need slow conduciton in one limb and unidirectional block in the other
<<PIC>>
abnormal transmembrane leak depolarizes cells too early.
common
calcium overloading of cells results in membrane potential oscillation which can trigger activation. This is through the Na-Ca exchanger, which can move both ions in both directions. Delayed afterdepolarization
Supraventricular tachycardias
narrow QRS complexes
physiologic.
exercise, epinephrine, blood loss
extremely common; 5% of people over 70, 10% of people over 80%
very frequent atrial ectopy can trigger fribrillation, using triggered or automatic.
an abnormal atrium, scarred and stretched, is easily put into fibrillation by triggers, due to easy reentry
irregularly irregular rapid pulse.
AV node will only allow so many beats through.
young folks ~200 bpm, deacreases with age.
can cause atrial thrombus in appendage
can also get tachycardia-induced cardiomopathy
some people can be asymptomatic. other people feel terrible. symptoms can include angina (if with CAD), CHF (if with valvular disease), fatigue, syncope/lightheadedness
Anticoagulation should be used if there is increased risk of
macroreentry
electrical activity loops around right atria around
AV Nodal Reentry
most common (60%) cause of paroxysmal SVT
inputs to AV node from atrium can have different enough properties to cause atrial reentry
excellent prognosis, but can be annoying
AV Reentry
accessory pathway across valvular
30% of paroxysmal SVT
ectopic atrial tachycardia
triggered or automatic focus
Ventricular
usually activated through muscle itself - reentry, generating a wider QRS
most ventricular tacy occurs in the setitng of a prior MI. Surviving tracts within infarction scar....
monomorphic, polymorphic, or Torsades des Pointes
others
Treatments
paroxysmal SVT
atrial fibrillation and flutter
ventricular tachycardia