Syncope Flashcards
General definition of syncope
transient loss of consciousness and postural tone
General underlying cause of all syncope
global cerebral hypofusion
Time course of syncope
Onset is rapid, duration brief, and recovery spontaneous and complete
Epidemiology of syncope
Lifetime incidence 35%
F > M
More after 70 yo
Pathophysiology of syncope
Decrease venous return -> diminished CO and BP -> baroreceptors in carotid sinus and AA provoke reflex -> increased sympathetic and decreased vagal -> peripheral vasoconstriction to promote venous return and CO -> failure results in hypoperfusion, occurs at 50mmHg -> cessation of blood flow for 6-8 sec results LOC
Categories of syncope
1) Neurally mediated - reflex, transient change in hemostatic reflexes
2) Neurogenic orthostatic hypotension - autonomic, chronically impaired homeostatic reflexes
3) Cardiogenic - cardiac conditions cause a decrease in CO
Initial eval of all syncope patients
History: Witnesses, precipitating events, associated sx, and medical Hx
PE: cardio/neurologic exam, vital signs (orthostatic)
ECG if any cardiac suspicion
identifies cause in 50%
helps risk stratify the remainder
Usual labs to dx syncope
CBC, BMP, UA
RF for adverse outcomes of syncope
- Abnormal ECG
- H/O heart disease
- Systolic <30
- Older age
- FHX sudden cardiac death
How to treat syncope patients with high-risk criteria
admit for eval and cardiac monitoring
Cause of neurally mediated syncope
transient change in autonomic efferent activity
- increased parasympathetic excitation = bradycardia
- increased sympathetic inhibition = vasodilation
MUST HAVE INTACT AUNTONOMIC NS
Which syncope is benign, usually associated with known trigger
neurally mediated
Subtypes of NMS
1) vasovagal syncope (common faint)
2) situational reflex syncope (triggers include fear, intense emotion, unpleasant sight/odor)
Tx for NMS
Reassurance, avoid provocative stimuli, IV fluids prn
Prodromal sx of syncope
Caused by autonomic activation -> diaphoresis, pallor, palpitations, nausea, hyperventilation
orthostatic hypotension
reduction of at least 20 systolic or 10 diastolic within 3 min of standing
2 classifications of orthostatic hypotension
Volume depletion
Neurogenic (Autonomic)
Volume depletion orthostatic hypotension
- Occurs within 15 secs of standing
- Mismatch between CO and PVR
- Compensatory increase in HR
- Supine Hypertension uncommon
- Caused by volume depletion, vasodilatation, or decreased CO
Neurogenic/Autonomic orthostatic hypo
- Occurs within 3 mins of standing
- Sympathetic vasoconstrictor (autonomic) failure
- Usually NO compensatory increase in HR
- Supine Hypertension common
- Caused by central neurodegenerative disorders and peripheral neuropathies
predisposing factors of NOH
Postprandial, elderly
Presyncope symptoms
- Commonly in neurogenic orthostatic hypotension
- Caused by hypoperfusion/ischemia of various structures
- dizziness, lightheadedness, weakness, fatigue, and visual/auditory disturbances, headache, cognitive slowing
Dx studies for NOH
- Tilt table test
- HR (parasympathetic) and BP (sympathetic) response to Valsalva
- Thermoregulatory sweat response (sympathetic cholinergic)
Tx of NOH
- Remove reversible causes
- Patient education: staged moves from supine to upright, isometric counter measures, raising head of bed, warn about hypotension after meals
- Optimize intravascular volume with fluid and salt intake
Which type get prodromal symptoms?
neurally mediated syncope (vasovagal)
Which type get presyncope sx?
neurogenic orthostatic hypotension
Central neurodegenerative disorders that cause orthostatic hypotension
Alzheimer’s, Lewy Bodies disorders (Parkinson’s, dementia), stroke
Peripheral neurodegenerative diseases that cause orthostatic hypotension
DM, amyloidosis, spinal cord injury
