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The exact number of cases of shock that present to the ED in the U.S. is difficult to ascertain due to the insensitivity of clinical parameters, current definitions, and lack of a central database repository. Previous estimates propose that approximately 1 million cases of shock are seen in the ED each year in the U.S.1 These estimates are largely based upon the assumption that hypotension, defined as a systolic blood pressure <90 mm Hg is consistent with shock in adults. Based upon a low blood pressure, the incidence of hypotension that present to American EDs is approximately 5.6 million cases/year.2


The mortality attributed to clinical shock varies depending on the inciting event. Septic shock has an estimated mortality of 40% to 60%. Cardiogenic shock has an estimated mortality of 36% to 56%.3 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.5 The definition and treatment of shock continues to evolve, but the general approach to a patient in the initial stages of shock follows similar principles regardless of the inciting factors or etiology.


Shock is circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and oxygen demand (consumption). This physiologic state leads to a reduction in effective tissue perfusion with its attendant biochemical, bioenergetic, and subcellular sequelae. Reduction in effective perfusion can be global or local, and the result is suboptimal substrate use at the cellular or subcellular level.6


Knowledge of the principles of oxygen delivery and consumption is important for understanding shock. Arterial oxygen content is the amount of oxygen bound to hemoglobin plus the amount dissolved in plasma. Oxygen is delivered to the tissues by the pumping function [cardiac output (CO)] of the heart. This is dependent upon the interplay of cardiac inotropy (speed and shortening capacity of myocardium), chronotropy (heart contraction rate), and lusitropy (ability to relax and fill heart chambers). Determinants of inotropy include autonomic input from sympathetic activation, parasympathetic inhibition, circulating catecholamines, and short-lived responses to an increase in afterload (Anrep effect) or heart rate (Bowditch effect).7 Increases in inotropic state help to maintain stroke volume at high heart rates.7 Under certain conditions, such as shock states, higher levels of epinephrine will be produced and reinforce adrenergic tone. Epinephrine levels are significantly elevated during induced hemorrhagic shock, then are subsequently reduced to almost normal levels after normal blood pressure is restored.8 Furthermore, previous studies have also shown that an acidotic milieu as may be found in shock further compromises ventricular contractile force and blood pressure.9 Both chronotropy and lusitropy are both influenced by sympathetic input. Norepinephrine interacts with cardiac β1-receptors, resulting in increased cyclic adenosine monophosphate. This leads to a process of intracellular signaling with an increased heart rate (chronotropy) and sequestration of calcium, leading to myocardial relaxation.7


Systemic oxygen delivery (Do2) is the product of the arterial oxygen content ...

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