Exam 1 lecture 3 Flashcards
Phase 4 of ventricular action potentials
resting potential. membrane is permeable t potassium through leak channels, outward flow of potassium ions generate the Ik2p current. Inward rectifer outward potassium current Iir. Em approx. for potassium (-96mv)
Phase 0
rapid opening of voltage gated sodium channels and inward sodium current, driving membrane potential in direction of sodium (+52)
Phase 1
closing of voltage gated sodium channels, coupled with voltage gated transient outward potassium current (Ito). Pulls membrane potential back to resting
Phase 2
Plateau, reduced outward potassium current (Ik1 or Iir) coupled with an inward calcium current (Ica (l)) through L type voltage gated calcium channels
Phase 3
repolarization. closure of L-type calcium channels, an increase in outward potassium current (Ik1), and rapid and slow voltage-gated delayed outward rectifier potassium current (Iks and Ikr). Delay in reporlarization allows for calcium channels to reactivate
why is delayed outward rectifier Ikr for potassium important for repolarization
hERG forms the major portion of voltage gated ion channel protein involved in Ikr. mutations can delay cardiac repolarization. In ECG, effect is LONG QT INTERVAL, or congenital long QT syndrome
what can congenital long QT syndrome cause
serious ventricular tachycardia and ventricular fibrillation
What else can cause congenital long QT syndrome
mutations in sodium and calcium channels
drugs that block hERG cause
acquired long QT syndrome, antiarrhythmics, anti-psychotic agents and antibiotics
inward rectifier
channels close as the cell depolarizes, (ooposite potassium channels which close when cell depolarizes). This is why rectifier current is reduced at plateau phase of cardiac action potential and increases again as cell repolarizes
directions of rectifier current
downward deflections are inward currents and upward deflections are outward currents
effective refractory period
during plateau phase, arrival of second depolarizing impulse has no effect
what follows effective refractory period?
relative refractory period: when sodium channels in membrane are unable to open when voltage is changed (when other are reset and ready to respond)
why dont cardiac muscle experience tetanus like the muscles do?
because the effective refractory period last quite a long time
when does calcium enter myocardial cells,
phase 2, during the plateau phase, triggers a release of more calcium from SR-> calcium concentration int he sarcoplasm increases-> calcium binds troponin which causes conformational change in tropomyosin, allowing mysoin to bind actin