Restriction of cardiac output results in an increase in heart rate and an alteration of stroke volume. The pulse pressure is narrow (making pulses harder to feel), and capillary refill is delayed. The liver is often enlarged, and jugular venous distention may be evident.
The principal abnormality in dissociative shock is the inability to deliver oxygen to tissues. Symptoms include tachycardia, tachypnea, alterations in mental status, and ultimately cardiovascular collapse.
Shock requires immediate resuscitation before obtaining laboratory or diagnostic studies. Following initial stabilization (including glucose administration if hypoglycemia is present), the type of shock dictates the necessary laboratory studies. All patients with shock may benefit from determination of a baseline arterial blood gas and blood lactate level to assess the impairment of tissue oxygenation. Measurement of mixed venous oxygen saturation aids in the assessment of the adequacy of oxygen delivery. In contrast to other forms of shock, patients with sepsis often have high mixed venous saturation values because of impairment of mitochondrial function and inability of tissues to extract oxygen. A complete blood count can potentially assess intravascular blood volume after equilibration following a hemorrhage. Electrolyte measurements in patients with hypovolemic shock may identify abnormalities from losses. Patients presenting in distributive shock require appropriate bacterial and viral cultures to identify a cause of infection. If cardiogenic or obstructive shock is suspected, an echocardiogram assists with the diagnosis and, in the case of tamponade, assists with placement of a pericardial drain to relieve the fluid. Patients with dissociative shock require detection of the causative agent (carbon monoxide, methemoglobin). The management of shock also requires monitoring of arterial blood gases for oxygenation, ventilation (CO2), and acidosis, and frequently assessing the levels of serum electrolytes, calcium, magnesium, phosphorus, and blood urea nitrogen (BUN).
SEE TABLE 40-1.
The key to therapy is the recognition of shock in its early,partially compensated state, when many of the hemodynamicand metabolic alterations may be reversible. Initial therapyfor shock follows the ABCs of resuscitation. Later therapycan then be directed at the underlying cause. Therapy shouldminimize cardiopulmonary work, while ensuring cardiacoutput, blood pressure, and gas exchange. Intubation, combined with mechanical ventilation with oxygen supplementation, improves oxygenation and decreases or eliminatesthe work of breathing but may impede venous return if distending airway pressures (positive end-expiratory pressure[PEEP] or peak inspiratory pressure) are excessive. Blood pressure support is crucial because the vasodilation in sepsismay reduce perfusion despite supranormal cardiac output.
Monitoring a child in shock requires maintaining access to the arterial and central venous circulation to record pressure measurements, perform blood sampling, and measure systemic blood pressure continuously. These measurements facilitate the estimation of preload and afterload. Regional monitoring with near infrared spectroscopy may allow early, noninvasive detection of alterations in perfusion.
Alterations in preload have a dramatic effect on cardiac output. In hypovolemic and distributive shock, decreased preload significantly impairs cardiac output. In these cases, early and aggressive fluid resuscitation is important and greatly affects outcome. In cardiogenic shock, an elevated preload contributes to pulmonary edema.