Hyperlactatemia and Cardiac Surgery

The normal blood lactate level is 0–2 mmol/L, and a value above 3–5 mmol/L is variably used to define hyperlactatemia. In cardiac surgical patients, hyperlactatemia can arise from both hypoxic and non-hypoxic mechanisms. The major non-hypoxic mechanism is likely stress-induced accelerated aerobic metabolism, in which elevated lactate results from a mass effect on the lactate/pyruvate equilibrium. The lactate/pyruvate ratio is normal (20). Lactate is a strong anion that is virtually fully dissociated at physiological pH. As such, increased lactate concentration reduces the strong ion difference and exerts an acidifying effect on the blood. Hyperlactatemia in cardiac surgery patients has been categorized as either early or late onset. Early-onset hyperlactatemia is that which develops in the operating room or very early following intensive care unit (ICU) admission. Early-onset hyperlactatemia is strongly associated with adverse outcome and probably arises as a consequence of both hypoxic (e.g., microcirculatory shock) and non-hypoxic (accelerated aerobic metabolism) mechanisms. By contrast, late-onset hyperlactatemia is a benign, self-limiting condition that typically arises within 6-12 hours of ICU admission and spontaneously resolves within 24 hours. Late onset hyperlactatemia occurs in the absence of any evidence of global or regional tissue hypoxia. The mechanism of late onset hyperlactatemia is not understood. Hyperlactatemia is a common accompaniment to treatment with β2-agonists such as epinephrine. Epinephrine-induced hyperlactatemia is thought to be due to accelerated aerobic metabolism and requires no specific intervention. Irrespective of the cause, the presence of hyperlactatemia should trigger a search for remedial causes of impaired tissue oxygenation, bearing in mind that normal—or even supranormal—indices of global oxygen delivery may exist despite regional tissue hypoperfusion

Anatomic, stage-based repair of secondary mitral valve disease

OBJECTIVE: Intervention for repair of secondary mitral valve disease is frequently associated with recurrent regurgitation. We sought to determine if there was sufficient evidence to support inclusion of anatomic indices of leaflet dysfunction in the management of secondary mitral valve disease. METHODS: We performed a systematic review and meta-analysis of published reports comparing anatomic indices of leaflet dysfunction with the complexity of valve repair and the outcome from intervention. Patients were stratified by the severity of leaflet dysfunction. A secondary analysis was performed comparing outcomes when procedural complexity was optimally matched to severity of leaflet dysfunction and when intervention was not matched to dysfunction. RESULTS: We identified 6864 publications, of which 65 met inclusion criteria. An association between the severity of leaflet dysfunction and the procedural complexity was highly predictive of satisfactory freedom from recurrent regurgitation. Patients were categorized into 4 groups based on stratification of leaflet dysfunction. Satisfactory results were achieved in 93.7% of patients in whom repair complexity was appropriately matched to severity of leaflet dysfunction and in 68.8% in whom repair was not matched to dysfunction (odds ratio, 0.148; 95% confidence interval, 0.119-0.184; P \u3c .0001). CONCLUSIONS: For patients with secondary mitral valve disease, satisfactory outcome from valve repair improves when procedural complexity is matched to anatomic indices of leaflet dysfunction. Anatomic indices of leaflet dysfunction should be considered when planning interventions for secondary mitral regurgitation. Routine inclusion of anatomic indices in trial design and reporting should facilitate comparison of results and strengthen guidelines. There are sufficient data to support anatomic staging of secondary mitral valve disease

Available Capacity of a Privately Owned Workstation

Cache Coherence Protocol for the DASH Multiprocessor. In Proc. of the 17th International Symposium on Computer Architecture, pages 148–159