Skip to Main Content


The exact number of cases of shock that present to the ED in the United States is difficult to ascertain due to the insensitivity of clinical parameters, current definitions, and lack of a central database repository. Previous estimates propose that more than 1 million cases of shock are seen in the ED each year in the United States.1 These estimates are largely based on the assumption that hypotension, defined as a systolic blood pressure <90 mm Hg, is consistent with shock in adults. Using this definition, the incidence of patients with hypotension that present to American EDs is approximately 5.6 million cases per year.2

Mortality depends on the inciting event. Septic shock has an estimated mortality of 40% to 60%.3 Cardiogenic shock has an estimated mortality of 36% to 56%.4 Approximately 30% to 45% of patients with septic shock and 60% to 90% of patients with cardiogenic shock die within 1 month of presentation.3,4 With a greater recognition and improved treatment, mortality from neurogenic shock has been reduced significantly. The definition of and treatment approach to shock continue to evolve, but the initial approach to a patient in shock follows similar principles, regardless of the inciting factors or cause.

Patients present to the ED in varying stages of critical illness and shock. These stages are confounded by age, comorbidities, and delays in presentation. A focus on early recognition, rapid diagnosis, and empiric resuscitation is essential. Therapy and patient stabilization may need to occur simultaneously with evaluation.


Shock is a state of circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and oxygen demand (consumption) resulting in end-organ dysfunction. Reduction in effective perfusion may be due to a local or global delivery deficiency or utilization deficiency with suboptimal substrate at the cellular or subcellular level.5 The mechanisms that can result in shock are frequently divided into four categories: (1) hypovolemic, (2) cardiogenic, (3) distributive, and (4) obstructive.


An understanding of the mechanisms of oxygen delivery and consumption is foundational to the treatment of shock. While the physiology is complex, familiarity with the basic principles, equations, and their interactions is essential (Tables 12–1 and 12–2). As noted in the cardiac output (CO) equation, CO is determined by heart rate and stroke volume. Stroke volume is dependent on preload, afterload, and contractility. The mean arterial pressure (MAP) demonstrates the impact that CO has on MAP (which can also be estimated with the formula: 2 × diastolic blood pressure + systolic blood pressure/3). This is important because there is a MAP threshold below which oxygen delivery is decreased. Systemic vascular resistance (SVR) directly impacts MAP, but also impacts afterload and thus CO. The physiologic mechanism of oxygen delivery to peripheral tissues (Do2) is described in the oxygen delivery equation. Recognize that blood pressure is not represented in this equation. Patients in shock may initially have normal blood pressures (cryptic shock), yet have other objective signs of shock ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.