If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock. Refractory
At Refractory stage (stage 4), the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much of the cellular ATP (the basic energy source for cells) has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. Because cells can only produce adenosine at a rate of about 2% of the cells total need per hour, even restoring oxygen is futile at this point because there is no adenosine to phosphorylate into ATP. Diagnosis
The diagnosis of shock is commonly based on a combination of symptoms, physical examination, and laboratory tests. Many signs and symptoms are not sensitive or specific for shock, thus many clinical decision-making tools have been developed to identify shock at an early stage. A high degree of suspicion is necessary for the proper diagnosis of shock. The first change seen in shock is increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire.
Colloids and crystalloids appear to be equally effective with respect to outcomes., Balanced crystalloids and normal saline also appear to be equally effective in critically ill patients. If the person remains in shock after initial resuscitation, packed red blood cells should be administered to keep the hemoglobin greater than 100 g/L.For those with hemorrhagic shock, the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension). Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, or until the patient has adequate mentation and peripheral pulses. Hypertonic fluid may also be an option in this group. Medications
Vasopressors may be used if blood pressure does not improve with fluids. Common vasopressors used in shock include: norepinephrine, phenylephrine, dopamine, and dobutamine. There is no evidence of substantial benefit of one vasopressor over another; however, using dopamine leads to an increased risk of arrhythmia when compared with norepinephrine. Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma but may be of use in neurogenic shock. Activated protein C (Xigris), while once aggressively promoted for the management of septic shock, has been found not to improve survival and is associated with a number of complications. Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued. The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes.