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Signa Vitae

Journal of Intensive Care and Emergency Medicine

The Role of Oxygen in Cardiac Arrest Resuscitation

Abstract

The heart is incapable of storing significant oxygen or substrates and thus is entirely dependent on a continuous delivery of flow in order to support its high metabolic state. Following cardiac arrest, myocardial tissue oxygen tension falls rapidly and aerobic production of ATP ceases. Without re-oxygenation of the ischemic myocardium, return of spontaneous circulation (ROSC) cannot be achieved. The oxygen paradox which has been described regarding other ischemia-reperfusion conditions seems to have application in cardiac arrest. It is clear that some level of oxygenation is necessary to achieve ROSC, however post ROSC there appears to be increased toxicity associated with hyperoxia. The optimal conditions for re-oxygenation in the setting of cardiac arrest remain ill defined at present.

Keywords: cardiac arrest, oxygen, myocard, oxygen delivery, Adenosine-5′-triphosphate (ATP), mitochondria, measurement of tissue oxygen, oxygen paradox

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Protecting mitochondrial bioenergetic function

Abstract

Reversal of cardiac arrest requires reestablishment of aerobic metabolism by reperfusion with oxygenated blood of tissues that have been ischemic for variables periods of time. However, reperfusion concomitantly activates a myriad of pathogenic mechanisms causing what is known as “reperfusion injury.” At the center of reperfusion injury are mitochondria, playing a critical role as effectors and targets of injury. Mitochondrial injury compromises oxidative phosphorylation and the ability to regenerate Adenosine-5′-triphosphate (ATP); i.e., bioenergetic function. Thus targeting mitochondria to protect bioenergetic function may represent a novel concept in resuscitation with the potential for altering clinical practice. We have identified sodium-hydrogen exchanger isoform-1 (NHE)-1 inhibition and erythropoietin as attractive candidate drugs for this purpose and demonstrated corresponding functional and clinical benefits. Further work on the subject may pave the way for further scientific discover focused on greater understating of underlying cell mechanisms, identification of additional and perhaps more potent strategies, and develop means for effective drug delivery.


Keywords:
cardiac arrest, reperfusion injury, mitochondria, bioenergetic function, left ventricular myocardial distensibility, sodium-hydrogen exchanger isoform-1 (NHE-1) inhibitors, erythropoietin

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Anesthetics and cardioprotection

Abstract

The prevalence of the cardiovascular disease significantly affects the outcome of both cardiac and non-cardiac surgery, and perioperative cardiac morbidity is one of the leading causes of death following anesthesia and surgery. The considerable incidence of myocardial infarction, congestive heart failure, myocardial ischemia, or serious dysrhythmias during the intraoperative or postoperative periods, has led many studies to examine medical factors and interventions for decreasing cardiac risk in patients with cardiovascular disease. An extensive amount of work has focused on whether any one anesthetic agent or technique is particularly beneficial for patients with coronary artery disease. Experimental studies conducted in our laboratory have clearly shown that volatile anesthetics may exert profound cardioprotection against myocardial ischemia and reperfusion injury. This article examines the recent evidence about the importance of mitochondria, reactive oxygen species and the KATP channels in cardioprotective signaling by volatile anesthetics. Moreover, the article addresses current concepts and controversies regarding specific roles of the mitochondrial and the sarcolemmal KATP channels in anesthetic-induced preconditioning.

Key words: preconditioning, volatile anesthetics, heart, coronary disease, ischemia, myocardial infarction, mitochondria.

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