Recognizing Shock

Shock is defined as a condition in which peripheral tissues and end organs do not receive adequate oxygen and nutrients. While it is sometimes used interchangeably with severe hypotension, shock does not only occur in the setting of severely low blood pressure. Importantly, the body will attempt to compensate for shock through various mechanisms, most commonly through increased heart rate. The heart rate will increase in an attempt to increase cardiac output (stroke volume x heart rate). Blood flow will be shunted from less vital organs such as the skin to more vital organs, such as the kidneys and the brain. In these cases, the child or the infant may be experiencing shock, but have high, normal, or low-normal blood pressure. This is called compensatory shock and may only persist for minutes to hours before progressing to frank uncompensated shock unless treatment is initiated. Without treatment, these compensatory systems can become overwhelmed and result in the child progressing quickly to critical hypotension and cardiac arrest. Therefore, the simple assessment of blood pressure is not a sufficient way to evaluate potential shock in pediatrics.

HYPOVOLEMICLow blood volume, often due to hemorrhage or fluid shifting out of vasculature
DISTRIBUTIVEBlood vessel dilation (e.g. septic shock)
CARDIOGENICHeart is not pumping adequately
OBSTRUCTIVEPhysical block of the blood flow
Table 18


Hypovolemic shock is the most common type of shock and perhaps the easiest to understand. Hypovolemic shock results from insufficient blood in the cardiovascular system. This can be due to hemorrhage externally, or into the peritoneum or into the gastrointestinal system. Hypovolemic shock in children can also occur from water loss, perspiration, diarrhea, vomiting, or when fluid moves into the tissues (third-spacing). In hypovolemic shock, preload to the heart is decreased (less volume to fill the heart), though contractility is normal or increased. Likewise, afterload is increased since the vessels have constricted in an attempt to increase blood pressure.

Possible tachypnea
Adequate or low blood pressure
Narrow pulse pressure
Slow capillary refill
Weak peripheral pulses
Normal central pulses
Possible decreased urine output
Decreased level of consciousness
Table 19


Distributive shock is a condition in which the majority of blood is inappropriately distributed in the vasculature. A common way to conceptualize distributive shock is as a condition in which the vasculature has relaxed and dilated to the point of inadequacy. The arterial blood supply needs to maintain a certain tension in order to maintain blood pressure. Likewise, the venous system must maintain tension as well, so as not to retain too much of the total blood supply. In distributive shock, the blood is not being maintained in the required and needed useful blood vessels. Distributive shock is most commonly caused by sepsis, anaphylaxis, or a neurological problem, all of which cause vascular dilation or loss of blood vessel tone. In distributive shock, the preload, contractility, and afterload vary depending on the etiology.

• Decreased preload• Decreased preload• Decreased preload
• Normal/decreased
• Contractility varies• Normal contractility
• Afterload varies• Afterload is low in left
ventricle and high in right
• Afterload is decreased
Table 20

Distributive shock is difficult to recognize because the signs and symptoms vary greatly depending on the etiology. Common symptoms include tachypnea, tachycardia, low to normal blood pressure, decreased urine output, and decreased level of consciousness.

Distributive shock is further categorized into warm and cold shock. If the person is experiencing warm shock, they commonly will have warm, erythematous peripheral skin and a wide pulse pressure in the setting of hypotension. If the person is experiencing cold shock, they commonly will have pale, vasoconstrictive skin and narrow pulse pressure hypotension. In each case, distributive shock is generally considered when the person is likely to have one of the three main causes: sepsis, anaphylaxis, or neurological problem


Cardiogenic shock is caused by inadequate contractility of the heart. One of the key differences between hypovolemic and cardiogenic shock is the work of breathing. In both cases, there will be tachypnea, but in hypovolemic shock the effort of breathing is only mildly increased. However, in cardiogenic shock, the work of breathing is often significantly increased as evidenced by grunts, nasal flaring, and the use of accessory thorax muscles. Also, since the heart is pumping ineffectively, blood remains in the pulmonary vasculature. This causes pulmonary congestion and edema, which can clinically be heard as crackles in the lungs and visualized as jugular vein distension. Pulses are often weak, capillary refill is slow, extremities are cool and cyanotic, and there may be a decrease in the level of consciousness.


Obstructive shock is similar to cardiogenic shock in that the impaired heart function is the primary abnormality. In cardiogenic shock, the contractility is impaired; but in obstructive shock, the heart is prevented from contracting appropriately. Common causes of obstructive shock are cardiac tamponade, tension pneumothorax, congenital heart malformations, and pulmonary embolism. Obstructive and cardiogenic shock is most easily distinguished by the contractility of the heart. In obstructive shock, heart contractility is normal, although pumping function is not. Cardiac tamponade is associated with muffled heart sounds since blood is present in the pericardial space. Pulsus paradoxus (e.g. a drop in blood pressure on inspiration) may also be present. Tension pneumothorax is a clinical diagnosis. The trachea may have deviated away from the side of the lesion, and there are absent breath sounds over the affected side of the chest. Consider a pulmonary embolism when the person is cyanotic and/or hypotensive, experiences chest pain, and has respiratory distress without lung pathology or airway obstruction. Risk factors include obesity, hormone use, family history of abnormal clotting, and coagulation factor abnormalities.