©2009 Mark Tuttle
Syncope









Syncope: transient loss of consciousness & postural tone + spontaneous recovery
Difficult to estimate the number of syncope patients, but there are many, and it’s
expensive
Those who suffer from severe/frequent fainting often die suddenly! Syncope is often
the only warning sign.
Things that cause you to pass out that can kill you:
o Ventricular tachycardia (VT) & ventricular fibrillation (VF) post-MI
o Heart block (very young  congenital (85% of their mothers have lupus); also
very old)
o Hypertrophic cardiomyopathy – most common cause of sudden death in young
ppl in USA. 50% have syncope as warning sign, 50% have no warning sign. (#2
most common is anomalous coronary arteries)
o Dilated cardiomyopathy – 10%
o Long QT – 5%
o Varies by region throughout the world
Narrowing of coronary arteries is a big cause of death
o ~45% of people our age have coronary blockages
 High fat diet, bad genes (Indians), etc
o Plaque: macrophages, oxidized/esterfied LDL, platelets, fibrin
 Covered by fibrous cap, which can rupture  occludes w/thrombosis
afterward  MI
Wolf-Parkinson-White Syndrome: accessory pathway (piece of muscle tissue) that
abnormally connects atria & ventricle, runs thru annulus fibrosis; failure of
development; cause of sudden death in athletes
Long QT: will kill if not treated. A channelopathy: a disturbance in ion channels of
myocytes.
o Long QT 1: K+ channel problem; die during exercise (esp. swimming)
 Many unexplained drownings
o Long QT 2: K+ channel problem; die from surprise
o Long QT 3: Na+ channel problem; die during sleep (most lethal)
 Many SIDS pt’s might be Long QT 3
Regatta Syndrome: similar to Long QT 3 (Na+ channel) except it’s more like a short QT.
Extremely prevalent in Asia.
o After syncope starts, dead w/in a few months
ANS
o
o
o
o
o
Has input from emotions (higher) as well as physiological (lower)
The ganglia of both parasymp and symp use Ach!
Parasymp ganglia are very close to where they’re going to innervate
Symp ganglia are more proximal to the spinal cord
Generally there’s a constant parasymp tone, and the symp varies
©2009 Mark Tuttle




o Mechanoreceptors (stretch)… 2/3 of all of them are in the posterior aspect of the
R and L ventricle. Heart is the major BP sensor, but every BV has them.
Skeletal muscle pump can raise BP 10 points… most people don’t use it all the time, but
it’s necessary for ppl w/autonomic dysregulation
o If the muscle pump fails in some pt’s, the heart is expecting blood for the next
beat… if it doesn’t come, the chamber collapses.
If R coronary artery is occluded, mechanoreceptors in heart get no O2  start signaling a
ton  tricks your brain into thinking your BP is very high  decreases sympathetic 
BP crashes to 0 + bradycardia  syncope
o Called veso-gerish response??
Postural Tachycardia Syndrome (POTS): impaired venous return, compensatory
tachycardia & ↑contractility to return blood to arterial side (blood pools in lower limbs
if standing)
o Follows viral infection
o In one form, pt’s get very tachycardic – is just a point mutation
 Causes failure in NE binding & thus cycling
o The other form, pt’s have autoimmune disorder
Ehlers-Danlos syndrome (EDS), ie. joint hypermobility
o Collagen disorder
o Causes ↑venous compliance



Reflex syncopes
Postural Tachycardia Syndrome (POTS)
Autonomic failure
o Pure autonomic failure – failure of ANS alone
 No somatic nn involvement
 Orthostatic hypotension
 Can’t urinate or shit or sweat or regulate body temp
o Multiple System Atrophy
 Autonomic failure + somatic nn. involvement: 100% mortality
 Types: Parkinsonian, Cerebellar, & Mixed

RV dysplasia: fat replaces myocardium



SSRI’s help some people
EPO helps others
Pacemakers that also sense BP work too