Shock is the inability to provide sufficient perfusion of oxygenated blood and substrate to tissues to meet metabolic demands. Oxygen delivery is directly related to the arterial oxygen content (oxygen saturation and hemoglobin concentration) and to cardiac output (stroke volume and heart rate). Changes in metabolic needs are met primarily by adjustments in cardiac output. Stroke volume is related to myocardial end-diastolic fiber length (preload), myocardial contractility (inotropy), and resistance of blood ejection from the ventricle (afterload) (see Chapter 145). In a young infant whose myocardium possesses relatively less contractile tissue, increased demand for cardiac output is met primarily by a neurally mediated increase in heart rate. In older children and adolescents, cardiac output is most efficiently augmented by increasing stroke volume through neurohormonally mediated changes in vascular tone, resulting in increased venous return to the heart (increased preload), decreased arterial resistance (decreased afterload), and increased myocardial contractility.
Acute hypovolemia is the most common cause of shock in children. It results from loss of fluid from the intravascular space secondary to inadequate intake or excessive losses (vomiting and diarrhea, blood loss, capillary leak syndromes, or pathologic renal fluid losses) (Table 40-1). Reduced blood volume decreases preload, stroke volume, and cardiac output. Hypovolemic shock results in increased sympathoadrenal activity, producing an increased heart rate and enhanced myocardial
CNS, Central nervous system.
contractility. Neurohormonally mediated constriction of the arterioles and capacitance vessels maintains blood pressure, augments venous return to the heart to improve preload, and redistributes blood flow from nonvital to vital organs. If hypovolemic shock remains untreated, the increased heart rate may impair coronary blood flow and ventricular filling, while elevated systemic vascular resistance increases myocardial oxygen consumption, resulting in worsening myocardial function. Ultimately, intense systemic vasoconstriction and hypovolemia produce tissue ischemia, impairing cell metabolism and releasing potent vasoactive mediators from injured cells. Cytokines and other vasoactive peptides can change myocardial contractility and vascular tone and promote release of other inflammatory mediators that increase capillary permeability and impair organ function further.
Abnormalities in the distribution of blood flow may result in profound inadequacies in tissue perfusion, even in the presence of a normal or high cardiac output. This maldistribution of flow usually results from abnormalities in vascular tone. Septic shock is the most common type of distributive shock in children. Other causes include anaphylaxis, neurologic injury, and drug-related causes (see Table 40-1).
Distributive shock may present with the systemic inflammatory response syndrome (SIRS), defined as two or more of the following: temperature greater than 38° C or less than 36° C; heart rate greater than 90 beats/min or more than two standard deviations above normal for age; tachypnea; or white blood count greater than 12,000 cells/mm3, less than 4000 cells/mm3, or greater than 10% immature forms.