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