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  • Shock is present when there is evidence of multisystem organ hypoperfusion; it often presents as decreased mean blood pressure.

  • Initial resuscitation aims to establish adequate airway, breathing, and circulation. Rapid initial resuscitation (usefully driven by protocol) is fundamental for improved outcome, since “time is tissue.”

  • A working diagnosis or clinical hypothesis of the cause of shock should always be made immediately, while treatment is initiated, based on clinical presentation, physical examination, and by observing the response to therapy.

  • Drug and/or definitive therapy for specific causes of shock must be considered and implemented early (eg, hemostasis for hemorrhage, revascularization for myocardial infarction, appropriate antibiotics, etc).

  • The most common causes of shock are high cardiac output hypotension, or septic shock; reduced venous return despite normal pump function, or hypovolemic shock; reduced pump function of the heart, or cardiogenic shock; and obstruction of the circulation, or obstructive shock. Overlapping etiologies can confuse the diagnosis, as can a short list of other less common etiologies, which are often separated by echocardiography and pulmonary artery catheterization.

  • Shock has a hemodynamic component, which is the focus of the initial resuscitation, but shock has also a systemic inflammatory component (ameliorated by rapid initial resuscitation) that leads to adverse sequelae including subsequent organ system dysfunction.

This chapter discusses shock with respect to the bedside approach: first with an early working diagnosis, then an approach to urgent resuscitation that confirms or changes the working diagnosis, followed by a pause to ponder the broader differential diagnosis of the types of shock and the pathophysiology of shock leading to potential adverse sequelae. Effective initial diagnosis and treatment at a rapid pace depend in large part on understanding cardiovascular pathophysiology.



Shock is present if evidence of multisystem organ hypoperfusion is apparent. Evidence of hypoperfusion includes tachycardia, tachypnea, low mean blood pressure, diaphoresis, poorly perfused skin and extremities, altered mental status, and decreased urine output. Hypotension has special importance because it commonly occurs during shock, because blood pressure is easily measured, and because extreme hypotension always results in shock. Important caveats are (1) relatively low blood pressure is normal in some healthy individuals and (2) systolic blood pressure may be preserved in some patients in shock by excessive sympathetic tone. In the latter case, it is important to anticipate that sedation will unmask hypotension. Further, cuff blood pressure measurements may markedly underestimate central blood pressure in low flow states.1 The focus of initial resuscitation is reversing the hemodynamic component of shock, which leads to tissue hypoxia and lactic acidosis. However, all types of shock are also associated with a systemic inflammatory component that is a key contributor to subsequent multisystem organ failure and death. The development of the systemic inflammatory component is minimized by rapid and adequate (usefully driven by protocol) initial resuscitation.2...

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