A-V Nodal Block in Acute Myocardial Infarction
The mechanism, clinical course and prognosis of conduction disturbances following acute myocardial infarction are closely related to the blood supply of the specific conduction system and the site of infarction (449,603,667,703,799). Conduction disturbances in the A-V node are usually associated with acute inferior myocardial infarction (424,667,703) presumably due to occlusion proximal to the origin of the A-V nodal artery. This artery is in 90% of cases a branch of the right coronary artery (401). The usual precursor of complete intranodal block in association with acute inferior myocardial infarction is type I second degree A-V block (449,603,703). The escape pacemaker during complete intranodal block is located just below the node (667) and usually produces an acceptable and dependable frequency (449,603,703). In contrast, conduction disturbances in the bundle branches are usually associated with acute anteroseptal infarction (424,449,603,667,703,799), presumably following occlusion proximal to the origin of the septal branches of the left anterior descending artery (401). Bifascicular block is the usual precursor of complete infranodal block complicating acute anteroseptal infarction (603,667,703). During complete infranodal block the escape pacemaker that emerges from the peripheral Purkinje-system is unstable and has a slow rate (424). The conduction disturbances in the bundle branch system will be discussed in the next chapter. Therefore in this chapter we will only consider conduction disturbances located in the A-V node. The generally accepted indications for atropine or pacemaker therapy in A-V block complicating acute inferior myocardial infarction are: 1. Stokes-Adams attacks; 2. a low ventricular rate (< 50/min); 3. powerfailure; and 4. bradycardia dependent ventricular arrhythmias (424,607,703).
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