Heart Block

Delayed conduction of electrical current as it passes through the conducting system

May occur at any level in the conducting system (AV node, Bundle of His or bundle branch)

Block in either AV node or the bundle → AV block

** Revision: PR interval

• From start of P wave to start of QRS complex
• → time taken for electrical message to travel from SA node →→→ ventricular muscle
• normally < 200 ms (3-5 sqs)
• an elongation of the PR interval

→ there is a problem with the conduction btw the SA node and ventricles → delay (elongated PR interval)

First degree HB

1. Impulse is delayed at the AV junction → prolonged PR interval
   1. Every impulse from the atria reaches the ventricles
2. Common with
   1. Increased vagal tone
   2. Athletic training
   3. Inferior MI
   4. Mitral valve surgery
   5. Myocarditis (e.g. Lyme disease)
   6. Electrolyte disturbances (e.g. Hyperkalaemia)
   7. AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone)
   8. May be a normal variant
3. ECG findings
   1. Rate depends in underlying rhythm
   2. Regular
   3. Normal P wave
   4. 1:1 AV conduction
   5. Prolonged PR interval > 200 ms (0.2s)
   6. Normal QRS (normal ventricular conduction pathway)
4. Benign → no Tx necessary
5. Normally does not cause symptoms – Unless associated with conduction disease elsewhere

Sinus bradycardia with 1st degree AV block. PR interval > 300 ms

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Second degree HB

Intermittent block of conduction btw the atria and ventricles – only some of the impulses are transmitted from the atria to the ventricles

Mobitz Type 1 (Wenckebach)

1. Characterised by a progressively ↑abnormally long delay at the AV node
2. Normal in athletes with high vagal tone
3. Nocturnal Wenckebach requires no Tx
4. Pathological causes
   1. AV nodal dysfunction
      1. drugs
      2. cardiac ischaemia
      3. Myocarditis
5. ECG findings
   1. Rate: depends on underlying rhythm
   2. Regularly irregular (predictable drop of ventricular beat)
   3. P wave present
   4. AV conduction ratio is varaible
   5. Gradual prolongation of PR interval, until one ventricular beat (QRS) is missed (dropped beat) → PR interval variable
6. Clinical Significance
   1. Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block
   2. Asymptomatic patients do not require treatment
   3. Symptomatic patients usually respond to atropine
   4. Permanent pacing is rarely required
   5. Progression to complete HB is rare

Mobitz Type II

1. Intermittent block that conducts some QRSs normally, but blocks other QRSs completely
2. Conduction fails suddenly and unexpectedly without a preceding prolongation of the PR interval
3. Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node)
4. While Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia), Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis)
5. Causes
   1. Anterior MI (due to septal infarction with necrosis of the bundle branches)
   2. Idiopathic fibrosis of the conducting system (Lenègre-Lev disease)
   3. Cardiac surgery, especially surgery occurring close to the septum e.g. mitral valve repair
   4. Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)
   5. Autoimmune (SLE, systemic sclerosis)
   6. Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)
   7. Hyperkalaemia
   8. Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
6. ECG findings
   1. Rate: depends on underlying rhythm
   2. Regularly irregular
   3. Normal P wave – P waves ‘march through’ at a constant rate
   4. AV conduction ratio  (X:X-1) e.g. 3:2, 4:3 etc – 
   5. Normal PR interval and QRS complex – PR interval in the conducted beats remains constant
   6. Dropped ventricular beat is sudden – unpredictable loss of ventricular conduction
7. Clinical Significance
   1. Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block
   2. Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac death
   3. The risk of asystole is around 35% per year
   4. Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker
   5. Progression to CHB is common → requires pacing

Interpretation

• LBBB
• Prolonged PR Interval (First Degree AV Block)
• Sinus Rhythm with bigeminal pattern due to 3:2 conduction of the P waves (Second Degree AV Block), the non-conducted P wave is in the roof of the T wave
• The PR Interval of the conducted P waves is the same and is accompanied by LBBB, so this AV Block is 3:2 Mobitz type II Second Degree AV Block (infranodal)

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Complete HB

1. Complete block of conduction btw the atria and ventricles
   1. Total dissociation btw atria and ventricles

• Atrial impulse not propagated to the ventricles
  • Atria is stimulated by one set of pacemaker cells e.g. SA node
  • Ventricles are stimulated by another pacemaker cell → often a lot slower than the atrial pacemaker
  • Severe bradycardia  → ↓↓COHaemodynamically unstable → requires pacing
  • As the pace-setting cells of the ventricles move further and further away from the atria
    • rhythm becomes > unstable
    • rate slows
    • QRS broadens
  • Therefore the rate and nature of the rhythm is determined by the origin of the escape rhythm
    • Junctional – high ventricular escape
      • High → conduction is swift, fast → narrow, normal more stable
    • Ventricular – low ventricular escape
      • low → slower conduction,  → unstable

• ECG findings
  • Separate rates for underlying sinus rhythm and for escape beat
  • Regular P waves
  • Regular QRS
  • No relationship btw p waves and QRS → atria and ventricles have dissociated activity (variable P:QRS ration)
  • Variable QRS width
    • Depends on the origin of the escape rhythm
      • Wide QRS complexes (120ms) = Ventricular escape
• Causes of heart block
  • Ischaemia
    • especially inferior AMI
      • median duration 2.5 hours
    • anterior AMI and CHB has poor outcome
  • Degenerative
    • most common cause of complete heart block in adults
    • Lev’s syndrome – calcification and sclerosis of fibrous cardiac skeleton (aortic / mitral valves)
    • Lenegre’s syndrome – primary sclerodegenerative disease of conducting system alone
  • Drugs
    • that cause sinus bradycardia
    • may contribute or less commonly be causative
    • 

• Management
  • no immediate treatment required if no haemodynamic compromise
  • withdrawal of contributing agents
  • correction of contributing electrolyte abnormalities
    1. especially hyperkalaemia
  • initially give 0.5 mg Atropine and assess response.
    • if response is inadequate, give further doses of Atropine 0.5 mg at a time to a maximum of 3 mg
    • if response is still inadequate, arrange external transcutaneous pacing
  • Electrical Pacing
    • initially transcutaneous in compromised patients
  • Chemical Pacing
    • Isoprenaline
      • bolus dose 20 – 40 µg IV
      • infusion – 0.5 – 20 µg/min
      • contraindicated in digoxin toxicity