Syncope - classification, etiology, pathogenesis, and clinical manifestations.
Syncope is a sudden, transient loss of consciousness and postural tone, due to transient global cerebral hypoperfusion, with spontaneous complete recovery.
Classification
- 1 Reflex (neurally mediated) syncope
Vasovagal syncope (most common).
Situational syncope (e.g., micturition, coughing).
Carotid sinus hypersensitivity.
- 2 Orthostatic hypotension syncope
Due to failure of autonomic reflexes to maintain blood pressure upon standing.
- 3 Cardiac syncope
Arrhythmias (e.g., bradycardia, tachyarrhythmia).
Structural heart disease (e.g., aortic stenosis, hypertrophic cardiomyopathy).
- 4 Cerebrovascular syncope (rare)
Vertebrobasilar insufficiency.
"Steal" syndromes.
Etiology (Causes)
Reflex syncope
Emotional stress, fear, pain.
Prolonged standing.
Situations that increase vagal tone (urination, defecation, swallowing).
Orthostatic hypotension
Volume depletion (e.g., dehydration, hemorrhage ).
Autonomic dysfunction (e.g., diabetic neuropathy, Parkinson disease).
Medications (e.g., antihypertensives, diuretics).
Cardiac causes
Arrhythmias:
- Sinus node dysfunction, atrioventricular block.
- Ventricular tachycardia or fibrillation.
Structural disease:
- Severe aortic stenosis → obstructed outflow.
- Myxoma blocking mitral valve.
Pathogenesis
- 1 Common mechanism: global cerebral hypoperfusion
Brain requires continuous blood flow; interruption for >8–10 seconds → loss of consciousness.
- 2 Reflex (neurally mediated) syncope
Trigger → abnormal reflex causing sudden vasodilation and/or bradycardia (via increased vagal tone or sympathetic withdrawal).
Leads to transient hypotension, decreased cerebral perfusion.
- 3 Orthostatic hypotension
On standing → pooling of blood in lower limbs.
Inadequate reflex sympathetic activation → failure to increase vascular tone and heart rate.
Reduced venous return → decreased cardiac output → cerebral hypoperfusion.
- 4 Cardiac syncope
Abrupt drop in cardiac output due to arrhythmias or structural obstruction.
Immediate reduction in cerebral blood flow.