Sudden Cardiac Arrest is the term used to describe a condition in which the heart suddenly stops pumping blood (carrying oxygen) to the various organs of the body.
When organs stop receiving blood, they develop ischemia – a term used to describe a severe energy imbalance that results from lack of oxygen. The severity of ischemia depends on how much oxygen an organ needs and for how long the lack of oxygen remains. Organs with the highest need of oxygen are the heart and the brain. These organs cannot tolerate lack of oxygen for more than a few minutes before irreversible damage occurs. With CPR, blood flow is artificially generated to deliver oxygen to these and other organs. The more effective CPR, the more oxygen is delivered. This is the reason why so much emphasis is given to starting CPR early and with maximal efficacy.
Yet, return of blood carrying oxygen – although absolutely necessary – is not problem-free. The returning blood carrying oxygen can damage organs that have been ischemic. This damage – known as reperfusion injury – can limit the maximal benefit expected from CPR. Several lines of research have shown that targeting reperfusion injury during CPR can reduce organ damage leading to higher resuscitation and survival rates; yet, currently there are no interventions clinically available to reduce reperfusion injury during CPR.
A top priority at Resuscitation Therapeutics is to bring to the CPR armamentarium pharmacological interventions to reduce reperfusion injury. Research has shown that pharmacological interventions able to reduce reperfusion injury helps preserve the viability of the heart muscle and therefore its capability to pump blood once cardiac activity is restored, leading to better hemodynamic function and survival. Research has also shown that mitochondria are at the center of reperfusion injury. Mitochondria are tiny organelles that live inside cells and enable extracting energy from nutrients in the presence of oxygen. Thus, pharmacological interventions that reduce reperfusion injury during CPR act by maintaining mitochondrial function and therefore the flow of energy that organs need to function properly.
Erythropoietin is the first pharmacological interventions being developed by Resuscitation Therapeutics to improve outcomes by reducing reperfusion injury. Erythropoietin activates intrinsic mechanism that protect mitochondria from reperfusion injury.
Ongoing Project - Learn more
Sodium – hydrogen exchanger isoform 1 (NHE-1) inhibitors are another option to reduce reperfusion injury. NHE-1 inhibitors protect mitochondria by limiting sodium-induced mitochondrial calcium overload and have been shown to be highly effective during CPR through years of preclinical research in the Founder’s laboratory.
Future development - Stay tuned