Aetiology
The aetiology of hypotension can be divided into 4 principal subtypes:
Hypovolaemic
Cardiogenic
Obstructive
Impaired peripheral vasoconstriction and/or distributive.
There may be a combination of causes for hypotension in any individual patient. For example, a patient with chronic liver disease who develops an upper gastrointestinal variceal bleed is likely to be at risk of hypotension because of hypovolaemia and impaired peripheral vasoconstriction. In addition, a low blood pressure (BP) measurement may be part of a normal physiological process (e.g., pregnancy).
Hypovolaemic
Volume depletion causes a decrease in venous return to the heart, leading to a drop in cardiac output and, subsequently, a lower mean arterial pressure. Neural and hormonal compensatory mechanisms may initially maintain BP. If hypovolaemia persists the patient develops orthostatic dizziness and tachycardia, followed by hypotension even when supine, and finally hypotensive shock.[9][10][11]
Hypovolaemic shock affects 30.8% of patients attending the emergency department with shock.[12]
Hypotension secondary to hypovolaemia could be due to:
Haemorrhage
overt haemorrhage (e.g., many cases of gastrointestinal bleeding, trauma)
concealed haemorrhage (e.g., aortic aneurysm rupture, retroperitoneal bleeding, ruptured ectopic pregnancy).
Non-haemorrhagic fluid depletion
gastrointestinal losses (e.g., diarrhoea, vomiting)
renal causes (e.g., excess diuretic use, dialysis-induced hypotension)
skin losses (e.g., massive sweating, burns)
respiratory losses (e.g., draining pleural effusions)
third-space sequestration (e.g., ascites).
Clinical signs of volume depletion are a result of the haemodynamic effects of the reduction in intravascular volume. Dehydration (loss of water) is associated with increased thirst, progressing when more severe to altered mental state and coma. Other signs of dehydration include dry mucous membranes and lack of axillary moisture. Dehydration and volume depletion are discrete entities, but may be present together at the same time.
Cardiogenic
Hypotension results from heart pump dysfunction (more commonly left-sided), causing a decrease in cardiac output in the setting of increased preload. The compensatory surges in catecholamines normally lead to increased systemic vascular resistance, maintaining BP.
However, in some instances (especially acute coronary syndrome), systemic vascular resistance decreases and hypotension develops.[13]
Causes include:
Acute coronary syndrome
Acute heart failure
Cardiac valvular lesions
Cardiac dysrhythmia.
The hypotension associated with carotid sinus syndrome (cardio-inhibitory subtype) is also cardiogenic in origin. It occurs when a bradyarrhythmia is provoked by carotid sinus massage.
Cardiogenic shock accounts for 14% of cases of shock presenting to the emergency department.[12]
Obstructive
Cardiac output can be reduced, and lead to hypotension even when cardiac pump function is normal. This can occur if there is obstruction to cardiac filling (e.g., with cardiac tamponade or tension pneumothorax) or obstruction to blood flow between the heart and lungs (e.g., with pulmonary embolism).[14] In such conditions, cardiac output falls despite systemic vascular resistance increases and normal volume status. Obstructive shock is uncommon, affecting 1% of patients attending the emergency department with shock.[12]
Impaired peripheral vasoconstriction and distributive change
Regulation of BP involves ongoing input from several systems, most importantly from circulating catecholamines and the alpha-1-adrenergic receptor system in arterioles. Hypotension in the presence of euvolaemia and normal cardiac output can arise if the homeostatic mechanisms that maintain vasoconstriction are impaired.
In some conditions (e.g., sepsis and anaphylaxis), impaired peripheral vasoconstriction is combined with loss of fluid to extravascular space (distributive change). Leakage of fluid from blood vessels to the extravascular space, due to increased vascular permeability, is brought about by the release of inflammatory cytokines.
Causes of hypotension due to impaired peripheral vasoconstriction and/or distributive change include:
Sepsis
Anaphylaxis
Severe acute pancreatitis (distributive change due to a systemic inflammatory response)[15]
Disorders directly affecting functioning of the autonomic nervous system
Chronic illnesses (e.g., diabetes mellitus, Parkinson's disease and multisystem atrophy, primary autonomic failure, Addison's disease, hypopituitarism, amyloidosis)
Acute illnesses (e.g., following acute stroke).
Accumulation of metabolites that influence the blood vessel function (e.g., chronic liver disease).
Medications (e.g., alpha-blockers, nitrates).
Syncope: this is a term used to describe a transient loss of consciousness and postural tone resulting from global cerebral hypoperfusion with spontaneous and complete recovery, and no neurological sequelae. Neurally mediated syncope refers to a heterogenous group of conditions in which there is a relatively sudden change in autonomic nervous system activity leading to a fall in BP, heart rate, and cerebral perfusion. It is typically preceded by prodromal symptoms of pallor, diaphoresis, nausea, and features of cerebral and retinal hypoperfusion, such as visual and auditory disturbances and cognitive slowing. Neurally mediated syncope incorporates vasovagal syncope, situational syncope (syncope occurring in specific situations; e.g., coughing, micturition, or with emotional stimuli), and carotid sinus syndrome.[6][16]
Nutritional deficiency states that produce autonomic and peripheral neuropathy (e.g., thiamine deficiency, vitamin B12 deficiency).
Exercise-associated collapse in endurance athletes due to lower extremity pooling of blood when exercise ceases.[17]
In a Danish cohort study of patients attending the emergency department with shock, 27.2% had distributive septic shock and 23.4% had distributive non-septic shock.[12]
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