For the myriad practitioners who come into contact with critically ill children, the term “shock” has acquired a unique lexicon. For example, a call to our pediatric intensive care unit from a community emergency department physician was highlighted by the comment: “I have a lethargic 3-month-old who looks ‘shocky’ to me.” A frantic page from one of our residents led to this exchange: “We have a 2-year-old down here who is developing diffuse petechiae—she really looks ‘septic’.” A 16-year-old admitted for worsening respiratory distress and an increasing oxygen requirement underwent echocardiography, which was read by the cardiologist as a “moderate-size pericardial effusion with no evidence of either right atrial compression or cardiac tamponade.” Are these physicians talking about different pathophysiologic entities in their respective patients? Not really. Each simply is describing one of the protean manifestations of a diverse and complex syndrome: circulatory shock. The primary function of the cardiovascular system is to provide oxygen and other substrate to the cells. Inextricably linked to this function is the timely and effective removal of the end products of a wide variety of metabolic processes. Circulatory shock or cardiovascular failure ensues when systemic oxygen and nutrient supply become acutely inadequate to meet the metabolic demands of the body’s organ systems. The resulting anaerobic state inefficiently generates intracellular adenosine triphosphate, causing accumulation of lactic acid, an objective indicator of the functional status of the circulatory system. The effects of impaired perfusion are reversible for a period of time, but ultimately reach a point of irreversible disruption of essential biochemical processes necessary to maintain cellular integrity. This malfunction of the energy-dependent cell membrane pumps leads to intracellular edema and acidosis and eventually cell death. On a macroscopic level, this state of global hypoxemia causes multisystem organ failure and ultimately the patient’s demise. The pathophysiologic pathway to cardiovascular failure results from impairment of cardiac output (CO), systemic vascular resistance (SVR), or both. It can be caused by a variety of direct-acting or systemic insults. CO is the product of heart rate and stroke volume. Stroke volume is determined by left ventricular filling pressure and myocardial contractility. SVR represents the impedance to left ventricular ejection (afterload) as well as the “tone” of the peripheral vasculature. In the lexicon of “shock,” a predominance of vasoconstriction is classified as “cold shock” and predominant vasodilation comes under the rubric of “warm shock.” The early recognition and management of the various types of circulatory failure are crucial to restoring adequate tissue perfusion before irreparable end-organ damage and a bradycardic/asystolic cardiac arrest occurs. This article reviews basic cardiovascular physiology in children, attempts to characterize the pathophysiologic derangements that occur with different types of circulatory shock, and examines a therapeutic regimen that comprises both general supportive measures as well as some of the newer, more specific agents being developed to reverse the immunologic and coagulation abnormalities that are being recognized increasingly as key players in the pathogenesis of circulatory failure.
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