From the Guidelines
Cardiopulmonary arrest can cause an increased white blood cell count due to the body's systemic inflammatory response to severe ischemia-reperfusion injury. During cardiac arrest, the body experiences severe physiological stress and tissue hypoxia, triggering an inflammatory response that mobilizes white blood cells from bone marrow reserves into circulation. This stress leukocytosis typically occurs within hours after resuscitation from cardiac arrest, as noted in the 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care 1. The white blood cell elevation is often characterized by an increase in neutrophils specifically, which are released as part of the body's systemic inflammatory response to the severe ischemia-reperfusion injury. Additionally, catecholamine release during cardiac arrest and resuscitation efforts stimulates demargination of white blood cells adhered to blood vessel walls, further contributing to the elevated count, as discussed in the context of post-cardiac arrest care 1. This leukocytosis following cardiac arrest is generally transient but can persist for days depending on the extent of tissue damage, presence of infection, and other complications. Some key points to consider include:
- The inflammatory response and subsequent leukocytosis are part of the body's immediate reaction to cardiac arrest and resuscitation.
- Clinicians should be aware that while an elevated white blood cell count is common after cardiac arrest, it must be interpreted in context, as it may also indicate developing complications such as infection or ongoing tissue damage.
- The management of post-cardiac arrest patients involves a comprehensive approach, including the assessment and mitigation of ischemia-reperfusion injury to multiple organ systems, as outlined in the guidelines 1.
- The use of specific interventions, such as targeted temperature management and ventilation strategies, may impact the patient's outcome and should be considered in the context of their individual needs and circumstances 1.
From the Research
Cardiopulmonary Arrest and White Blood Cell Count
- Cardiopulmonary arrest can lead to a systemic inflammatory response, which is characterized by an increase in white blood cell count (WBC) 2, 3, 4.
- Studies have shown that elevated WBC counts are associated with increased mortality and poor outcomes in patients who have experienced cardiopulmonary arrest 2, 5.
- The dynamics of WBC count changes after cardiopulmonary arrest are not well established, but research suggests that WBC counts tend to decay exponentially over time 3, 4.
- The relationship between WBC count and mortality is complex, with both high and low WBC counts being associated with increased mortality 2.
Inflammatory Response and Cardiopulmonary Arrest
- Cardiopulmonary arrest triggers a systemic inflammatory response, which is characterized by the release of various inflammatory markers, including interleukin-6 (IL-6) and procalcitonin 6, 5.
- The level of inflammatory response is associated with the severity of post-cardiac arrest syndrome (PCAS) and mortality 6, 5.
- Targeted temperature management (TTM) does not appear to modify the level of inflammatory response after cardiopulmonary arrest 6.
Prognostic Implications
- Elevated WBC counts and inflammatory markers, such as IL-6 and procalcitonin, are associated with increased mortality and poor outcomes in patients who have experienced cardiopulmonary arrest 2, 5.
- The predictive capability of inflammatory markers, such as procalcitonin and IL-6, can be used to identify high-risk patients and inform treatment decisions 5.