Last updated on December 13, 2018 at 14:48
The different shocks are discussed more in detail in pathophysiology topics, since this is more an overview topic.
A shock is the final common pathway for potentially lethal events, like myocardial infarction, pulmonary embolism, trauma and sepsis. Its characterized by severe systemic hypoperfusion of tissues, either by decreased cardiac output or reduced effective circulating blood volume. The consequences are impaired tissue perfusion and hypoxia of the cells, which leads to multiorgan failure. So, in other words, a shock is a whole-body circulatory failure. In theory it’s reversible, but prolonged shocks are often fatal.
Phases of shock
The phases are documented most clearly in hypovolemic shock but may apply to other forms as well. The phases are somewhat artificially divided, so they’re not easily separated.
1. Reversible, compensated phase
For different reasons (see the different types of shock below) will the cardiac output be severely reduced. This causes a sympathetic activation. The sympathetic activation will try to increase the cardiac output as compensation, and there will be a release of epinephrine, norepinephrine, ADH and angiotensin II, leading to peripheral vasoconstriction, tachycardia and renal fluid retention. Because of vasoconstriction in skin will the skin be cool and pallor, which is characteristic for shock (but not septic shock, where the opposite happens).
The vasoconstriction causes blood to be directed from non-vital organs to vital organs such as the brain and heart, because the coronaries and cerebral arteries aren’t affected by the sympathetic vasoconstriction.
2. Progressive phase
If the underlying cause isn’t corrected the shock passes into the progressive phase. The vasoconstriction persists, the tissue perfusion is still too low, making the cells switch to anaerob glycolysis and yielding lactate. This accumulation of lactate in blood will give a metabolic acidosis.
Metabolic acidosis causes vasodilation of the arterioles, which causes blood to pool in the microcirculation and flow very slowly. This worsens the cardiac output even further. Vital organs start to fail.
3. Irreversible phase
Without appropriate intervention will shock enter the irreversible phase. At this stage, not much can be done.
The hypoxic damage on cells will be so big in this stage that lysosomal enzymes will leak from the cells. The ischaemia of the bowel wall will allow bacterial flora from faeces to enter the blood stream. Myocardial contractile function worsens because of synthesis of nitric oxide (NO). All this together will superimpose the shock, and the increased necrosis of tissues will lead to failure of organs and death.
Types of shock
- Cardiogenic shock
A result from low cardiac output due to myocardial pump failure. It may be caused by acute myocardial infarction, ventricular arrhythmias and pulmonary embolism.
Results from low cardiac output due to blood loss or low plasma volumes, that can happen in extensive bleedings, diarrhoea, dehydration and severe burns.
- Septic shock
Microbial infections lead to systemic immune responses that cause arterial vasodilation and venous blood pooling, making the cardiac output decrease.
Systemic vasodilation and increased vascular permeability triggered by IgE hypersensitivity reaction (Hypersensitivity type I). Imagine someone with peanut hypersensitivity, they can die from this if they don’t get adrenalin as soon as possible.
Brain injuries and spinal cord injuries that lead to loss of vascular tone.
Cardiogenic shock occurs when the myocardial pump fails for any reason. When the pump fails, cardiac output decreases, which sends the patient into the first phase of shock.
Hypovolemic shock doesn’t have a complex pathomechanism either. Inadequate blood or plasma volume means not enough blood to supply the body.
Septic shock however, has a complex pathomechanism, however we won’t cover all the details of it. It isn’t even completely understood. The most common cause of septic shock are gram-positive bacteria, followed by gram-negative bacteria and lastly fungi. Infections don’t have to be systemic to cause septic shock; even localized infections can. A widespread inflammation induces a hypermetabolic state. Macrophages, neutrophils, dendritic cells, endothelial cells and complement components get activated.
The endothelial cell activation has three consequences. Thrombosis is induced, causing disseminated intravascular coagulopathy. Increased vascular permeability causes leakage of fluid into the tissues, causing oedema and lower blood volume. Lastly, vasodilation causes severe hypotension, which further reduces tissue perfusion.
These factors decrease the delivery of oxygen and nutrients to tissues that need them, contributing to organ dysfunction.
DIC – Disseminated intravascular coagulopathy
DIC is the sudden or a sneaky onset of widespread thrombosis within the microcirculation. It has two phases:
The first phase is called the thrombotic phase. Microthrombi form in capillaries of all organs due to the endothelial cell damage and stasis of blood flow. This extensive thrombosis depletes the blood of platelets and coagulation factors.
The second phase is the consumptional coagulopathy phase. Because there are no more platelets and coagulation factors will there be bleeding everywhere.
The thrombi are microscopic, but so many that they together can cause a circulatory insufficiency in brain, lungs, heart and kidneys. Capillary blood becomes filled with microthrombi so it resembles sludge, which obviously doesn’t circulate well.
DIC is not a primary condition but instead always appears secondary to other conditions, such as shock.
The DIC can be triggered by extrinsic pathway or intrinsic pathway:
Tissue factors that cause microthrombi gets into the blood. This can be caused by delivery complication, burns and trauma.
This is the most common form. Widespread endothelial damage, also called “sluggish capillaries”, can form microthrombi.
For example, in sepsis, endothelial necrosis and TNF together cause DIC. In shock will hypoxia cause endothelial necrosis which favours clotting.
Malignancy in tumours can activate factor X.
This condition may result in ischemic damages in the organs mentioned above, and haemorrhages as:
- Sheehan’s syndrome, where there is a pituitary necrosis caused by blood loss during and after child birth
- Waterhouse-Friderichsens’s syndrome, where there is apoplexy (severe bleeding) in adrenal glands, causing adrenal insufficiency and death.
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