Shock

Shock is one of the most frequently diagnosed and most complex clinical conditions encountered in the critically ill patient. Ongoing investigations have identified the mechanisms of various shock states to be complicated, yet based within the cellular foundation of normal, everyday existence. Although mortality from the shock states remains high, the focus on early aggressive resuscitation to defined end points has significantly enhanced a clinician's ability to improve patient outcome.
Definition
Although early definitions of shock lack scientific terminology, they compensate for this in their simplicity. Samuel Gross defined shock as a rude unhinging of the machinery of life. With improved understanding of cellular physiology and function, we now recognize the machinery of life to be the delivery and use of oxygen at the cellular level. Shock is currently best defined as a multifactorial syndrome resulting in inadequate tissue perfusion and cellular oxygenation.
The importance of regional blood flow to individual organ systems is the singular concept for recognizing both the obvious and subtler shock states. Perfusion may be decreased either systemically (hypotension) or limited to regional maldistribution (septic shock, in which global perfusion is normal or even elevated). Regardless of cause or severity, all forms of shock have the commonality of perfusion inadequate to meet metabolic demands at the cellular level. Decreased organ perfusion leads to tissue hypoxia, anaerobic metabolism, activation of an inflammatory cascade, and eventual organ dysfunction. The ultimate consequences of shock depend on the degree and duration of hypoperfusion, the number of organs affected, and the presence of prior organ dysfunction. The challenges to the intensivist are identification of the hypoperfused state, its cause, and rapid restoration of cellular perfusion. This chapter reviews the current methods for diagnosing, monitoring, and treating the various shock states.
Physiology
During the past few decades, significant progress has been made in elucidating the cellular basis for shock. Whereas hypoperfusion and cellular ischemia were previously thought to be sufficient to cause shock, they are now recognized as being the initiating triggers for a complex physiologic cascade. Cellular hypoxia predisposes tissues to reperfusion injury leading to local vasoconstriction, thrombosis, regional malperfusion, release of superoxide radicals, and direct cellular damage. Subsequent activation of neutrophils and release of proinflammatory cytokines result in cellular injury, organ dysfunction, and frequently death.
Early diagnosis of cellular ischemia with prompt restoration of tissue perfusion and oxygenation is essential to ameliorating this inflammatory process and improving outcomes. The underlying cause may be quite evident, as in the case of upper gastrointestinal hemorrhage, or may be occult, as in the case of intraabdominal solid viscus injury from blunt trauma. Due to the significant morbidity and mortality associated with delayed shock resuscitation, the intensivist must commonly begin appropriate management before all clinical information or diagnostic studies are available. As a result, the intensivist must possess a solid understanding of the most likely shock states, their clinical presentation, and the necessary therapeutic interventions.
Classification