from Part IV - Therapy of sudden death
Published online by Cambridge University Press: 06 January 2010
Introduction
Shock is a complex entity traditionally defined as a state in which the oxygen utilization or consumption needs of tissues are not matched by sufficient delivery of oxygen. This mismatch commonly results from states of altered tissue perfusion. From this perspective, cardiopulmonary arrest represents the most extreme of shock states.
Figure 38.1 represents the basic relationship between oxygen consumption (VO2) and oxygen delivery (DO2) that is pertinent to individual organs as well as to the whole body. VO2 can remain constant over a wide range of DO2, because most tissue beds are capable of efficiently increasing the extraction of oxygen. This will be reflected by decreasing venous oxygen saturation from each organ. When DO2 reaches a critical threshold, however, tissue extraction of oxygen cannot be further increased to meet tissue demands. At this point VO2 becomes directly dependent on DO2 (DO2crit) and cells begin to convert to anaerobic metabolism, as manifested by increases in certain metabolic products such as lactate, NADH, and reduced cytochrome oxidase. The point of DO2crit is the point of dysoxia or ischemia at which tissue DO2 cannot meet tissue oxygen demand. Oxygen debt can be defined as the amount of cumulative difference of VO2 between baseline and that spent below DO2crit. As discussed later, the level of accumulated oxygen debt in shock states is critically linked with survival.
Several unique physiologic aspects and principles of cardiac arrest and CPR exist that limit the usefulness of many monitoring modalities, some of which will be more useful in the postresuscitation period. These include the following.
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