The American journal of emergency medicine
-
Lactic acidosis is a marker of tissue hypoperfusion and impairs oxygen delivery. High lactate levels are associated with altered systemic hemodynamics, tissue hypoperfusion, and altered cellular metabolism. Increased lactate levels have also been reported as a complication of β-adrenergic agents administered during asthma therapy. ⋯ Previous studies have suggested that administration of β agonists can lead to lactic acidemia in the absence of hypoxia or shock, but it is the highest level of lactate that we found in the literature. In sepsis and shock, lactic acidosis is used as a marker of disease severity. In this case, it is not necessarily the sign of an immediate gravity.
-
We examined the impact of primary stroke center (PSC) certification on emergency department (ED) use and outcomes within an integrated delivery system in which EDs underwent staggered certification. ⋯ Stroke center certification was associated with significant changes in ED admission and radiographic utilization patterns, without measurable improvements in survival.
-
A 39-year-old man with HIV presented to the emergency department for evaluation of dyspnea accompanied by fever, diffuse chest discomfort, dry cough, and fatigue for past 1 week. The patient described his dyspnea as exertional progressing over 1 week to rest dyspnea. He was prescribed antiretroviral therapy but was noncompliant. ⋯ Vital signs included a temperature of 101°F, heart rate of 115 beats per minute, respiratory rate of 16 per minute, and pulse oxygenation of 91% on room air. Lung examination revealed decreased breath sounds bilaterally, and the remainder of the examination was unrevealing. Laboratory findings revealed leukocytosis and increased serum lactate dehydrogenase of 577 U/L (90-190 U/L), and chest radiograph showed a right lower lobe infiltrate and perihilar, bilateral interstitial infiltrates (Fig. 1A).
-
This study aimed to determine whether (a) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); (b) with the duration of VF, the degree of the imbalance would be greater; and (c) there was a relationship between the level of MMP-9 or TIMP-1 and the cardiac function. ⋯ There was an imbalance between TIMP-1 and MMP-9 after CPR. It may partly contribute to the postresuscitation cardiac dysfunction.