After World War II, Carl Wiggers simulated hemor-rhagic shock in dogs by connecting a large bottle to the femoral artery of an anesthetized dog with a length of flexible tubing. If the bottle was suspended 136 cm above the heart, the dog's blood pressure (100 mm Hg) would be just enough to push blood up the tubing to the reservoir but little would enter. If the reservoir was lowered to 54 cm above the heart, blood quickly flowed out of the dog and into the reservoir. This continued until enough blood had been shed to lower the mean arterial pressure to 40 mm Hg. It was noted that after several hours of this hypotension the blood would begin to flow out of the bottle and back into the dog. When all the blood had returned, the arterial pressure then began to decline and the dog quickly died. This progression of injury in which the animal required more and more volume just to maintain a pressure of 40 mm Hg was referred to as decompensation. The decompensation phase is due to injury to the peripheral vascular beds from a prolonged period of inadequate blood flow. During the compensated phase, the cardiovascular reflexes attempt to maintain the circulation by vasoconstriction of the systemic arterioles and veins and stimulation of the heart. During decompensation, vascular tone actually falls below normal because of autoregulatory escape from the sympathetic constriction and production of vasodilatory cytokines by the ischemically injured peripheral tissues. These substances include histamine, kinins, nitric oxide, tumor necrosis factor, prostaglandins, and interleukins. As will be seen later, an increase in capillary permeability will also cause fluid to shift into the extravascular space.
Wiggers also noted that after a period of hypotension the bottle could be elevated to restore the cardiac output and blood pressure. If the deficit in cardiac output had been mild, then the dog would recover uneventfully. If the deficit had been severe, however, a normal arterial pressure could not be maintained for long and the dog would again become hypotensive and eventually die. This was termed the irreversible phase of shock. Of course, what was irreversible yesterday may be reversible today, for the management of the shock patient has steadily improved over the years.
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