djorgenmorris

1. Dysrhythmias Originating
Within the AV Junction
 AV junction serves two important physiological
purposes:
 Slows the impulse between the atria and the
ventricles
 Backup pacemaker if the SA node or cells higher in the
conductive system fail to fire

2. Dysrhythmias Originating within the
AV Junction (AV Blocks)
 AV Blocks
 Locations
 At the AV node
 At the Bundle of His
 Below the Bundle of His
 Classifications
 First-Degree AV block
 Type I Second-DegreeAV
block
 Type II Second-DegreeAV
block
 Third-DegreeAV block

3. Usually <0.12
seconds
QRS
>0.20 SecondsPRI
NormalP Waves
SA node or atrial
Pacemaker
Site
Usually regularRhythm
Depends on
underlying rhythm
Rate
First-Degree AV Block
Rules of Interpretation
AV Blocks

4. AV Blocks
 First-Degree AV Block
 Etiology
 Delay in the conjunction of an impulse through the AV node
 May occur in healthy hearts, but often indicative of ischemia at
the AV junction
 Clinical Significance
 Usually not significant, but new onset may precede a more
advanced block
 Treatment
 Generally, none required other than observation
 Avoid drugs that may further slowAV conduction

5. AV Blocks
Usually <0.12 secondsQRS
Increases until QRS is
dropped, then repeats
PRI
Normal, some P waves
not followed by QRS
P Waves
SA node or atrialPacemaker Site
Atrial, regular;
ventricular, irregular
Rhythm
Atrial, normal;
ventricular, normal to
slow
Rate
Type I Second-Degree AV Block
Rules of Interpretation

6. AV Blocks
 Type I Second-DegreeAV Block
 Etiology
 Also called Mobitz I, orWenckebach
 Delay increases until an impulse is blocked
 Indicative of ischemia at the AV junction
 Clinical Significance
 Frequently dropped beats can result in cardiac compromise
 Treatment
 Generally, none required other than observation
 Avoid drugs that may further slowAV conduction
 Treat symptomatic bradycardia

7. AV Blocks
Normal or >0.12
seconds
QRS
Constant for conducted
beats, may be >0.21 secondsPRI
Normal, some P waves
not followed by QRS
P Waves
SA node or atrialPacemaker Site
May be regular or
irregular
Rhythm
Atrial, normal;
ventricular, slow
Rate
Type II Second-Degree AV Block
Rules of Interpretation

8. AV Blocks
 Type II Second-Degree AV Block
 Etiology
 Also called Mobitz II or infranodal
 Intermittent block of impulses
 Usually associated with MI or septal necrosis
 Clinical Significance
 May compromise cardiac output and is indicative of MI
 Often develops into full AV blocks
 Treatment
 Avoid drugs that may further slowAV conduction
 Treat symptomatic bradycardia
 Consider transcutaneous pacing
 Atropine

9. AV Blocks
Normal or >0.12
seconds
QRS
Constant for conducted
beats, may be >0.21 secondsPRI
2 P waves for each
QRS
P Waves
SA node or atrialPacemaker Site
RegularRhythm
Atrial, normal;
ventricular, slow
Rate
2:1 AV Block
Rules of Interpretation

10. AV Blocks
 2:1 AV Block
 Etiology
 Second degree AV block where there are two P waves for each
QRS
 Associated with acute myocardial infarction and septal
necrosis
 Clinical significance
 Can compromise cardiac output
 Can develop into full AV block
 Treatment
 Prepare for transcutaneous pacing
 Atropine

11. 0.12 seconds or greaterQRS
No relationship to QRSPRI
Normal, with no
correlation to QRS
P Waves
SA node and AV
junction or ventricle
Pacemaker
Site
Both atrial and
ventricular are regular
Rhythm
Atrial, normal;
ventricular, 40–60
Rate
Third-Degree AV Block
Rules of Interpretation
AV Blocks

12. AV Blocks
 Third-Degree AV Block (Complete Heart Block)
 Etiology
 Absence of conduction between the atria and the ventricles
 Results from AMI, digitalis toxicity, or degeneration of the
conductive system
 Clinical Significance
 Severely compromised cardiac output
 Treatment
 Transcutaneous pacing for acutely symptomatic patients
 Treat symptomatic bradycardia
 Avoid drugs that may further slowAV conduction

13. Dysrhythmias Originating in
the AV Junction
 Dysrhythmias
 Premature junctional contractions
 Junctional escape complexes and rhythm
 Junctional bradycardia
 Accelerated junctional rhythm
 Characteristics of all junctional rhythms
 Inverted P Waves in Lead II
 PRI of <0.12 Seconds
 Normal QRS Complex Duration

14. Usually normalQRS
Normal if P occurs
before QRS
PRI
Inverted, may occur
after QRS
P Waves
Ectopic focus in the
AV junction
Pacemaker Site
Depends on
underlying rhythm
Rhythm
Depends on
underlying rhythm
Rate
Rules of Interpretation
Premature Junctional Contractions
Dysrhythmias Originating in
the AV Junction

15. Dysrhythmias Originating in
the AV Junction
 Premature Junctional Contractions
 Etiology
 Single electrical impulse originating in the AV node
 May occur with use of caffeine, tobacco, alcohol,
sympathomimetic drugs, ischemic heart disease, hypoxia, or
digitalis toxicity, or may be idiopathic
 Clinical Significance
 Limited, frequent PJCs may be precursor to other junctional
dysrhythmias
 Treatment
 None usually required

16. Usually normalQRS
Normal if P occurs
before QRS
PRI
Inverted, may occur
after QRS
P Waves
AV junction
Pacemaker
Site
Irregular in single
occurrence, regular
in escape rhythm
Rhythm
40–60Rate
Junctional Escape Complexes
and Rhythms
Rules of Interpretation
Dysrhythmias Originating in
the AV Junction

17. Dysrhythmias Originating in
the AV Junction
 Junctional Escape Complexes and Rhythms
 Etiology
 Results when the AV node becomes the pacemaker
 Results from increased vagal tone, pathologically slow SA
discharges, or heart block
 Clinical Significance
 Slow rate may decrease cardiac output, precipitating angina
and other problems
 Treatment
 None if the patient remains asymptomatic
 Treat symptomatic episodes with atropine or pacing

18. Usually normal, may
be greater than 0.12
QRS
Normal if P occurs
before QRS
PRI
Inverted, may occur
after QRS
P Waves
AV junctionPacemaker Site
Irregular in single
occurrence, regular in
escape rhythm
Rhythm
Less than 40Rate
Junctional Bradycardia
Rules of Interpretation
Dysrhythmias Originating in
the AV Junction

19. Dysrhythmias Originating in
the AV Junction
 Junctional Bradycardia
 Etiology
 Junctional dysrhythmia with a heart rate less than the intrinsic
rate of the AV node
 Increased vagal tone, pathological slow SA node discharge,
heart block, intrinsic disease
 Clinical Significance
 Decreased cardiac output
 Treatment
 Prepare for transcutaneous pacing
 ConsiderAtropine

20. NormalQRS
Normal if P occurs
before QRS
PRI
Inverted, may occur
after QRS
P Waves
AV junctionPacemaker Site
RegularRhythm
60–100Rate
Accelerated Junctional Rhythm
Rules of Interpretation
Dysrhythmias Originating in
the AV Junction

21. Dysrhythmias Originating in
the AV Junction
 Accelerated Junctional Rhythm
 Etiology
 Results from increased automaticity in the AV junction
 Often occurs due to ischemia of the AV junction
 Clinical Significance
 Usually well tolerated, but monitor for other dysrhythmias
 Treatment
 None generally required in the prehospital setting