Results of the Multidisciplinary Critical Care Knowledge Assessment Program, 1995.
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Biomedical subjects
Publications and source records attributed to J L Zimmerman.
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The discovery of new tools adds to the human experience, but our newfound ability to communicate and share knowledge and wisdom almost instantaneously results in a factorial increase in the collective wisdom of a global community. Computer networks continue to expand and reach into every corner of the globe. This global information network has the potential to affect many aspects of society. This paper presents a brief history and overview of the Internet and network application tools and discusses some of the ethical issues that need to be addressed as the Internet grows to touch every part of our lives.
BACKGROUND: Ruling out myocardial infarction in patients coming to the emergency room with chest pain is hindered by the lack of a specific early diagnostic marker. Less than 30 percent of patients admitted to coronary care units have infarction, resulting in substantial unnecessary expenditures. We developed a rapid assay of the subforms of creatine kinase MB (CK-MB) and prospectively analyzed its sensitivity and specificity in diagnosing myocardial infarction in the first six hours after the onset of chest pain. METHODS: In 1110 consecutive patients who came to the emergency room with chest pain, blood samples were collected every 30 to 60 minutes until at least 6 hours after the onset of symptoms; in patients who were then admitted to the hospital, samples were collected every 4 hours for up to 48 hours. The samples were analyzed for CK-MB subforms, and the diagnosis of myocardial infarction was confirmed by conventional CK-MB analysis. RESULTS: Of the 1110 patients evaluated, 121 had myocardial infarction. The sensitivity of the assay of CK-MB subforms to detect myocardial infarction in the first six hours after the onset of symptoms was 95.7 per cent, as compared with only 48 percent for the conventional CK-MB assay; the specificity was 93.9 percent among patients hospitalized without myocardial infarction and 96.2 percent among those sent home. Among the patients with myocardial infarction, definitive results of the subform assay were available a mean (+/- SD) of 1.22 +/- 1.17 hours after their arrival in the emergency room. CONCLUSIONS: The assay of CK-MB subforms reliably detected myocardial infarction within the first six hours after the onset of symptoms, and its use could reduce admission to the coronary care unit by 50 to 70 percent, thereby reducing costs.
OBJECTIVE: To evaluate the effects of HA-1A, a human monoclonal antiendotoxin antibody, in septic patients with ARDS. DESIGN: Substudy of a multicenter, double-blinded, placebo-controlled trial of HA-1A in septic patients. PATIENTS: 63 septic patients with ARDS at the time of study entry. INTERVENTION: A single intravenous injection of HA-1A (100 mg) or placebo. RESULTS: A quantitative radiographic score, the PaO2/FIO2 ratio and an index of the severity of ARDS did not show a significant difference between the treatment and placebo groups at 3, 5 and 7 days after treatment. The duration of endotracheal intubation did not differ between the two groups. 15 of 30 HA-1A treated patients (50%) and 23 of 33 placebo-treated patients (69.7%) died within 28 days. The daily mortality was always lower in the HA-1A group, but this difference was not statistically significant at 28 days. The 28-day survival curves for the two treatment groups adjusted by covariate analysis were not significantly different (p = 0.07). Using logistic regression, a significant independent effect of HA-1A treatment was detected upon the early survival rate at 7 days (p = 0.03) but not at 14 and 28 days. CONCLUSION: A single injection of HA-1A in septic patients with ARDS did not reverse acute respiratory failure or improve long-term survival.
OBJECTIVES: We sought to determine whether there might be acute changes in hemodynamics attributable to HA-1A, a monoclonal antibody to endotoxin, in patients with presumed Gram-negative sepsis. DESIGN: Post hoc analysis of a multicenter, randomized, double-blind, placebo-controlled study. PATIENTS: A total of 543 patients with severe sepsis presumed to be caused by Gram-negative bacteria who were enrolled in a clinical trial to evaluate the efficacy and safety of HA-1A human monoclonal antibody. INTERVENTIONS: Patients were randomly assigned to receive either 100 mg of HA-1A or placebo. MEASUREMENT AND MAIN RESULTS: Patients were grouped by the study drug, HA-1A, or placebo, and the presence or absence of Gram-negative bacteremia. Hemodynamic variables were monitored from before, until 72 hrs after infusion of the study drug. For the entire study population (n = 543), no changes over time attributable to study drug were noted in the mean arterial pressure (p > .19), heart rate (p > .53) or the need for vasopressor administration (p > .62). One hundred ninety-seven patients underwent pulmonary artery catheterization and had hemodynamic data available from before the infusion of HA-1A or placebo until at least 12 hrs after infusion. Evaluating all 197 patients on an intent to treat basis demonstrated no significant differences over time in cardiac index (p > .15), oxygen delivery index (p > .43), or left ventricular stroke work index (p > .48) between patients who received HA-1A and those patients receiving placebo. Grouping patients by the presence of Gram-negative bacteremia and study drug received also failed to demonstrate any significant difference attributable to HA-1A in mean arterial pressure (p > .54), heart rate (p > .84), cardiac index (p > .13), oxygen delivery index (p > .05), or left ventricular stroke work index (p > .48) between populations. CONCLUSION: There is no apparent relationship between the administration of HA-1A, the presence of Gram-negative bacteremia, and hemodynamic profiles over the 72-hr study period.
The evolution of family therapy from a cybernetic metaphor to a narrative metaphor has led us to think differently about therapy, about clients, and about ourselves as therapists. In this article we pursue how this different way of thinking has informed a theoretical understanding of a narrative therapy approach and consequently has opened space for different ways of working clinically. We begin by tracing the evolution to narrative; we consider the implications of social constructionism and its political effects; and we complete the discussion by focusing on narrative theory. We then show how the clinical work follows logically and is coherent with the theoretical considerations. We describe, and illustrate with clinical examples, an innovative approach to working with couples and families with adolescents. In this work we pay attention to the larger cultural stories, including gender constructions, and to personal stories that persons have created to make meaning out of their experience as they interact with one another in a reciprocal meaning-making process. Interventions focus on externalizing the problem narrative that is influencing the client(s), mapping the effects of the problem pattern and/or the totalizing view persons might have of others, and creating space for client(s) to notice preferred actions and intentions. Finally, we close the loop by asking questions of ourselves and others about the effects of working from a narrative metaphor.
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OBJECTIVES: To determine the safety, pharmacokinetics, and activity of an anti-tumor necrosis factor (TNF)-alpha monoclonal antibody in severe sepsis. DESIGN: Open-label, prospective, phase II multicenter trial with escalating doses of a murine monoclonal antibody (CB0006). SETTING: Twelve academic medical center intensive care units in the United States and Europe. PATIENTS: Eighty patients with severe sepsis or septic shock who received standard supportive care and antimicrobial therapy in addition to the anti-TNF antibody. INTERVENTIONS: Patients were treated intravenously with one of four dosing regimens with CB0006: 0.1 mg/kg, 1.0 mg/kg, 10 mg/kg or two doses of 1 mg/kg 24 hrs apart. MEASUREMENTS AND MAIN RESULTS: The murine monoclonal anti-TNF antibody was well tolerated despite the development of anti-murine antibodies in 98% of patients. No survival benefit was found for the total study population, but patients with increased circulating TNF concentrations at study entry appeared to benefit by the high dose anti-TNF antibody treatment. Increased interleukin (IL)-6 levels predicted a fatal outcome (p = .003), but TNF levels were not found to be a prognostic indicator. TNF levels were higher (206.7 +/- 60.7 vs. 85.9 +/- 26.1 pg/mL; p < .001) and outcome was poor (41% vs. 71% survival; p = .007) in patients who were in shock at study entry when compared with septic patients not in shock. CONCLUSIONS: The murine anti-TNF-alpha monoclonal antibody CB0006 has proven to be safe in this clinical trial and may prove to be useful in septic patients with increased circulating TNF concentrations. Further studies are needed to determine efficacy and the ultimate clinical utility of this immunotherapeutic agent in sepsis.
OBJECTIVE: To evaluate the in vivo performance of a continuous intra-arterial blood gas monitor as compared with in vitro arterial blood gases for measurements of PaO2, PaCO2, and arterial pH. DESIGN: Consecutive patient enrollment. SETTING: Medical intensive care unit of a county teaching hospital. PATIENTS: Five critically ill patients. INTERVENTIONS: All patients had a fiberoptic sensor placed through a 20-gauge cannula inserted into the radial artery. Sensor and arterial blood gas measurements were monitored up to 68 hrs. Arterial blood gases were analyzed on two blood gas analyzers. MEASUREMENTS AND MAIN RESULTS: A total of 104 arterial blood gases were obtained for comparison of sensor measurements with blood gas analyzer values. Comparison of the sensor values with the blood gas analyzer values showed bias and precision values of -0.021 and 0.037 for arterial pH, 1.74 and 6.06 torr (0.23 and 0.81 kPa) for PaCO2, and -5.89 and 13.19 torr (-0.79 and 1.76 kPa) for PaO2, respectively. Comparison of the two blood gas analyzer measurements showed bias and precision values of -0.030 and 0.010 for arterial pH, 1.96 and 2.55 torr (0.26 and 0.34 kPa) for PaCO2, and -5.77 and 17.15 torr (-0.77 and 2.29 kPa) for PaO2, respectively. No complications attributable to the sensor were detected. CONCLUSIONS: The performance of this fiberoptic continuous intra-arterial blood gas monitor is comparable to that of blood gas analyzers and compares favorably with previously reported studies utilizing other sensors in reliably and reproducibly approximating PaO2, PaCO2, and arterial pH values. This monitoring capability was accomplished with no patient morbidity. Further study is indicated to confirm these initial results and to establish the role of a continuous intra-arterial blood gas monitor in critically ill patients.
OBJECTIVE: To determine the occurrence rate of complications and mortality in patients with severe asthma requiring endotracheal intubation and mechanical ventilation. DESIGN: Retrospective review of medical records from September 1982 to July 1988. SETTING: Urban, teaching hospital serving primarily indigent patients. PATIENTS: Fifty-seven adult patients with asthma requiring tracheal intubation and mechanical ventilation. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Fifty-seven patients requiring tracheal intubation and mechanical ventilation during 69 hospital admissions were identified. Medication noncompliance and upper respiratory tract infections were recorded as the most frequent precipitating events for exacerbation of asthma. Forty-nine intubations were initiated because of a clinical diagnosis of respiratory distress, but multiple indications were present in 42 admissions. One or more complications occurred in 31 episodes of endotracheal intubation and mechanical ventilation (45%). Death occurred in four (6%) of 69 admissions. Three of the four deaths occurred in patients who had a cardiorespiratory arrest before hospital admission. CONCLUSIONS: While complications occurred in 45% of patients with severe asthma requiring intubation and mechanical ventilation, the mortality rate was low. We conclude that intubation and mechanical ventilation in patients with life-threatening asthma are safe and beneficial interventions.
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The pathogenesis of acute myocardial ischemia or infarction following cocaine abuse is not known. Cocaine causes an increase in circulating catecholamines. Therefore alpha-adrenergic mediated focal or generalized coronary artery spasm has been presumed to be the likely mechanism to induce ischemia. However, coronary vasospasm in chronic cocaine abusers has not been demonstrated angiographically. Moreover, it has been observed that patients commonly manifest ischemic changes hours up to a week after abusing cocaine. In order to evaluate direct effects of cocaine on coronary vasculature, 6 chronic cocaine abusers admitted with prolonged chest pain and electrocardiographic ST- and T-wave changes were studied. Cocaine administered intravenously (maximum 32 mg) produced subjective sensation of central nervous stimulation (the "high") in all patients. However there was no significant change in coronary artery diameter (assessed by computer-assisted quantitative technique), myocardial perfusion (assessed by contrast echocardiography) or left ventricular wall motion (assessed by two-dimensional echocardiography) as compared with the baseline values. Coronary sinus flow (thermodilution) showed an upward trend, a probable reflection of a significant increase in cardiac output (average 62%, p less than 0.007). Despite a significant elevation in heart rate (average 56%, p less than 0.007), mean systemic arterial pressure (average 12%, p less than 0.05) and rate-pressure product (average 69%, p less than 0.005), no symptomatic or acute electrocardiographic changes were observed. It is concluded that recreational doses of cocaine do not cause focal or generalized coronary vasospasm or reduced myocardial perfusion in patients who present with chest pain temporally related to cocaine.(ABSTRACT TRUNCATED AT 250 WORDS)
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STUDY OBJECTIVES: To describe the clinical and ECG features of cocaine abusers evaluated in the emergency department and admitted to the medical coronary care unit with chest pain consistent with myocardial ischemia. DESIGN: A four-month retrospective review of all cocaine abusers who presented to the ED with chest pain and a diagnosis of possible myocardial infarction. SETTING: Urban county hospital. TYPE OF PARTICIPANTS: Forty-eight adult cocaine abusers admitted with chest pain. MEASUREMENTS AND MAIN RESULTS: Patients included 34 men and 14 women with a mean age of 29 +/- 7.3 years. The average duration of cocaine abuse in 28 patients for whom it was reported was 5 +/- 4.8 years. Chest pain occurred within one hour of cocaine abuse in 13 admissions (27%), more than one hour after abuse in 13 admissions (27%), and it was not recorded in 23 admissions (47%). Initial ECGs were evaluated in all patients and revealed significant repolarization abnormalities consisting of abnormal ST segment elevations in 18 (37%) and T-wave inversions in 20 (41%) that often persisted on subsequent ECGs. Three patients sustained acute myocardial infarctions. CONCLUSIONS: Our findings confirm a small but significant incidence of myocardial infarction in cocaine abusers presenting to the ED with chest pain. The chronicity of cocaine abuse, the persistence of ECG abnormalities, and the variable temporal relationship of chest pain to cocaine abuse suggest possible chronic myocardial changes as etiologies of ischemia.
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Although the strategies of early embryogenesis differ greatly among multicellular eukaryotes, there are certain parallels in structure, form, and function that cross even kingdom lines: the extreme heat sensitivity of zygotes and very early embryos, followed by the acquisition of thermotolerance during subsequent development, is one such parallel. The heat sensitivity may be so extreme that even moderate increases in temperature result in lethality (generally associated with the earliest phases of embryogenesis), or the effects may be less severe, resulting in defects in development but not in lethality. Mechanistically, and molecularly, these two forms of thermosensitivity appear to have different origins. On the one hand, outright lethality appears to result from an inability to induce heat shock genes and proteins; on the other hand, heat-induced developmental defects appear to result from an alteration in expression of non-heat shock genes and from a delay in the overall developmental program that generally accompanies the cell's response to heat shock. This review is focused on the developmental regulation of the heat shock response during early embryogenesis and on the impact of this regulation on the development of both animal and plant embryos. The two basic issues that we address here are (i) the expression of heat shock genes in the absence of heat shock during embryogenesis and (ii) the expression (or lack of expression) of heat shock genes after deliberate exposure of the embryos to heat shock and the consequences of this expression on its subsequent survival and development.