Biomedical subjects
R P Dellinger
Publications and source records attributed to R P Dellinger.
Placebo and inhaled nitric oxide mortality the same in ARDS clinical trial.
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Programs, partnerships, and patient care: moving Society of Critical Care Medicine and critical care forward. The Presidential Address from the 27th Educational and Scientific Symposium of the Society of Critical Care Medicine.
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Inhaled nitric oxide: can we deliver?
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Tumor necrosis factor in septic shock and multiple system trauma.
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Blood gas monitoring.
Arterial blood gas (ABG) measurements are one of the most frequently requested laboratory examinations in critically ill patients. ABGs include measurement of pHa, PaCO2, PaO2, and oxyhemoglobin saturation. These measurements allow for assessment of the nature, progression, and severity of metabolic and respiratory disturbances.
Fundamental critical care support: another merit badge or more?
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Post hoc analyses in sepsis trials: a formula for disappointment?
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Continuous intra-arterial blood gas monitoring.
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Nitric oxide inhibition in the treatment of septic shock.
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Clinical outcome end points and assessment of mechanical ventilation innovations.
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Treatment of gram-negative septic shock with an immunoglobulin preparation: a prospective, randomized clinical trial.
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Initial evaluation of a new intra-arterial blood gas system in humans.
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.
Airway management and nosocomial infection.
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Endotracheal intubation and mechanical ventilation in severe asthma.
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.
The practice of critical care medicine. A national survey report. ACCP Council on Critical Care.
Aggressive reimbursement reform has been an imposing directive for care providers of ICU medicine. Timely knowledge of actual care routines obtained from a large sample of actively practicing physicians should be mandatory when developing any guidelines or practice standards. A questionnaire was therefore designed by the steering committee of the ACCP Council on Critical Care and sent to its members. The 1,294 responses were analyzed for demographics of the individual practitioner, local aspects of ICU staffing and policies, reimbursement, and a specific practice issue, nutrition. The typical respondent was aged 41 to 50 (41 percent), was a pulmonary subspecialist (68 percent), was not critical care certified (55 percent), worked 25 to 50 percent of his or her total time in the ICU (40 percent), and would continue ICU practice despite poor reimbursement (82 percent). Physicians practiced within a group (53 percent), in a 100- to 500-bed hospital (69 percent), with house staff available (60 percent), and predominantly cared for Medicare patients (55 percent). The following data may allow better judgments to be made pertaining to the implementation of care policies in the current ICU environment.
Clinical trials in adult respiratory distress syndrome.
The need for randomized clinical trials in adult respiratory distress syndrome (ARDS) is now recognized. With this recognition comes the need for researchers to implement proper trial design and for the clinician to be able to interpret results as they apply to clinical practice. The heterogeneity of ARDS as related to etiology, stage, and severity creates the potential for maldistribution of patients in the clinical trial. Likewise, a particular intervention may benefit or not benefit a patient based on these variables. Choosing a minimum of end-points (ideally one) for hypothesis testing is important. The optimal end-point for hypothesis testing pertinent to clinical impact is all-cause mortality at a certain time point (usually 14 or 28 days). Unblinded trials are suboptimal, but necessary, with interventions such as mechanical ventilation treatment modalities. Given these circumstances, treatment protocols should be utilized in both groups. Cooperation of the basic scientist and the clinical scientist is ideal for direction of research in ARDS. Industry funding of ARDS clinical trials is now typical and needed. Under these circumstances, it is important to prevent inappropriate industry influence on trial design, data analysis, data interpretation, and data presentation. The investigator must remain above reproach and the informed consent process must be of the highest standard.
Does cocaine cause coronary vasospasm in chronic cocaine abusers? A study of coronary and systemic hemodynamics.
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)