To be able to explain the differences in pathophysiology behind the different types
of heart block
To be able to recognise the different signs on ECG trips of heart blocks
Click to CompleteTo be able top describe and the causes and understand the clinical
significance of the different types of heart block
To complete the heart block quiz to demonstrate understanding of the
above objectives
A first degree heart block is defined by a P-R interval longer than 0.2 seconds (5 small squares)
It occurs when the spread of excitation between the SA node and the ventricles takes longer than normal
There are two types of second degree heart block:
Type 1 (Mobitz I or Wenckebach)
Is when the PR interval lengthens each time and eventually after the longest PR interval there is a missing QRS complex, this cycle then repeats
The difference is more obvious if you compare the first PR interval in the cycle to the last.
Mobitz I is usually due to reversible conduction block at the level of the AV node:
- Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse
- This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block)
Causes of Mobitz I
- Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
- Increased vagal tone (e.g. athletes) - hence can be a normal finding
- Inferior MI
- Myocarditis
- Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)
Clinical Significance
Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance
and with low risk of progression to third degree heart block
- Asymptomatic patients do not require treatment
- Symptomatic patients usually respond to atropine
- Permanent pacing is rarely required
Type 2 (Mobitz II)
Is when there are non-conducted p-waves (not preceded by a QRS complex),
there is no PR prolongation and the QRS complex is usually wide
Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cellssuddenly and unexpectedly fail to conduct a supraventricular impulse
The PR interval in the conducted beats remains constant
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)
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
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 of Mobitz II
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
Treatment: Mobitz II mandates immediate admission for cardiac monitoring,
backup temporary pacing and insertion of a permanent pacemaker
Complete heart block (third degree heart block) occurs when
all of the supraventricular impulses fail to spread to the ventricles
The ventricles then have to generate their own wave of excitation (escape rhythm)
Alternatively, the patient may suffer ventricular standstill leading to syncope
(if self-terminating) or sudden cardiac death (if prolonged)
Typically the patient will have severe bradycardia with independent atrial and ventricular rates, i.e. AV dissociation
On an ECG, both the P-P and QRS-QRS intervals are regular
See the diagram below, where the QRS complexes are not coordinated with the
p waves as they should be (the red lines are not equal to or coordinated
with the blue lines)
The ventricular rate is usually around 40 whereas the atrial rate is
around 100 BPM
Pathophysiology
Complete heart block is essentially the end point of either Mobitz I or Mobitz II AV block
It may be due to progressive fatigue of AV nodal cells as per Mobitz I (e.g. secondary to increased vagal tone in the acute phase of an inferior MI)
Alternatively, it may be due to sudden onset of complete conduction failure throughout the His-Purkinje system, as per Mobitz II (e.g. secondary to septal infarction in acute anterior MI)
The former is more likely to respond to atropine and has a better overall prognosis
Causes of complete heart block
Inferior myocardial infarction
AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin)
Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease)
Clinical significance
Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac death
They require urgent admission for cardiac monitoring, backup temporary pacing and
usually insertion of a permanent pacemaker
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