A quantitative analysis of the acidosis of cardiac arrest: a prospective observational study
A quantitative analysis of the acidosis of cardiac arrest: a prospective observational study
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DOI：
10.1186/cc3714
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发表时间：
2005-08-01
期刊：
影响因子：
15.1
通讯作者：
Bellomo, R
中科院分区：
文献类型：
--
作者：
Makino, J;Uchino, S;Bellomo, R
代谢性酸中毒在心脏骤停患者中很常见，通常认为主要是由高乳酸血症引起的。然而，单纯的高乳酸血症并不能解释代谢性酸中毒的原因。最近，Stewart Figge方法被发现在解释和量化各种临床情况下的酸碱变化是有用的。这种新颖的定量方法也可能为心脏骤停酸中毒的因素提供有用的见解。我们认为，高乳酸血症不是心脏骤停酸中毒的唯一原因，其他因素在其发展中起着重要作用。方法前瞻性纳入东京某三级医院急诊科收治的院外心脏骤停患者105例和轻伤患者28例（对照组）。血清钠、钾、离子钙、镁、氯化物、乳酸、白蛋白、磷酸盐和血气在到达急诊科后尽快测量，随后使用Stewart - Figge方法进行分析。结果与对照组相比，心脏骤停患者有严重的代谢性酸中毒（标准碱过量- 19.1 vs - 1.5; P < 0.0001）。他们也有高钾血症、低氯血症、高乳酸血症和高磷血症。心脏骤停患者阴离子间隙和强离子间隙也较高。以对照组为参照，乳酸是酸中毒的最强决定因素（- 11.8 meq/ l），其次是强离子间隙（- 7.3 meq/ l）和磷酸盐（- 2.9 meq/ l）。低氯血症（+ 4.6 meq/ l）、高钾血症（+ 3.6 meq/ l）和低白蛋白血症（+ 3.5 meq/ l）的碱化作用减弱了代谢性酸中毒。结论院外心脏骤停患者代谢性酸中毒的病因复杂，并非单纯由高乳酸血症引起。此外，补偿变化自发发生，减轻了其严重性。
Introduction Metabolic acidosis is common in patients with cardiac arrest and is conventionally considered to be essentially due to hyperlactatemia. However, hyperlactatemia alone fails to explain the cause of metabolic acidosis. Recently, the Stewart Figge methodology has been found to be useful in explaining and quantifying acid - base changes in various clinical situations. This novel quantitative methodology might also provide useful insight into the factors responsible for the acidosis of cardiac arrest. We proposed that hyperlactatemia is not the sole cause of cardiac arrest acidosis and that other factors participate significantly in its development.Methods One hundred and five patients with out-of-hospital cardiac arrest and 28 patients with minor injuries ( comparison group) who were admitted to the Emergency Department of a tertiary hospital in Tokyo were prospectively included in this study. Serum sodium, potassium, ionized calcium, magnesium, chloride, lactate, albumin, phosphate and blood gases were measured as soon as feasible upon arrival to the emergency department and were later analyzed using the Stewart - Figge methodology.Results Patients with cardiac arrest had a severe metabolic acidosis ( standard base excess - 19.1 versus - 1.5; P < 0.0001) compared with the control patients. They were also hyperkalemic, hypochloremic, hyperlactatemic and hyperphosphatemic. Anion gap and strong ion gap were also higher in cardiac arrest patients. With the comparison group as a reference, lactate was found to be the strongest determinant of acidosis (- 11.8 meq/ l), followed by strong ion gap (- 7.3 meq/ l) and phosphate (- 2.9 meq/ l). This metabolic acidosis was attenuated by the alkalinizing effect of hypochloremia (+ 4.6 meq/ l), hyperkalemia (+ 3.6 meq/ l) and hypoalbuminemia (+ 3.5 meq/ l).Conclusion The cause of metabolic acidosis in patients with out-of-hospital cardiac arrest is complex and is not due to hyperlactatemia alone. Furthermore, compensating changes occur spontaneously, attenuating its severity.