Electrophysiology Lecture 4 -- Clinical Arrhythmia 2 Flashcards

1
Q

Prevalence trend of atrial fibrillation

A

Prevalence directly related to age (older = more)

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2
Q

What determines the APD in fast channel tisue?

A

Na+ channel recovery

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3
Q

What determines the APD in slow channel tissue?

A

Ca++ channel recovery

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4
Q

Atrial fibrillation exhibits mostly what kidn of reentry?

A

Irregularly irregular reentry

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5
Q

Describe the rate of firing in atrial fibrillation

A

Rapid and irregular firings at 400 - 600 bpm

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6
Q

Maximum beat rate that the AV node can conduct. What effect does this have on atrial fibrillation?

A

150 bpm

AV node filtering since the 400 - 600 bpm firing in the atria cannot pass into the ventricles

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7
Q

Typical untreated ventricular response to atrial fibrillation

A

130 - 150 bpm

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8
Q

Ventrical response to atrial fibrillation involving a fast channel tissue bypass

A

Firing > 150 bpm = increased response

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9
Q

3 potential negative consequences of atrial fibrillation

A
  • Impaired cardiac performance
  • Symptoms (palpitations, chest discomfort, dyspnea)
  • Stroke
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10
Q

Potential consequence of maintaining beat rate over 100 bpm due to atrial fib

A

Congestive heart failure

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11
Q

Potential concentration of maintaining beat rate over 120 bpm due to atrial fib

A

Tachycardiomyopathy

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12
Q

Cause of stroke due to atrial fibrillation

A

Stasis of blood in left atrial appendage leads to clot formation. Dislodgment of thrombus –> brain = stroke

NOTE: single most important cause of stroke in elderly

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13
Q

What is the method to predict stroke risk for atrial fib patients?

A

CHADS2 score

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14
Q

Explain CHADS2

A

Note that age 65 may also be a good cutoff

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15
Q

If CHADS = 1 or higher, what kind of treatment is recommended?

A

Anticoagulation

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16
Q

Classic proposed mechanism for atrial fib

A

Multiple simultaneous functional reentrant circuits

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17
Q

2 mechanisms proposed for atrial fib apart from the classic mechanism

A
  1. Rapidly firing single ectopic focus, driving atria so fast that different regions respond at different rates according to max frequency they can support, producing fibrillatory response
  2. Single very rapid local reentry circuit, producing fib response as in 1
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18
Q

2 treatment approaches for atrial fibrillation

A

Rate control

Rhythm control

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19
Q

How to control rate in atrial fib

A

Leave patient in AF, but control ventricular response (i.e. slow conduction in AV node, for example)

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20
Q

How to control rhythm in atrial fib

A

Stop AF if needed (usually by electrical cardioversion)

If needed to prevent recurrence (often is), give antiarrhythmetic drugs, or if they fail, perform atrial tissue ablation targeted to arrhythmogenic regions

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21
Q

3 types of drugs for rhythm control (i.e. in atrial fib)

A
  • Class I (propafenone, flecainide)
  • Class II/ beta-blocker (sotalol)
  • Amiodarone
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22
Q

3 types of drugs frp rate control (i.e. in atrial fib)

A
  • Beta-adrenoceptor blockers
  • Calcium channel blockers (diltiazem, verapamil)
  • Digitalis
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23
Q

Purpose of electrica cardioversion

A

Synchronise cardiac electrical activity and “resetting it” = effective for terminating >99% of sustained tachyarrythmias, including atrial fib

24
Q

How to deliver electrical cardioversion for supraventricular arrhythmias (such as atrial fib)

A

Shock should be synchronized with the QRS to avoid delivery during T wave (when some ventricular muscle is repolarized and some not)

25
Q

Potential consequence of delivering electrical cardioversoin during T wave

A

Can induce chaotic ventricular reentry and ventricular fibrillation

26
Q

How to prevent recurrance of atrial fibrillation

A

Increase refractory period

27
Q

Describe the firing in atrial flutter

A

A single atrial macroreentrant circuit in atrium (most commonly right), typically at 250 - 300 bpm

28
Q

Atrial flutter exhibits mostly what kind of reentry and why?

A

Rate is slower than in atrial fib, so atria cn respond 1:1 (rapid and regular)

29
Q

Atrial fibrillation ECG

A
30
Q

Atrial flutter ecg

A
31
Q

Which type of control approach is more used in treating atrial flutter?

A

Rate control is harder for AFL, so rhythm control more commonly used (best response to class I and class III antiarrhythmics)

32
Q

Most successful and curative method for atrial flutter

A

Ablation

33
Q

Why is ablation most often the first choice for prevention of recurrance over antiarrhythmic drugs for atrial flutter?

A

Single circuit usually allows critical anatomical component to be identified so easy to ablate

34
Q

Stroke risk for atrial flutter

A

Comparable to atrial fib (same principles apply, i.e. CHAS2 > 1 = anticoagulants)

35
Q

Define ventricular tachycardia

A

Rapid rhythm arising from a region in the ventricles, most typically 150 - 180 bpm

36
Q

Causes of ventricular tachycardia

A
  • Enhanced automaticity
  • DADs
  • EADs
  • Reentry
37
Q

VT due to enhanced automaticity is seen most likely in what condition?

A

Acute MI

38
Q

What does VT due to enhanced automaticity repond well to?

A

Class I antiarrhythmetics (i.e. intravenous lidocaine)

39
Q

VT due to DADs is most likely seen in which conditions?

A

Conditions of cardiac hypertrophy and failure (i.e. hypertrophic cardiomypathies, CHF), which cause abnormal Ca++ handling

40
Q

Give an example of a specific genetic context in which DAD-induced VT is seen

A

Ryanodine receptor mutation in catecholaminergic polymorphic VT (CPVT)

41
Q

DAD-induced VT responds to what kind of antiarrhythmic drug?

A

Class I

42
Q

Class I effect (i.e. relevant to DAD-induced VT)

A

Prevents DAD from reaching threshold and may also prevent abnormal RyR2 Ca++ release

43
Q

Conditions associated with EAD-induced VT

A
  • Conditions that prolong APD/QT interval (i.e. Long QT Syndrome); can be congenital or acquired
44
Q

Example of acquired EAD-VT

A

Drugs that prolong APD, especially class III drugs

45
Q

Examples of congenital EAD-VT

A

Genetic conditions that enhance plateau Na+ current (LQT3) or reduce phase 3 K+ current (LQT1, LQT2)

46
Q

What exacerbates the risk of EAD-induced VT?

A

Concomitant factors tending to prolong QT (slow heart rate, hypokalemia, hypomagnesemia)

47
Q

How to treat EAD-induced VT

A

Focus on underlying conditions:

  • Beta-blockers useful in LQT1 and 2
  • Increasing HR rate induces QT and may help (i.e. temp. pacemaker in emergency situation)
48
Q

When does reetrant VT tend to occur?

A

In presence of reentry substrate like a myocardial scar, most commonly post-MI

49
Q

Drugs that reetrant VT is most likely to respond to

A

Class III

50
Q

Drugs that reetrant VT is unlikely to respond to

A

Class I

51
Q

When can direct-current cardioversion be used for VT?

A

Terminate VT when severe hemodynamic compromise is life-threatening

52
Q

Define ventricular fibrillation

A

Chatoci ventricular rhythm with no effective cardiac pumping

53
Q

Lethality of ventricular fibrillation

A

Lethal within minutes in the absence of cardiac massage/ CPR (requires emergency cardioversion)

54
Q

How does ventricular fibrillation occur?

A
  • De novo as a result of a predisposing condition (acute MI, congenital ion-channel mutation)
  • A result of degeneration of VT
55
Q

How to prevent recurrence of ventricular fibrillation

A

Resuscitated individuals from VF generally require implantation of a defibrillator (drug therapy not reliable enough)