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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—listen for rales or gallops. Feel for enlarged liver or spleen.
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Shock is a reflection 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. 19-1). 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.
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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 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 (e.g., 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 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.
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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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In contrast, the shock response results from decreased oxygen and energy substrate delivery. The levels of cortisol and catecholamines are 5 to 10 times higher in the shock state compared with the stress response.2 Intravascular volume is preserved and oliguria results. Supraphysiologic levels of cortisol and catecholamines with glucagon cause hyperglycemia. Ironically, hyperglycemia in sepsis is considered potentially harmful since research suggests that it impairs neutrophil function,3,4 acts as a procoagulant, induces cellular apoptosis, increases risk of infection, and impairs wound healing.3
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Shock can be subcategorized into compensated and hypotensive ...