AV Block

AV Block

CAUSES OF AV BLOCK

  1. AV Block….Congenital causes, e.g. Congenital gumma, maldevelopment of the bundle. cyst, ventricular septal defect or maldevolepment of the bundle.AV Block
  2. Acquired causes:

a ) Coronary arterial disease with or without hypertension. br Drugs, e.g. Digitalis, Quinidine, Beta blockers, Ca- channel blockers, etc.

  1. c) Aortic-stenosis.
  2. d) Carditis due to Rheumatic fever, Diphtheria.

e)Disordered atrial rhythms, e.g. atrial fibrillation and flutter (functional block).

  1. f) Idiopathic fibrosis of the conducting system.
  2. g) Cardiomyopathy and endomyocardial fibrosis.
  3. h) Fibrosis of the AV junction without any significant coronary artery disease is possibly the most commoncause.
  4. i) Dystrophica myotonia.
  5. j) Chagas disease.
  6. k) Lyme carditis.

Cardiac surgery

  1. m) Infiltrative disease.

AV Block…The site of AV block may not be necessarily located in the AV node. It may be located in the atrial myocardium near the node (AN region), in the AV node proper (N region) or in the bundle of His, closure to the node (NH region) or sometimes the site of lesion may be located more distally in Bundle of His or its branches. Proximal blocks are said to be more benign than the distal blocks.

TYPES

Fist degree or Latent heart block (1° AV block)

Here, all SA impulses are allowed to pass through the AV node but the time is prolonged. ECG will show an increased P-R interval even beyond the upper level of normality (0.2 sec.))Clinically one should suspect first degree heart block if the first sound is muffled in presence of tachycardia.

Second degree or Partial heart block

Here, from time to time, some SA impulses are not allowed to pass through the AV node. Thus atria contract but not the ventricles resulting in absence of heart sounds and missing of pulse but jugular venous pulsation shows ‘a’ wave only. This may occur at regular intervals giving rise to 2 1 or 3 1 heart blocks or may occur irregularly. The P-R intervals may sometimes progressively increase till the beat is dropped which is called Mobitz type I block or Wenckebach block.)This is comparatively benign in type and does, not progress to complete heart block. Apart from above, Mobitz Type 1 block may occur in normal individuals with increased vagal tone. Sometimes again P-R interval remains either normal or increased but is fixed; this is called Mobitz type II block. This has a bad prognosis as it may lead to Stokes-Adams attack. Mobitz type II block may be due to fibrosis of the conducting system (Lenegre’s disease) or it may be due to fibrocalcific affection of the conducting system (Lev’s disease). This is always due to organic disease and usually involves the infranodal conduction system. During exercise the heart rate may not increase due to block. ECG will show the characteristic changes with presence of P waves only but no associated QRS complexes. In Wenchebach’s type progressive lengthening of P-R intervals is seen till QRS complex is dropped. The characteristic ECG shows QRS complexes occurring in regular grouping (grouped beating) which is separated by the blocked beat. Thus RR interval progressively shortens. This Wenckebach’s type is typically seen in posterior and inferior myocardial infarction.AV Block

There is also progressive decrease in conduction velocity called ‘decremental conduction.’ Usually only a single impulse is blocked and the cycle is repeated. However longer pauses may be interrupted by escape beats arising from AV node and ventricle. Repetition of such cycles results in group beating and Wenckebach’s periodicity. The degree of increase in PR interval becomes progressively less with each conducted beat However the PP interval is constant.

Phird degree or Complete heart block

Here, no SA impulse is allowed to pass through the AV node. Therefore, ventricles generate their own rhythm at a regular rate of 36-40 per minute, called idioventricular rhythm from a pace-maker called Idioventricular pace-maker located close to the AV node.

Important features of Complete heart block

Pulse Rate-36 to 40 per minute.

Rhythm regular.

Nolume high.

Tension-high.

Condition of the arterial wall-may be sclerosed.

Character-may be collapsing. Due to wide pulse pressure.

This pulse is a fixed pulse. i.e. its rate will not change after exercise, fever, Amylnitrite inhalation or Atropine injection. There is also changing systolic blood pressure.

Carotid artery may show carotid dance at a rate of 36-40 per minute. Jugular veins show atrial pulsations at a rate of 72 per minutes and from time to time a giant pulsation is seen, called cannon pulsation. This is due to occurrence of atrial contraction immediately after ventricular contraction.

Auscultation of mitral area

The intensity of the first sound is muffled; but from time to time it is accentuated called explosive 1st Heart sound or bruit de cannon. This is due to occurrence of ventricular contraction immediately after atrial contraction. Sometimes the first sound is very faint. Rarely a mid- diastolic murmur called rythand;s murmur may be audible. Atrial sounds (S4) may also be audible

ECG shows slow regular QRS complexes (36 to 40 per minute) with regular occurrence of P waves at higher rates without a fixed P-R relationship. When the block is at the AV node, the pace-maker is located within the bundle of His and this gives narrow QRS complexes with a fairly rapid rate. When the block is infranodal the pacemaker is located in the bundle branch, hence the QRS complexes are wider and the rate is slow. So, Stokes-Adams attacks are common.

TREATMENT OF AV Block

In symptomatic patients of l0 AV block dual chamber pacemaker therapy is often considered provided no treatable causes are present

Mobitz type I block is usually benign and do not progress to complete heart block. However in symptomatic cases atropine 0.5 mg IV every 2 minutes to a maximum of 0.04 mg/kg may be given. If symptoms are persistent without any treatable causes whatsoever permanent pacing is indicated.

Mobitz type II block-Temporary transvenous pacing is usually required in haemodynamically unstable patients. Atropine is usually not effective and may worsen the condition by increasing sinus rate causing higher degree of block.

3° block or complete block requires permanent pacing. A temporary transvenous pacing is only done when permanent pacemaker is delayed.

.AV Block.

Recent Posts

  • Respiratory Diseases

TYPES OF SPECIFIC PNEUMONIAS

TYPES OF SPECIFIC PNEUMONIA Staphylococcal Pneumonia TYPES OF SPECIFIC PNEUMONIA It may be a primary respiratory infection or secondary to…

2 months ago
  • Respiratory Diseases

ACUTE LOBAR PNEUMONIA

ACUTE LOBAR PNEUMONIA It is the commonest of all specific pneumonias. AETIOLOGY Predisposing causes Age: All ages but 50% of…

2 months ago
  • Respiratory Diseases

BRONCHIAL ASTHMA

BRONCHIAL ASTHMA DEFINITION OF BRONCHIAL ASTHMA BRONCHIAL ASTHMA is a chronic reversible inflammatory destructive disease of the airways characterised by…

2 months ago
  • Respiratory Diseases

BRONCHIECTASIS

BRONCHIECTASIS DEFINITION BRONCHIECTASIS is a condition of permanent abnormal dilatation of the larger bronchi. AETIOLOGY AND PATHOGENESIS Acquire Obstruction Obstruction…

2 months ago
  • Respiratory Diseases

CHRONIC BRONCHITIS

CHRONIC BRONCHITIS DEFINITION OF CHRONIC BRONCHITIS Chronic bronchitis may be defined as a disease characterised by cough and sputum for…

2 months ago
  • Respiratory Diseases

ACUTE TRACHEO BRONCHITIS

ACUTE TRACHEO BRONCHITIS DEFINITION ACUTE TRACHEO BRONCHITIS is Acute inflammation of Tracheo bronchial tree caused by various organisms (bacteria and…

2 months ago