Using a systolic blood pressure <90 mm Hg as criteria, 0.4% to 1.3% of patients presenting to EDs are in shock.1 Mortality depends on the inciting event. Septic shock has an estimated hospital mortality of 26%.2 Cardiogenic shock has an estimated hospital mortality of 39% to 48%.3,4 Neurogenic shock occurs in <20% of spinal cord injuries (cervical, 19.3%; thoracic, 7%; lumbar, 3%).5 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 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.6-8 The mechanisms that can result in shock are frequently divided into four categories: (1) hypovolemic, (2) distributive, (3) cardiogenic, and (4) obstructive.
The four categories of shock can be described in terms of their respective physiologic changes and common causes, recognizing that a single etiology may manifest the clinical findings of more than one shock type (Table 12-1).9,10 Hypovolemic shock occurs when decreased intravascular fluid or decreased blood volume causes decreased preload, stroke volume, and cardiac output (CO). Severe blood loss (hemorrhage) can cause decreased myocardial oxygenation, which decreases contractility and CO. This action may lead to an autonomic increase in the systemic vascular resistance (SVR). Hypovolemic shock can also occur due to volume loss from other etiologies. In distributive shock, there is relative intravascular volume depletion due to marked systemic vasodilatation. This is most commonly seen in septic shock.6 Compensatory responses to decreased SVR may include increased CO (increased contractility and heart rate) and tachycardia. The concurrent decreased SVR results in a decreased preload and may hinder CO overall. In sepsis, up to 40% of patients may have a transient cardiomyopathy characterized by decreased contractility and increased mortality.6 Anaphylaxis, adrenal insufficiency, and neurogenic shock are additional causes of distributive shock. In cardiogenic shock, the left ventricle fails to deliver oxygenated blood to peripheral tissues due to variances in contractility, as well as preload, afterload, and right ventricular function.8 Myocardial infarction is the most common cause of cardiogenic shock. Dysrhythmias are another common cause because they can lead to a decreased CO. Bradyarrhythmias result in low CO, and tachyarrhythmias can result in decreased preload and stroke volume. Patients with cardiogenic shock may soon develop clinically evident infection (up to 46%) and/or demonstrate an inflammatory response similar to but less pronounced than with septic ...