Electrophysiology II Flashcards
SA node
- pacemaker activity
- normal initiation site of cardiac excitation
- 60-100/min
- phase 0, 3, 4
phase 0 of SA
rapid depolarization due to Ica voltage dependent L channels
phase 3 of SA
-slower repolarization due to inactivation of Ica and activation of delayed V dep K
phase 4/ pacemaker activity
- interaction between Ica T channels, Ik, and If (h)
- If is net inward current that activates in response to hyperpolarization (when membrane gets back to neg, it sets off)
- has inward Na and outward K- depolarization in response to hyperpolarization
- when cell repolarizes, hyperpolarization opens cation channel and Na in and K out- depol
L type calcium channel
- low threshold -40
- slow inactivation and long lasting
- large channel size
- SA pacemaker and AV conduction and excitation contraction coupling
- contraction of smooth muscle
T type calcium channel
- high threshold -70 (goes open sooner and starts AP)
- fast inactivation/ doesnt last long
- small channel size
- SA node pacemaker and proliferative signaling
- contraction in smooth muscle
three mechanisms that can slow the SA pacemaker
- decreased rate of depol (K out slower takes longer to get to neg and the If channel to open)
- diastolic hyperpolarization- more hyperpol means takes more to get to threshold
- increased threshold-takes longer to get there
ANS regulation of SA node
-neuronal PNS and SNS
PNS regulation of SA node
- vagal break
- vagus nerve, cholinergic (Ach)
- muscarinic receptor (M2) metabotropic
- vagus–>Ach released–> Ach activates M2–> activated Gi protein and decreases cAMP which:
- reduces inward If (less depol)
- reduces inward Icat (less AP)
- threshold of Ical more pos (harder to get Ical to open, less Ca in)
- rate slows down
SNS regulation
- adrenergic, norepi
- B1 adrenergic receptors, metabotropic
- B1 receptor activated from norepi–>adenylate cyclase activated–> increase cAMP which:
- increase If (more depol faster- threshold faster)
- increases Icat (more Ca in)
- threshold of Ical more negative (easier to set off AP)
- increases rate
atropine
- blocks M2- no vagal activation to slow HR, Ach can’t bind
- no drop in HR
propanolol
- B blocker, no SNS sim because norepi can’t bind
- no speed up
- not as dramatic as atropine
atropine plus propanolol
- equivalent of removing ANS
- shows how parasympathetic really wins out most of the time over SNS
cardioselective beta blockers
- block B1
- bradycardia
block M2
-tachycardia
nerve- inhibit AchE
-bradycardia b/c more Ach around to bind and activate M2
block uptake of NE
-tachycardia (more norepi around to bind to beta)
atrial muscle AP
- phases 0-4
- short plateau because of long Ica and Ikur (ultrarapid)
- no intrinsic pacemaker
- ca entry from plateau promotes contraction and refractory period permits filling
AV node
- APs similar to SA
- from SA to AV in 30 ms
- intrinsic activity of 40/min
- delay b/n atria and ventricles is 90 ms
- Ca upstroke
- SP small
- slow upstroke
- few gap junctions
- conduction velocity low
- PNS decreases firing rate and conduction V
- SNS increases firing rate and conduction V, but both really controlled by SA node
bundle branches/ purkinje fibers
- highest conduction velocity in heart
- 4m/s, 80X nodes, 4X muscle
- AP similar to muscle cells but
- also have If about 20/ min and irregular
ventricular muscle APs
- similar to atrial
- no intrinsic pacemaker activity
- orderly, spatiotemporal process
- from bottom to top
- coordinated contraction of ventricular muscle cells that produces efficient ejection of blood
- inside to outside, 3 layers have different APs- see slide
coordinated contration
- wave of electrical excitation
- contraction coupled to electrical excitation
- heart consists of 2 electrical syncytia
propagation of cardiac APs
- gap junctions
- connexins
- electrical coupling of cardiac cells
- need to reach threshold for AP in neighboring cell
- current flows from A to B and passes AP through gap junction, flows back through membrane as capacitance
