Circulatory shock is defined as an inadequate blood flow throughout the body. In the absence of mechanisms that function to maintain blood pressure within a normal range of values, blood pressure decreases dramatically. As a consequence, tissues can suffer from damage as a result of too little delivery of oxygen to cells. Severe circulatory shock can damage vital body tissues to the extent that death of the individual occurs.
Depending on its severity, shock can be divided into three separate stages: (1) the nonprogressive or compensated stage, (2) the progressive stage, and (3) the irreversible stage. All types of circulatory shock exhibit one or more of these stages, regardless of their causes. There are several causes of shock, but hemorrhagic, or hypovolemic, shock issued to illustrate the characteristics of each stage.
In compensated shock, the blood pressure decreases only a moderate amount, and the mechanisms that regulate blood pressure function to successfully to reestablish normal blood pressure and blood flow. The baroreceptor reflexes, chemoreceptor reflexes, and ischemia within the medulla oblongata initiate strong sympathetic responses that result in intense vasoconstriction and increased heart rate. As the blood volume decreases, the stress-relaxation response of blood vessels causes the blood vessels to contract and helps sustain blood pressure. In response to reduced blood flow through the kidneys, increased amounts of renin are released. The elevated renin release results in a greater rate of angiotensin II formation, causing vasoconstriction and increased aldosterone release from the adrenal cortex. The aldo-sterone, in turn, promotes water and salt retention by the kidneys, conserving water. In addition, ADH is released from the posterior pituitary gland and enhances the retention of water by the kidneys. Because of the fluid shift mechanism, water also moves from the interstitial spaces and the intestinal lumen to restore the normal blood volume. An intense sensation of thirst increases water intake, also helping to elevate normal blood volume.
In mild cases of compensated shock, the baroreceptor reflexes can be adequate to compensate for blood loss until the blood volume is restored, but in more severe cases all of the mechanisms described are required to compensate for the blood loss.
In progressive shock, the compensatory mechanisms are not adequate to compensate for the loss of blood volume. As a consequence, a positive-feedback cycle develops in which the blood pressure regulatory mechanisms are not able to compensate for circulatory shock. As circulatory shock becomes worse, regulatory mechanisms become even less able to compensate for the increasing severity of the circulatory shock. The cycle proceeds until the next stage of shock is reached or until medical treatment is applied that assists the regulatory mechanisms in reestablishing adequate blood flow to tissues.
During progressive shock, the blood pressure declines to a very low level that is not adequate to maintain blood flow to the cardiac muscle; thus the heart begins to deteriorate. Substances that are toxic to the heart are released from tissues that suffer from sever ischemia. When the blood pressure declines to a very low level, blood begins to clot in the small vessels. Eventually blood vessel dilation begins as a result of decreased sympathetic activity and because of the lack of oxygen in capillary beds. Capillary permeability increases under ischemic conditions, allowing fluid to to leave the blood vessels and enter the interstitial spaces, and finally intense tissue deterioration begins in response to inadequate blood flow.
Without medical intervention, progressive shock leads to irreversible shock. Irreversible shock leads to death, regardless of the amount or type of medical treatment applied. In this stage of shock, the damage to tissues, including cardiac muscle, is so extensive that the patient is destined to die even if adequate blood volume is reestablished and blood pressure is elevated to its normal value. Irreversible shock is characterized by decreasing function of the heart and progressive dilation of peripheral blood vessels.
Patients suffering from shock are normally placed in a horizontal plane, usually with the head slightly lower than the feet, and oxygen is often supple. Replacement therapy consists of transfusions of whole blood, plasma, artificial solutions called plasma substitutes, and physiological saline solutions administered to increase blood volume. In some circumstances, drugs that enhance vasoconstriction are also administered. Occasionally, such as in patients in anaphylactic shock, antiiflammatory substances such as glucocorticoids and antihistamines are administered. The basic objective in treating shock is to reverse the condition so that progressive shock is arrested, to prevent it from progressing to the irreversible stage, and to cause the condition to be reversed so that normal blood flow through tissues is reestablished.