Klabunde 1 Flashcards
Resting membrane ventricular myocyte ______: Resting membrane potential (Em) is determined by:
-90mV concentrations of +/- ions across the cell membrane electric gradient relative permeability of cell membrane to ions ionic pumps
What main pump maintains ionic gradient:
What main pump maintains ionic gradient: Electrogenic : 3 Na out for every 2 K in, creating the negative potential w/in the cell
Cardiac tissue hypoxia and cardiac glycosides (ie: digoxin) do what to Na-K-ATPase pumps, causing RMP to become ______:
inhibited Na-K-ATPase RMP is more positive (partially depolarized)
Phase 0 Phase 1 Phase 2 Phase 3 Phase 4
Phase 0 Depolarization – Fast Na Phase 1 Transient outward K Phase 2 Plateau – L-type Ca Phase 3 Delayed rectif. Ikr (K in or out?) OUT Phase 4 Inward rectif. Ikr (K in)
Refractory period Effective (absolute) refractory period phases: Why? Relative refractory period
During phase 0, 1, 2, and part of 3, that cell is unexcitable h-gates are still closed At the end of ERP (end of phase 3) Suprathreshhold depolarization required to stimulate AP Not all the Na channels have recovered to resting state based on Em When activated: decreased phase 0 slope and lower amplitude
Phase 0 Phase 3 Phase 4
L-type Ca Delayed rectif. K If funny channels
Non-nodal cell RMP determined by:
K concentrations (slow leak out) K electric gradient (K+ drawn to –ve intracell.) relatively permeability memb. to K (not Na+ or Ca++) ionic pumps (NA/K ATPase, delayed Ikr)
RMP nodal cell Threshold
-64 -40
RMP non-nodal: Threshold potential ______: Depolarizes to ______mV:
-90 -70mV +30mV
Norepi binds to ____ receptor: B1 coupled to ____: stimulatory G protein (Gs): Gs activates _____ second messenger: cAMP act via:
B1 stimulatory G protein (Gs): adenylates cyclate increasing cAMP
- increases slow Na “pacemaker current” If “funny current”
- earlier opening of L-type Ca (phase 4)
- Shorter repolarization is also shortened
AcH binds to ____ receptor: M2 coupled to ____: Gi inhibits _____ second messenger: Decreased cAMP act via:
M2 inhibitory G protein (Gi): adenylates cyclate decreasing cAMP
- inhibiting slow Na “pacemaker current” If “funny current”
- Activates KAcH channels which hyperpolarize cells
…. So we went from nodal vs non-nodal AP (phases), RMP, threshold potential, and regulation (ANS and SNS) how does AP conduct cell-to-cell: how does this differ from vascuar myocytes: how does this AP result in the heart contracting
gap junctions located at intercalated discs syncytium
- non-conducting connective tissue separates/stalls AP
- slows conduction to 0.05m/s allows atrial contraction
Arrhythmias are generated via 3 mechanisms:
Abnormal automaticity
Triggered activity (EAD, DAD)
Reentry – conduction pathway prematurely stimulated by prev.AP
Abnormal automaticity, Effects which phase of AP:
phase 0 i.e. blocked by drugs (digitalis) i.e. inactivated by depolarization secondary to hypoxia Depresses slope, “fast response” converted to “slow response”
- Triggered activity EAD (early afterdepolarization) end of phase ____: DAD (delayed afterdepolarization) end phase ____:
Phase 3 – Na channels still blocked, Ca++ carries depolarizing current
Phase 3/start phase 4 – elevations in intracellular Ca++ secondary to ischemia or excess catecholamines