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Andrew D Bersten

Publications and source records attributed to Andrew D Bersten.

16 recordsLinked to original sources
PubMed2006

Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis.

BACKGROUND: Non-invasive positive pressure ventilation (NIPPV), using continuous positive airway pressure (CPAP) or bilevel ventilation, has been shown to reduce the need for invasive mechanical ventilation in patients with acute cardiogenic pulmonary oedema. We assessed additional benefits of NIPPV in a meta-analysis. METHODS: Meta-analysis comparison in acute cardiogenic pulmonary oedema was undertaken to compare (1) CPAP with standard therapy (oxygen by face-mask, diuretics, nitrates, and other supportive care), (2) bilevel ventilation with standard therapy, and (3) bilevel ventilation with CPAP, incorporating randomised controlled trials identified by electronic and hand search (1966-May, 2005). In 23 trials that fulfilled inclusion criteria, we assessed the effect of NIPPV on hospital mortality and mechanical ventilation, estimated as relative risks. FINDINGS: CPAP was associated with a significantly lower mortality rate than standard therapy (relative risk 0.59, 95% CI 0.38-0.90, p=0.015). A non-significant trend towards reduced mortality was seen in the comparison between bilevel ventilation and standard therapy (0.63, 0.37-1.10, p=0.11). We recorded no substantial difference in mortality risk between bilevel ventilation and CPAP (p=0.38). The need for mechanical ventilation was reduced with CPAP (0.44, 0.29-0.66, p=0.0003) and with bilevel ventilation (0.50, 0.27-0.90, p=0.02), compared with standard therapy; but no significant difference was seen between CPAP and bilevel ventilation (p=0.86). Weak evidence of an increase in the incidence of new myocardial infarction with bilevel ventilation versus CPAP was recorded (1.49, 0.92-2.42, p=0.11). Heterogeneity of treatment effects was not evident for mortality or mechanical ventilation across patients' groups. INTERPRETATION: In patients with acute cardiogenic pulmonary oedema, CPAP and bilevel ventilation reduces the need for subsequent mechanical ventilation. Compared with standard therapy, CPAP reduces mortality; our results also suggest a trend towards reduced mortality after bilevel NIPPV.

Continuous Positive Airway Pressure↗
PubMed2006

Pulmonary haemorrhage associated with negative-pressure pulmonary oedema: a case report.

Negative-pressure pulmonary oedema caused by upper airway obstruction after tracheal extubation is well recognised, but extensive pulmonary haemorrhage is rare. We report a case of post-extubation, laryngospasm-induced pulmonary oedema with associated pulmonary haemorrhage. The patient required mechanical ventilation with high positive end-expiratory pressure.

Airway Obstruction↗
PubMed2005

Meta-analysis of controlled trials of ventilator therapy in acute lung injury and acute respiratory distress syndrome: an alternative perspective.

OBJECTIVE: The role of protective ventilation in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is controversial. Evidence was sought from published randomised trials for a consistent treatment effect of protective ventilation and any covariate modification. DESIGN: Meta-analysis of protective ventilation trials in ALI/ARDS and meta-regression of covariates on treatment effect (log odds ratio), with respect to 28-day mortality. Heterogeneity impact on the meta-analysis was assessed by the H statistic (substantial impact, >1.5) and graphical analysis. Five trials with a total of 1,202 patients were considered. MEASUREMENTS AND RESULTS: Average 28-day mortality was 0.40 in the treatment group (protective ventilation, n=605) vs. 0.46 in the control group (control ventilation, n=597). The treatment effect (odds ratio) was: fixed-effects, 0.71 (95% CI 0.56-0.91, p=0.006; heterogeneity, p=0.06) and random effects: 0.80 (95% CI 0.49-1.31, p=0.37). Heterogeneity impact (H statistic=1.50) was adjudged as modest. The treatment effect was significant and (a) favoured protective ventilation for a tidal volume less than 7.7 ml/kg predicted (treatment group) and a mean plateau pressure of 30 cmH(2)O or higher (control group) but was not influenced by plateau pressure 21-30 cmH(2)O (treatment group) and (b) depended upon plateau pressure difference greater than 5-7 cmH(2)O between protective ventilation and standard ventilation. CONCLUSIONS: Overall treatment effect estimate favoured protective ventilation but did not achieve statistical significance. Protective ventilation depended upon threshold levels of tidal volume, plateau pressure, and plateau pressure difference.

Acute Disease↗
PubMed2005

Circulating surfactant protein-B levels increase acutely in response to exercise-induced left ventricular dysfunction.

1. As a result of its enormous surface area and necessary thinness for gas exchange, the alveolocapillary barrier is vulnerable to mechanical disruption from raised pulmonary microvascular pressure (Pmv). 2. Because surfactant protein-B (SP-B) leaks into the blood stream from the alveoli in response to alveolocapillary barrier damage and exercise leads to increased Pmv, we sought to determine whether exercise results in increased plasma SP-B. Moreover, in the setting of exercise-induced left ventricular dysfunction, the consequent increase in left heart filling pressure and, therefore, P(mv) would be expected to further increase plasma SP-B levels. 3. Twenty consecutive subjects referred for treadmill exercise stress echocardiography (ESE) had venous blood sampled immediately before and after ESE for batch atrial natriuretic peptide (ANP) and SP-B assay. Echocardiographic measures of pulmonary haemodynamics (pulmonary artery flow acceleration time (pafAT) and right ventricular outflow tract velocity time integral (rVTI)) were also taken pre- and post-exercise. 4. Although circulating ANP levels increased following exercise (P < 0.001), there was no change in circulating SP-B levels in the entire cohort. 5. Ten subjects had a positive ESE for ventricular dysfunction. Although circulating ANP was increased post-exercise in both the negative and positive ESE groups (P < 0.05 and P < 0.01, respectively), circulating SP-B only increased post-exercise in the positive ESE group (P < 0.05). Echocardiographic parameters supported an increment in P(mv) in the cohort with exercise-induced left ventricular dysfunction because this group had an increase in pafAT (P < 0.05; reflecting pulmonary artery pressure) and no change in rVTI. 6. Physical exertion associated with a Bruce protocol ESE is insufficient to increase circulating SP-B, despite evidence of increased left atrial and pulmonary vascular pressure. However, in the setting of exercise-induced myocardial dysfunction, there is a detectable increase in circulating SP-B. 7. The exaggerated increase in pulmonary vascular pressure in exercise-induced myocardial dysfunction may result in increased SP-B leakage from the alveoli into the circulation by altering the integrity of the alveolocapillary barrier to protein.

Atrial Natriuretic Factor↗
PubMed2004

Plasma surfactant protein-B: a novel biomarker in chronic heart failure.

BACKGROUND: In chronic heart failure (CHF), elevated pulmonary microvascular pressure (P(mv)) results in pulmonary edema. Because elevated P(mv) may alter the integrity of the alveolocapillary barrier, allowing leakage of surfactant protein-B (SP-B) from the alveoli into the circulation, we aimed to determine plasma levels of SP-B in CHF and their relation to clinical status. METHODS AND RESULTS: Fifty-three outpatients with CHF had plasma SP-B and N-terminal proBNP (NT-proBNP) assayed, in addition to a formalized clinical assessment at each clinic review over a period of 18 months. The control group comprised 19 normal volunteers. Plasma SP-B was elevated in CHF (P<0.001), and levels increased with New York Heart Association classification (P<0.001). SP-B correlated with objective clinical status parameters and NT-proBNP. During follow-up, major cardiovascular events occurred in patients with higher plasma SP-B (P<0.01) and NT-proBNP (P<0.05). Furthermore, on conditional logistic regression analysis, only SP-B was independently associated with CHF hospitalization (P=0.005). The 53 patients underwent a total of 210 outpatient visits. When the diuretic dosage was increased on clinical grounds, SP-B had increased 39% (P<0.001) and NT-proBNP had increased 32% (P<0.001). Conversely, at the next visit, SP-B fell 12% (P<0.001), whereas NT-proBNP fell 39% (P<0.001). CONCLUSIONS: Plasma SP-B is increased in CHF, and levels are related to clinical severity. Furthermore, within individual patients, SP-B levels vary with dynamic clinical status and NT-proBNP levels. Because plasma SP-B is independently associated with CHF hospitalization, it may, by virtue of its differing release mechanism to NT-proBNP, be a clinically useful biomarker of the pulmonary consequences of raised P(mv).

Aged↗
PubMed2003

Effect of inspiratory flow pattern and inspiratory to expiratory ratio on nonlinear elastic behavior in patients with acute lung injury.

Ventilatory modes employing different inspiratory flow patterns and inspiratory to expiratory ratios may alter lung strain in acute lung injury patients. To determine whether variations in lung strain existed between pressure-controlled, volume-controlled, and pressure-controlled inverse ratio modes of ventilation, we randomly applied each for 30 minutes in 18 acute lung injury patients, keeping tidal volume, respiratory rate, fractional inspired oxygen, and total positive end-expiratory pressure constant. After each mode, a multiple linear regression analysis of dynamic airway pressure and airflow was performed with a volume-dependent single compartment model of the equation of motion, and an index of nonlinear elastic behavior was calculated. In five additional patients, concurrent dynamic computerized axial tomography scanning at juxtadiaphragmatic and subcarinal levels was added. Although static mechanics, oxygenation, and hemodynamics were no different between pressure-controlled, volume-controlled, and pressure-controlled inverse ratio ventilation, we found significant differences in nonlinear behavior. This was least with pressure-controlled followed by volume-controlled ventilation, and pressure-controlled inverse ratio ventilation had the greatest nonlinear elastic behavior. Dynamic computerized axial tomography analysis revealed more overinflated units in the left subcarinal slice with pressure-controlled inverse ratio ventilation. Ventilator flow pattern and inspiratory to expiratory ratio independently influence lung strain in acute lung injury; however, further studies are needed to determine the biologic significance.

Aged↗
PubMed2003

Infarct-induced chronic heart failure increases bidirectional protein movement across the alveolocapillary barrier.

Chronic heart failure (CHF) is associated with adaptive structural changes at the alveolocapillary barrier that may be associated with altered protein permeability. Bidirectional protein movement across the barrier was studied in anesthetized rats with infarct-induced CHF by following (125)I-labeled albumin ((125)I-albumin) flux into the alveoli and the leakage of surfactant protein (SP)-B from the alveoli into the circulation. Three groups were studied: controls [0% left ventricular (LV) infarction], moderate infarct (25-45% LV infarction), and large infarct (>46% LV infarction). Wet and dry lung weights increased in the large infarct group (both P < 0.001), consistent with increased lung water and solid lung tissue. (125)I-albumin flux increased across the endothelial (P < 0.001) and epithelial (P < 0.01) components of the alveolocapillary barrier in the large infarct group. Plasma SP-B increased 23% with moderate infarcts (P < 0.05) and 97% with large infarcts (P < 0.001), independent of alveolar levels. Lavage fluid immune cells (P < 0.01) and myeloperoxidase activity (P < 0.05) increased in the large infarct group, consistent with inflammation. Bidirectional protein movement across the alveolocapillary barrier is increased in CHF, and alveolar inflammation may contribute to this pathophysiological defect.

Animals↗
PubMed2003

Prolonged alveolocapillary barrier damage after acute cardiogenic pulmonary edema.

OBJECTIVES: To determine whether acute cardiogenic pulmonary edema is associated with damage to the alveolocapillary barrier, as evidenced by increased leakage of surfactant specific proteins into the circulation, to document the duration of alveolocapillary barrier damage in this setting, and to explore the role of pulmonary parenchymal inflammation by determining if circulating tumor necrosis factor-alpha is increased after acute cardiogenic pulmonary edema. DESIGN: Prospective, observational study. SETTING: Critical care, cardiac intensive care, and cardiology wards of a tertiary-care university teaching hospital. PATIENTS: A total of 28 patients presenting with acute cardiogenic pulmonary edema and 13 age-matched normal volunteers. INTERVENTIONS: Circulating surfactant protein-A and -B and tumor necrosis factor-alpha were measured on days 0 (presentation), 1, 3, 7, and 14. Clinical markers of pulmonary edema were documented at the same times. MEASUREMENTS AND MAIN RESULTS: Surfactant protein-A and -B were elevated on day 0 compared with controls (367 +/- 17 ng/mL vs. 303 +/- 17 and 3821 +/- 266 ng/mL vs. 2747 +/- 157 [mean +/- sem], p <.05), and although clinical, hemodynamic and radiographic variables improved rapidly (p <.001), surfactant protein-A and -B rose further until day 3 (437 +/- 22, p <.001, 4642 +/- 353, p <.01). Tumor necrosis factor-alpha was elevated at presentation (p <.05), doubled by day 1 (6.98 +/- 1.36 pg/mL, p <.05), remained elevated on day 3 (5.72 +/- 0.96 pg/mL, p <.05), and peak levels were related to chest radiograph extravascular lung water score (r(p) = 0.64, p =.003). CONCLUSIONS: Although the initial increase in plasma surfactant protein-A and -B may represent hydrostatic stress failure of the alveolocapillary barrier, the prolonged elevation, when hemodynamic abnormalities have resolved, and the delayed elevation of tumor necrosis factor-alpha are consistent with pulmonary parenchymal inflammation, which may further damage the alveolocapillary barrier. This prolonged physiologic defect at the alveolocapillary barrier after acute cardiogenic pulmonary edema may partly account for the vulnerability of these patients to recurrent pulmonary fluid accumulation.

Acute Disease↗
PubMed2002

Conventional coagulation and thromboelastograph parameters and longevity of continuous renal replacement circuits.

OBJECTIVE: To determine the relationship between conventional and thromboelastograph (TEG) coagulation parameters and continuous renal replacement therapy (CRRT) circuit longevity. DESIGN: Conventional coagulation and TEG parameters were measured at the commencement of and during CRRT. Time to circuit cessation was measured and only circuits reaching a predetermined rise from baseline in the pressure gradient across the haemofilter were diagnosed as failing due to clotting. All other circuits were excluded from analysis. SETTING: A general critical care unit of a metropolitan tertiary hospital. PATIENTS AND PARTICIPANTS: Fourteen consecutive patients requiring CRRT were studied. The CRRT technique used was continuous veno-venous haemodialysis. INTERVENTIONS: Thromboelastograph measurements were made prior to the commencement of CRRT and daily thereafter for each circuit. The international normalised ratio (INR), activated partial thromboplastin time (APTT) and platelet numbers were measured at commencement and 8 hourly thereafter. Heparin was used for anticoagulation unless considered contraindicated. MEASUREMENTS AND RESULTS: Forty-seven circuits with a mean (SD) circuit life of 33.0 (30.2) h were entered. Twenty-five circuits fulfilled circuit clotting criteria; the mean circuit life was 30.8 (22.1) h. Heparin anticoagulation was found to prolong circuit life significantly despite adequate mean circuit life, 33.2 (35.7) h, in heparin-free circuits. The starting APTT and the TEG variables reaction time (R) and coagulation time (RK) were significantly correlated. The starting APTT, starting RK and mean time taken for the amplitude to increase from 2 to 20 mm (K) were predictive of circuit life. None of these variables predicted which patients would need heparin. CONCLUSION: While TEG variables more closely predicted circuit longevity than conventional coagulation variables, the clinical benefit of TEG monitoring of anticoagulation for CRRT would appear to be minimal.

Acute Kidney Injury↗
PubMed2002

Endotoxin induces respiratory failure and increases surfactant turnover and respiration independent of alveolocapillary injury in rats.

Although endotoxin-induced acute lung injury is associated with inflammation, alveolocapillary injury, surfactant dysfunction, and altered lung mechanics, the precise sequence of these changes is polemic. We have studied the early pathogenesis of acute lung injury in spontaneously breathing anesthetized rats after intravenous infusion of Salmonella abortus equi endotoxin. The animals became hypoxic, and airway resistance, tissue resistance, lung elastance, and static compliance all deteriorated well before any change in alveolar neutrophils, macrophages, lung fluid (99mTc-labeled diethylenetriamine pentaacetic acid), or 125I-albumin flux, which were only appreciably increased at 8.5 hours. Lung elastance deteriorated before airway resistance, indicating that the compliance change was specific rather than caused by reduced lung volume. The subcellular and alveolar content of surfactant proteins A and B, cholesterol, disaturated phospholipids, and phospholipid classes remained normal in the face of a dramatic increase in the synthesis and turnover of 3H-disaturated phosphatidylcholine. Our findings indicate that the increase in surfactant disaturated phospholipid turnover reflects, at least in part, an approximately five-fold increase in "sigh frequency." We suggest that endotoxin has direct effects on tissue resistance and lung elastance independent of surfactant composition and that the initial respiratory failure results primarily from endotoxin-induced ventilation/perfusion mismatch independent of edema or alveolocapillary injury per se.

Airway Resistance↗
PubMed2002

Incidence and mortality of acute lung injury and the acute respiratory distress syndrome in three Australian States.

To determine the incidence and 28-d mortality rate for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) using the 1994 American-European Consensus Conference definitions, we prospectively screened every admission to all 21 adult intensive care units in the States of South Australia, Western Australia, and Tasmania (total population older than 15 yr of age estimated as 2,941,137), between October 1 and November 30, 1999. A total of 1,977 admissions were screened of which 168 developed ALI and 148 developed ARDS, which represents a first incidence of 34 and 28 cases per 100,000 per annum, respectively. The respective 28-d mortality rates were 32% and 34%. The most common predisposing factors for ALI were nonpulmonary sepsis (31%) and pneumonia (28%). Although the incidences of ALI and ARDS are higher and the mortality rates are lower than those reported from studies in other countries, multicenter international studies are required to exclude methodological differences as the cause for this finding.

Causality↗
PubMedDate not supplied

Determinants of serum levels of surfactant proteins A and B and Clara cell protein CC16.

Increased leakage of surfactant proteins A and B (SP-A and SP-B) and Clara cell secretory protein (CC16) from the air spaces into the circulation occurs in a range of respiratory conditions. However, circulating levels depend not only on the rate of entry into the circulation, but also on the rate of clearance. In order to clarify the role of the kidney in the clearance of these proteins, serum levels were related to markers of glomerular filtration in 54 non-smoking patients with varying degrees of renal dysfunction, none of whom had respiratory disease or were receiving dialysis at the time of sampling. Serum SP-A was related to SP-B (r = 0.53, p < 0.001) and to CC16 (r = 0.33, p < 0.02). Similarly, SP-B was related to CC16 (r = 0.39, p < 0.004). Stepwise multiple linear regression analysis suggested that serum SP-A and SP-B are influenced by age (approximately 20 and approximately 25% of variance, respectively), whereas CC16 is determined by renal function and, to a lesser extent, by body weight (approximately 63% of variance in total). We conclude that CC16 is cleared from blood by the renal route, whereas SP-A and SP-B are not. Serum SP-A and SP-B are influenced by age, which we speculate reflects increased damage to the alveolocapillary barrier.

Adolescent↗