Electrophysiology Lecture 3 -- Clinical Arrhythmia 1 Flashcards

(33 cards)

1
Q

Significance of a wide QRS complex

A

There is either a block somewhere in the ventricular conducting system, or the rhythm is originating somewhere in the ventricles (“ventricular source”) = activation pattern is different from when the impulse traverses the conducting system from the AV node or above

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2
Q

What is the usual cause of premature beats with narrow QRS complexes

A

Early atrial firing (atrial premature beats, APBs; atrial premature complexes, APCs; or premature atrial complexes, PACs – all mean the same thing)

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3
Q

Usual origin of premature extra beats with wide QRS complexes

A

In the ventricles (ventricular premature beats, VPBs; or ventricular premature complexes, VPCs; or premature ventricular complexes, PVCs – all the same)

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4
Q

Define atrial (supraventricular) tachycardia

A

Fast rhythms (>100 bpm) that generally have narrow QRS complexes

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5
Q

Define ventricular tachycardias

A

Fast rhythms (>100 bpm) that generally have wide QRS complexes

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6
Q

Potential consequence of pathological bradyarrhythmia

A

Clinically significant = syncope Severe = cardiac arrest

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7
Q

Define sick sinus syndrome

A

Sinus node intermittently fails to fire –> sinus pauses or sinus arrest (stops altogether)

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8
Q

Typical consequence of sick sinus syndrome

A

Syncope (rarely sudden death)

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9
Q

Population most affected by sick sinus syndrome

A

Tends to occur in the elderly, more rarely with ion channel gene mutations

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10
Q

ECG of sick sinus syndrome

A

No P wave Abnormal pause Abnormal atrial complex

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11
Q

Define first degree atrioventricular block

A

Slowing of atrial-ventricular conduction, no blocked beats

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12
Q

ECG of first degree atrioventricular block

A

Long PR interval

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13
Q

Define second degree AV block

A

Some beats fail to conduct. Has 2 subtypes:

  1. Mobitz Type 1 (also called Wenkebach block)
  2. Mobitz Type 2
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14
Q

Define Mobitz Type I

A

Progressive PR lengthening on a beat-to-beat basis until conductoin to the ventricles fails (“blocked P wave”). Cycle begins again.

Problem is almost always in the AV node and rarely progresses to third degree block

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15
Q

Define Mobitz Type 2

A

Blocked P waves occur without gradual PR lengthening

QRS duration usually long because of disease ni the His-Purkinje system, commongly progresses to third degree block and an indication for pacemaker

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16
Q

Define third degree AV block

A

Also called “complete AV block”; no sinus impulses get to ventricles, almost always requires pacemaker

17
Q

Define paroxysmal supreventricular tachcardia

A

Reentrant arrhythmias involving the AV node that occur randomly

18
Q

What is the most common reentrant arrhythmia in individuals with otherwise normal hearts

A

AV node reentry

19
Q

Why is AV node reentry so common in individuals with otherwise normal hearts?

A

Slow confuction in the AV node makes stable reentry much more likely

20
Q

Most common form of AV node reentry

A

AV node reentrant tachycardia

21
Q

Describe the direction of electrical activity in AV node reentry

A
  • Atria are fired whenever im[ulse goes up to the top of the AV node (retrograde direction)
  • Ventricles are fired whenever impulse goes dow nthe AV node (antegrade direction)
  • Maintained by reentry in AV node fast-channel tissue (note that the tissue is still slow-channel, just one side is faster than the other)
22
Q

Length of normal fast channel tissue

A

L = CT x V

L = 0.3 s x 1 m/s = 0.3 m

23
Q

Length of normal slow channel tissue

A

L = CT x V

L = 0.3 s x 0.3 m/s = 0.009 m = 9 mm

24
Q

How to stop AV node reentry?

A

Depress AV nodal (slow channel) conduction to make the reentering impulse block (die out)

25
How to depress AV nodal conduction (2 methods)
1. Block calcium channels mediating AV node conduction (intravenous calcium channel blocker) 2. Hyperpolarize AV node cells by enhancing K+ current so that their action potentials are further away from threshold and calcium current is insufficient to allow continued firing
26
2 ways to hyperpolarize AV node cells
1. Pharmacologically enhancing K+ current (intravenous adenosine, IKado; or increasing IKAch) 2. Enhancing vagal tone
27
2 ways to enhance vagal tone
1. Via a physiological maneuver like Valsalva or carotid sinus massage 2. Digitalis administration (not very effective acutely)
28
Define Wolff-Parkinson-White
AV reentry going in one direction, the other which goes through a bypass tract (abnormal congenital fast-tissue connection between atria and ventricles, through fibrous tissue)
29
Most common pathway of conduction in Wolff-Parkinson-White
Goes down (antegradely) through AV node Back (retrogradely) through bypass tract
30
Parts of the Wolff-Parksinson-White macroreentrant circuit
Atrial tissue between bypass and AV node Ventricular tissue between AV node and bypass
31
How to terminate Wolff-Parkinson-White
Attack the weakest link of circuit, usually AV node (slow channel tissue)
32
How to pharmacologically prevent recurrences of AV node reentry or reentry involving bypass
Pharmacological therapy directed against AV node (i.e. calcium channel blockers) or for WPW, fast-channel tissue in the bypass tract (Na+ channel blockers or class III agents)
33
How to prevent AV node reentry or reentry involving bypass recurrences non-pharmacologically
Treatment of choice for patients not easily controlled with drugs = * AV node reentry = interventional catheter-based procedure to ablate one of the AV node pathways * Bypass = Ablation has 95% cure rate with rare complications