Refractory Period & Pacemakers Flashcards
What is the hierarchy of pacemaker activity?
SA node (primary, fastest) latent atrial pacemakers AV node His bundle (junctional) bundle branches Purk fibers
What are the mechs involved in SA node pacemaker activity?
- T-type Ca current
- hyperpolarization-activated inward current (I-f) [funny!]
- deactivation of k current (I-k)
- inward Na/Ca exchange current activated by intracell SR Ca release
When are premature beats elicited?
diff times during the RRP (vulnerable period)
-the earlier, the smaller AP amplitude and rate of rise
What is the R on T phenomena?
a premature beat (R wave) that occurs during the RRP (T-wave) of the previous beat
leads to re-entry that cause Premature ventricular contraction (PVC)
example of “non-sustained ventricular tachycardia)
So what’s this atrial fibrillation thing?
It’s when the atria are beating really hard but not all the impulses are going through the ventricles
why? cuz post-depolarization refractoriness
But still a bunch going though! like 120 bpm (compared to atria at 200bmp)
on EKG will see: bunch of p’s followed by qrs
irregularly irregular rhythm
What is post-depolarization refractoriness?
The refractory period of a slow response is longer than the AV node AP duration
the AP is done but the cells are still in the refractory period
- the Ca channels are not yet fully functional so even if an AP comes through it won’t have any effect
- the longer u give the cell to recuperate, better the chance to elicit an AP
How do you slow ventricular rate in a pt with atrial fibrilation?
Ca channel blockers to lengthen the refractory period even more (so less impulses go through the ventricles)
also give b blockers to slow sympathetics
The rate (interval) at which the heart is beating will determine, to some extend, the duration of the cardiac AP. Explain
well, the faster the HR, the shorter the AP duration will be (Q-T)
why? you want systole to happen really fast to give diastole a lil extra time (to fill the ventricles before the next beat)
What causes prolonged Q-T syndrome?
- bradycardia: pathologically slow HR
- hypokalemia: low extracell K, so to prevent it from leaving u get anomalous rectification and a decr in K permeability
- harder to leave so prolong the AP - quinidine
- congenital e.g. h-gate dont close normally or K channels dont turn on
What is diastolic depolarization?
automaticity! the SA node kinda does its own thing: generate spontaneous AP
also known as pacemaker phase, phase 4
What contributes to diastolic depolarization?
- T type Ca current: bring Ca in to start the signaling
- funny current: activates on hyperpolarization, inward current
- deactivation of I-K current (so can finish depolarization)
- Inward Na/Ca exchange current
- activated by intracell SR Ca release
What contributes to purk fiber depolarization?
- funny current
2. deactivation of K+ current
What mechs can you use to change HR?
- change the slope of diastolic depolarization:
- sympathetics (NE) increase the slope so can reach threshold faster and create AP => faster heart rate
- parasymp (Ach) lower the slope so lower the HR - change in maximum diastolic potential: most negative, lowest point- aka if increase it a bit would be easier to bring on an AP
- change threshold: with drugs, but can make easier/harder to generate an AP
- pacemaker shift: they each have diff rates so if a diff one becomes the main one u will change the HR
What is overdrive suppression?
The SA node beats intrinsically faster and this suppressed other latent pacemakers
-if u stop the SA node, u get lil break before another pacemaker picks up the heartbeat
How does vagal nerve stimulation control HR?
Ach! (parasympathetics)
inhibits pacemakers within the SA node, AV node, atria
How?
-incr K+ permeability: leave [make -] -> slow HR
-decrease cAMP synthesis: inhibit slow inward L-type current an funny current (help with depolarization)
-decrease the slope of diastolic depolarization (slower to get to threshold)
-hyperpolarizes maximum diastolic potential (slower to get to threshold)
