©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)

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