The basic definition of myocardial ischemia is a greater myocardial tissue oxygen demand than oxygen supply. During short-term ischemic episodes, the heart's defense mechanism seeks to remedy this imbalance by downregulating myocardial contractile function and, concomitantly, increasing the rate of glycolysis (anaerobic energy production). Consequently, sar-colemmal glucose transport increases, and intracellular acido-sis resulting from a buildup of the glycolytic breakdown products causes further inhibition of the contractile apparatus.
Even though energy production continues in the absence of oxygen, the glycolytic pathway is an inefficient means for producing adenosine triphosphate (ATP). As an ischemic episode becomes more severe or prolonged, the heart becomes unable to produce enough energy via glycolysis, and cellular necrosis ensues. For example, 10 min of ischemia result in about 50% depletion of ATP, and after approx 30 min of normothermic ischemia without significant collateral blood flow, irreversible damage or necrosis may occur (1). Anatomically, the most vulnerable layer of the heart is the subendocardium; because of the higher systolic wall stress in this layer compared to the mid- and epicardial layers, there exists a relatively greater metabolic demand.
Was this article helpful?
This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.