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Prognostic value of lactate in out-of-hospital cardiac arrest: a prospective cohort study

02 April 2022
Volume 14 · Issue 4

Abstract

Background:

The prognostic role of lactate in out-of-hospital cardiac arrest (OHCA) remains unclear.

Aims:

To explore serum lactate as a predictor of return of spontaneous circulation in patients experiencing OHCA after arrival at hospital.

Methods:

This 13-month prospective observational cohort study involved patients aged ≥18 years. Serum lactate levels were measured during cardiopulmonary resuscitation before ROSC. Patients were divided into two groups by lactate level: Group 1, low (≤9.9 mmol/l) and Group 2, high (≥10 mmol/l).

Findings:

105 patients were included, 50 in group 1 and 55 group 2. Median lactate were 7.4 mmol/l and 14.2 mmol/l respectively. More patients in group 1 were found with ventricular fibrillation (40% versus 14.5%; P≤0.01), obtained ROSC more quickly (37 minutes 38 seconds versus 39 minutes 13 seconds; P=0.79) and achieved short-term survival (survived >24 hours) (40% versus 23.5%; P=0.32), versus group 2; prediction of survival did not reach statistical significance.

Conclusion:

Lower lactate levels in OHCA appear to be associated with better short-term outcomes but the cut-off points regarding survival remain unclear.

Out-of-hospital cardiac arrest (OHCA) is a major public health concern in industrialised countries, with high mortality rates (Zhou et al, 2018). UK emergency medical services treat 30000 OHCAs annually (Perkins and Brace-McDonnell, 2015) but the survival rate remains persistently low. High-quality cardiopulmonary resuscitation (CPR) and early defibrillation, where indicated, are essential to achieve optimal outcomes (Deakin et al, 2010).

Sudden OHCA results in cessation of cardiac function with haemodynamic collapse leading to anaerobic metabolism (Dadeh and Nuanjaroan, 2018). In anaerobic conditions, tissue hypoxia leads to an accumulation of lactate (Mizock and Falk, 1992).

Patients who have had an OHCA are hypoxic, hypoperfused and experience hyperlactataemia, most likely caused by ischaemia and inflammation resulting from ischaemia-reperfusion injury (Donnino et al, 2007; Cocchi et al, 2011), which is a surrogate marker for hypoxic insult (Orban et al, 2017).

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