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Acute M.I. With Right Bundle Branch Block and Atrial Pacing

This ECG was taken from a 78-year-old man who was experiencing chest pressure in the morning, after having left shoulder pain since the night before. He has a history of hypertension and hypercholesterolemia, and has an implanted pacemaker.

What does the ECG show?  The ECG shows an atrial paced rhythm, with two premature beats, beats number 5 and 12.  These are probably PVCs.  The patient has a functioning AV conduction system, so the paced atrial beats are conducting through the AV node and producing QRS complexes.  In the interventricular conduction system, the impulse encounters right bundle branch block. This causes each QRS to have an “extra” wave attached at the end, representing slightly delayed depolarization of the right ventricle.  Instead of an “rS” pattern in V1, for example, we see “rSR’ “.  The slight delay causes the QRS to be widened, as we are measuring the two ventricles separately, rather than synchronously.

There is definite ST segment elevation in V2 and V3, and the shape of the ST segment is straight, having lost it’s normal “concave upward” appearance.  In an ECG taken three minutes later, the STE extends to V4.

Do the pacemaker or the right bundle branch block prevent us from diagnosing an ST-elevation M.I.?  The answer to that is a resounding “NO!” Pacemakers can sometimes make it difficult to assess ST elevation because ventricular pacing causes ST segment changes.  Pacing the right ventricle causes a depolarization delay in the left ventricle as the impulse travels “cell to cell” across the LV.  This means an RV-paced beat will resemble a PVC from the RV.  When LV depolarization is altered, repolarization will also be altered, causing ST elevation in leads with negative QRS complexes, and ST depression is leads with upright QRSs. These are called discordant ST changes. These changes are proportionate to the height or depth of the QRS, with very minimal or no ST changes in leads with short or biphasic QRS complexes.  We don’t have to worry about that in this situation – the pacemaker is not pacing the ventricles.

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Takotsubo Cardiomyopathy

This ECG is taken from an elderly woman with chest pressure radiating to left shoulder for 30 minutes.  She also complained of nausea with vomiting.  Her family offered a history of  unspecified cardiac disease, hypertension, hypercholesterolemia, and dementia.

The ECG shows ST elevation in Leads I and aVL, with reciprocal ST depression in Leads III and aVF.  ST segments have an abnormally flat shape in Leads aVL, II, III, aVF, V5 and V6.

She was admitted to the hospital and sent to the cath lab.  Her arteries were found to be clear, and Takotsubo cardiomyopathy was diagnosed.  See also.

 

Our thanks to Lew Steinberg and Palm Beach Gardens Fire Rescue for donating this interesting ECG.

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Inferior Wall M.I. With Right Ventricular M.I.

This ECG was recorded from a 75-year-old man with substernal chest pain and diaphoresis.  It shows a pretty classic picture of acute inferior wall M.I. The second ECG is a repeat tracing with the V4 wire moved to the V4 Right position, and it is positive for right ventricular M.I.  The patient was found to have a 100% occlusion of the right coronary artery, which was opened and stented in the cath lab.

There are several other examples of IWMI with RVMI in our archives, so we will confine this commentary to the ECG signs that make these tracings so typical of right coronary artery occlusion. Once you are familiar with the typical pattern of IWMI / RVMI, it is easy to see, even when the ST elevation is subtle (as this one certainly is NOT).

Signs of IWMI in these ECGs are

·         ST elevation in inferior leads II, III and aVF.

·         Reciprocal ST depression in leads I and aVL. 

Signs of RVMI in these ECGs are:

·         ST elevation in V4 right.

·         ST elevation in V1 without ST elevation in V2.

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Inferior Wall M.I. and Right Bundle Branch Block

These ECGs were taken from a 76 year-old-man who was complaining of chest pressure for 20 minutes.  He had a remote history of coronary artery bypass graft surgery.

This case has several good teaching points, including:

Significant artifact.  The limb leads show artifact which is severe enough to hamper our assessment of the j point location. Every effort should be made to eliminate artifact.  Some measures that might help are:

        *  clean and slightly "rough up" the skin where the electrode will be placed.  A rough wash cloth or gauze pad will work.

        *  shave hair if necessary.

        *  avoid areas of movement if possible.  Precordial electrodes must be placed in specific spots, but limb leads may be placed anywhere on the limb or on the trunk if it is impossible to avoid movement on the limbs.

       *   use fresh electrodes that have been protected from drying out.

Subtle STEMI changes.   This patient has an inferior wall M.I., which was confirmed as a complete occlusion of the right coronary artery in the cath lab.  The ST elevation in Leads II, III, and aVF is subtle, and more difficult to measure because of the artifact.  However, the SHAPE of the ST segments is a giveaway - they are very straight.  A convex-upward shape is normal (see Lead I).  Also, Lead aVL shows typical ST DEPRESSION, as a reciprocal view of the STE in Lead III.  More ST depressions can be seen in Leads V1 through V3, and they end abruptly there.  These localized ST depressions represent a reciprocal view of the posterior (also called lateral) wall, and represent an "extension" of the inferior wall M.I. up the back of the heart.  A V4 Right lead was obtained and shows no measurable ST elevation, but the shape is straight to slightly "frowning", indicating that the right ventricle may soon have STE.  Repeat ECGs should be obtained to watch for more definite ST elevations.

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Simultaneous Occlusions in LAD and Diagonal

This ECG was obtained from a 35-year-old man who was complaining of crushing substernal chest pain which radiated down his left arm for the last ten minutes. He was diaphoretic, and described his pain as a “10” on the 1-10 scale. He got only modest relief from IV fentanyl.

He was transported to a full-service cardiac hospital, where he underwent angioplasty of simultaneous 100% occlusions of his proximal left anterior descending artery and diagonal artery. He was noted to have apical akinesia with a 35% ejection fraction.

He continued to improve following angioplasty, and was discharged home with an external defibrillator vest.

The ECG shows ST elevation in V2, V4, V5, and V6, which makes us suspect that the V2 and V3 wires were switched accidentally.  This reflects damage in the anterior wall of the LV. There is also very marked ST elevation in I and aVL, reflecting damage in the high lateral wall. There is reciprocal ST depression in the inferior leads aVF and III.  Fortunately, there are no pathological Q waves, which would indicate permanent damage from necrosis of the myocardium.

You can see films from his procedure in Heart Art, labeled “Simultaneous Occlusive Lesions in LAD and Diagonal”.

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Inferior Wall M.I. With Wide QRS and Complete AV Block

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

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Anterior Wall M.I. With Bifascicular Block

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.

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Acute M.I. In Patient With Pacemaker

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. 

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Inferior-lateral M.I. With QRS Fragmentation

SUBTLE ST CHANGES   This ECG was obtained from an 87-year-old man who was experiencing chest pain.  Due to the subtle ST elevation in Leads II, III, aVF, V5, and V6, (inferior- lateral walls) the ECG was transmitted to the hospital by the EMS crew, and the cath lab was activated.  The patient denied previous cardiac history. 

In addition to the subtle ST elevation, there is ST depression in V1 through V4, which represents a reciprocal view of the injury in the inferior-posterior-lateral wall.  Because the anterior wall is superior in its position in the chest, it is opposite the inferior/posterior wall, and can show ST depression when the inferior-posterior area has ST elevation. This ECG was the 6th one done during this EMS call.  Prior to this one, the ST segments were elevated less than 1 mm.  This is a good example of the value of repeat ECGs during an acute event.  

RIGHT VENTRICULAR M.I.?     This ECG was done with V4 placed on the right side, to check for right ventricular M.I., which is a protocol for this EMS agency. When the right coronary artery is the culprit artery (about 80% of IWMIs), RVMI is likely.  In RVMI, we would usually see reciprocal ST depression in Leads I and aVL, but the STE is very subtle here, so the depression would likely be also.  When the culprit artery is the left circumflex artery (<20%), lateral lead ST elevation is more likely, as we see here in V5 and V6. 

WHAT ABOUT RHYTHM?     The rhythm is sinus with PACs.  PACs are considered to be benign in most situations, but in a patient with acute M.I., any dysrhythmia can be concerning. The QT interval, measured as QTc (corrected to a heart rate of 60 bpm), is slightly prolonged at .458 seconds (458 ms).  Over .440 seconds is considered prolonged in men, and over .500 sec. places the patient at increased risk of developing torsades de pointes.  CAD and myocardial ischemia can lead to this modest increase in QTc.

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