HEART BLOCKS IN ECG

1. HEART BLOCKS
Dr.G.VENKATA RAMANA
MBBS DNB FAMILY MEDICINE

3. • In first-degree AV block, conduction through the AV node is slower
than usual and the PR interval is therefore prolonged

5. • First-degree AV block is a common feature of vagally
induced bradycardia, as an increase in vagal tone
decreases AV nodal conduction
• It may also be a feature of:
• Ischaemic heart disease
• Hyperkalemia or hypokalemia
• Acute rheumatic myocarditis
• Lyme disease
• Drugs
• Beta blockers
• Rate-modifying calcium channel blockers
• Digoxin
• No specific treatment is necessary for first-degree AV
block in its own right

6. If the PR interval gradually lengthens with each beat, until one P wave
fails to produce a QRS complex, the patient has Mobitz type I AV block

7. • When Mobitztype I AV block occurs at the level of the AV
node it is generally regarded as ‘benign’,and a
permanent pacemaker is not required unless the
frequency of ‘dropped’ ventricular beats causes a
symptomatic bradycardia
• When the block is infranodal (as identified by
electrophysiological testing) there is a stronger indication
for pacing, even if patients are asymptomatic
• Mobitz type I AV block may require pacing prior to
surgery

10. • Mobitz type II AV block
• Characteristic features are:
• Most P waves are followed by a QRS complex
• The PR interval is normal and constant
• Occasionally, a P wave is not followed by a QRS
complex.
• Mobitz type II AV block is thought to result from abnormal
conduction belowthe AV node (infranodal) and is
considered more serious than Mobitz type I as it can
progress without warning to third-degree (complete)
heart block
• Referral to a cardiologist is therefore recommended, as a
pacemaker may be required

13. 2:1 AV block
Special form of second-degree heart block in which alternate P
waves are not followed by QRS complexes
Usually requires pacing

15. • Third-degree AV block
• In third-degree AV block (‘complete heart block’), there is
complete interruption of conduction between atria and
ventricles, so that the two are working independently
• QRS complexes usually arise as the result of a
ventricular escape rhythm in which the QRS complexes
are usually broad
• However, if the level of AV block is located in or just
below the AV node, a junctional escape rhythm may
arise with narrow QRS complexes
• Third-degree AV block usually requires pacing

18. • Causes of third-degree AV block
• Congenital
• Acquired
• Drug toxicity (e.g. anti-arrhythmics)
• Fibrosis/calcification of the conduction system
• Myocardial ischemia / Infarction
• Infection (e.g. Lyme disease)
• Myocardial infiltration (e.g. amyloid, sarcoid)
• Metabolic disorders (e.g. hypothyroidism)
• Neuromuscular diseases (e.g. myotonic muscular
dystrophy)
• Cardiac procedures (e.g. ablation procedures, aortic
valve surgery)

19. SA block
• If impulses are blocked from exiting the SA node, SA block
(or SA ‘exit’ block) is said to occur
• Because the impulse cannot leave the SA node, the atria
do not depolarize and therefore a P wave is missing
• SA block is different to sinus arrest
• In sinus arrest, the SA node does not depolarize at all; in
SA block, the SA node does depolarize, but the impulse
does not reach the rest of the atria
• Both conditions lead to one or more missing P waves
• However, in SA block the intrinsic rhythm of the SA node is
maintained, so when the SA block resolves and a P wave
finally does appear, it appears in the expected place
• In contrast, in sinus arrest the SA nodal rhythm is reset,
and so the reappearance of the P wave is unpredictable

21. Left bundle branch block
• In left bundle branch block (LBBB) conduction down the
left bundle has failed, and so the left ventricle cannot be
depolarized in the normal way via its Purkinje fibres
• However, the right ventricle can still depolarize normally
via the still-functioning right bundle
• The right ventricle therefore depolarizes first (and does
so in its normal rapid way via its Purkinje fibres), but then
this wave of depolarization spreads slowly across to the
left ventricle, going from myocyte to myocyte, until the
left ventricle has also depolarized
• This delay in left ventricular activation causes
interventricular dyssynchrony, with the right ventricle
depolarizing (and contracting) before the left ventricle,
which has a deleterious effect on left ventricular function

26. • Causes of left bundle branch block
• Ischemic heart disease
• Cardiomyopathy
• Left ventricular hypertrophy
• Hypertension
• Aortic stenosis
• Fibrosis of the conduction system
• The presence of LBBB is almost invariably an indication
of underlying pathology

27. Right bundle branch block
• In RBBB conduction down the right bundle has failed,
and so the right ventricle cannot be depolarized in the
normal way via its Purkinje fibres
• However, the left ventricle can still depolarize normally
via the still-functioning left bundle
• The left ventricle therefore depolarizes first (and does so
in its normal rapid way via its Purkinje fibres), but then
this wave of depolarization spreads slowly across to the
right ventricle, going from myocyte to myocyte, until the
right ventricle has also depolarized
• As with LBBB, this delay in right ventricular activation
causes interventricular dyssynchrony

32. • Causes of right bundle branch block
• Ischemic heart disease
• Cardiomyopathy
• Atrial septal defect
• Ebstein’s anomaly
• Pulmonary embolism (usually massive)

33. Remembering the name ‘William Marrow’ should
help you recall that:
• In LBBB, the QRS looks like a ‘W’ in lead V1 and
an ‘M’ in lead V6 (William)
• In RBBB, the QRS looks like an ‘M’ in lead V1
and a ‘W’ in lead V6 (Marrow)