©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 à 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 à occludes w/thrombosis afterward à 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 Has input from emotions (higher) as well as physiological (lower)
o The ganglia of both parasymp and symp use Ach!
o Parasymp ganglia are very close to where they’re going to innervate
o Symp ganglia are more proximal to the spinal cord
o Generally there’s a constant parasymp tone, and the symp varies
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 à start signaling a ton à tricks your brain into thinking your BP is very high à decreases sympathetic à BP crashes to 0 + bradycardia à 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