Chapter 4: Shock

INTRODUCTION

Shock is a profound state of circulatory failure that leads to a reduction in delivery and impaired utilization of oxygen and other nutrients at the end-organ level. At first, these changes cause reversible injury and, if prolonged, lead to irreversible cellular damage.^1,2 Shock is a common syndrome encountered in the intensive care unit (ICU) and is associated with a high mortality rate.^1-3 Consequently, early recognition, prompt exploration of its etiology, and effective management of shock can greatly influence clinical outcomes.

Fundamentally, shock is a state of circulatory collapse relating to an aberration in preload (hypovolemic shock), pump function (cardiogenic and obstructive shock), or afterload (distributive shock). Early signs of shock include alterations in vital signs (tachycardia, tachypnea, and hypotension) and clinical evidence of end-organ hypoperfusion. Specifically, end-organ hypoperfusion can manifest as an acute alteration in mental status, a decrease in capillary refill, and a decrease in urine output (< 0.5 mL per kg of body weight per hour). Laboratory abnormalities may include alterations in lactate levels and mixed venous oxygen saturations.

INITIAL APPROACH TO A PATIENT IN SHOCK

The initial approach to a patient in shock involves an assessment of the cause as well as simultaneous management of the shock (Tables 4-1 and 4-2). As resuscitative efforts are initiated, a close examination of the available history, clinical examination, laboratory findings, and radiographs is warranted. As noted above, shock is characterized by a hypoperfused state, manifested by low blood pressure (BP). Both cardiac output (CO) and systemic vascular resistance (SVR) contribute to BP, as demonstrated by the equation BP = CO × SVR. The various types of shock are characterized by distinct alterations in either or both parameters. A thorough understanding of this relationship is advantageous when managing a patient in shock.