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INTRODUCTION

Shock is the clinical condition of organ dysfunction resulting from an imbalance between cellular oxygen supply and demand. This life-threatening condition is common in the intensive care unit (ICU). There are a multitude of heterogeneous disease processes that can lead to shock. The organ dysfunction seen in early shock is reversible with restoration of adequate oxygen supply. Left untreated, shock transitions from this reversible phase to an irreversible phase and death from multisystem organ dysfunction (MSOF). The clinician is required to identify the patient with shock promptly, make a preliminary assessment of the type of shock present, and initiate therapy to prevent irreversible organ dysfunction and death. In this chapter, we review a commonly used classification system that organizes shock into four major types based on the underlying physiologic derangement. We discuss the initial assessment utilizing the history, physical examination, and initial diagnostic testing to confirm the presence of shock and determine the type of shock causing the organ dysfunction. Finally, we will discuss key principles of initial therapy with the aim of reducing the high morbidity and mortality associated with shock.

PATHOPHYSIOLOGY OF SHOCK

The cellular oxygen imbalance of shock is most commonly related to impaired oxygen delivery in the setting of circulatory failure. Shock can also develop during states of increased oxygen consumption or impaired oxygen utilization. An example of the impaired oxygen utilization is cyanide poisoning, which causes uncoupling of oxidative phosphorylation. This chapter will focus on the approach to the patient with shock related to inadequate oxygen delivery.

In the setting of insufficient oxygen supply, the cell is no longer able to support aerobic metabolism. With adequate oxygen, the cell metabolizes glucose to pyruvate, which then enters the mitochondria where ATP is generated via oxidative phosphorylation. Without sufficient oxygen supply, the cell is forced into anaerobic metabolism, in which pyruvate is metabolized to lactate with much less ATP generation (per mole of glucose). Maintenance of the homeostatic environment of the cell is dependent on an adequate supply of ATP. ATP-dependent ion pumping systems, such as the Na+/K+ ATPase, consume 20–80% of the cell’s energy. Inadequate oxygen delivery and subsequent decreased ATP disrupt the cell’s ability to maintain osmotic, ionic, and intracellular pH homeostasis. Influx of calcium can lead to activation of calcium-dependent phospholipases and proteases, causing cellular swelling and death. In addition to direct cell death, cellular hypoxia can cause damage at the organ system level via leakage of the intracellular contents into the extracellular space activating inflammatory cascades and altering the microvascular circulation.

DETERMINANTS OF OXYGEN DELIVERY

Since shock is the clinical manifestation of inadequate oxygen delivery compared to cellular needs, we will review determinants of oxygen delivery (DO2). Disease processes affecting any of the components of oxygen delivery have the potential to lead to the development of shock. Disturbances to key determinants of oxygen delivery form the ...

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