Shock is a state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia. At the outset, the cellular injury is reversible; however, prolonged shock eventually leads to irreversible tissue injury and is often fatal.
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Table 4.3 Three Major Types of Shock
Type of Shock Clinical Examples Principal Pathogenic Mechanisms
Arrhythmia Failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure, or obstruction to outfow
Shock may complicate severe hemorrhage, extensive trauma improvements in care, the mortality remains at a stagger- or burns, myocardial infarction, pulmonary embolism, and microbial sepsis. Its causes fall into three general categories (
Table 4.3
Cardiogenic shock results from low cardiac output as a result of myocardial pump failure. It may be caused by myocardial damage (infarction), ventricular arrhythmias, extrinsic compression (cardiac tamponade) (Chapter 12), or outflow obstruction (e.g., pulmonary embolism).
Hypovolemic shock results from low cardiac output due to loss of blood or plasma volume (e.g., resulting from hemorrhage or fluid loss from severe burns).
Septic shock is triggered by microbial infections and is associated with severe systemic inflammatory response syndrome (SIRS). In addition to microbes, SIRS may be triggered by a variety of insults, including burns, trauma, and/or pancreatitis. The common pathogenic mechanism is a massive outpouring of inflammatory mediators from innate and adaptive immune cells that produce arterial vasodilation, vascular leakage, and venous blood pooling. These cardiovascular abnormalities result in tissue hypoperfusion, cellular hypoxia, and metabolic derangements that lead to organ dysfunction and, if severe and persistent, organ failure and death. The pathogenesis of shock is discussed in detail below.
Less commonly, shock can result from a loss of vascular tone associated with anesthesia or secondary to a spinal cord injury (neurogenic shock). Anaphylactic shock results from systemic vasodilation and increased vascular permeability that is triggered by an immunoglobulin E–mediated hypersensitivity reaction (Chapter 5).
Septic shock is responsible for 2% of all hospital admissions in the United States. Of these, 50% require treatment in intensive care units. The number of cases in the United States exceeds 750,000/year and the incidence is rising, which is ironically due to improvements in life support for critically ill patients, as well as the growing ranks of immunocompromised hosts (because of chemotherapy, immunosuppression, advanced age, or human immunodeficiency virus infection) and the increasing prevalence of multidrugresistant organisms in the hospital setting. Despite ing 20% to 30%.
Septic shock is most frequently triggered by gram-positive bacterial infections, followed by gram-negative bacteria and fungi. Hence, an older synonym, “endotoxic shock,” is no longer appropriate.
The ability of diverse microorganisms to cause septic shock is consistent with the idea that a variety of microbial constituents can trigger the process. As mentioned in Chapter 3, macrophages, neutrophils, dendritic cells, endothelial cells, and soluble components of the innate immune system (e.g., complement) recognize and are activated by several substances derived from microorganisms. After activation, these cells and factors initiate a number of inflammatory responses that interact in a complex, incompletely understood fashion to produce septic shock and multiorgan dysfunction (
Fig. 4.19