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Flashcards in Electrical Activity Deck (10):

Generation of AP in Ventricle Cells (4 parts)

* Resting membrane potential = -90 mV (mainly based on K+ efflux - IK1 current); STABLE
* Kir2.1 channel protein

* Upstroke - Na+ influx once threshold of -65 mV reached
* Threshold —> voltage-gated m gate opens —> once near +40 mV inactivation h gate shuts
* All-or-nothing; positive feedback b/c as Na+ enters cell the cell becomes more positive which opens more Na+ channels

* Plateau - K+ efflux, Ca++ influx, Na+ current and Na/Ca exchangers all contribute
* L type Ca++ channels
* IK1 current dec in plateau b/c higher potential BUT there are 2 other TIME DELAYED K efflux currents at this time (IKr and IKs - rapid and slow repolarizing currents)

* Refractory Period - unable to propagate new AP
* Full Recovery Time = effective refractory period (no AP) + relative refractory period (higher threshold for AP)


How are L Type Ca++ Channels inactivated?

1- Ca++ dependent (high Ca++ in cell turns off L type channels faster)

2- Voltage dependent


Generation of AP in SA Node Cells

* Resting membrane potential is NOT stable; slowly depolarizes until reaches threshold for another AP (-45 mV); this slow depolarization is called pacemaker potential

* 2 Possible Mechanisms
* I. Funny channel - cAMP and hyper-polarization turns on HCN channel protein; positive influx of Ca++ and Na+
* II. Ca++ Clock -
* Spontaneous release of Ca++ from SR —> Ca/Na exchange to remove Ca from cell —> net depolarization (b/c 3 Na+ in for 1 Ca++ out) —> depolarization act L type channels —> AP then SR reloaded w/ Ca++ from cytosol and it starts again


2 Ways Cardiac Musc Cells are Diff Than Skeletal Musc Cells

* Cardiac muscle cannot contract w/ just Ca++ from SR (needs extracellular Ca++ influx too)

* Plateau instead of rapid repolarization by K+ efflux


3 Steps of Excitation-Contraction Coupling in Ventricles

* 1- Na+ upstroke depolarizes cell membrane —> depolarizes T tubules

* 2- Depolarization opens voltage-gated L type Ca++
channels —> Ca++ influx

* 3- Inc Ca++ in cell causes inc Ca++ release from SR via RYR2 (“calcium induced calcium release”)


How is Ca++ removed from cardiac muscle cell?

* Pumped back into SR via SERCA2 (requires ATP)

* Na+/Ca++ exchanger (3 Na+ in for 1 Ca++ out - overall depolarizes cell); extra Na+ then removed by Na-K pump

* Ca++ transporters on cell membrane surface (requires ATP)


Staircase/Bodwitch Effect

* Changing HR changes force of contraction in about 12 incremental steps (12 beats)
* Inc HR = Inc Force (positive inotropic effect)

* How?
* Inc HR means AP duration is shorter; less time for Ca++ efflux so overall Ca++ accumulates in cell


How does sympathetic NS affect electrical activity?

* Affects ventricles the most

* Activates channels —> reaches AP threshold faster —> inc firing frequency/HR
* Force of contraction inc but duration dec
* Adrenaline binds beta1 adrenergic receptor —> activates adenylyl cyclase —> inc cAMP—> activate protein kinases …
* Funny channel activation
* Phosphorylate phospholamban so no longer blocks SERCA2
* Phosphorylate RyR2 for inc Ca++ release
* Phosphorylate/activate L type channels
* Inc K+ efflux for more rapid repolarization


How does parasympathetic NS affect electrical activity?

* Affects SA node cells > AV node cells > ventricle cells

* Vagus —> Ach
* Binds Gi (inhibitory G protein) —> inc cGMP which inhibits adenylyl cyclase from making cAMP (ONLY COUNTERS EFFECTS OF ADRENALINE)
* Creates K+ efflux that hyper polarizes cells so less steep pacemaker potential; takes longer to reach AP threshold


What happens in channelopathies in general?

QT prolongation —> Torsade de Pointes
* How?
* Prolonged AP —> more Ca++ influx via L type channels
* Compensate w/ Na-Ca exchanger which has net depolarization effect —> makes AP duration even longer
* SR becomes overloaded w/ Ca++ —> spontaneous release from SR —> triggers EADs (early after-depolarizations); oscillations in Ca++ conc in cell —> EADs