This ECG is from a 66-year-old woman who called 911 for a complaint of chest pain for the past four hours. She also complained of nausea, vomiting, and diarrhea for that time. She was pale and diaphoretic, and her BP was 77/43 sitting up, improving to 90/54 reclining. She denied “cardiac” history.  Her medications included:  aspirin, an SSRI, cilostazol, amlodipine, umeclidinium and vilanterol inhaler, atorvastatin, levothyroid, and metoprolol. We don’t have a previous ECG.  The EMS crew followed their chest pain protocol and delivered the patient to a facility with an interventional cath lab, but they did not designate a “STEMI Alert” because of the wide QRS.  It is their protocol to use the term “STEMI Alert” only when no M.I. mimics, such as left bundle branch block, are present. 

What does this ECG show?     There is an underlying sinus rhythm at 75 bpm.  There is AV dissociation, with regular, wide QRS complexes at a rate of 44 bpm.   This meets the criteria for complete heart block (third-degree AV block).  The morphology of the QRS complexes meets the criteria for left bundle branch block (wide, upright in Leads I and V6, negative in V1).  At a rate of 44 bpm, several options for this escape rhythm are possible:  1)  junctional escape with LBBB, 2) junctional escape with intraventricular conduction delay due to AMI,  and 3) idioventricular escape rhythm.   Also, in the presence of IWMI, AV node ischemia is very likely, resulting in AV blocks at the level of the AV node.  CHB at the AV node would result in junctional escape rhythm, and CHB below that, in the fascicles of the bundle branches, would result in idioventricular escape. The issue for this patient, and ANY patient, is cardiac output, and we see several reasons for cardiac output to be lower:

·         Wide QRS

This ECG is taken from an 82-year-old man who called 911 because of chest pain.  He has an unspecified “cardiac” history, but we do not know the specifics. 

WHAT IS THE RHYTHM?  The heart rate is 69 bpm, and there are P waves before every QRS complex. The underlying rhythm is regular, with one premature beat that is wide without a P wave.  The PR interval is slightly prolonged at .25 seconds.  The rhythm is normal sinus rhythm with first-degree AV block and one PVC. 

WHY THE WIDE QRS?   The QRS complex is wide at .14 seconds. The QRS in V 1 has a wide R wave after a small Q wave.  This in consistent with right bundle branch block pattern, with loss of the normal initial small r wave (pathological Q waves).  The diagnosis of RBBB is further corroborated by the wide little S waves in Leads I and V6.  The QRS frontal plane axis is -66 degrees per the machine, and clearly “abnormal left” because the QRS in Lead II is negative, while the QRS in Leads I and aVL are positive.  This is left anterior fascicular block, also called left anterior hemiblock.  The combination of RBBB and LAFB is a common one, as the two branches have the same blood supply.  It is also called bi-fascicular block. 

WHAT ABOUT THE ST SEGMENTS?  The ST segments in leads V2 through V6 are elevated, and their shape is very straight, as opposed to the normal shape of coved upward (smile). Even though the amount of ST elevation at the J points appears subtle, the shape of the segments, the fact that they appear in related leads, and the fact that the patient is an elderly male with chest pain all point to the diagnosis of ANTERIOR WALL ST elevation M.I. (STEMI).  Additional ST changes include a straight shape in Leads I and aVL and ST depression in V1 and aVR.  

PATIENT OUTCOME  The patient was transported to a cardiac center, where he received angioplasty in the cath lab.  The left coronary artery was found to be occluded, and was repaired and stented.  He recovered without complications and was sent home in a few days.

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. 

Intermittent chest pain.     This series of three ECG were taken from a 41-year-old man with a two-week history of intermittent chest pain.  At the time of the first ECG, 12:05 pm, he was pain-free.  We see a sinus tachycardia at 102 bpm, and has just come under the care of paramedics. There is a very subtle ST sagging and T wave inversion in Lead III, and no other ST changes. He had an uneventful trip to the hospital.

On arrival at the Emergency Department, just before he was unloaded from the ambulance (12:15), he experienced chest pain.  An ECG was obtained, which shows ST elevation in V1 through V4, as well as in Leads I and avL.  There are reciprocal ST depressions in Leads III and aVF. 

The patient was taken into the ED, where his symptoms abated, and a third ECG was obtained (12:19). The third ECG looks very much like the first one. V5 and V6 have T waves that appear flat, or even inverted, but there is some baseline artifact making it hard to see them. 

Diagnosis confirmed       Based on the patient’s presentation, and the second ECG, he was taken immediately to the cath lab. A 100% occluding lesion with a clot was discovered in the mid LAD.  The clot was removed with suction, and the lesion stented.  A 40% narrowing was discovered in the RCA.  

Repeat ECGs whenever possible       This series of ECGs offers a compelling argument for performing repeat ECGs.  This can be especially important when symptoms are waxing and waning.  Sometimes, a clot can completely occlude an artery, then “float” to another position, allowing blood flow to resume.  Sometimes, the artery constricts around the lesion, causing occlusion, then relaxes.  Had the rescue crew not repeated the ECG at 12:19, there may have been a delay in this young patient receiving interventional care.