Excerpt from Shock, Distributive

Synonyms, Key Words, and Related Terms: distributive shock, end-organ dysfunction, hypotension, systemic vascular resistance, SVR, septic shock, systemic inflammatory response syndrome, SIRS, toxic shock syndrome, TSS, anaphylaxis, drug reactions, toxin reactions, transfusion reaction, heavy metal poisoning, addisonian crisis, hepatic insufficiency, neurogenic shock

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Background: Shock is defined as a clinical syndrome due to inadequate tissue perfusion that results in end-organ dysfunction. Shock is categorized according to etiology, including cardiogenic, hypovolemic, compressive/obstructive shock (eg, cardiac tamponade and pulmonary embolism), distributive shock (eg, severe sepsis, pancreatitis, anaphylaxis), endocrine (eg, adrenal insufficiency, hyper or hypothyroid), neurogenic, and shock due to other miscellaneous causes (eg, carbon monoxide).

Distributive shock is characterized by decreased systemic vasomotor tone, usually qualified as a decreased systemic vascular resistance (SVR). With fluid resuscitation, effective circulating volume increases and often creates a hyperdynamic pattern and increased cardiac output associated with a low-to-normal blood pressure. This form of shock is referred to as distributive; in this setting, autoregulation and the pattern of peripheral blood flow distribution are disrupted. If hypotension also develops, then blood flow to pressure-dependent organs, such as the kidney, gut, and liver decreases despite an increase in baseline total blood flow. This gives rise to the paradoxical increase in mixed venous O₂ saturation (SvO₂) associated with signs of organ ischemia (metabolic acidosis and hyperlactatemia).

Septic shock, which is due to a complex systemic inflammatory response to infection, is the most commonly encountered form of distributive shock. In the United States, this is the most common cause of noncardiac death in intensive care units (ICUs). Other causes of distributive shock include systemic inflammatory response syndrome (SIRS) due to noninfectious inflammatory conditions; toxic shock syndrome (TSS); anaphylaxis; drug or toxin reactions, including insect bites, transfusion reaction, and heavy metal poisoning; Addisonian crisis; hepatic insufficiency; and neurogenic shock due to brain or spinal cord injury.

Pathophysiology: The decreased tissue perfusion in distributive shock is due to several factors that reduce peripheral vasomotor tone and vasoresponsiveness. Acute septic shock presents as a hypodynamic hypotensive state as the circulating inflammatory response targets the vascular endothelium–vascular smooth muscle interface. The main factor that induces this initial shock state is an increase in the unstressed volume of the peripheral capacitance vessels (eg, splanchnic circulation), as more blood is sent to otherwise underperfused low metabolic activity vascular beds. This results in a decrease in effective circulatory volume.

Additionally, since the inflammatory response is initially spread through the blood stream, the vascular endothelium is specifically targeted. Impaired vascular endothelial integrity results in increased capillary permeability with extravascular loss of protein-rich intravascular volume into the interstitium. Myocardial dysfunction and complete cardiovascular collapse, probably related to intracellular energy failure and apoptosis, represent the final stages of fatal septic shock. Since impaired myocardial contractility, if present, develops in the setting of reduced afterload and fluid resuscitation, load-dependent measures of cardiac performance, such as left ventricular ejection fraction, stroke volume, and cardiac output, are often maintained. Controversy exists as to whether left ventricular dilation, if present, is an adaptive process or an epiphenomenon of fluid resuscitation, but it has little prognostic significance.

The hemodynamic changes of distributive shock may be subdivided into early or late; these are primarily characterized by the evolution of changes in contractility and dilation of peripheral small vessels and the impact of resuscitation efforts. Early septic shock (warm or hyperdynamic) is characterized by peripheral vasodilation that causes flushed warm extremities with a compensatory in .....