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What are the components underlying every "reentry" tachycardia?
How does current normally move?

Two conduction pathways: one slowly conducting with a short refractory time, one more rapidly conducting with a longer refractory time.
Normally, current travels down the rapidly conducting path to the ventricles, but also back up the slowly conducting path to cancel that impulse.
(this really benefits from images/videos - check out the lecture if this doesn't make sense0


How does a slow and a fast pathway turn into tachycardia, initially?

A premature impulse from the SA node reaches the fast/slow branchpoint at just the right time such that the fast pathway is still refractory, but the impulse can propagate through the slow pathway.
The impulse from the slow path goes back up the fast path, leaving it refractory, so the next impulse from higher up again can't travel down the fast path... and so you're in a loop.


So you've got impulses conducting through the slow path to the ventricles now. Why does this increase heart rate?

The impulse that travels up the fast path can cause the atria to depolarize (from bottom to top -> inverted P wave on inferior leads).
That atrial depolarization can spread via the slow path back to the ventricles, causing another systole at a rate exceeding that generated by the SA node.


All this fast path, slow path stuff is pretty vague. What are some locations where this "reentry" process can happen? (name 4)

Wolff-Parkinson-White syndrome: accessory electrical connection from atrium to ventricle ("fast path" relative to AV node).
Within the AV node itself.
Ventricular infarct.
Within the atrium (atrial flutter).


How many people have multiple AV nodal pathways?

About 1/3 of people have an extra "slow" pathway in the AV node.


What does Wolff-Parkinson-White (WPW) syndrome look like in "pre-excitation" i.e. before a reentry tachycardia happens? (describe the path of depolarization and relevant ECG features)

SA impulses -> atria.
Atrial impulses take the fast, accessory path to ventricles, making the PR interval... pretty much 0.
Initial ventricular depolaration has a broad, notched "delta wave."
The QRS is wide (with axis shift depending on where the connection is), as the ventricles depolarize from one side through myocytes. The end of the QRS is usually narrow as impulses reach the His-Purkinje system and finish ventricular propagation more rapidly.


How does normal, sinus WPW transition to supraventricular tachycardia (more specifically, Atrial-ventricular reentrant tachycardia - AVRT)? Describe conduction path and relevant ECG features.

A premature atrial complex (PAC) is too early for conduction through accessory path. Conduction occurs through the AV node / His purkinje, but by the time it reaches accessory path, accessory path has recovered.
Impulse goes back up to atria -> atrial depolarization from bottom up (causing inverted P wave in inferior leads) -> through AV node again -> tachycardic loop.
The R-P interval is very short due to rapid anterograde conduction.
Also, note that this produces a regular tachycardia.


I'd ask you about the conduction circuit in ventricular tachycardia... but I'm not sure about how it works myself.

Autonomous ventricular depolarization currents around scar tissue... go up His-Purkinje to the atria... then form a circuit and come back down. (Do they hit the SA node? Or...)
(we'll see it in small group, hopefully)


What's happening in atrial flutter?
What does this look like on ECG (in a clockwise flutter)?

Circuit is traveling in loop around atrium... (this is more regular, and distinct from A fib), occasionally this gets conducted to the AV node.
On ECG, there's a "saw-tooth" P wave that is negative in leads II, III, and aVF (i.e. the current is going upward).


2 ways to treat a reentry circuit? (Drugs that accomplish this.)

Prolong refractoriness. (Class III K+ channel blocker)
Decrease conduction velocity. (Na+ channel blocker)


Treatment for WPW-related tachycardias?

Catheter ablation of the accessory pathway.


What happens in atrial tachycardia?

A focus of tissue has aberrant automaticity and drives atrial depolarization, which then conducts normally.
The P waves are present and the PR intervals are normal.
(I guess the only difference here is the faster rate? Maybe the P weirds have abnormal shapes, depending on the location of the focus)


Should you try to directly address sinus tachycardia?

Probably not. Better to address the underlying cause.


What does "triggered activity" refer to? What is its primary cause?

Another action potential that occurs during or just after a cell's refractory period... and propagates.
The primary cause of this is too much intracellular Ca++.
(due to, e.g. digoxin toxicity)


Will torsades des pointes jump out at you on ECG?

Yep. It's a form of triggered activation tachycardia.


Where does A-fib initiate?
How does it propagate?

Automaticity in atrium.
It propagates by multiple wavelet reentry - lots of microcircuits.


Why doesn't A fib kill the ventricles?

The AV node acts as a gate keeper, and only lets an occasional impulse through, at irregular intervals.


What does A fib look like on ECG?

P waves are gone - just undulations.
R waves are at irregular intervals.


What happens in Ventricular fibrillation?

QRS replaced by chaotic circulating wavelets.
No significant contraction -> loss of consciousness and death.


How does the QRS help you distinguish supraventricular vs. ventricular tachycardia?

Supraventricular: usually narrow QRS (early QRS of AVRT may be wide, though)
Ventricular: usually wide QRS


What's going on in ventricular tachycardia?
Significant ECG features?

Analogous to atrial tachycardia, there's a focus of ventricular cells that is initiating depolarization spontaneously from within the cells.
Tachycardia with wide QRS (also QRS is independent of P waves).


Why is ventricular tachycardia fast, given that ventricular escape rhythm is slow?

There's reentry happening: the depolarization spreads back up to the atria, AV node, forming a circuit.
(unlike in A fib, the AV node lets all or most of these impulses through... probably because the AV node is being stimulated less frequently and a regular intervals)


What's going on in atrial flutter?
Significant ECG features?

Sort of similar to A fib, but in a regular wave of depolarization that circles around the atria. AV node lets impulse through at regular intervals, but doesn't necessarily let them all through.
On ECG, there are negative, "saw-tooth" P waves in infererior leads (II, III, and aVF). Not every P wave leads to a QRS, but QRS's are induced at regular intervals.


2 mechanisms to treat a reentry circuit?
Drugs classes that do this?

Prolong refractoriness - Class III K+ channel blockers.
Decrease conduction velocity - Class I Na+ channel blockers.


How might you treat AVRT with a procedure?

Catheter ablation of the accessory pathway.


Review: Which is fast/slow - SA node or His-Purkinje system phase 4 upstroke?
Which ion is used in each?

Phase 4 upstroke speed dictates automaticity.
SA node phase 4 upstroke is relatively fast, and mediated by Ca++.
His-purkinje phase 4 upstroke is relatively slow, and mediated by Na+ (not to be confused the rapid Na+-mediated phase 0 upstroke).


What's going on in atrial tachycardia?
Significant ECG features?

Ectopic foci of automaticity in right or left atria -> set pace at a rate faster than the SA node.
The P waves may look abnormal, depending on where in the atria the ectopic focus is. Otherwise ECG looks normal (normal PR, P waves precede each QRS, etc.), just fast.


Review: What is does normal P wave morphology look like on ECG?

P waves should be upright in leads I and II, and biphasic in lead V1.


Treatment for sinus tachycardia?

Address the underlying cause.


What causes early and delayed afterdepolarizations?

Too much cytosolic Ca++.