stage of shock occurs when MAP decreases by 10 to 15 mm Hg from baseline. Kidney and hormonal compensatory mechanisms are activated because cardiovascular responses alone are not enough to maintain MAP and supply oxygen to vital organs.
The ongoing decrease in MAP triggers the release of renin, antidiuretic hormone (ADH), aldosterone, epinephrine, and norepinephrine to start kidney compensation. Urine output decreases, sodium reabsorption increases, and widespread blood vessel constriction occurs. ADH increases water reabsorption in the kidney, further reducing urine output, and increases blood vessel constriction in the skin and other less vital tissue areas. Together these actions compensate for shock by maintaining the fluid volume within the central blood vessels.
Tissue hypoxia occurs in nonvital organs (e.g., skin, GI tract) and in the kidney, but it is not great enough to cause permanent damage. Acid-base and electrolyte changes occur in response to the buildup of metabolites. Changes include acidosis (low blood pH) and hyperkalemia
refractory stage of shock occurs when too much cell death and tissue damage result from too little oxygen reaching the tissues. Vital organs have extensive damage and cannot respond effectively to interventions, and shock continues. So much damage has occurred with release of metabolites and enzymes that damage to vital organs continues despite interventions.
The sequence of cell damage caused by massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS). Once the damage has started, the sequence becomes a vicious cycle as more dead and dying cells open and release metabolites. These trigger small clots (microthrombi) to form, which block tissue perfusion and damage more cells, continuing the devastating cycle. Liver, heart, brain, and kidney function are lost first. The most profound change is damage to the heart muscle.
Manifestations are a rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation. Therapy is not effective in saving the patient's life, even if the cause of shock is corrected and MAP temporarily returns to normal.
Severe sepsis is sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion (Dellinger et al., 2013). It represents the progression of sepsis with an amplified SIRS (see Fig. 37-4). All tissues are involved and are hypoxic to some degree. Some organs are experiencing cell death and dysfunction at this time. Microthrombi formation is widespread with clots forming where they are not needed. This process uses up or consumes much of the available platelets and clotting factors, a condition known as disseminated intravascular coagulation (DIC). The amplified SIRS and cytokine release increase capillary leakiness, injure cells, and increase cell metabolism. Damage to endothelial cells reduces anticlotting actions and triggers the formation of even more small clots, increasing DIC. Anaerobic metabolism continues, and cell uptake of oxygen is poor. The continued stress response triggers the continued release of glucose from the liver and causes hyperglycemia. The more severe the response, the higher the blood glucose level (Kleinpell et al., 2013; Schell-Chaple & Lee, 2014).
Despite the severity of this stage and the fact that it may be present for 24 hours or more, it is often missed. One of the reasons it may be missed is that the cardiac function is hyperdynamic in this phase. The pooling of blood and the widespread capillary leak stimulate the heart, and cardiac output is increased 751with a more rapid heart rate and an elevated systolic blood pressure. In addition, the patient's extremities may feel warm and there is little or no cyanosis. Even though the patient may "look" better, the pathologic changes occurring at the tissue level are serious and have caused significant damage. The WBC count at this time may no longer be elevated.
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