Electrophysiology Lecture 3 -- Clinical Arrhythmia 1 Flashcards Preview

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Flashcards in Electrophysiology Lecture 3 -- Clinical Arrhythmia 1 Deck (33):
1

Significance of a wide QRS complex

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

2

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

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

3

Usual origin of premature extra beats with wide QRS complexes

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

4

Define atrial (supraventricular) tachycardia

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

5

Define ventricular tachycardias

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

6

Potential consequence of pathological bradyarrhythmia

Clinically significant = syncope Severe = cardiac arrest

7

Define sick sinus syndrome

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

8

Typical consequence of sick sinus syndrome

Syncope (rarely sudden death)

9

Population most affected by sick sinus syndrome

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

10

ECG of sick sinus syndrome

No P wave Abnormal pause Abnormal atrial complex

11

Define first degree atrioventricular block

Slowing of atrial-ventricular conduction, no blocked beats

12

ECG of first degree atrioventricular block

Long PR interval

13

Define second degree AV block

Some beats fail to conduct. Has 2 subtypes:

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

14

Define Mobitz Type I

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

15

Define Mobitz Type 2

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

16

Define third degree AV block

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

17

Define paroxysmal supreventricular tachcardia

Reentrant arrhythmias involving the AV node that occur randomly

18

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

AV node reentry

19

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

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

20

Most common form of AV node reentry

AV node reentrant tachycardia

21

Describe the direction of electrical activity in AV node reentry

  • 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

Length of normal fast channel tissue

L = CT x V

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

23

Length of normal slow channel tissue

L = CT x V

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

24

How to stop AV node reentry?

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