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Chapter 9

Shock

Joseph Cuschieri and Darren Bowe

Key Points

1 Shock is the clinical syndrome that results from inadequate tissue perfusion from numerous causes:

hypovolemic, cardiogenic, extracardiac obstructive, and distributive.

2 Hypovolemic shock due to ongoing blood and/or plasma loss leads to progressive cardiovascular

deterioration, ultimate hypotension, oliguria, confusion, irreversible cell injury, and death.

3 Cardiogenic shock results in decreased tissue perfusion due to intrinsic pump failure.

4 Extracardiac obstructive shock attenuates cardiac pump function due to external compression of

inflow and outflow (tamponade, tension pneumothorax, etc.).

5 Septic and traumatic shock, forms of distributive shock, are systemic inflammatory responses to

infection or tissue injury with cellular breakdown, producing severe hypotension requiring massive

volume resuscitation and high risk of multiple organ failure and death.

6 Complications of an episode of shock include ischemia–reperfusion injury from oxidant stress;

potential secondary immunosuppression with enhanced nosocomial infection risk; hypothermia and

coagulopathy; and multiple organ failure syndrome, including abdominal compartment syndrome

(ACS).

7 Treatment of shock requires goal-directed volume resuscitation with treatment of the underlying

etiology and careful monitoring of adequacy of end-organ perfusion to avoid under- and

overresuscitation.

1 The current accepted concept of shock was first described in 1929 by Walter B. Cannon1 as inadequate

blood flow that results in cellular hypoxia. Persistence of cellular hypoxia results in dysfunction at both

cellular and organ levels. Although shock can result from a number of etiologies, it was Blalock who

first described the four major causes we still refer to today, which are hematogenic, neurogenic,

cardiogenic, and vasogenic.2

Prior to this, the concept of shock was not understood since the nature and purpose of the heart and

circulatory system were either unknown or misunderstood. Galen was the first to explore the purpose of

the heart and circulatory system. He proposed that the arteries carried blood, not air, as previously

thought, away from the heart. However, he incorrectly believed that arterial blood within the

circulatory system subsequently dissolved in the body to release nutrients. Blood returning to the heart

was not due to recirculation, but rather was rapidly remanufactured by the liver. Additionally, since

much of his dissection work was carried out in frogs, he concluded falsely that the heart had only two

chambers and blood passed from the right to left chamber through invisible pores in the septum.3

These conclusions remained unchallenged for nearly 1,500 years until Vesalius, in the 17th century.

Through a series of dissections, he demonstrated that blood did not flow directly from the right to left

ventricle. Although he provided elaborate drawings of the body’s network of blood vessels, he did not

anticipate that blood circulated through the body and was unable to discern the heart’s purpose. Shortly

thereafter, Harvey moved beyond anatomy and studied physiology; he discovered the closed nature of

the circulation and concluded that the heart was the main pumping mechanism. Although the

microscope had not yet been invented, he proposed the existence of capillaries that connect the arterial

and venous system.3

Due to this improved understanding of the circulatory system, the condition of shock due to blood

loss and other etiologies were carefully being observed and explored. During the 18th century, military

surgeons such as Henri le Dran (1740) noted that injured soldiers left unattended for several hours

suddenly deteriorated as if there had been a secousse (jolt) to the system, which probably led to use of

the word “shock.”1 Surgeons began to notice that even when a wounded extremity was amputated, the

physiologic effects of the injury often continued, and shock was increasingly recognized as a distinct

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