Shock is a state of circulatory dysfunction that results in insufficient oxygen delivery and other substrate to meet tissue metabolic demands.1 Inadequate oxygen delivery leads to a shift to anaerobic metabolism, eventually resulting in lactate production and metabolic acidosis.2 If this state persists, it can lead to multiple organ dysfunction and death.
If unrecognized and untreated, shock progresses through three phases due to inadequate oxygen delivery.
Compensated: Homeostasis is maintained by the body’s compensatory mechanisms.
Increases in systemic vascular resistance and cardiac output through sympathetic nervous system activation and neurohormonal mechanisms lead to maintenance of blood pressure.
In younger children, cardiac output is maintained by increases in heart rate, leading to tachycardia.
Oxygen delivery is optimized by increasing oxygen extraction at the tissue level and maintaining blood flow to vital organs (e.g., heart, brain, and kidneys).
Blood flow to the gastrointestinal tract may be compromised.
Increased oxygen consumption leads to increased carbon dioxide (CO2) production, often resulting in an increased respiratory rate for CO2 elimination.
Early stages of all types of shock may be difficult to differentiate from the patient’s normal status.
Tachycardia may be the only sign of shock.
Uncompensated: Despite the body’s compensatory mechanisms, cardiovascular compromise occurs, leading to inadequate microvascular perfusion.
This state is characterized by an imbalance of oxygen delivery (DO2) and oxygen consumption (VO2).
Decreasing mixed venous oxygen saturation (SVO2) reflects a decrease in oxygen delivery relative to oxygen consumption.
Cellular metabolism and function deteriorate, leading to organ system dysfunction and metabolic acidosis from lactic acid production.
Increased lactate production can be seen in all forms of uncompensated shock.
As this phase evolves, the body loses the ability to maintain blood pressure due to cardiovascular compromise.
In children, hypotension is a late and ominous sign that may reflect up to a 25% to 40% loss of circulating blood volume.
Irreversible: Terminal or irreversible shock results from damage to key organs of such magnitude that death occurs. This occurs even if therapy returns cardiovascular parameters to normal.
Classification of Shock
Type of Shock | Primary Derangement | Common Causes |
Hypovolemic | Decreased circulating blood volume due to internal or external losses |
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Distributive | Vasodilation, venous pooling, decreased preload Maldistribution of regional blood flow |
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Cardiogenic | Decreased myocardial contractility and cardiac pump failure |
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Obstructive | Mechanical obstruction to ventricular outflow |
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Dissociative | Oxygen not released from hemoglobin |
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Early detection of shock states is crucial to treatment and outcome because delayed recognition can lead to organ failure and death. A thorough history and physical are essential. Frequent repeat examinations are necessary with careful attention paid to each organ system (Table 28-2). Early signs of shock may be subtle.
Organ System Dysfunction in Shock
System | Symptoms in Compensated Shock | Symptoms in Uncompensated Shock |
Central nervous system | Restless, lethargic, anxious | Agitated/confused, coma |
Respiratory | ā Ventilation | āā Ventilation |
Cardiovascular | Tachycardia | Tachycardia or bradycardia, |
Normotension or hypertension | Hypotension | |
Delayed (cold shock) or bounding (warm shock) pulses | Diminished to absent peripheral pulses | |
Metabolism | Compensated metabolic acidemia | Uncompensated metabolic acidemia |
Gastrointestinal tract | Impaired motility | Ileus |
Kidney | Oliguria (<0.5 mL/kg/hour) | Oliguria/anuria |
Skin | Cool extremities, delayed capillary refill | Mottled, cyanotic, cold extremities |