Aetiology
There are four different categories of shock.
Distributive (failure of vasoregulation): causes include sepsis, anaphylaxis, and brainstem or spinal injury (neurogenic).
Cardiogenic (pump dysfunction): most commonly occurs after myocardial infarction but other causes include tachyarrhythmias (e.g., atrial fibrillation or ventricular tachycardia), bradyarrhythmias, toxic substances (e.g., alcohol, recreational drugs), non-adherence with salt/fluid intake or medications, excessive rise in blood pressure, infection (e.g., pneumonia, infective endocarditis, sepsis), and acute mechanical causes (e.g., myocardial rupture, chest trauma, acute valvular incompetence).[3]
Hypovolaemic (loss of intravascular volume): haemorrhagic causes include gastrointestinal bleeding and trauma.[18][19] Non-haemorrhagic causes include burns and diabetic ketoacidosis.
Obstructive (barriers to cardiac flow or filling): a pulmonary embolism may restrict pulmonary blood flow; cardiac tamponade and tension pneumothorax cause cardiac filling restriction.
Patients may have a combination of the above categories of shock. For example, a patient with sepsis may have septic shock (distributive shock), septic cardiomyopathy (cardiogenic shock), and a degree of hypovolaemia (hypovolaemic shock).
Pathophysiology
Hypoperfusion is a lack of adequate oxygen delivery at a cellular level, due to decreased blood flow and oxygen delivery, or increased tissue oxygen demand without a homeostatic increase in blood flow to supply the required oxygen for organ tissue. When blood flow supply cannot meet demand, hypoperfusion results. Low oxygen delivery from poor blood flow or low blood oxygen saturation impairs basic metabolic functions of cells and organs.
Hypoperfusion triggers a systemic stress response, including tachycardia and peripheral vasoconstriction. Once physiological compensation mechanisms are overwhelmed, organ dysfunction ensues, followed by organ failure, irreversible organ damage, and death.
In septic shock, pathological peripheral vasodilation caused by the septic state may result in a relative loss of perfusion pressure due to loss of systemic vascular resistance (vascular regulation). This may lead to secondary coronary ischaemia and cardiac dysfunction. The resulting vascular and cardiac impairment may contribute to the progression of shock.
In cardiogenic shock, tissue hypoperfusion resulting from loss of cardiac output induces tissue (cellular) inflammation.[20] Shock may self-perpetuate by inducing additional cellular-level shock response such as cell-toxic cytokines, which results in systemic inflammatory response syndrome.
Low blood pressure is an indirect, imprecise measure of perfusion. This is illustrated by decreased cellular oxygen delivery in hypertensive crisis, where high arterial resistance actually reduces cardiac output and perfusion. Tissue hypoxia may be present without low blood pressure.[2]
Classification
Pathological mechanism
Shock is most commonly classified by cause.
Cardiogenic (pump dysfunction): may occur after myocardial infarction, due to cardiomyopathy, arrhythmia, or cardiac valve pathology.
Hypovolaemic (loss of intravascular volume): due to haemorrhage, dehydration, gastrointestinal or third space losses.
Distributive (failure of vasoregulation): results in a fall in systemic vascular resistance with vasodilation and, classically, warm peripheries, as occurs in sepsis and anaphylaxis.
Obstructive (barriers to cardiac flow or filling): a pulmonary embolus may restrict flow; cardiac tamponade and tension pneumothorax cause a cardiac filling restriction.
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