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  • Tachycardia and pallor must be considered “shock” until proven otherwise.
  • Decompensated shock with hypotension can be clinically recognized by altered mental status. Hypotension is an ominous sign and heralds cardiac arrest.
  • Hypovolemia is the most common cause of shock worldwide.
  • Although septic shock is categorized as “distributive,” it also has a component of cardiac dysfunction and hypovolemia.
  • Congenital cardiac lesions that are dependent on a patent ductus arteriosus for survival include those with left ventricular outflow obstruction such as coarctation of the aorta, critical aortic stenosis, and hypoplastic left heart.
  • Effortless tachypnea may be an attempt to correct for the metabolic acidosis caused by anaerobic metabolism from shock.
  • Tissue perfusion (capillary refill) can be used as a surrogate marker for cardiac output.
  • Early, aggressive therapy for shock is necessary to restore tissue perfusion and oxygenation.
  • If a patient in shock has no hepatomegaly, no rales on auscultation of the lungs, and clear and distinct heart sounds, early and aggressive isotonic fluid delivery with 20 mL/kg boluses to 60 mL/kg or more is the first line of therapy.

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Shock is a reflection of acute depletion of energy (ATP) secondary to 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 blood (Fig. 25–1). Disease processes creates 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.

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Figure 25-1.
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Factors influencing oxygen delivery.

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

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The next compensatory mechanism is the redirection of blood from nonvital to vital organs through increasing systemic vascular resistance. Blood is shunted away from the skin, gut, kidneys, and muscle and this is clinically reflected by cool extremities, delayed capillary refill, and decreased urine output. Other 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.

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The physiologic “fight or flight” response to stress involves central and sympathetic nervous system activation. Adrenocorticotropic hormone is released from the central nervous system to produce cortisol while the sympathetic nervous system releases ...

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