Shock

Shock is a life-threatening condition and to provide the best treatment, nursing care needs to focus on the cause of shock. Different types of shock and their causes are discussed to provide a better understanding of the nursing priorities involved.     

Shock

Inevitably, a patient in shock will present to your office. The findings may be obvious, or they may show the more subtle changes of mild tachypnea, tachycardia, and/or changes in mental status. In either event, the perfusion pressure either has already decompensated or will do so momentarily. Whether you initiate therapy then and there might well determine whether your patient will survive. Accordingly, each office should have available for the pre-hospital management of shock those items listed in Table 3. As clinicians, you must be prepared to begin treatment in your office. Although the hospital, particularly the intensive or coronary care unit, is the appropriate setting for the management of shock, therapy must be initiated as soon as and wherever the diagnosis is made. In this situation, an ounce of prevention is indeed worth a pound of cure. Shock, whether it develops insidiously or precipitously, is a state of inadequate tissue perfusion that, if misdiagnosed or treated inadequately, will inevitably result in death.     

Shock liver

The clinical syndrome of "shock liver," also known as ischemic hepatitis, is characterized by sudden elevation (to more than 20 times the upper limit of normal) of SGOT and SGPT in response to cellular anoxia, followed by resolution to near normal levels within seven to ten days. In our experience with ten cases, systemic hypotension was documented in only four, but processes characterized by decreased cellular perfusion were identified in all and included cardiac failure or arrhythmia, sepsis, cerebrovascular accidents, renal failure, and chronic obstructive pulmonary disease. We were also able to document the transient rise in serum bilirubin and alkaline phosphatase levels and prolonged prothrombin time that followed the transaminase elevations by 24 to 48 hours in most cases, followed by rapid resolution. In neither of the two cases in which tissue was available by biopsy after resolution of the biochemical abnormalities did we find the classic histologic picture of necrosis in zone 3 ("centrilobular necrosis"). The clinical picture of shock liver is so characteristic and resolves so rapidly that there should be no confusion with other causes of marked elevations of transaminase levels.