AV Block: 2nd degree, Mobitz II (Hay block)

AV Block: 2nd degree AV block, Mobitz II (Hay Block)

Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I).

Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I).
The PR interval in the conducted beats remains constant.
The P waves ‘march through’ at a constant rate.
The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc).

Arrows indicate “dropped” QRS complexes (i.e. non-conducted P waves)

ECG Example of Mobitz II

Mechanism

Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node).
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).
Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd degree AV block is produced by intermittent failure of the remaining fascicle (“bilateral bundle-branch block”).
In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.
In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes.
Unlike Mobitz I, which is produced by progressive fatigue of the AV nodal cells, Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse.
There may be no pattern to the conduction blockade, or alternatively there may be a fixed relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block.

Causes of Mobitz II

Anterior MI (due to septal infarction with necrosis of the bundle branches).
Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease).
Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)
Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).
Autoimmune (SLE, systemic sclerosis).
Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).
Hyperkalaemia.
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.

Clinical Significance

Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block.
Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac death.
The risk of asystole is around 35% per year.
Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker.

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