Flashcards in Intro to Cardiac Electrophysiology Deck (15):
What is the only electrical connection between the atria and the ventricles (normally)? What structure ensures this?
The AV node is the only electrical connection between the atria and ventricles -which also makes it vulnerable to block.
The fibrous skeleton of the heart provides electrical insulation. (there are congenital defects that can create other connections)
How do atrial myocyte refractory periods (depolarization plateaus) compare to those of ventricle myocytes?
Atrial myocytes have shorter refractory periods.
If the AV node is blocked, what sets the pace in the ventricle, given every myocyte is capable of its own spontaneous contractions?
Purkinje fibers (which have long refractory periods)
Two main currents that result in SA automaticity?
Decreasing I(k) - meaning, less K+ going out.
Increasing I(Ca) - meaning, more Ca++ coming in.
I(f)... is a minor player here.
What main current is responsible for Purkinje automaticity?
How does the range of voltages at which depolarization spontaneously occurs vary between SA node cells and Purkinje fibers? Significane?
SA node: -50 to -70 mV
Purkinje: -70 to -90 mV
Purkinje fibers normally don't have enough time to get that polarized unless there's some sort of block (e.g. AV block), so their pace is set by the SA node.
(This also accounts for Purkinje fibers' slower intrinsic rate??)
2 reasons for why the SA node sets the Purkinje fibers' pace unless blocked?
Differences in intrinsic rate - Purkinje fibers are slower.
What does overdrive suppression of Purkinje pacemakers refer to?
Activation of the Na+/K+ pump in Purkinje fibers-> hyperpolarization -> inhibition of automaticity.
What ion is responsible for a "fast response" AP? Which heart tissues have fast responses?
Atria, ventricles, and His / Purkinje
What ion is responsible for "slow response" AP? Which heart tissues have slow responses?
SA and AV nodes
What's the most important determinant of how excitable an cardiac myocyte is?
(note that during cardiac surgery, KCl is injected to stop the heart from beating)
How does conduction speed change in fibers surviving infarction? Why? How does this look on electrogram?
Conduction is slower due to a reduced number of gap junctions.
On electrogram, the action potential plateau looks jagged due to the late upstrokes of many fibers.
(and normal electrogram curve shows all the fibers having their AP synchronously)
4 mechanisms for slow conduction in arrhythmogenic substrates? (why does each happen?)
Depolarization of resting potential -> Na+ channel inactivation. (High extracellular K+)
Blockade of Na+ channel. (drugs)
Reduced gap junction conductance. (high Ca++ inhibits connexons, e.g. acute infarction)
Reduced number of gap junctions (e.g. fibers surviving infarction)
What is the definition of Effective Refractory Period (ERP)?
Time following depolarization when a stimulus cannot elicit a *propagating* AP.