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USMLE Step 1 Cheat Sheet: The Ultimate Guide to Antiarrhythmics for the USMLE Step 1

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by Alec Palmerton, MD in Cheat Sheet
USMLE Step 1 Ventricular Myocyte Action Potential

In my work as an instructor/tutor for the USMLE Step 1, one of the most common requests is to discuss antiarrhythmics. By the end of this USMLE Step 1 lesson, you will be able to answer the following questions:

  1. What would be the effects of class I antiarrhythmics on cardiac depolarization? Why? Nodal, non-nodal, or both?
  2. What would be the effects of class III antiarrhythmics on ventricular myocyte action potential? Why?
  3. Class III antiarrhythmics – main effect on EKG intervals? Why? What does this increase the risk of?
  4. What would be the effects of class IA antiarrhythmics on cardiac depolarization? Why?
  5. What would be the effects of calcium channel blockers on heart rate? Why does this make sense?
  6. Calcium channel blockers would affect which EKG interval in particular? Why?
  7. What would be the overall effect of ACh on heart rate and conduction via the AV node? Why?

Note: this lesson builds on a previous lesson on ion channel physiology.

We will begin by considering ventricular myocyte action potentials, then move on to consider the special case of nodal tissue.

Ready for the recall-type USMLE Step 1 questions?

What effect would opening Na+ channels have on a cardiac cell’s membrane potential?

Depolarization (membrane potential more positive)

What effect would opening Ca++ channels have on a cardiac cell’s membrane potential?

Depolarization

What effect would opening K+ channels have on a cardiac cell’s membrane potential?

Repolarization (become more negative)

Ventricular myocyte action potential – how many phases are there? What are they?

5 total

Phase 0, 1, 2, 3, and Phase 4
USMLE Step 1 Ventricular Myocyte Action Potential

On an EKG, the P-wave corresponds to what?

Atrial depolarization

On an EKG, the QRS complex corresponds to what?

Ventricular depolarization

On an EKG, the T wave corresponds to what?

Ventricular repolarization

Phase 0 – Which ion channel(s) open/close? Effects on overall membrane potential?

Voltage-gated Na+ channels open → depolarization

Phase 1 - Which ion channel(s) open/close? Effects on overall membrane potential?

Voltage gated Na+ channels close / voltage-gated K+ channels open → initial repolarization

Phase 2 – Which ion channel(s) open/close? Effects on overall membrane potential?

K+ still open, but voltage-gated Ca++ channels open → plateau phase (have K+ moving OUT, while Ca++ moves IN→ minimal net movement of charges)

Phase 2 – most closely corresponds to what on EKG? Why does this make sense?

ST segment

The ST segment is typically flat, which would make sense, since during the plateau phase, there is minimal change in the net membrane potential

Phase 3 – Which ion channel(s) open/close? Effects on overall membrane potential?

Even more K+ channels open (voltage-gated “slow” K+ channels), voltage-gated Ca++ channels closed → ventricular repolarization

Phase 3 – most closely corresponds to what on EKG?

T wave (ventricular repolarization)

NOTE: atrial repolarization also occurs, but is NOT typically seen on the EKG, as the atrium is much smaller, and the repolarization would be obscured by the presence of the large QRS

Phase 4 – Which ion channel(s) open/close? Effects on overall membrane potential?

K+ channels open → membrane potential at resting potential (negative)

Class I antiarrhythmics – affect what ion channel(s)/receptors?

Na+

IA, IB, or IC – which affects another ion channel? Which ion channel is this?

IA ALSO blocks K+ channels, in addition to Na+ channels

Wait!

I strongly recommend that you attempt to answer the final questions by yourself first, before looking at the answers.  Remember, the USMLE Step 1 exam will test your ability to make connections on the spot. The more practice you have, the higher your score!  Then, when you think you might know the answer (or are completely stumped), look at the answers below!

Ready for the recall-type USMLE Step 1 questions?

What would be the effects of class I antiarrhythmics on cardiac depolarization? Why? Nodal, non-nodal, or both?

Slows phase 0 depolarization in non-nodal tissue

Recall that nodal tissue does NOT use Na+ (only uses Ca++) in phase 0 depolarization

USMLE Step 1 Class Ic Antiarrhythmic

Class IC antiarrhythmics will slow down depolarization, flattening the slope of Phase 0. Note that Class IA will have similar effects on Phase 0 depolarization

What would be the effects of class III antiarrhythmics on ventricular myocyte action potential? Why?

Class III antiarrhythmics would slow Phase 3 repolarization, since K+ channels mediate this repolarization

USMLE Step 1 Class III Antiarrhythmics

Class III antiarrhythmics delay Phase 3 repolarization by blocking the K+ channels necessary for repolarization. Note that Class IA antiarrhythmics will have similar effects on Phase 3 repolarization, as they also block K+ channels.

Class III antiarrhythmics – main effect on EKG intervals? Why? What does this increase the risk of?

Prolonged QT interval

Slows repolarization, so will prolong time between QRS complex (ventricular depolarization), and T wave (ventricular repolarization).

This will increase risk of TORSADES DE POINTES (you MUST know this for Step 1)

What would be the effects of class IA antiarrhythmics on cardiac depolarization? Why?

Slow phase 0 in non-nodal tissue

Prolong QT interval (also blocks K+ channels)

Next, we move on to discuss nodal tissue.

Ready for the recall-type USMLE Step 1 questions?

Nodal tissue action potential – how many phases are there? What are they?

3 total

Phase 0, 3, and Phase 4

Phase 0 – Which ion channel(s) open/close? Effects on overall membrane potential?

Voltage-gated Ca++ channels open → depolarization

Phase 0 – why is the action potential determined by Ca++ channels, and not Na+ channels?

(This is a review from a previous article)

In order to activate Na+ channels generally in the heart, you must first REMOVE INACTIVATION from them (double-negative, I’m sorry). In order to remove inactivation, you must have a more negative membrane potential. This is ONLY possible in non-nodal tissue, because of the presence of the special K+ channel, called IK1.

In other words, nodal tissues HAS Na+ channels (oddly enough), but it does NOT use them, because the membrane potential does NOT become negative enough to remove inactivation of the Na+ channels.

Ca++ channels do not have this sort of regulation, and thus will be active in nodal tissue.

What is the next phase to occur following Phase 0?

Phase 3

Note there is NO phase 1 or 2 in nodal tissue

Phase 3 – Which ion channel(s) open/close? Effects on overall membrane potential?

Ca++ channel inactivation, K+ channels open → repolarization

Phase 4 – Which ion channel(s) open/close? Effects on overall membrane potential?

“Leaky” Na+ / Ca++ channels → slow depolarization

Phase 4 – what will happen eventually following slow depolarization? What Phase will this correspond to?

Slow depolarization via leaky Na+ and Ca++ channels → pass voltage threshold for voltage-gated Ca++ channel opening → depolarization (phase 0)

What special K+ channels are present in nodal tissue that are absent in ventricular tissue? What causes them to open, and what would be the effect?

In nodal tissue (both SA and SA nodes), there are special K+ channels called IKG channels. When ACh binds to these channels, they will open → K+ efflux → hyperpolarization

What is the normal pathway of conduction through the heart, starting with the SA node?

SA node → atrium → AV node → His Purkinje system → ventricles

USMLE Step 1 Normal Conduction

When the conduction signal moves from SA node to atrium, what causes the atrial depolarization?

SA node will depolarize the atrial tissue surrounding it, since they are electrically connected

What structures allow for depolarization of the atrium in response to SA nodal depolarization? How?

Gap junctions.

Allows for direct connection of cytoplasm between adjacent cells. This allows for the direct transfer of ions (and thus the wave of depolarization) from one cell to the next.

What allows for depolarization of the AV node?

Gap junctions connecting it to atrial tissue allow for transfer of action potential from atrial tissue → AV node

What does normal sinus rhythm mean?

Rhythm originates in the SA node

What determines the heart rate assuming a normal sinus rhythm (i.e. the rhythm originates in the SA node)?

Slope of the phase 4 depolarization in the SA node

In other words, if the slope of the phase 4 depolarization is HIGHER → reach depolarization threshold FASTER → have MORE depolarizations in a given time period (i.e. heart rate ↑)

What determines the speed of conduction through the AV node?

Slope of the phase 0 depolarization through the AV node

Why does it make sense that it is phase 0 and NOT phase 4 depolarization that will determine this?

It is a question of HOW you reach the depolarization threshold

In the case of the SA node, phase 0 depolarization is reached because of SPONTANEOUS depolarization during phase 4. In other words, leaky Na+ and Ca++ channels → slow depolarization → reach depolarization threshold

In contrast, the AV node is depolarized directly following atrial depolarization. Note that this is NOT spontaneous, and is in fact triggered by the atrial depolarization itself.

Class II antiarrhythmics – affect what ion channel(s)/receptors?

β blockers

Class IV antiarrhythmics – affect what ion channel(s)/receptors?

Ca++ channel blockers

Wait!

I strongly recommend that you attempt to answer the final questions by yourself first, before looking at the answers.  Remember, the USMLE Step 1 exam will test your ability to make connections on the spot. The more practice you have, the higher your score!  Then, when you think you might know the answer (or are completely stumped), look at the answers below!


Almost there! Think about how nice it will be to finally understand the antiarrhythmics section in First Aid!!

What would be the effects of calcium channel blockers on heart rate? Why does this make sense?

HR ↓Slope of phase 4 depolarization ↓ → reach threshold slower → fewer depolarizations in a given time period → HR ↓

Calcium channel blockers would affect which EKG interval in particular? Why?

PR interval ↑ by slowing phase 0 depolarization

Takes longer for signal to travel between atrium (P wave) to ventricle (QRS complex), because conduction through the AV node is slower → interval between P and QRS (PR interval) ↑

What would be the overall effect of ACh on heart rate and conduction via the AV node? Why?

ACh binds IKG channels → K+ efflux ↑ → hyperpolarization → require more cation influx to get same level of depolarization → slow conduction through AV node and slow heart rate

What should you do next?

  1. Turn the narrative, “Pathogenesis to Presentation” questions into Anki cards by copy/pasting the question/answer into the “Front” and “Back” fields in Anki.  Do the same for the fundamental facts that you were unfamiliar with, to maximize your chances of USMLE Step 1 success!  Remember: the USMLE is a test of understanding, so the better you can understand these questions, the better your score!
  2. Add reverse cards when appropriate to your Anki cards
  3. Re-word the questions/explanations as desired, and BOLD the important text to make it easier to review in the future
  4. Learn something new?  Something unclear?  Comment below!
  5. If you liked this post, please consider sharing it on Facebook/Twitter!  I judge the utility of these posts by the number of comments / shares they receive, so if you’d like more, or would like a particular topic addressed, please let us know!

Photos by: ZaaFari,Silvia3, and Kalumet.

Want FREE Cardiology Flashcards?

Cardiology is key for impressive USMLE scores. Master cardiology from a Harvard-trained anesthesiologist who scored USMLE 270 with these 130+ high-yield flash cards. You’ll be begging for cardio questions - even if vitals make you queasy.

Subscribe