If bradycardia persists or there are contraindications to isoproterenol, pacemaker placement is indicated. A transcutaneous pacemaker can be positioned on the chest wall before insertion of a temporary pacing lead. Indications for temporary pacing include symptomatic bradycardias occurring during sinus node dysfunction, carotid hypersensitivity, complete heart block, and after cardiac surgery. Pacing may be used prophylactically during second-degree atrioventicular block or with right heart catheterization in a patient with left bundle branch block.
Patients with symptomatic bradycardia (asystole, sinus bradycardia, sinus pauses, type I second-degree atrioventicular block) associated with hypotension and unresponsive to atropine are treated with transvenous pacing. Patients who demonstrate increased likelihood of progression to complete heart block by either involvement of the bundle branches (see below) or type II second-degree atrioventicular block also require transvenous pacing.
Indications for temporary pacemaker insertion during myocardial infarction are based on the patient's hemodynamic status and symptoms during bradycardia, and the likelihood of the development of complete heart block with an inadequate escape mechanism ( Table 1). The type of heart block and its severity in acute myocardial infarction is dependent on the coronary artery involved. The dominant coronary artery (right coronary artery in 90 per cent of patients and left circumflex in 10 per cent) gives rise to the posterior descending artery which supplies the atrioventicular node, the proximal bundle of His and the proximal right bundle. The left anterior descending artery, through its septal perforators, supplies the left bundle branch and left anterior fascicle, and the right bundle branch beyond its origin. The left posterior fascicle receives a dual blood supply. During inferior myocardial infarction, atrioventicular nodal ischemia often leads to PR prolongation and type I second-degree atrioventicular block. If there is complete heart block, this occurs progressively and the escape complex is often narrow. Sinus bradycardia can also be caused by either sinoatrial ischemia or reflex bradycardia. These conduction abnormalities are often responsive to atropine or can lead to accelerated junctional rhythms. During anterior myocardial infarction, manifestation of bundle branch involvement is secondary to extensive involvement of one or both of the bundle branches. Complete heart block appears suddenly and is a manifestation of infranodal block. The most common preceding bundle branch involvement in this setting is right bundle branch block and left anterior hemiblock, followed by type II second-degree atrioventicular block and new bilateral bundle branch block. Isolated left anterior hemiblock or right bundle branch block is less likely to progress to complete heart block.
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