This ECG is taken from an elderly man who has a history of complete heart block and AV sequential pacemaker.  On the day of this ECG, he presented to the Emergency Department with chest pain and shortness of breath. His vital signs were stable and within normal limits.  We do not have information about his treatment or outcome. 

I don’t see spikes.  How do we know this is a paced rhythm?  The ECG clearly shows the presence of an AV pacemaker.  There are very tiny pacer “spikes”, probably best seen in Leads III, aVF, aVL, and most of the precordial leads.  Other ECG signs that this is a paced rhythm are:  wide QRS at about .16 seconds (160 ms); abnormal left frontal plane axis; regular rhythm with AV dissociation (there are P waves seen occasionally that have no fixed relationship to the QRS complexes).  Also, V6 is negative.  That rules out left bundle branch block unless the electrodes are misplaced.  There are no capture beats in this strip.  The patient appears to be, at least right now, 100% dependent on the paced rhythm. 

Why does the presence of a pacemaker make it harder to diagnose an M.I. from the ECG?  Wide-QRS rhythms, such as right-ventricular paced rhythms, left bundle branch block, and ventricular ectopic rhythms, usually have “discordant ST and T wave changes”.  That is, when the QRS is positive (upright), the ST and T wave are negative.  The reverse is also true:  when the QRS is negative and wide, the ST and T wave changes are positive (ST elevation).  This is not true for right bundle branch block because the conduction delay that causes the widening of the QRS is in the right ventricle, and the ST segment is reflecting the LEFT ventricle’s repolarization.  Discordant ST changes can make it difficult to determine from the ECG alone that there is an ST elevation M.I. (STEMI).  Diagnosis usually must be made from patient presentation, ECG changes over time, and cardiac enzymes – or more definitively from cardiac angiogram. Pacemakers that produce narrow QRS complexes do not cause discordant ST changes. 

This ECG is from a 54-year-old woman who had an M.I. one week prior to this tracing.  She did not receive interventional treatment, as it was not available where she lived when this happened years ago.  Her ECG shows the signs of healing injury, as well as probable permanent damage. 

Where was this M.I.?      The affected leads are all of the precordial leads (V1 through V6), as well as I and aVL.   The precordial leads reflect the anterior and low lateral walls of the heart, and Leads I and aVL show us the high lateral wall.  This area is perfused by the left coronary artery, and she had a proximal lesion. 

What ST and T wave changes are present?    All of the leads listed above show a flattening of the ST segments.  While they are no longer elevated (the acute injury is over), they are flat and almost convex upward.  This shape is usually abnormal, and it has persisted even though the acute injury is subsiding.  The T waves in the anterolateral leads are all inverted.  This represents reperfusion of the injured tissue.  Whether the offending clot is removed by invasive procedure, thrombolytic drugs, or natural degradation, the tissue that is still alive will reperfuse. 

This is an ECG from a 95 year old man who was recovering from an anterior-septal wall M.I.  Other clinical data for this patient has been lost, except that he suffered a new right bundle branch block during this M.I.  The ECG shows pathological Q waves in V1, V2, and V3, consistent with permanent damage (necrosis) in the anterior septal wall.  The ST segments in those leads are coved upward.  Even though the J points are not elevated, this ST segment shape suggests recent injury.  The classic RBBB pattern is present:  wide QRS, rSR' pattern in V1, and wide little s waves in I and V6.  It is not known why the overall voltage is low in this patient.