Lisps Review Flashcards
Ca channel blockers inhibit
L-type channels. This slows the upstroke of AP and the plateau. Thus it is responsible for conduction.
3 K+ channels in heart?
IK channel: phase 3 repolarization
ITO channel: phase 1 repolarization
IK1 channel: BACKGROUND CURRENT that determines RMP. This channel is not “on or off”…not voltage “gated”, but voltage “dependent”…during depolarization free Mg2+ plugs K+ channel. This is why conduction decreases over depolarization. RESPONSIBLE FOR PLATEAU OF AP.
What does hyperkalemia do to Vg Na channels?
Reduces their rate of activation, slowing inward Na+ current. Promotes conduction block, and re-entry.
Triggered activity. 2 Types?
DAD: abnormal release of Ca from SR (overloaded, like in digitalis toxicity)…Ca/Na exchanger compensates by inward Na current, which promotes depolarization that can possibly hit threshold.
EAD - more serious. Long depolarization. EAD caused by long AP, which causes EAD (positive feedback). Acidosis or ischemia, or quinones, can increase length of AP.
Diastolic depolarization determines…
pacemaker rate. Only part of AP that has to do with rate. Has nothing to do with conduction.
Upstroke of AP determines…
conduction. Pertains to synchrony of cells contractions. Eg. QRS conduction
Refractory period determines…
duration of AP. Has nothing to do with conduction either.
Ventricular rate is determined by
AV node
2 things that can depolarize resting membrane potential
- Ischemia/infarct (local K+ buildup)
- Hyperkalemia
Both promote slurred QRS, and re-entry
Space constant is positively determined by
Size of cell and number of nexal connections (His-Purkinje has biggest space constant)
What determines shape of QRS
normal conduction through His-purkinje system
Autonomics effect sinus rhythm how?
Val Salva maneuver or cold water on face → high vagal stimulation → suppresses arrhythmia (eg. Wolf-Parkinson-White) → lowers O2 demand on heart
What does an L-type Ca blocker do to AV node?
Slows upstroke of AP, thus slower conduction.
