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INTRODUCTION

We greatly appreciate the author of the fourth edition chapter Jonathan K. Marr, MD. This fifth edition chapter is an update of his previous chapter.

HIGH-YIELD FACTS

  • Tachycardia and pallor should be treated as shock until proven otherwise.

  • Effortless tachypnea signifies respiratory compensation for metabolic acidosis.

  • Hypotension in pediatrics heralds impending cardiac arrest.

  • Hypovolemic shock is the most common cause of shock worldwide.

  • Early and aggressive therapy for shock is necessary to restore oxygenation and tissue perfusion.

  • Overaggressive fluid resuscitation in cardiogenic shock can be harmful; assess for rales, gallops, or hepatosplenomegaly.

Shock is a manifestation of inadequate oxygen and substrate delivery to cells relative to metabolic demand. Oxygen delivery depends on multiple variables and includes heart rate, preload, contractility, afterload, hemoglobin content, oxygen saturation, and dissolved oxygen in the blood (Fig. 20-1). Disease processes create alterations in the above variables and the body has developed compensatory mechanisms to adjust. When the ability to adjust is exceeded, there is progression to impairment of organ function, irreversible organ failure, and death.

FIGURE 20-1.

Factors influencing oxygen delivery.

Children differ from adults with respect to their anatomy and physiology. In infants, cardiac output is dependent on heart rate since stroke volume is relatively fixed. In contrast, insufficient cardiac output is often due to low stroke volume. Maintaining oxygen delivery to tissues activates compensatory mechanisms. The first line of defense in maintaining cardiac output is tachycardia and this is often the first subtle sign of shock.1 Common reasons for tachycardia in the emergency department other than shock include fever, pain, anxiety, hypoxia, and medications (e.g., albuterol).

The next compensatory mechanism is the redirection of blood from nonvital to vital organs through increasing systemic vascular resistance (SVR). Blood is shunted away from the skin, gut, kidneys, and muscle, and is clinically reflected by cool extremities, delayed capillary refill, and decreased urine output. Mechanisms such as increase in contractility and increasing smooth muscle tone to move blood from the venous system to the heart are other ways to augment increases in cardiac output.

Variation in these compensatory mechanisms is observed in the distinct presentations of shock when comparing adults and children. The majority of adults present in shock with evidence of low systemic vascular tone and normal or increased cardiac output with tachycardia, described as “warm shock”; whereas almost half of children presenting in shock have evidence of low cardiac output and elevated SVR with cool extremities, described as “cold shock.”2

The physiologic fight-or-flight response to stress involves central and sympathetic nervous system activation. Catecholamines increase cardiac output by increasing heart rate and stroke volume, and the result is an increase in blood pressure. Glucagon is also released to provide glucose via glycogenolysis and gluconeogenesis.

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