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Search Results: 1 - 10 of 95294 matches for " Stephen W Trzeciak "
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Association between inhaled nitric oxide treatment and long-term pulmonary function in survivors of acute respiratory distress syndrome
R Phillip Dellinger, Stephen W Trzeciak, Gerard J Criner, Janice L Zimmerman, Robert W Taylor, Helen Usansky, Joseph Young, Brahm Goldstein
Critical Care , 2012, DOI: 10.1186/cc11215
Abstract: ARDS survivors (N = 92) from a large-scale randomized, placebo-controlled study evaluating mortality after either 5 ppm iNO or placebo for up to 28 days were assessed six months post-treatment. Pulmonary function testing across seven parameters was conducted.At 6 months post-treatment, results indicated significantly better absolute values for iNO versus placebo for mean ± SD total lung capacity (TLC, 5.54 ± 1.42 vs. 4.81 ± 1.00; P = 0.026). There were also significantly better values for mean ± SD percent predicted values for a) forced expiratory volume in 1 second (FEV1, 80.23 ± 21.21 vs. 69.51 ± 28.97; P = 0.042), b) forced vital capacity (FVC, 83.78 ± 19.37 vs. 69.84 ± 27.40; P = 0.019), c) FEV1/FVC (96.14 ± 13.79 vs. 87.92 ± 19.77; P = 0.033), and d) TLC (93.33 ± 18.21 vs. 76.10 ± 21.84; P < 0.001). Nonsignificant differences were found in absolute FEV1, FEV1/FVC, FVC, forced expiratory flow from 25% to 75% of FVC, functional residual capacity, and CO diffusion.ARDS patients surviving after treatment with low-dose iNO had significantly better values for select pulmonary function tests at six months post-treatment than placebo-treated patients. Further trials are warranted to determine the effects of iNO on chronic lung function in ARDS survivors, a factor in long-term morbidity and quality of life in this population.A Double-blind, Randomized, Placebo-controlled, Dose-response Study of Inhaled Nitric Oxide in the Treatment of Acute Respiratory Distress Syndrome. NCT number: ISRCTN53268296Inhaled nitric oxide (iNO) is a vasodilator indicated for treatment of term and near-term neonates with hypoxic respiratory failure associated with clinical or echocardiographic evidence of pulmonary hypertension. In these patients, iNO has been shown to improve oxygenation and reduce the need for extracorporeal membrane oxygenation therapy [1]. NO binds to and activates cytosolic guanylate cyclase, thereby increasing intracellular levels of cyclic guanosine 3',5'-monophosphate
Clinical manifestations of disordered microcirculatory perfusion in severe sepsis
Stephen Trzeciak, Emanuel P Rivers
Critical Care , 2005, DOI: 10.1186/cc3744
Abstract: Microcirculatory blood flow is markedly impaired in sepsis [1-3], and microcirculatory dysfunction plays a pivotal role in the development of the clinical manifestations of severe sepsis and septic shock. In the past, direct visualization of microcirculatory networks was only possible in experimental models of sepsis using intravital videomicroscopy, which is not possible in human subjects. Newly developed imaging technologies, such as orthogonal polarization spectral (OPS) imaging, have brought the ability to directly visualize the microcirculation to the bedside. Microcirculatory imaging, however, is still investigational in human sepsis and has not yet been incorporated into routine clinical practice. The purpose of this review, therefore, is to bridge the experimental and clinical aspects of microcirculatory science, and discuss the concepts that can be incorporated into bedside assessments of patients with severe sepsis and septic shock.Although the hemodynamic profile and clinical management of septic shock are typically characterized solely in terms of global hemodynamic (i.e. macrovascular) parameters, it is the microcirculation that is responsible for delivering blood flow from the cardiovascular system to the tissues. After conventional cardiovascular support measures achieve restoration of an acceptable arterial blood pressure in a septic shock patient, a clinician may be falsely reassured that the patient is clinically 'stable'. However, there are a myriad of possible pathogenic mechanisms occurring in the microcirculation that are difficult to detect with conventional clinical means and are, in effect, hidden from the clinician. In fact, much of the pathophysiology of severe sepsis can be explained by 'what lies beneath' in the microcirculation [4]. In severe sepsis this can include: (1) global tissue hypoxia [5]; (2) pan-endothelial cell injury [6]; (3) activation of the coagulation cascade [7]; and (4) "microcirculatory and mitochondrial distress synd
Clinical review: Emergency department overcrowding and the potential impact on the critically ill
Robert M Cowan, Stephen Trzeciak
Critical Care , 2005, DOI: 10.1186/cc2981
Abstract: Critical care begins immediately upon recognition of the critically ill (or potentially critically ill) patient, who has been defined as 'any patient who is physiologically unstable, requiring constant and minute-to-minute titration of therapy according to the evolution of the disease process' [1]. Therefore, the spectrum of critical care is not limited to the care that is provided within the confines of the intensive care unit (ICU). Rather, critical care begins (and is often necessitated) outside the ICU setting [2]. The nature of the illness rather than the location of the patient defines the need for critical care [1]; therefore, critical care patients are best defined physiologically rather than geographically. Outside the ICU and postoperative recovery rooms, critical care is most commonly provided in the emergency department (ED) [3].Critical care constitutes a significant and growing proportion of ED practice [4-6]. Studies conducted in urban US EDs have reported that more than 150 days of critical care time are provided in an ED annually [5,6]. Many EDs have optimized their ability to deliver certain aspects of critical care for very specific scenarios, such as trauma, acute cerebrovascular accidents, and acute myocardial infarctions (AMIs). Although EDs are designed to provide emergent stabilization and initial therapy for critically ill patients, most EDs do not have ICU-level resources for optimal longitudinal critical care delivery (such as uninterrupted 1 : 1 nursing care, focused subspecialty expertise, and invasive hemodynamic monitoring). Currently, the provision of critical care in the ED is increasing (in terms of both frequency and duration), largely because of ED overcrowding [5,7].This review describes the causes and effects of ED overcrowding in the USA; explores the potential impact this has on the care of the critically ill ED patient; and identifies possible solutions, focusing on innovations in ED based critical care.In order to meet the i
The association of near-infrared spectroscopy-derived tissue oxygenation measurements with sepsis syndromes, organ dysfunction and mortality in emergency department patients with sepsis
Nathan I Shapiro, Ryan Arnold, Robert Sherwin, Jennifer O'Connor, Gabriel Najarro, Sam Singh, David Lundy, Teresa Nelson, Stephen W Trzeciak, Alan E Jones, the Emergency Medicine Shock Research Network (EMShockNet)
Critical Care , 2011, DOI: 10.1186/cc10463
Abstract: This prospective, observational study comprised a convenience sample of three cohorts of adult patients (age > 17 years) at three urban university emergency departments: (1) a septic shock cohort (systolic blood pressure < 90 after fluid challenge; the "SHOCK" cohort, n = 58), (2) a sepsis without shock cohort (the "SEPSIS" cohort, n = 60) and emergency department patients without infection (n = 50). We measured the StO2 initial, StO2 occlusion and StO2 recovery slopes for all patients. Outcomes were sepsis syndrome severity, organ dysfunction (SOFA score at 24 hours) and in-hospital mortality.Among the 168 patients enrolled, mean initial StO2 was lower in the SHOCK cohort than in the SEPSIS cohort (76% vs 81%), with an impaired occlusion slope (-10.2 and 5.2%/minute vs -13.1 and 4.4%/minute) and an impaired recovery slope (2.4 and 1.6%/second vs 3.9 and 1.7%/second) (P < 0.001 for all). The recovery slope was well-correlated with SOFA score at 24 hours (-0.35; P < 0.001), with a promising area under the curve (AUC) for mortality of 0.81. The occlusion slope correlation with SOFA score at 24 hours was 0.21 (P < 0.02), with a fair mortality AUC of 0.70. The initial StO2 was significantly but less strongly correlated with SOFA score at 24 hours (-0.18; P < 0.04), with a poor mortality AUC of 0.56.NIRS measurements for the StO2 initial, StO2 occlusion and StO2 recovery slope were abnormal in patients with septic shock compared to sepsis patients. The recovery slope was most strongly associated with organ dysfunction and mortality. Further validation is warranted.NCT01062685Severe sepsis currently accounts for > 500,000 emergency department (ED) visits [1] and over 750,000 cases annually in the United States [2]. While the etiologies and presentations of sepsis remain extremely heterogeneous, the disease pathophysiology comprises a dysregulated host response, activation of the inflammatory and coagulation cascades, tissue hypoxia, cellular dysfunction, organ dysfunction
Arterial pressure optimization in the treatment of septic shock: a complex puzzle
Alan E Jones, Stephen Trzeciak, R Phillip Dellinger
Critical Care , 2010, DOI: 10.1186/cc8194
Abstract: In the previous issue of Critical Care Dünser and colleagues presented the results of post-hoc analysis that add another piece to the puzzle of understanding optimal arterial pressure goals in the treatment of sepsis [1]. The authors examine data from a control group of severe sepsis patients enrolled in an interventional trial that mandated hemo dynamic management to specific therapeutic targets, one of which was achievement of a mean arterial pressure (MAP) of 70 mmHg or higher through the use of vasopressors. Dunser and colleagues analyzed the association between the average MAP, both as a continuous variable and grouped into quartiles, and mortality. What they found was no association between average MAP, or MAP quartiles above 70 mmHg, and 28-day mortality. They did, however, report an association between vasopressor load and mortality.In his classic text Physiology of Shock published in 1950, Dr Carl J Wiggers wrote 'In short, there are no patho-gnomonic signs of shock ... The instability of a patient's condition, along with progressive deterioration, constitutes the best evidence of shock. In the assessment of such determination, the trend of arterial pressures remains one of our best criteria' [2]. For over a century, arterial hypotension has been intensely studied as a central cause of organ hypoperfusion and subsequent organ injury in critically ill patients. This includes patients with hemorrhage [2], heterogeneous populations of pre-hospital patients [3] and emergency department patients [4], and specific disease states such as pulmonary embolism [5], acute myocardial infarction [6], post-cardiac arrest syndrome [7], and sepsis [8]. Because of both the universal availability of its measurement and its association with severity of illness, medical care providers frequently use blood pressure to communicate with each other about the hemodynamic stability of patients.We agree with the authors' contention that consensus recommendation of a goal for MAP as a
J/$ψ$ and $ψ(2S)$ measurement in $p$+$p$ collisions at $\sqrt{s} =$ 200 and 500 GeV in the STAR experiment
Barbara Trzeciak
Physics , 2014, DOI: 10.1088/1742-6596/612/1/012038
Abstract: In this paper, results on the J/$\psi$ cross section and polarization measured via the dielectron decay channel at mid-rapidity in $p+p$ collisions at $\sqrt{s}$ = 200 and 500 GeV in the STAR experiment are discussed. The first measurement of $\psi(2S)$ to J/$\psi$ ratio at $\sqrt{s}$ = 500 GeV is also reported.
J/$ψ$ measurements in the STAR experiment
Barbara Trzeciak
Physics , 2014,
Abstract: In this paper, we present recent STAR J/$\psi$ results. J/$\psi$ nuclear modification factors ($R_{AA}$) in Au+Au collisions at $\sqrt{s_{NN}} =$ 200, 62.4 and 39 GeV and in U+U collisions at $\sqrt{s_{NN}} =$ 193 GeV are measured and compared to different theoretical calculations. We also report J/$\psi$ elliptic flow ($v_{2}$) results in Au+Au collisions at $\sqrt{s_{NN}} =$ 200 GeV and the first $\psi(2S)$ to J/$\psi$ ratio measurement in $p+p$ collisions at $\sqrt{s} =$ 500 GeV.
J/$ψ$ and $ψ(2S)$ measurement in p+p collisions at $\sqrt{s} =$ 200 and 500 GeV with the STAR experiment
Barbara Trzeciak
Physics , 2015,
Abstract: In this paper, results on the J/psi cross section and polarization measured via the dielectron decay channel at mid-rapidity in p+p collisions at 200 and 500 GeV in the STAR experiment are discussed. Also, first measurements of the J/psi production as a function of the charged-particle multiplicity density and of psi(2S) to J/psi ratio at 500 GeV are reported.
J/$ψ$ polarization measurements in p+p collisions at $\sqrt{s}$ = 200 and 500 GeV with the STAR experiment
Barbara Trzeciak
Physics , 2015,
Abstract: In these proceedings, measurements of J/psi polarization in p+p collisions at 200 and 500 GeV via the dielectron decay channel at mid-rapidity with the STAR experiment are discussed. At 200 GeV the polarization parameter, $\lambda_{\theta}$, related to the polar anisotropy is obtained in the helicity frame as a function of transverse momentum, 2 < $p_{T}$ < 6 GeV/c, and compared to different model predictions. A new J/psi polarization measurement at 500 GeV extends the previous analysis to a wide transverse momentum range of 5 < $p_{T}$ < 16 GeV/c. Also, the polarization parameter related to the azimuthal anisotropy, $\lambda_{\phi}$, is extracted in addition to $\lambda_{\theta}$, in two reference frames: the helicity and Collins-Soper frames. This allows for the frame invariant parameter calculation vs $p_{T}$ in these two frames.
J/$ψ$ polarization in p+p collisions at $\sqrt{s}$ = 200 GeV in STAR
Barbara Trzeciak
Physics , 2012, DOI: 10.5506/APhysPolBSupp.5.549
Abstract: In this paper, J/$\psi$ polarization at mid-rapidity in $p+p$ collisions at $\sqrt{s}$ = 200 GeV measured in the STAR experiment at RHIC is reported. J/$\psi$ production is analyzed via the dielectron decay channel. J/$\psi$ polarization is extracted from the decay angular distribution in the helicity frame. The J/$\psi$ polarization is measured at transverse momentum range (2 - 6) GeV/c and is found to be consistent with $NLO^+$ Color Singlet Model ($NLO^+$ CSM), Color Octet Model (COM) predictions and with no polarization within current uncertainties.
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