Everything "EP" Flashcards

IBHRE/CCDS

1
Q

What is a “Rheobase”?

A

The lowest point on a strength duration curve at an infinitely long pulse duration. Ex.: For cardiac pacing, rheobase is usually reached between 1 and 2 milliseconds; at shorter durations, threshold rises.

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2
Q

What is “Chronaxie Time”?

A

This is the pulse width at twice the rheobase value and approximates the most efficient stimulation pulse duration.

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3
Q

What is “Strength Duration Curve”?

A

The quantity of charge, current, voltage, or energy required to stimulate the heart at a series of pulse durations.

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4
Q

What is the Formula to calculate “Charge”?

A

C (charge) = I x T (“I” is the symbol for current) (multiply mean current times pulse duration (“T” = time)).

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5
Q

What is the Formula to calculate “Energy”?

A

E (energy) = I x V x T (in microjuoules: multiply mean current by mean voltage by pulse duration.

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6
Q

What is the “Functional Refractory Period” (FRP)?

A

The coupling interval which first results in a measurable degree of delay in impulse conduction.

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7
Q

What is the “Effective Refractory Period” (ERP)?

A

The longest coupling interval to be associated with block.

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8
Q

What is the “Resting (transmembrane) Potential”?

A

The voltage difference between the inside and outside of the cell fiber.

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9
Q

What is “Action Potential”?

A

The cellular characteristics of depolarization and re-polarization. The action potential consists of 5 phases.

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10
Q

What are the five phases of action potential?

A

Phase 0: the depolarization phase: during this phase, the rapid sodium channels are stimulated to open, causing the resting transmembrane potential to spike from about -90mV to about 0mV.
Phase 1: Early re-polarization.
Phase 2: Plateau Phase - mediated by the slow calcium channels, essentially disrupts and delays the re-polarization started in phase 1 and prolongs the refractory period.
Phase 3: The end of re-polarization. (Note: the period beginning at the end of phase 0 through the end of phase 3 is the refractory period of cardiac tissue).
Phase 4: The resting phase. It is during this phase that, in some cardiac cells, ions leak back and forth between membranes and cause a gradual increase in the transmembrane (resting) potential. When the potential (voltage) reaches the threshold voltage, the cell depolarizes. This spontaneous depolarization is called “automaticity.”

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11
Q

Any likely questions related to Atrial Natriuretic Peptide/Brain Natriuretic Peptide (ANP/BNP)

A

It’s a substance produced by the atrium when the muscle is subjected to higher than normal pressure (such as closing against a closed tricuspid valve) - suggestive of increased levels of ANP/BNP may be pointing to VVI(R) pacing or loss of atrial capture (or synchrony) as the culprit.

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12
Q

What is AVNRT?

A

Type of SVT confined within the AV junction requiring a fast pathway plus a slow pathway with unidirectional block in one of the pathways. P-waves are absent from the surface ECG due to the junctional rhythm.

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13
Q

AVNRT Rule of thumb:

A

Ablate the SLOW pathway. Ablation of the fast pathway significantly increases the risk of complete heart block.

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14
Q

Sites used for ablation of the slow pathway range from the mid septal region between the compact AV node and the coronary sinus os to the posteroseptal region around the os. A successful ablation is indicated by what?

A

1.) An accelerated junctional rhythm with 1:1 VA conduction during the burn.
2.) An increase in refractoriness of the anterograde AV node.
3.) Elimination or alteration in dual AV nodal physiology. (The retrograde AV nodal conduction is usually unchanged after slow pathway ablation)

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15
Q

What are complications of FAST pathway ablations?

A

1.) High-grade (2nd/3rd degree) heart block.
2.) Marked first-degree heart block.
3.) Pseudo-pacemaker syndrome caused by prolonged AV conduction times resulting in atrial contraction during AV valve closure.
4.) Persistence of atypical AV nodal reentry implying slow pathways as both the anterograde and retrograde limbs of the tachycardia.

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16
Q

What are clinical presentations of AVNRT?

A

Palpitations, dizziness, syncope, rapid regular pounding in the neck is common in AVNRT but not in other SVTs, and polyuria - due to increased levels of Atrial Natriuretic peptide (ANP).

17
Q

What is a typical ECG presentation of AVNRT?

A

Regular, narrow QRS complex tachycardia, and no visible P-wave, or P-wave located in the terminal portion of the QRS.

18
Q

What are helpful ECG patterns with AVNRT?

A

r’ (r-prime) pattern in lead V1, pseudo S-waves in leads II, III, or aVF, and no discernible P-wave separate from the QRS complex.

19
Q

What are some other diagnostics with AVNRT?

A

Typical AVNRT is rarely induced with ventricular pacing in the EP lab, while this is the rule for Atypical AVNRT, administration of adenosine during the tachycardia helps to differentiate an atrial tachycardia from AVNRT - if the AV block is produced while the atrial rhythm continues unchanged, this is highly suggestive of an atrial origin of the tachycardia, and the earliest activation at the low intertribal septum during tachycardia is consistent with AVNRT.

20
Q

When is there a good indication for a permanent pacemaker?

A

The patient is symptomatic, the heart rate is less than 40 BPM, systole of greater than 3 seconds is documented despite the patient possibly being asymptomatic.

21
Q

What is a “slew rate”?

A

The peak slope of an electrogram signal.

22
Q

What is the formula for slew rate?

A

dV/dt, or Voltage (in millivolts) divided by time (in milliseconds).