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Anterior wall M.I.

Anterior Wall M.I. With Ventricular Bigeminy

Sat, 07/21/2018 - 17:29 -- Dawn

The Patient     This ECG was obtained from a 51-year-old man who presented to EMS with acute chest pain. He had a history of hypertension, 40 pack-year smoker.

Hospital Course     He was diagnosed with anterior wall STEMI and taken to the cath lab.  He was rated Killips Class 1 (no evidence of congestive heart failure), TIMI risk score 4  (14% risk of all-cause 30-day mortality).  He underwent primary percutaneous coronary intervention (PCI) of the proximal left anterior descending coronary artery (LAD).

Ten days post PCI, the patient had ventricular arrhythmias and went into cardiac arrest, but was resuscitated. He continued to have occurrences of non-sustained ventricular tachycardia (VT), progressing to sustained VT.  Electrolytes were monitored and corrected when necessary. The patient expired before any further diagnosis was made.

ECG Interpretation    The rhythm is sinus at a rate of about 80 bpm (first two beats).  The PR interval is about .18 seconds.  The QRS duration is about .10 seconds.  After the second sinus beat, ventricular bigeminy occurs. Every other sinus beat is obscured by the PVCs.  By the end of the strip, the underlying sinus rhythm has slowed slightly.

The ECG signs that the ectopic beats are ventricular are:  lack of P waves associated with the premature beats, QRS width about .16 seconds, and compensatory pauses.  The axis of the sinus beats is around 60 degrees (normal), but the axis of the premature beats is difficult to determine due to the low voltage and biphasic QRS complexes in the frontal plane leads.  It is also difficult to determine ST and T wave changes in the PVCs for the same reason.

Catastrophic Event With Bradycardia

Sun, 04/22/2018 - 14:46 -- Dawn

The Patient:    Paramedics were summoned to the home of a 74-year-old woman who had a complaint of shortness of breath.  She was found sitting, alert and oriented, with labored respirations at 30/min. She stated that the shortness of breath came on suddenly. She denied any cardiac or pulmonary medical history, and said she took no medications. The patient was ambulatory.  Her skin was cool and moist.  Her SpO2 on room air was 85%, improving to 90% on oxygen via 15 lpm non-rebreather mask.  Her lungs sounded clear.

 

When the patient was moved to the transport vehicle, she suddenly became nonverbal, with a leftward gaze. Her pupils were noted to be unequal and non-reactive (we do not know which was larger).  Her BP was 67/43.

 

During transport, her heart rate declined into the 20’s and became apneic and pulseless.  Recorded BP was 46/25. CPR was done until and after arrival at the hospital, where efforts to resuscitate were halted after some time.

 

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

Wed, 01/24/2018 - 22:08 -- Dawn

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.

Simultaneous Occlusions in LAD and Diagonal

Sun, 07/30/2017 - 16:03 -- Dawn

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”.

Anterior Wall M.I. With Bifascicular Block

Sat, 03/25/2017 - 15:13 -- Dawn

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.

Acute M.I. In Patient With Pacemaker

Wed, 01/04/2017 - 21:07 -- Dawn

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. 

Teaching Series: Acute Anterior Wall M.I.

Sun, 06/26/2016 - 15:33 -- Dawn

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.

Recent M.I.

Wed, 04/20/2016 - 23:07 -- Dawn

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. 

Anterior Wall M.I.

Sun, 07/26/2015 - 13:10 -- Dawn

This is a very interesting ECG taken from an acute M.I. patient.  Your basic level students will be able to appreciate the ST elevation in V1 through V3. Although the elevations are not very high, there are plenty of other abnormalities that point to acute STEMI: the ST segments are flat and there are marked ischemic T waves in the lateral leads: V4 through V6 and I and aVL.  The patient was suffering an acute episode of chest pain.

It is also noticeable that R wave progression in the precordial leads (V1 through V6) is not optimal, as there is still a significant S wave in V6.  We do not know if this is an electrode placement issue or not.  The QT interval is just at the high limit of normal.  
For your more advanced students, aVR has ST elevation.  It is not reciprocal of an ST depression in Lead II.  Research has shown that ST elevation in aVR and V1, especially when the ST elevation is greater in aVR, is a strong indication of proximal LCA or a Left Main occlusion.  Unfortunately, we do not have cath results for this patient.  In acute M.I. patients,  higher mortality rate has been associated ST elevation in aVR.

For more information about ST elevation in aVR, click here: https://login.medscape.com/login/sso/getlogin?urlCache=aHR0cDovL3d3dy5tZWRzY2FwZS5jb20vdmlld2FydGljbGUvNTg5Nzgx&ac=401

and here:  http://content.onlinejacc.org/cgi/content/full/38/5/1355

 

Left Main Coronary Artery Obstruction

Mon, 05/11/2015 - 01:15 -- Dawn

Today’s ECG of the WEEK comes from Sebastian Garay, Paramedic.  He presented it on his excellent website CardioCareConcepts.com, and was kind enough to share it with the ECG Guru.  It is a great example of LEFT MAIN CORONARY ARTERY lesion with ST elevation in aVR and V1.

The patient was a 68 year old man who presented with a sudden onset of chest pain, followed by cardiac arrest.  He was revived by the use of an automatic external defibrillator (AED).  The initial 12-Lead ECG shows atrial fibrillation with a rapid response of 102 bpm.  There are prominent ST ELEVATIONS in aVR and somewhat more subtle STEs in V1.  These leads reflect the base of the septum, which is the area perfused by the proximal left coronary artery.  A lesion in this area is sometimes in the LEFT MAIN coronary artery, or both the proximal LCA and the circumflex.  Both of these types of lesions carry a very high mortality rate.

The widespread ST depressions reflect the injury current, which is being directed upward and toward the patient’s right shoulder, causing a reciprocal depression in all leads except aVR, V1 and Lead III.

This patient arrived in the Emergency Dept. in grave condition and was taken to the cath lab, where an occlusive lesion was found in the LEFT MAIN coronary artery.  He later died from this severe injury.

We recommend further reading on this topic, as there has been a large body of research on ECG findings of ST elevation in aVR.  Here are some links of interest:

 

Dr. Smith’s Blog;   JACC Online; ScienceDirect.com.

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