L8 Cardiac Pacemaker Mechanisms Flashcards
Hierarchy of cardiac pacemaker activity
[[fastest]] SA node -> latent atrial/vent pacemakers -> AV node/His junction -> Septal bundle -> Purkinje fibers [[slowest]]
SA node is the boss that beats at the appropriate rate in the human body. If it goes bad, the next in line is the latent, etc.
Automaticity
Definition: the fact that the heart can generate an impulse by itself.
How do you determine from an EKG what pacemaker is firing?
The speed of the HR
Ionic mechanisms in SA node vs. purkinje fiber pacemaker activity
SA node: multiple mechanisms
1. T-type Ca current
2. hyperpolarization-activated inward Na current from I(f)
I(f) is the only current in all pacemakers, also funny bc activated the opposite way of most, upon hyperpolarization
3. deactivation of I(k)
4. inward Na/Ca exchange current activated by SR Ca release (Na current contributes to formation of next AP)
Purkinje Fibers:
Use only the Na current from I(f) and the deactivation of the I(k) channels to stop K current out
How can you ∆ HR?
Change the slope of diastolic depolarization -
===NE acts on this via B adrenergics to increase HR===
Change the threshold potential - making it easier or harder to depol.
Change the diastolic maximum potential - (the most negative point of repolarization before another AP) changes how easy it is to depolarize up to threshold ====Ach decreases this and slows HR===
How does a change in HR look like on an EKG?
R-R interval is reduced/increased
Overdrive suppression
The idea that when a pacemaker is stimulated faster than its normal rate and then suddenly stopped, it’ll take a little bit of time until another pacemaker jumps in and takes over
Ach impact on HR
Vagal stimulation inhibits pacemakers in SA, AV, and atria regions. Increases K permeability,
decreases cAMP,
inhibits L-type Ca current,
decreases slope of diastolic depol.,
hyperpolarizes the maximum diastolic potential
All these things slow heart rate
NE impact on HR
NE stimulates ALL pacemakers.
Increases slow inward L-type Ca current,
Increases cAMP
increases slope of diastolic depol.
All give a faster HR
Sinus arrhythmia
A normal variability in pacemaker cycle length due to the varied vagal contributions to the SA node with respiration.
Inhale, stretch receptors inhibit vagal stimulation and HR increases/ cycle SHORTENS.
Exhale, opposite happens. cycle LENGTHENS
Good to be in good aerobic health because sinus arrhythmia helps prevent bad arrhythmias
Changes in SA node pacemaker rate are shown on the EKG by…
the entire R-R interval would change…
Change in pacemaker location would manifest in an EKG as a sudden difference in cycle length/HR
How would Symp nerve activity affect an EKG recording?
Symp affects the HR and slope of diastolic depolarization, which would make the AP quicker to occur