Journal of Blood Disorders & Transfusion

White Blood Cell Dynamics and Their Role in Post Cardiac Arrest

Elena Heldin^* Department of Hematology, Lund University, Lund, Sweden
^*Correspondence: Elena Heldin, Department of Hematology, Lund University, Lund, Sweden, Email:

Received: 29-Aug-2025, Manuscript No. JBDT-25-30355; Editor assigned: 01-Sep-2025, Pre QC No. JBDT-25-30355 (PQ); Reviewed: 15-Sep-2025, QC No. JBDT-25-30355; Revised: 22-Sep-2025, Manuscript No. JBDT-25-30355 (R); Published: 29-Sep-2025, DOI: 10.4172/2155-9864.25.S16.079

Description

Cardiac arrest continues to be a major cause of mortality worldwide and although advances in emergency response have improved immediate survival, long-term outcomes remain variable. One-year mortality after cardiac arrest depends on multiple factors including neurological recovery, organ function, underlying health status and the magnitude of physiological stress following resuscitation. Among the many clinical parameters assessed during hospitalization, the White Blood Cell (WBC) count has gained attention as a possible indicator of long-term survival. Because the WBC count reflects inflammatory and immune activity, two processes central to post-cardiac arrest physiology, its association with one-year mortality has become an important area of investigation.

Cardiac arrest results in an abrupt halt of blood flow, rapidly depriving tissues of oxygen. When circulation is restored through cardiopulmonary resuscitation and Return of Spontaneous Circulation (ROSC), the body undergoes widespread reperfusion injury. This injury activates a cascade of inflammatory reactions, metabolic disturbances and oxidative stress. These harmful processes together contribute to postcardiac arrest syndrome, a condition that can persist for days or weeks. The brain is particularly sensitive to oxygen deprivation and neurological injury often dictates long-term survival. However, other organs including the kidneys, heart and liver may also experience persistent dysfunction. Because these injuries arise from a strong inflammatory and immune response, laboratory indicators that reflect such changes can offer insight into long-term outcomes. WBC count is one such indicator, easily measured and widely available in all clinical settings.

The WBC count represents the total number of leukocytes circulating in the blood. After cardiac arrest, leukocytes play an active role in modulating inflammation, eliminating damaged cells and responding to physiological stress. The production and release of leukocytes from bone marrow increase rapidly as the body reacts to ischemia and reperfusion. Elevated WBC count after ROSC is often considered a sign of heightened systemic inflammation. A high WBC count reflects strong inflammatory activation. After ROSC, reperfusion triggers numerous inflammatory pathways involving cytokine release, endothelial activation and oxidative reactions. When this response is excessive, recovery becomes more difficult. Persistent inflammation can worsen brain injury, contribute to secondary organ damage and reduce overall survival probability.

Individuals with elevated WBC counts often exhibit more extensive neurological impairment. Because the severity of brain injury influences long-term outcomes more than any other factor, the association between increased WBC and one-year mortality is understandable. Severe neurological insult activates widespread systemic responses, including leukocyte mobilization, which may partly explain this pattern. Additionally, elevated WBC count has been associated with cardiac dysfunction following ROSC. The myocardium is vulnerable to reperfusion injury and inflammatory cells that infiltrate the heart can worsen contractile dysfunction. Individuals who experience such complications may have reduced survival rates over the following year.

Although elevated WBC counts are commonly studied, low counts may also predict poorer outcomes. A decreased WBC count can represent bone marrow exhaustion, inadequate immune function, or a prolonged immunosuppressive phase resembling late-stage sepsis. After cardiac arrest, some individuals experience downregulation of leukocyte production and activity. Immunosuppression after cardiac arrest increases susceptibility to secondary infections, a significant contributor to late mortality. Respiratory infections, bloodstream infections and urinary tract infections frequently occur in individuals requiring prolonged hospitalization or intensive care support. Those with low WBC counts may be less capable of mounting an effective response to such infections, worsening long-term survival rates.

The timing of WBC measurement plays an important role in evaluating its association with long-term outcomes. The most closely examined timeframes include immediately after ROSC, within the first 24 hours and during the initial 72 hours. The earliest values reflect the immediate systemic reaction to ischemia and reperfusion. High counts at this stage frequently correspond with longer resuscitation times, more severe metabolic derangements, or profound tissue injury.

WBC count serves as an accessible and informative indicator of systemic response following cardiac arrest. Elevated or markedly reduced levels reflect physiological stress, inflammatory burden, or immune dysfunction, all of which are associated with increased one-year mortality. Although WBC count should not be viewed as an isolated predictor, it enhances broader clinical assessment and may identify individuals requiring closer observation and follow-up.