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Block C - Circulation > Electrophysiology Lecture 2 -- Mechanisms of arrhythmia > Flashcards

Electrophysiology Lecture 2 -- Mechanisms of arrhythmia Flashcards

1
Q

Define bradycardia

A

HR <60 bpm

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2
Q

Define tachycardia

A

HR >100 bpm

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3
Q

2 examples of physiologic arrhythmias

A

Sinus bradycardia in a trained athlete Sinus tachycardia during exercise

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4
Q

Two types of pathologic arrhythmias

A

Ectopic complexes (ectopic beats) Ectopic tachycardias

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5
Q

Definition of ectopic complex

A

A beat that arises from a site other than the sinus node (may be atrial, AV nodal/junctional, or ventricular)

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6
Q

2 types of premature ectopic complexes

A

Premature atrial ectopic complexes/beats (PACs, APCs, APBs) Premature ventricular ectopic complexes/beats (PVCs, VPCs, VPBs)

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7
Q

Location of ectopic tachycardias

A

Arise from a site other than the sinus node (in atrium or ventricles)

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8
Q

4 types of ectopic tachycardias

A

Paroxysmal Nonparoxysmal Sustained Nonsustained

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9
Q

Define a paroxysmal ectopic tachycardia

A

Start and stop abruptly, usually by initiating or terminating factor

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10
Q

Define a nonparoxysmal ectopic tachycardia

A

Present constantly, tend to appear or disappear by gradual changes in rate

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11
Q

Define a sustained ectopic tachycardia

A

Continuing for prolonged period or until stopped by an intervention

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12
Q

Define a nonsustained ectopic tachycardia

A

Terminating spontaneously

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13
Q

Most common types of ectopic tachycardia

A

Ventricular tachycardia (VT) Paroxysmal atrial tachycardia (PAT)

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14
Q

2 types of automaticity in pathologic arrhythmias + subgroups

A

Enhances Abnormal forms – Early Afterdepolarizations – Delayed afterdepolarizations

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15
Q

3 ways automaticity can be enhanced

A

Less negative diastolic potential (closer to threshold) Steeper slope of phase 4 More negative threshold (closer to max diastolic potential)

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16
Q

2 ways of suppressing enhanced automaticity

A

Make threshold potential more positive Antagonize components that enhance automaticity

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17
Q

Example of how to make the threshold potential more positive

A

Suppress: - current needed to fire cell during phase 0 - Ca++ current in SA/VA nodes - Na+ current in HP system

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18
Q

Example of how to antagonize compound that enhance automaticity

A

Beta blockers in situations where beta-adrenergic stimulation contributes to enhanced automaticity

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19
Q

AP curve of early afterdepolarizations

A
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20
Q

AP curve of delayed afterdepolarizations

A
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21
Q

How does an early afterdepolarizatoin occur?

A

When the action potential has been parkedly prolonged, causing Ca++ current to depolarize cell.

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22
Q

Around what phase does an early afterdepolarization occur?

A

On the plateau phase (2) of the action potential (before full repolarization)

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23
Q

Potential consequence of early afterdepolarization

A

Ventricular tachycardia, often with characteristic ECG appearance (“Torsades de Pointes”)

24
Q

Define Torsades de Pointes

A

ECG appearance characteristic of EAD-induced VT, which is a rapid VT with alternation of the points of the QRS

25
Q

3 common factors that cause EAD-induced arrhythmias

A

Factors that increase APD:

  • Certain antiarrhythmic drugs that block K+ channels involved in repolarization
  • Slow heart rate
  • Hypokalemia (low EC K+)
26
Q

What largely determines the QT interval on a ECG

A

Ventricular APD

27
Q

Common ECG association to EAD-Induced afterdepolarizations

A

Marked QT prolongation (“long QT syndrome”)

28
Q

3 ways to treat EAD-induced arrhythmias

A
  • Eliminate reversible factors (i.e. drug therapy) that may be causative or contributory
  • Treat hypokalemia if present
  • Increase HR (i.e. electrical pacemaker or isoproterenol)
29
Q

Cause of delayed afterdepolarizations (DAD)

A

Cellular calcium overload in fast channel tissues –> diastolic spillover of Ca++ from SR release channels (ryanodine receptors)

30
Q

What causes ryanodine (RyR2) receptors to open?

A

High intra-SR Ca++ concentrations

31
Q

What are two pathological situations where RyR2 is hypersensitive to intra-SR Ca++?

A

CHF

Come RyR2 mutations

32
Q

Define a premature beat

A

Premature activation of an action potential if an afterdepolarization reaches threshold

33
Q

When can DAD’s cause a tachycardia?

A

A series of afterdepolarizations which reach a threshold

34
Q

4 factors enhancing DAD’s and how they contribute to the problem

A
  • Increase HR, premature complexes (increase intracellular Ca++)
  • Hypercalcemia (increase intracellular Ca++)
  • Catecholamines (increase intracellular Ca++, increase RyR2 sensitivity to Ca++)
  • Mutations of RyR2 –> hypersentivity to Ca++
35
Q

2 ways to treat DAD-induced arrhythmias

A
  • Eliminate reversible contributory or causative factors
  • Various drugs can reduce DAD’s
36
Q

Purpose of Ca++ antagonists for DAD-induced arrhythmia

A

Reduce calcium entry during each action potential (may be problematic with negative inotropy)

37
Q

What is the importance of re-entrant cardiac arrhythmias

A

Cause of many important cardiac arrhythmias, including many that are implicated in sudden cardiac death

38
Q

2 examples of drugs that can reduce DAD’s

A

Ca++ antagonists (i.e. verapamil)

Na+ channel blockers (i.e. lidocaine, quinidine)

39
Q

Purpose of Na+ channel blockers for DAD-induced arrhythmias

A

Make threshold potential more positive, so harder for DAD to reach threshold

40
Q

Diagram of normal activation of cardiac rhythm

A
41
Q

Diagram of re-entrant cardiac arrhythmia

A
42
Q

Where can re-entrant arrhythmias occur?

A

Anywhere in the heart provided there are two pathways connected proximally (X) and distally (Y)

Also, anywhere with fibers interconnected at more than one point

43
Q

Where is a common anatomic arrangement for reentrant arrhythmias?

A

AV node (there can be 2 distinct alternative conduction pathways)

44
Q

Necessary impulse condition for a reentrant arrhythmia to occur

A

Impulse must first arrive from X at a time when one pathway (B) is still refractory, but the other (A) has recovered excitability

45
Q

Why is a premature beat much more likely than a sinus beat to encounter refractoriness in a pathway conducive to reetrant arrhythmia?

A

Refractory period is usually over wel before the next expected sinus beat

46
Q

Why is timing crucial for a reentrant arrhythmia to occur?

A

If the premature beat arrives too early, both A and B will be refractory

47
Q

Impulse pathway if the distal end of pathway B has recovered excitability

A

Can travel retrogradely over pathway B –> arrive at proximal end of pathway A

48
Q

Impulse pathway is the proximal end of pathway A has recovered excitability after retrogradely flowing through B

A

Propagation antegradely down pathway A

49
Q

How can one premature impulse initiate a self-sustaining tachycardia?

A

If reetrance can be sustained; distal end of B and proximal end of A always regain excitability when the reentrant impulse reaches them

50
Q

3 conditions necessary for reentrance

A
  • Premature beats
  • Differences in refractoriness between alternate pathways
  • Conduction which is slow enough so that the reentrant impulse never encounters refractory tissue (would be blocked)
51
Q

Equation for the time to complete one circuit of the reetrant pathway

A

T = L/V

where:

  • T = time
  • L = total length of reetrant pathway
  • V = conduction velocity
52
Q

Time condition for successful sustained reentry

A

T > RP

(L/V > RP)

Circuit time has to be longer than the longest refractory period

53
Q

Consequence of the circuit time not being longer than the longest refractory period

A

The impulse would leave the area of greatest refractoriness and return to it before excitability is restored

54
Q

How can reentrant arrhythmias be terminated or prevented?

A

Increasing the refractory period so that it exceeds conduction time (short refractoriness increases re-entrant likelihood)

55
Q

Effect of conduction on reentrant arrhythmia likelihood

A

Fast conduction (V large) makes reentry less likely

Slow conduction facilitates reentry (EXCEPT when sufficient to completely block conduction in reentry circuit)

Block C - Circulation (26 decks)

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