Journal of critical care
-
Journal of critical care · Mar 1996
Comparative StudyA comparison between the acute effects of nitric oxide synthase inhibition and fluid resuscitation on myocardial function and metabolism in entotoxemic dogs.
Nitric oxide (NO) synthase inhibitors increase mean arterial pressure (MAP) and systemic vascular resistance (SVR) in animal models of sepsis and in humans with septic shock. However, NO synthase inhibitors may cause coronary vessel constriction leading to myocardial ischemia and increased mortality in endotoxemic animals. This study was designed to test the acute effect of NG-nitro-L-arginine (L-NAME) on left ventricular (LV) function and coronary blood flow in a dog model of endotoxemia. ⋯ We conclude that although L-NAME at 30 mg/kg causes vasoconstriction, its effects on coronary blood flow and LV function were not significant.
-
Journal of critical care · Mar 1996
Diagnosis and therapy of acute respiratory distress syndrome in adults: an international survey.
In an attempt to identify the range of opinions influencing the diagnosis and therapy of patients with the adult respiratory distress syndrome (ARDS), a postal survey was mailed to 3,164 physician members of the American Thoracic Society Critical Care Assembly. The questionnaire asked opinions regarding the factors important in the diagnosis of ARDS and its treatment. Thirty-one percent of physicians surveyed responded within 4 weeks, the vast majority of which were board certified or eligible in Internal Medicine, Pulmonary Disease, and/or Critical Care Medicine. ⋯ It was reported that modest levels of positive end-expiratory pressure (PEEP) were used in incremental fashion as FiO2 requirements increased. Perceived indications for insertion of pulmonary artery catheters and compensation of the effects of PEEP on the pulmonary artery occlusion pressure varied widely among the responders. We conclude that reported practice patterns regarding the care of ARDS patients vary widely even within a relatively homogenous group of critical care practitioners.
-
Journal of critical care · Mar 1996
Pulmonary lactate release in patients with sepsis and the adult respiratory distress syndrome.
Elevated arterial lactate concentrations in patients with sepsis have been interpreted as evidence of peripheral, nonpulmonary tissue hypoxia. These patients often develop pulmonary failure manifested by the acute respiratory distress syndrome (ARDS). As the result of tissue hypoxia or inflammation, the lungs of patients with sepsis and ARDS may become a source of lactate release into the circulation. ⋯ The lungs of patients with sepsis and ARDS may produce lactate. Pulmonary lactate release correlates with the severity of lung injury. The contribution of pulmonary lactate release should be considered when interpreting arterial lactate concentration as an index of systemic hypoxia.
-
Nitric oxide (NO) is a major regulator of vascular tone, blood pressure, and blood flow, and plays a significant role in disease states associated with hemodynamic alterations. However, the role of NO in association with the effects of brain death (BD) has not yet been evaluated. ⋯ The decreases in pulmonary and systemic vascular resistance, pulmonary impedance, and cardiac function associated with BD are not related to major changes in the NO pathway. NO may not play a key role in the early changes after BD.
-
Journal of critical care · Mar 1996
Effect of alpha-adrenoreceptor stimulation on the diaphragmatic oxygen delivery-consumption relationship.
In the vascularly isolated canine hemidiaphragm, we tested the hypothesis that alpha-adrenoreceptor stimulation may influence diaphragmatic function and O2 extraction during reductions in O2 delivery (QO2di). ⋯ These results indicate that alpha-adrenoreceptor activation may increase the tension generated by the diaphragm as well as its oxygen consumption and oxygen extraction. Although this may be beneficial during moderate reductions in oxygen delivery, in more severe shock states, activation of these receptors by endogenous or exogenously administered catecholamines may hasten the development of delivery limitation of VO2di and compromise the ability to sustain ventilation.