When the end organs and peripheral tissues fail to absorb the nutrients and oxygen necessary to maintain their function, it can lead to shock. Though this term is frequently used interchangeably with severe hypotension, it happens beyond the event of severely low blood pressure.
An increase in heart rate may be observed as the body tries to compensate for the shock event. To increase cardiac output, the heart rate will become faster than normal. The blood flow will be limited to less vital organs (skin, for example), preferencing more crucial organs such as the brain and kidneys. In cases such as these, the patient may have high, normal, or low-normal blood pressure while experiencing shock. This is event is called “compensatory shock” and may last for minutes to hours before developing to frank uncompensated shock in the event that treatment is delayed. Without further intervention, this can quickly develop into critical hypotension and cardiac arrest. Mere evaluation of the blood pressure is therefore not an effective way to predict shock in children and infants.
|Types of Shock|
|HYPOVOLEMIC||Low blood volume, often due to hemorrhage or fluid shifting out of vasculature|
|DISTRIBUTIVE||Blood vessel dilation (e.g. septic shock)|
|CARDIOGENIC||Heart is not pumping adequately|
|OBSTRUCTIVE||Physical block of the blood flow|
The most common type of shock, and the easiest to understand, is hypovolemic shock. Insufficient blood in the cardiovascular system causes hypovolemic shock. This is caused by hemorrhage into the gastrointestinal system, into the peritoneum, or externally. Diarrhea, vomiting, perspiration, water loss, and fluid moving into tissues (third-spacing) are all causes of hypovolemic shock in children.
The preload to the heart is decreased (e.g., the heart requires less volume to fill), though contractility is normal or increased in hypovolemic shock The vessels have constricted to try to increase blood pressure, causing afterload to increase.
|SIGNS OF HYPOVOLEMIC SHOCK|
|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|
When the majority of blood is inappropriately distributed in the vasculature, it is a condition known as distributive shock. Conceptualize a condition in which the vasculature has relaxed and dilated to the point of inadequacy, and you have a common understanding of distributive shock. In order to keep blood pressure up, a certain tension must be maintained by the arterial blood supply. Likewise, so that it doesn’t retain too much of the total blood supply, the venous system must also keep tension up. In conditions of distributive shock, blood is not being maintained in the needed and required useful blood vessels. Anaphylaxis, sepsis, and neurological problems, all of which result in a loss of blood vessel tone or vascular dilation, are all common causes of distributive shock. The afterload, contractility, and preload vary depending on the etiology in distributive shock.
|Septic Shock||Analphylactic Shock||Neurogenic Shock|
|• Decreased preload||• Decreased preload||• Decreased preload|
|• Contractility varies||• Normal contractility|
|• Afterload varies||• Afterload is low in left
ventricle and high in right
|• Afterload is decreased|
Because there is a great variance depending on the etiology of the signs and symptoms, distributive shock can be difficult to recognize. Decreased level of consciousness, decreased urine output, low to normal blood pressure, tachycardia, and tachypnea are common symptoms.
Warm and cold shock are more specific categories of distributive shock. Narrow pulse pressure hypotension and pale, vasoconstricted skin are signs of a person experiencing cold shock; in contrast, a wide pulse pressure in the setting of hypotension and a warm, erythematous peripheral skin are common amongst individuals experiencing warm shock. If an individual has an instance of sepsis, a neurological problem, or anaphylaxis, this is when he or she is generally considered to be experiencing distributive shock.
Inadequate contractility of the heart causes cardiogenic shock. The work of breathing is a key difference between hypovolemic and cardiogenic shock. The effort of breathing is only mildly increased in hypovolemic shock, even though there will be tachypnea in both. The use of accessory thorax muscles, nasal flaring, and grunts show a significant increase in the work of breathing, evincing cardiogenic shock. Blood also remains in the pulmonary vasculature, since the heart is pumping ineffectively. This can cause crackles in the lungs, which looks like jugular vein distension, as a result of pulmonary congestion and edema. There may be a decrease in the level of consciousness, extremities are cyanotic and cool, capillary refill is slow, and the pulse is often weak.
The primary abnormality in obstructive shock is the impaired heart function, making it similar to cardiogenic shock. The difference is that the contractility is impaired in cardiogenic shock; whereas in obstructive shock, the heart is prevented from contracting appropriately. Congenital heart malformations, pulmonary embolism, tension pneumothorax, and cardiac tamponade are common causes of obstructive shock.
The contractility of the heart is the easiest way to distinguish between obstructive and cardiogenic shock. When dealing with obstructive shock, pumping function is not normal, while heart contractility remains normal. Blood is present in the pericardial space, creating muffled heart sounds that are associated with cardiac tamponade. There may also be a drop in blood pressure on inspiration, or pulsus paradoxus. A clinical diagnosis would be tension pneumothorax. Over the affected side of the chest, there are absent breath sounds, and there is a deviation from the side of the lesion by the trachea. When the person has respiratory distress without lung pathology or airway obstruction, experiences chest pain, or is cyanotic and/or hypotensive, consider a pulmonary embolism. Risk factors include obesity, hormone use, family history of abnormal clotting, and coagulation factor abnormalities.