The compensatory mechanisms described above are quite effective at maintaining critical organ perfusion even in the face of severe hemorrhage. Animal studies demonstrate complete recovery without intervention in animals bled as much as 40 percent of their estimated blood volumes. However, if the hemorrhage is not controlled, a vicious cycle of increased myocardial work and decreased perfusion eventually develops. Progressive increases in heart rate shorten diastole, with a resultant decrease in myocardial perfusion and oxygenation as well as cardiac filling and output. The low perfusion state increases acidemia, which in turn decreases myocardial contractility.
Eventually, cardiac output becomes inadequate to maintain cellular oxygen delivery, and characteristic changes occur. The first cellular response to hypoperfusion is an attenuation of the cell membrane and an increase in sodium influx. Adenosine triphosphate (ATP) is utilized to maintain function of the sodium-potassium pump; during periods of low flow, however, it cannot be regenerated in sufficient quantities through the normal oxygen-dependent pathways. As the supply of oxygen and high-energy substrates diminishes, the cells revert to anaerobic metabolism to generate ATP, resulting in the accumulation of lactic acid. As ATP availability decreases, sodium continues to enter the cells, causing progressive swelling first of the cytoplasm, then the endoplasmic reticulum, and finally the mitochondria. Eventually the cells undergo clumping of mitochondria, loss of membrane integrity, and death.
There appears to be a point of no return for individual cells as well as for the overall organism in shock. Although this point is well defined for the cell, the clinician caring for patients in shock is less able to identify this landmark. It has been suggested that a sudden and substantial decrease in oxygen consumption may be a reliable marker of irreversible shock.
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