Chapter 4 Shock
1 What blood pressure defines shock in the pediatric patient?
Shock is not defined by the blood pressure or by any other vital sign. Shock exists when the patient’s metabolic demand exceeds the body’s ability to deliver oxygen and nutrients. This occurs most commonly when metabolic demand is normal or slightly elevated but delivery of oxygen and nutrients is dramatically reduced. Examples include excessive blood loss (hemorrhage) or excessive fluid loss (diarrhea). The shock state can and often does exist in the presence of a “normal” blood pressure.
Bell LM: Shock. In Fleisher GM, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 51–62.
KEY POINTS: DEFINITION OF SHOCK
1 Shock is a condition in which the patient’s metabolic requirements are unmet.
2 The shock state is a complex interplay between the physiologic insult and the host’s response to that insult; both play a role.
3 In its earliest phase, shock might be recognized only by abnormal results of laboratory tests that measure tissue acid–base status (e.g., serum lactate). Overt clinical signs are seen as the shock state progresses.
2 How can shock be recognized?
To recognize shock, consider both the consequences of inadequate perfusion and the patient’s compensatory mechanisms. The clinical manifestations of shock are those of inadequate perfusion and compensation. Inadequate perfusion of the brain results in an alteration in the child’s level of consciousness. Inadequate perfusion of the kidneys results in decreased urine output.
As perfusion decreases, compensatory changes occur. These changes improve delivery of oxygen and nutrients and direct blood flow to the vital organs. The first compensatory mechanism is usually an increased heart rate. Since cardiac output is equal to the rate multiplied by the stroke volume, an increased heart rate can maintain cardiac output in the face of decreased stroke volume. Additionally, peripheral vasoconstriction helps to maintain blood flow to the central organs and to the brain. The patient therefore has pale, cool extremities and a delayed capillary refilling time. This increased vascular tone also affects the measured blood pressure. The diastolic pressure is slightly elevated, so the difference between the systolic and diastolic pressures—the pulse pressure—is smaller. This is referred to as a “narrowed” pulse pressure.
To compensate for both the decreased oxygen delivery and the acidosis created by underperfusion of peripheral tissues, the respiratory rate increases. The blood pressure eventually falls, but this is a late finding and may signal that the shock state is irreversible.
3 What are the stages of shock?
Shock is a spectrum of illness, so any division into discrete segments is somewhat artificial. However, shock is usually divided into two stages: compensated shock and uncompensated shock.
4 What is compensated shock?
In early shock, various physiologic changes allow continued delivery of oxygen and nutrients to the heart, kidneys, brain, and other vital organs. Tachycardia is usually the first compensatory mechanism. The increased heart rate helps to maintain cardiac output in the face of low blood volume, excessive vasodilation, or pump failure. Increased vasomotor tone shunts blood away from the skin and the extremities to more vital organs. In compensated shock, the patient is able to continue to meet his or her metabolic demand, even if only marginally.
5 Are there exceptions to the compensatory mechanisms described above?
Yes. In septic shock the patient sometimes develops so-called warm shock or warm distributive shock. In this state the patient has flushed skin and bounding pulses associated with a hyperdynamic precordium. This state can be explained by the cascade of inflammatory mediators that is responsible for the condition called septic shock. Likewise, in neurogenic shock, loss of sympathetic tone can result in bradycardia in the face of profound hypotension.
6 What is uncompensated shock?
If the shock state progresses without interruption, the patient’s compensatory mechanisms eventually fail. Hypoperfusion of organ systems causes acidosis and further release of inflammatory mediators. As blood flow to the brain decreases, the patient can become irritable or stuporous and eventually slips into coma. Likewise, decreased renal blood flow causes decreased urine output and finally results in anuria. The gastrointestinal tract is similarly affected, so the patient often has decreased bowel motility followed by distention and edema of the bowel wall. As tissue ischemia and acidosis progress, the inflammatory mediators cause diffuse vascular injury and capillary leakage. The pulmonary bed is especially sensitive to this type of injury. Damage to the pulmonary tissues exacerbates tissue hypoxemia. The ultimate result of progressive shock is multiorgan system failure and acute respiratory distress syndrome. At some point during this process the patient’s blood pressure falls.
7 What are the types (or mechanisms) of shock?
There are multiple mechanisms for shock. These include:
Hypovolemic shock: Hypovolemia, such as might occur with blood loss, vomiting, and/or diarrhea, decreases perfusion to the tissues and leads to shock.
Distributive or vasodilatory shock: This type of shock is the final common pathway of a variety of conditions that result in vasodilation. Neurogenic distributive shock is caused by a spinal cord injury that eliminates sympathetic innervation to the blood vessels, causing profound vasodilation and bradycardia. Accidental ingestion of vasodilating medications can also result in distributive shock. Anaphylaxis results in vasodilation, and, although anaphylaxis has many other components, shock is a part of the clinical picture. Septic shock is largely distributive in nature but is a complex process (see below).
Cardiogenic shock: Pump failure is the primary mechanism for cardiogenic shock. Decreased myocardial contractility makes adequate delivery of oxygen and nutrients impossible. Since children are very dependent on a normal heart rate to produce an adequate cardiac output, drugs and other conditions that cause bradycardia can lead to shock. The patient will have evidence of congestive heart failure, such as rales on pulmonary auscultation and peripheral edema. Viral myocarditis, hypertrophic cardiomyopathy, and certain myocardial depressant drugs can cause cardiogenic shock.
Septic shock: Many consider septic shock to be another form of distributive shock. In septic shock, a stimulus causes the formation of inflammatory mediators that result in profound vasodilation and shock. However, some of these mediators also directly depress myocardial activity; thus, septic shock can have features of both distributive and cardiogenic shock.
Jones AE, Craddock PA, Tayal VS, Kline JA: Diagnostic accuracy of left ventricular function for identifying sepsis among emergency department patients with nontraumatic, symptomatic, undifferentiated hypotension. Shock 24:513–517, 2005.
8 Is the pathophysiology of shock really that simple?
No, it is exceedingly complex. What we refer to as “shock” is the final common pathway for a variety of physiologic insults. Whether the process starts with acute blood loss or with an overwhelming infection, eventually the host mounts a response to the insult, and this response—at least in some cases—seems to contribute to the shock state.
9 What usually initiates septic shock?
The most common and potent initiator of the inflammatory cascade called septic shock is exposure to endotoxin. Endotoxin is the lipopolysaccharide (LPS) coat of gram-negative bacteria. Other bacterial and viral agents can also start this process. Examples include certain viral proteins and teichoic acid.
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