Cardiac Arrest

What is cardiac arrest?

Cardiac arrest is a sudden and unexpected cessation of normal heart function, leading to the stopping of blood circulation. In cardiac arrest, the heart’s electrical system malfunctions, causing it to stop beating effectively. This condition is life-threatening and requires immediate intervention to restore normal heart rhythm and circulation. If left untreated, cardiac arrest can quickly lead to death.

During cardiac arrest, the heart may enter a chaotic rhythm called ventricular fibrillation (VF) or it may stop beating altogether (asystole). In either case, blood flow to vital organs, including the brain, is severely compromised, leading to loss of consciousness, cessation of breathing, and ultimately, irreversible damage if not treated promptly.

What is the relationship between cardiac arrest and oxidative stress?

Oxidative stress plays a significant role in the pathophysiology of cardiac arrest and its consequences. Here’s how oxidative stress is related to cardiac arrest:

• Ischemia-Reperfusion Injury: Cardiac arrest results in the cessation of blood flow to the heart muscle (ischemia), leading to a lack of oxygen and nutrients. When blood flow is restored (reperfusion) following resuscitation efforts, it can lead to the generation of reactive oxygen species (ROS) and oxidative stress. This process, known as ischemia-reperfusion injury, contributes to tissue damage, inflammation, and cell death in the heart muscle.

• Myocardial Stunning: Myocardial stunning refers to reversible dysfunction of the heart muscle following a period of ischemia and reperfusion. Oxidative stress plays a role in the development of myocardial stunning by promoting oxidative damage to cellular components, impairing energy metabolism, and disrupting contractile function in the heart muscle. This oxidative stress-induced dysfunction can contribute to the overall severity of cardiac arrest and may affect recovery outcomes.

• Arrhythmias: Oxidative stress can predispose the heart to arrhythmias, including ventricular fibrillation (VF) and ventricular tachycardia (VT), which are common causes of cardiac arrest. ROS can alter the electrical properties of cardiac cells, leading to abnormal conduction and excitability, and increasing the risk of arrhythmias. Additionally, oxidative stress can impair the function of ion channels and regulatory proteins involved in cardiac rhythm control, further promoting arrhythmogenesis.

• Reperfusion Injury: Following successful resuscitation from cardiac arrest, reperfusion of blood flow to the heart can paradoxically exacerbate tissue injury through the production of ROS and oxidative stress. Reperfusion injury can contribute to myocardial damage, inflammation, and microvascular dysfunction, impairing recovery and increasing the risk of complications such as heart failure and arrhythmias.

• Systemic Effects: Cardiac arrest and subsequent resuscitation can lead to systemic effects beyond the heart, including systemic inflammation, endothelial dysfunction, and multiorgan dysfunction syndrome. Oxidative stress plays a central role in mediating these systemic effects by promoting inflammation, vascular dysfunction, and cellular injury in various organs and tissues throughout the body.

Overall, oxidative stress is intimately involved in the pathophysiology of cardiac arrest and its consequences, including myocardial injury, arrhythmogenesis, and systemic dysfunction.