Shock is a medical emergency which can result in organ damage and death. A complex physiological response is triggered by decreased tissue perfusion. There are 4 types of shock depending on underlying cause: hypovolemic, cardiogenic, obstructive, and distributive, which encompasses anaphylactic, septic, and neurogenic shock. The 4 stages of shock are initial, compensatory, progressive, and refractory.
The initial stage may be difficult to recognize due to subtle or absent symptoms. Something has led to a decrease in tissue perfusion. Cardiac output is so low, cells experience hypoxia. Without sufficient oxygen and nutrients, tissues switch from aerobic metabolism to anaerobic metabolism. A by-product of anaerobic metabolism is lactic acid. Normally, the liver deals with lactic acid. But during shock, the liver's not working optimally. Lactic acid builds up in the bloodstream, dropping blood pH and causing acidosis.
Next is the compensatory stage. Compensatory mechanisms try to release substances that increase cardiac output or increase blood volume to increase tissue perfusion. The body attempts to increase cardiac output and blood pressure with the SNS and RAS.
Baroreceptors sense a drop in blood pressure and stimulate the SNS. The SNS releases catecholamines epinephrine and norepinephrine. These catecholamines cause vasoconstriction, increased blood pressure, and increased heart rate. Less blood goes to non-vital organs, more blood is routed to vital ones. The drop in blood pressure results in decreased capillary hydrostatic pressure. This triggers an increase in venous blood by shifting fluid from the interstitial compartment to the intravascular compartment.
Baroreceptors also stimulate the vagus nerve, which stimulates the release of antidiuretic hormone from the posterior pituitary gland, preventing water from leaving the kidneys and thus increasing blood volume.
The RAS kicks into gear. A reduction in blood flow to the kidneys triggers them to convert prorenin in blood to renin. Renin is released into circulation, where it converts angiotensinogen from the liver, to angiotensin I. With the help of ACE, angiotensin I is converted to angiotensin II. Angiotensin II is a vasoconstrictive peptide which narrows both arteries and veins. Angiotensin II also triggers the release of aldosterone from the adrenal cortex, which makes the kidneys retain more sodium and water and increase potassium excretion - more retention of water in the bloodstream and increased blood pressure.
Compensatory mechanisms increase cardiac output and blood volume. But some compromises are made. Perfusion is decreased to the GI tract, so it slows. There is decreased perfusion to the skin, which makes it cold and clammy (exception to this is if the person is in septic shock).
Decreased perfusion results in parts of the lungs not getting perfusion, which means no gas exchange in those parts. There is a mismatch between ventilation and perfusion and blood oxygen levels decrease so the person hyperventilates.
The body can only maintain compensatory mechanisms for a limited time.
During the progressive stage, compensatory mechanisms have failed. They no longer maintain adequate tissue perfusion, which leads to worsening tissue damage. The body progresses towards MODS. No more compensation means low cardiac output and low tissue perfusion. Cells do not receive oxygen, succumbing to cell hypoxic injury.
Capillary permeability increases - this is key to the pathology of this stage. The barrier between intravascular and interstitial space is broken down. Fluid and protein are drawn into the interstitial space, resulting in major edema. This depletes blood volume, decreases cardiac output and tissue perfusion.
What happens in various organs? When the brain doesn't receive adequate perfusion, there is a major mental status change. Heart cells begin to die, including those of the electrical conduction system. This results in cardiac dysrhythmias. In the lungs, ARDS develops. Increased capillary permeability in alveolar sacs, the site of gas exchange, results in their collapse. This results in fluid in the lungs, lower oxygen levels, high respiratory rate, and respiratory failure. The person requires intubation and mechanical ventilation in order to keep breathing. In the GI tract, ulcers form as the cells that protect the gut’s lining from its own acid stop working. This results in massive gastrointestinal bleeding. Liver’s cells are also dying. Since the liver produces most clotting factors, clotting doesn’t work well.
There is also disseminated intravascular coagulation. Small clots form in vessels, further blocking blood flow to organs. These clots deplete platelets and clotting factors, resulting in massive and uncontrolled bleeding.
The fourth and final stage of shock is the refractory stage, characterized by poor tissue perfusion, hypotension, and organ failure. Despite aggressive resuscitation efforts, the person is unlikely to survive.
