a multidisciplinary surgical ICU. METHODS: Data were gathered from April to September 2000 and from April to September 2002 before and after introduction of nurse/therapist-driven weaning. VAP was identified by chest radiography, clinical presentation, Gram's stains, and cultures from tracheal aspirates or bronchoalveolar lavage. Infection control practitioners diagnosed VAP. Failed extubation was defined as reintubation within 72 hours. RESULTS: Overall, there was a 2:1 ratio of male patients to female patients. The total number of patients and days of mechanical ventilation increased, but the use ratio (ventilator days/ICU days) fell from 0.47 to 0.33. Patients failing extubation fell from 43 (in 2000) to 25 (in 2002). From these patients, 17 cases of VAP occurred in 2000 and 5 in 2002. Mean age (40 years), Injury Severity Score (24), and ICU LOS (5.7-7.4 days; p = not significant) were unchanged in injured patients. ICU discharge was frequently delayed because of the need for subsequent respiratory care. CONCLUSION: Protocol-driven weaning reduces use of mechanical ventilation and VAP. Injured and general surgical patients show reduction in complications, but shorter ICU LOS depends on resources elsewhere in the health care system.

Adult↗
PubMed2003

Ventilator-induced lung injury.

Ventilator-induced lung injury has been established as a significant risk to patients receiving PPV. Animal studies have provided definitive experimental data that support the existence of VILI. Clinical studies have implied the role of VILI in ARDS and ALI patients. In patients who have ARDS or ALI, however, VILI cannot be distinguished from exacerbation of the primary condition. Animal and clinical studies that clearly show elevated levels of cytokines when PPV is applied beyond certain limits support the concept that an inflammatory process is activated by PPV. Whether the induction of inflammatory mediators contributes to the mortality or morbidity of the ventilated patient has not been established. A potential role for anti-inflammatory therapeutic agents is promising. Therefore, the following considerations can guide the clinical care of ventilator patients: Alveolar pressure exposure (plateau pressure) should be limited to less than 32 cm H2O. Positive end-expiratory pressure should be applied to avoid end-expiratory collapse and reopening. Tidal volume should be set at approximately 6 mL/kg or further guided by plateau pressure limitation. Although studies suggest that reducing Ti, flow, and f may be important in avoiding VILI, there are no current guidelines. The results of preliminary studies investigating the preventative potential of respiratory acidosis, prone positioning, or careful vascular pressure management seem promising. Inflammatory response in VILI has been established, but a role for intervention, such as general or specific suppression of the response, has not been established.

Animals↗
PubMed2002

Oscillations and noise: inherent instability of pressure support ventilation?

Pressure support ventilation (PSV) is almost universally employed in the management of actively breathing ventilated patients with acute respiratory failure. In this partial support mode of ventilation, a fixed pressure is applied to the airway opening, and flow delivery is monitored by the ventilator. Inspiration is terminated when measured inspiratory flow falls below a set fraction of the peak flow rate (flow cutoff); the ventilator then cycles to a lower pressure and expiration commences. We used linear and nonlinear mathematical models to investigate the dynamic behavior of pressure support ventilation and confirmed the predicted behavior using a test lung. Our mathematical and laboratory analyses indicate that pressure support ventilation in the setting of airflow obstruction can be accompanied by marked variations in tidal volume and end-expiratory alveolar pressure, even when subject effort is unvarying. Unstable behavior was observed in the simplest plausible linear mathematical model and is an inherent consequence of the underlying dynamics of this mode of ventilation. The mechanism underlying the observed instability is "feed forward" behavior mediated by oscillatory elevation in end-expiratory pressure. In both mathematical and mechanical models, unstable behavior occurred at impedance values and ventilator settings that are clinically realistic.

Adult↗
PubMed2002

Recent advances in emergency life support.

With additional international input, recent changes in emergency life support are reflected in updated guidelines for Advanced Cardiac Life Support (ACLS) from the American Heart Association and new technology in the arena of vascular access and emergency airway management. These changes will expand nurses' ability to provide advanced levels of care, even in the prehospital situation, and represent a more rigorous evidence-based approach than ever before. As early morbidity and mortality in emergency situations are frequently associated with complications associated with airway management and vascular access, recent development in these areas are reviewed along with evolution in ACLS guidelines.

Adult↗
PubMed2002

Pulmonary microvascular fracture in a patient with acute respiratory distress syndrome.

OBJECTIVE: To present electron micrographs of lung tissue obtained from a patient exposed to high ventilatory pressures in the context of pulmonary dysfunction and pulmonary hypertension. DESIGN: Case report. SETTING: Adult intensive care unit of a university-affiliated teaching hospital. PATIENTS: A patient exposed to high-pressure mechanical ventilation during support for acute respiratory distress syndrome; the acute respiratory distress syndrome in this case was secondary to septic shock. MEASUREMENTS AND MAIN RESULTS: Scanning electron micrographs of lung tissue, focusing on the internal alveolar surfaces. FINDINGS: Multiple gross disruptions of the alveolar walls, suggestive of stress fractures. CONCLUSION: High-pressure mechanical ventilation may promote fracturing of the alveolar blood:airspace barrier.

Aged↗