Patients in septic shock require immediate cardiorespiratory stabilization with large volumes of intravenous (IV) fluids, infusion of vasoactive drugs, and, often, endotracheal intubation and mechanical ventilation.
Empiric IV antimicrobial therapy should be immediately directed toward all potential infectious sources.
The drugs used for hemodynamic support of patients with sepsis have adverse effects on splanchnic circulation. Accordingly, the ideal hemodynamic therapy in these patients has not been determined. After adequate fluid resuscitation, therapy with dopamine may be initiated, followed by norepinephrine when dopamine fails. Alternatively, therapy may be initiated with norepinephrine, with dobutamine used if inotropic support is needed. The use of epinephrine as a single agent in septic shock is not recommended.
Manipulation of oxygen delivery by increasing the cardiac index has either yielded no improvement or has worsened morbidity and mortality. Routine use of hemodynamic drugs to raise cardiac output to supranormal levels is not recommended.
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Stages of sepsis based on American College of Chest Physicians/Society of Critical Care Medicine Consensus Panel guidelines.
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Pathogenesis of sepsis and multiorgan failure.
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Venn diagram showing overlap of infection, bacteremia, sepsis, systemic inflammatory response syndrome (SIRS), and multiorgan dysfunction.
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Acute respiratory distress syndrome (ARDS) present in this chest x-ray (CXR) film is a common organ system affected in multiorgan failure of sepsis.
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Acute respiratory distress syndrome (ARDS) shown in this chest x-ray (CXR) film is a common complication of septic shock. Note bilateral airspace infiltration, absence of cardiomegaly, vascular redistribution, and Kerley B lines.
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Organizing phase of diffuse alveolar damage (ARDS) secondary to septic shock shows diffuse alveolar injury and infiltration with inflammatory cells.
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Organizing diffuse alveolar damage in a different location showing disorganization of pulmonary architecture.
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A high-power view of organizing diffuse alveolar damage (ARDS) shows hyperplasia of type II pneumocytes and hyaline membrane deposits.
