HEART BLOCKS IN ECG AND HOW TO INTEPRET IN ECG?

HEART BLOCKS IN ECG

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

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

3. 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 A cute rheumatic myocarditis Lyme disease D rugs B eta blockers R ate-modifying calcium channel blockers Digoxin No specific treatment is necessary for first-degree AV block in its own right

4. 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

5. 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

6. Mobitz type II AV block Characteristic features are: M ost P waves are followed by a QRS complex T he PR interval is normal and constant O ccasionally , 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

7. 2:1 AV block S pecial form of second-degree heart block in which alternate P waves are not followed by QRS complexes U sually requires pacing

8. 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

9. Causes of third-degree AV block Congenital Acquired D rug toxicity (e.g. anti- arrhythmics ) F ibrosis/calcification of the conduction system M yocardial ischemia / Infarction I nfection (e.g. Lyme disease) M yocardial infiltration (e.g. amyloid, sarcoid ) Metabolic disorders (e.g. hypothyroidism ) N euromuscular diseases (e.g. myotonic muscular dystrophy) Cardiac procedures (e.g. ablation procedures, aortic valve surgery )

10. 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

11. 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

12. 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

13. 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

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

15. 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 )