Phases of Shock - Compensatory

Shock is a state of circulatory failure that happens when the organs and body tissues do not receive enough blood flow to support their oxygen and metabolic demands, putting them at risk of hypoxia and cellular injury. Shock is a continuum of events that progresses through several stages, including compensated, decompensated or progressive, and irreversible shock. 

The compensatory phase of shock refers to the initial stage of shock when the body is still able to compensate for the decrease in tissue perfusion despite a loss of intravascular fluid volume or cardiac dysfunction. 

During the compensatory stage, compensatory mechanisms (e.g., increased heart rate, increased heart contractility, and/or vascular constriction) are able to maintain cardiac output (i.e., the amount of blood pumped out by the heart per minute) and blood pressure, thereby ensuring perfusion to vital organs, such as the brain and the heart. 

Compensated shock is the initial stage of shock when a series of compensatory mechanisms are able to counter the decrease in tissue perfusion. Damage to the tissues and organs may be reversible and further deterioration can be prevented if shock is addressed during the compensated stage. However, if the cause of shock is not addressed promptly, these compensatory mechanisms may become overwhelmed and unable to support adequate tissue perfusion, resulting in decompensated shock. During decompensated shock, signs and symptoms of organ dysfunction begin to appear (e.g., decreased urination, confusion, cold and clammy skin, irregular heart rhythms, etc.), and damage to the tissues becomes irreversible. Finally, if shock persists for too long, vital organs such as the brain, heart, and kidneys may begin to shut down, leading to multiple organ failure. 

There are four types of shock depending on the underlying cause: hypovolemic; cardiogenic; obstructive; and distributive, which encompasses anaphylactic, septic, and neurogenic shock. Hypovolemic shock occurs as a result of a decrease in intravascular volume, which can be caused by severe bleeding, fluid losses from vomiting or diarrhea, renal losses, or burns among other causes. Next, cardiogenic shock occurs when a direct injury to the heart, such as a myocardial infarction (MI), prevents the heart from pumping blood efficiently. Obstructive shock occurs when a mechanical obstruction, like cardiac tamponade (i.e., compression of the heart, caused by the build-up of fluid, blood, or air in the pericardium), tension pneumothorax, or a pulmonary embolism prevents the heart from filling properly and pumping enough blood through the cardiovascular system. Finally, distributive shock occurs when blood vessels vasodilate excessively and become leaky. When distributive shock is caused by an allergic reaction, it is called anaphylactic shock; when it is a result of a severe infection, it is called septic shock; and when it is caused by damage to the nervous system, it is called neurogenic shock. 

In compensated shock, a number of physiological responses are activated in order to restore perfusion, so there may be tachycardia and tachypnea; however, blood pressure is typically normal. Because the body is attempting to ensure blood supply to vital organs, blood is shunted away from non-vital organ systems, such as the skin, kidneys, and gastrointestinal tract, and towards the brain and heart. As a result, individuals may present with cold and clammy skin, weak peripheral pulses, delayed capillary refill, decreased bowel sounds, and decreased urinary output. At this stage, individuals are likely to be alert and awake, but they may present with early signs of decreased oxygen supply to the brain, such as anxiety, irritability, or restlessness. 

Diagnosis of compensated shock involves monitoring individuals to detect early signs of hypoperfusion, including low or declining blood pressure, tachycardia, or decreased urinary output. Monitoring is usually followed by additional tests, including an echocardiogram, an electrocardiogram (ECG), and/or a chest X-ray to identify the precipitating cause of shock. Routine diagnostic investigations also include laboratory tests to identify decreased oxygen levels; electrolyte abnormalities; and signs of end-organ damage, like decreased renal function, elevated lactate levels, and blood pH disturbances. 

Initial treatment of shock involves supportive measures, including supplemental oxygen; intravenous fluids; and medications, like norepinephrine or dopamine, to improve the cardiac output and blood pressure. Definitive treatment is aimed at addressing the underlying cause of shock when possible.

Shock is a state of insufficient blood flow that affects the whole body, putting organs at risk for hypoxia, cellular injury, and ultimately organ failure. The compensated stage of shock refers to the initial stage of shock when the body is still able to compensate for the decrease in tissue perfusion by a series of physiological mechanisms. Signs and symptoms of compensated shock include a normal blood pressure; tachycardia; tachypnea; and evidence of peripheral vasoconstriction, such as cold and clammy skin, weak peripheral pulses, delayed capillary refill, and decreased urinary output. If recognized and treated, compensated shock is more likely to be reversible. This stage is also more likely to respond to therapy when compared to decompensated shock, which is associated with irreversible end-organ damage and organ failure.