CHAPTER 28 Shock Emergencies
I. GENERAL STRATEGY
Shock is not a disease, but a clinical manifestation of the body’s inability to perfuse its tissues adequately.1 Shock is recognized as a systemic response to a clinical insult (illness or injury) resulting in inadequate tissue perfusion and decreased oxygen to the cells. Shock can occur from alterations in circulating volume (hypovolemic), alterations in cardiac pump function (cardiogenic), alterations in peripheral vascular resistance or redistribution of blood in the periphery (distributive), and alterations in the blood’s ability to perfuse major organs such as the heart and lungs (obstructive). No matter what the cause of shock is, the final common pathway, when interventions fail, is multiple organ failure and eventually death.
The pathophysiologic alterations that occur during shock may be roughly divided into three stages: compensated, uncompensated, and irreversible.1–4 These stages are summarized in Table 28-1.
| Stage | Pathophysiology |
|---|---|
| Compensated (nonprogressive) stage | Various receptors sense the drop of systemic pressure, initiating a cascade of physiologic changes. Homeostatic compensatory mechanisms mediated by the sympathetic nervous system are activated to restore adequate tissue perfusion and preserve vital organ function in the brain and the heart. Oxygen delivery (DO2) to nonvital organs is not sufficient to meet cellular demand (measured as oxygen consumption [VO2]). To remain viable, the cell will convert from aerobic to anaerobic metabolism. Although initially beneficial, this conversion results in a drastic reduction in energy production and accumulation of lactic acid, the byproduct of anaerobic metabolism. The resulting lactic acidemia begins to cause cellular damage. Preexisting conditions such as chronic obstructive pulmonary edema or cardiovascular disease as well as the age of the patient will cause additional stress during this process. |
| Uncompensated (progressive) stage | The compensatory mechanisms begin to fail to maintain adequate tissue perfusion in the vital organs. Mechanisms that were initially helpful become ineffective and cause additional tissue damage. Cellular derangement and death within all organ systems begin to occur at this point. Additional pathologic responses to the shock state (e.g., severe lactic acidemia and inflammatory/immune system activation) may lead to multiple system deterioration or failure. Even if DO2 is sufficient, some cells may not be able to use the oxygen as a result of cellular damage. |
| Irreversible (refractory) stage | The final stage of shock is the critical point at which no treatment can reverse the process. Cellular destruction is so severe that death is inevitable. At this stage, specific causes of shock are indistinguishable. Each patient’s shock state is unique, and its clinical progression may be altered by several factors. These include the cause of shock, patient age, severity and duration of hypoperfusion, and the presence of underlying disease. |
A. Assessment
1. Primary and secondary assessment/resuscitation (see Chapters 1 and 31)
C. Planning and Implementation/Interventions
F. Age-Related Considerations
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