Electrophysiology Lecture 3 -- Clinical Arrhythmia 1 Flashcards

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
Q

How to depress AV nodal conduction (2 methods)

A
  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
Q

2 ways to hyperpolarize AV node cells

A
  1. Pharmacologically enhancing K+ current (intravenous adenosine, IKado; or increasing IKAch)
  2. Enhancing vagal tone
27
Q

2 ways to enhance vagal tone

A
  1. Via a physiological maneuver like Valsalva or carotid sinus massage
  2. Digitalis administration (not very effective acutely)
28
Q

Define Wolff-Parkinson-White

A

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
Q

Most common pathway of conduction in Wolff-Parkinson-White

A

Goes down (antegradely) through AV node

Back (retrogradely) through bypass tract

30
Q

Parts of the Wolff-Parksinson-White macroreentrant circuit

A

Atrial tissue between bypass and AV node

Ventricular tissue between AV node and bypass

31
Q

How to terminate Wolff-Parkinson-White

A

Attack the weakest link of circuit, usually AV node (slow channel tissue)

32
Q

How to pharmacologically prevent recurrences of AV node reentry or reentry involving bypass

A

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
Q

How to prevent AV node reentry or reentry involving bypass recurrences non-pharmacologically

A

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