Effects of Early Hemodynamics, Oxygen Metabolism, and Lactate Dynamics on Prognosis of Post-Cardiac Arrest Syndrome

Effects of Early Hemodynamics, Oxygen Metabolism, and Lactate Dynamics on Prognosis of Post-Cardiac Arrest Syndrome

Cardiac arrest (CA) is a significant global public health concern, with an annual incidence of 0.5 to 1.5 per 1000 individuals. Despite advancements in cardiopulmonary resuscitation (CPR) guidelines by the American Heart Association (AHA) and the International Liaison Committee on Resuscitation, the survival rate and percentage of patients with favorable neurological outcomes post-CA remain relatively low. The AHA 2010 CPR guidelines emphasize the importance of treating post-cardiac arrest syndrome (PCAS) in the intensive care unit (ICU) as the fifth link in the CA survival chain. PCAS is a complex pathophysiological process that includes brain injury, myocardial dysfunction leading to hemodynamic instability, and systemic ischemia/reperfusion response resulting in lactate accumulation. These factors critically influence the survival and neurological prognosis of CA patients in the early stages. This study aimed to assess the effects of early hemodynamics, oxygen metabolism, and lactate dynamics during PCAS on 28-day survival rates and neurological outcomes.

The study was conducted with approval from the Ethics Committee of Beijing Chaoyang Hospital, Capital Medical University. Data from patients admitted to the ICU of Beijing Chaoyang Hospital between January 2012 and July 2019 were analyzed. Inclusion criteria comprised patients who achieved successful resuscitation after out-of-hospital cardiac arrest (OHCA), were aged 18 years or older, and had serum lactate levels measured within two hours after the return of spontaneous circulation (ROSC). Exclusion criteria included pregnancy, malignant tumors, survival for less than two hours, or CA caused by major trauma.

Patient demographics, resuscitation details, and clinical treatment data were collected. Continuous electrocardiography, pulse oximetry, and systemic arterial blood pressure measurements were used to monitor all OHCA patients. Treatment followed the AHA 2010 CPR guidelines. Vital signs and arterial blood gas analysis, including mean arterial pressure (MAP), heart rate (HR), serum lactate levels, arterial pH, partial oxygen pressure (PaO2), and partial carbon dioxide pressure (PaCO2), were recorded at admission (within two hours after ROSC) and three days later (72 hours after ROSC). Lactate clearance was calculated as the percentage reduction in lactate levels from admission to 72 hours post-ROSC. Patients were followed until death or up to 28 days. Neurological prognosis was assessed using the cerebral performance category (CPC) score, with a favorable outcome defined as a CPC score of 1 to 2.

Baseline characteristics and index events were described for both survival and non-survival groups. Continuous data were presented as means with standard deviations or medians with interquartile ranges, depending on data normality. Categorical variables were expressed as numbers and percentages. Differences in variables were assessed using Student’s t-test, the Wilcoxon rank-sum test, or the Chi-squared test, as appropriate. Univariate and multivariate Cox regression analyses identified risk factors for 28-day mortality and predictors of good neurological outcomes. Statistical significance was set at P < 0.05, and analyses were performed using IBM SPSS Statistics 22.

A total of 1383 patients with ROSC after CA were initially recruited. After exclusions, 1150 patients were enrolled, with 476 in the 28-day survival group and 674 in the non-survival group. Notably, 44.1% of non-survivors died within 72 hours. The primary cause of OHCA was cardiac in nature, with reperfusion therapy and therapeutic hypothermia equally distributed between the groups. The survival group had a higher proportion of male patients, younger age, and more shockable rhythms compared to the non-survival group. Additionally, the survival group required less mechanical ventilation and had a shorter time to ROSC.

Hemodynamic and metabolic parameters were significantly different between the groups. On day one, the survival group had higher MAP. At 72 hours post-ROSC, the survival group exhibited lower HR, higher MAP, and lower doses of vasopressors (noradrenaline and dopamine). Blood gas analysis revealed no significant differences in PaO2 and PaCO2 between the groups on day one. However, by day three, the survival group had higher pH and PaO2 but lower PaCO2. Lactate levels at admission were significantly lower in the survival group, and lactate clearance was better compared to the non-survival group.

Neurological outcomes were more favorable in the survival group, with 53.8% achieving good neurological prognosis at 28 days. The survival group showed higher rates of favorable neurological outcomes on both day one and day three compared to the non-survival group. Cox regression analysis identified greater lactate clearance as a significant predictor of lower 28-day mortality risk. Other significant variables included time to ROSC, non-shockable rhythm, 72-hour HR, and MAP. Lactate clearance was the sole predictor of good neurological outcomes.

The study highlights the importance of early hemodynamic and metabolic monitoring in PCAS patients. Despite improvements in CA-ROSC success rates, survival discharge rates and favorable neurological outcomes remain suboptimal. PCAS care focuses on mitigating systemic ischemia-reperfusion injury and non-specific inflammation. However, the distinction between PCAS and septic shock, particularly regarding early vasopressor use, is crucial. Enhancing oxygen metabolism and reducing blood lactate levels are key factors influencing PCAS survival and neurological damage.

Systemic organs in PCAS patients undergo significant changes during ischemia-reperfusion, including impaired cardiac function, hemodynamic instability, oxygen debt, and lactate accumulation due to insufficient tissue perfusion. Inadequate lactate clearance leads to tissue acidosis, brain damage, and multiple organ dysfunction. Excessive vasopressor use exacerbates microcirculatory hypoxia, increasing lactic acid production and underutilization, thereby worsening outcomes. Therefore, early monitoring of hemodynamics and lactate levels is essential.

This large-scale retrospective study analyzed the impact of hemodynamics, oxygen metabolism, and lactate dynamics on PCAS patients, using 28-day survival and good neurological outcomes as primary endpoints. The findings suggest that while high doses of vasopressors may improve hemodynamics, they do not enhance 28-day mortality or neurological outcomes. Instead, maintaining a steady and ideal MAP with reasonable vasopressor doses is beneficial for PCAS treatment.

The study has several limitations. First, it is a single-center retrospective study, which may introduce bias. Second, cumulative adrenaline levels used in pre-hospital CPR were not collected. Third, lactate and blood gas data during resuscitation were limited. Fourth, invasive hemodynamics and continuous lactate monitoring were not performed in the first 72 hours post-ROSC, and resuscitation fluid volume was not calculated.

In conclusion, close monitoring of oxygen metabolism, hemodynamics, and lactate metabolism within 72 hours post-ROSC is vital for PCAS patients. High doses of vasopressors, while improving hemodynamics, do not enhance 28-day mortality or neurological outcomes. Early and appropriate management of these parameters is crucial for improving survival and neurological prognosis in PCAS patients.

doi.org/10.1097/CM9.0000000000001807

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