CV09 Electrophysiology Flipped Session 011321 PDF

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Notes for physiology flipped session on heart electrophysiology, Block 3....

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Al i z a yJ a l i s i GUSOM Cl a s sof2 0 2 4 Hello and welcome to this year’s edition of Cardiac Electrophysiology! This was a flipped session organized by learning objective. Emphasized/unique info is in yellow. Connections to other courses are in green. 1. Discuss the relationship between the sequence of electrical activity and mechanical activity in the heart Depolarization of automaticity cells (SA, AV, Purkinje) always precedes the contraction of the myocytes. That is why the peak of the AP precedes the maximum contractile response. The AP of automaticity cells overlaps that of myocytes to prevent tetanus.

a. What is the normal sequence of depolarization in the heart, starting at the SA node and ending at the ventricular epicardium? (LO #7 in Dr. P’s slides)

2. *HY* Draw a typical ventricular cell action potential, LIST the phases, DESCRIBE the membrane ionic movements and conductance changes that underlie each phase. Below is my best attempt to condense all the scary current/voltage graphs from the slides. Source: Netter’s Essential Physiology by Mulroney and Myers!

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3. DESCRIBE action potential shape and ionic movements for AV and SA nodal (1), atrial and purkinje cells (2) and compare them to those in the ventricular cell (2). Dr. Partridge said that he just wants us to know the 2 types of AP shapes and ionic movements for nodes (1) and cells (2). See above for the ionic movements for (2).

4. DESCRIBE factors (action potential upstroke velocity (A), cell geometry (B), and intercellular coupling (C)) that affect conduction velocity in different regions in the heart. (A)Greater action potential upstroke velocity = greater velocity of conduction of that action potential. (B)Larger cell diameter means faster conduction velocity. The Smallest Diameter Award goes to the AV node - its teeny diameter slows down conduction velocity allowing for that nifty delay between atrial and ventricular contraction.

Al i z a yJ a l i s i GUSOM Cl a s sof2 0 2 4

(C)Intercellular coupling refers to cell-cell junctions. If there are more gap junctions connecting cells, more ions will be able to flow through them in a given period of time thereby increasing the conduction velocity. 5. DESCRIBE the effects of sympathetic and parasympathetic stimulation on pacemaker action potentials and control of heart rate. And, funny channels are suppressed, leading to a longer phase 4. https://www.nature.com/articles/s 41598-018-19719-x

Catecholamines activate the funny channel, leading to a shorter phase 4  HR speeds up because it takes less time to reach Ca2+ TP for myocyte contraction. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116039/

6. PREDICT the effects that increasing K+ concentration will have on ventricular action potential shape and conduction velocity. Let’s say you have a patient with hyperkalemia due to kidney disease. Or maybe a patient who is having an acute MI and their extracellular K+ concentration is going up. How does the K+ affect their heart function?

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Revisiting our AP curve from LO #2, we see that in Phases 1 and 2, outward diffusion of K+ by way of rectifier channels (while other ions are moving in) is necessary to prevent rapid repolarization/ incomplete contractile response. But if you already have more K+ out than in, the rate of this outward diffusion will gradually decrease.. We see this in the figure above as a reduction in the depolarization achieved in Phase 0, a loss of the typical spike seen in phase 1 and shortening of phase 2 of the AP (more rapid repolarization). At the myocyte level, this means decreased contractility (see graph in LO#1). The AP conduction velocity will also decrease because the upstroke velocity will decrease (Na+ does not come in as readily) and gap junctions will close. This means a decreased rate of contraction. 7. (added in by yours truly) APPLY what you have learned about electromechanical coupling in the heart to EXPLAIN the pathophysiology underlying myocardial ischemia. The explanation for LO#6 details steps 5, 6 7 in the process below. 1 2 3 4

Additional Details 3. The K+ channels open in response to low ATP. 4. The Na+/K+ ATPase fails without ATP, so K+ begins to leak out.

5 6 7

This is a protective mechanism that prevents the spread of the MI across the heart!

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