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Marked Bradycardia With Bifascicular Block

The Patient:    This ECG was taken from an elderly woman. Unfortunately, we do not know any details about the case.  That acknowledged, there are many interesting aspects to this ECG.

The ECG:  The first thing we notice is the severe bradycardia – almost certain to be symptomatic.  The rate is 32 bpm and the rhythm is regular.  There are no P waves.  This is a junctional rhythm, slightly slower than expected from junctional escape.

The QRS shows the presence of right bundle branch block.  Each QRS on the ECG starts as a narrow complex, but then adds an “extra” wave onto the end – the delay caused by the right ventricle depolarizing late.  The terminal delay is very noticeable in V1 as an R’ wave, and in Leads I and V6 as a small, wide s wave.  There is right axis deviation, so the diagnosis of bifascicular block (RBBB and left posterior fascicular block) can be made.

V2 through V6 show fragmentation of the QRS complexes and a loss of voltage and R wave progression.  This points to anterior wall M.I. We can’t know the age of the M.I. without clinical correlation, but the ST segments in those leads are very flat, with uniformly symmetrical inverted T waves all the way to V6.  All of these signs indicate recent injury.  An anterior M.I. can cause the bifascicular block we are seeing, since the bundle branches begin in the septum.

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Catastrophic Event With Bradycardia

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.

 

Dawn's picture

Anterior Wall M.I.

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

 

Dawn's picture

Left Main Coronary Artery Obstruction

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.

Dawn's picture

Anterior Wall M.I.

This ECG was taken from a 60 year old man who was complaining of severe substernal chest pain, radiating to his left arm and a non-productive cough.  There was some initial discussion among the EMS crew  about the possibility of the ECG showing a "benign early repolarization" pattern because of the concave upward ("smiling") ST segments.  They also considered a diagnosis of pericarditis, because the ST segments seem widespread.  The baseline artifact makes it difficult to evaluate for PR segment depression or Spodick's Sign.

The patient's age (60 years) and troubling symptoms (chest pain radiating to the left arm) ruled out BEP for the paramedics.  The ST segment elevations are pretty widespread - Leads V3, V4, V5, V6, I and II all show some STE.  There are also "hyperacute" T waves in the leads with STE.  There are ST abnormalities ranging from flattening of the shape to depression, but the bottom line is this patient is a 60-year-old man with substernal chest pain radiating down his left arm!

The patient was treated in the ambulance with chest pain protocols, and was transferred to a hospital with an interventional cath lab.  The patient was conculusively diagnosed with an acute M.I. and underwent angioplasty.

This is a good ECG to demonstrate subtle changes when, combined with patient presentation, can help us diagnose a coronary event.  It helps us emphasize that not all STEMIs will have dome-shaped, "tombstone" ST segments, and that patient symptoms, history, and age are important to consider.

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Teaching Series: Anterior Wall M.I.

A series of ECGs can be a valuable addition to any teacher's collection.  This series follows a 75-year-old woman through three days, during which she experienced an acute anterior wall M.I., a catheterization with angioplasty and stents placement.

In the first ECG, taken at 4:09 am, the patient has presented to the Emergency Dept. with a complaint of chest pain. (Other details are no longer available).  Although there is some baseline artifact, it appears that the rhythm is sinus rhythm with one PAC (7th beat).  There is subtle but measurable ST elevation in V1, V2, and V3 (anterior-septal leads).  The shape of the STE in V1 is noticeably coved upward.  Even aVR has some STE, with coving.  There is equally subtle ST depression in Leads II, III, and aVF (inferior leads).  Fortunately, there are no pathological Q waves at this point, which would be an indication of necrotic tissue in the area of the M.I. (anterior-septal wall).

The patient was taken to the cath lab, where it was found that she had a 100% mid-left anterior descending artery occlusion, which was opened and stented.  She also was found to have widespread coronary artery disease, with the left circumflex artery 25% occluded (stented), the right coronary artery (which was dominant) proximately occluded 50% and stented, and the posterior descending artery 75% occluded (stented).

The second ECG, taken at 6:29 the same morning, after the cath procedure, shows some ST elevation with coving remaining in V1 through V3, and also aVR, but now with the loss of R waves in V1 and V2 and loss of R wave voltage in V3.  This represents the formation of pathological Q waves, and can be a permanent change in many cases.

The third ECG, taken two days later in the cardiac step-down unit, shows improvement, and progression toward healing.  The ST segments are still shaped in a slightly coved-upward shape, but they are less elevated.  The R waves have returned.  The T waves in V1-V3 are inverted.  The deeply inverted T waves of V2 and V3, especially, and classic for ischemia, and we even see the "ischemic zone" extending across the anterior-lateral wall, including V4 through V6 and Leads I and aVL.

The patient did very well to discharge, and we don't have followup after that.

 

 

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Extensive Anterior-lateral M.I. With Right Bundle Branch Block

This ECG depicts an extensive and ultimately, fatal, injury.  There is marked ST segment elevation in Leads V2 through V6 (anterior wall).  There is also ST elevation in Leads I and aVL (high lateral wall).  The ST elevation in aVR is indicative of a very proximal lesion in the left coronary artery, which supplies the anterior wall, including the anterior portion of the septum, the high lateral wall, and, in this case, the low lateral wall.  The inferior leads, II, III, and aVF, show reciprocal ST depression.

This is an old ECG - the computer readings of the rate and intervals is lost, as is the grid.  But the rate here appears to be about 80 bpm and the QRS is widened.  There is a right bundle branch block ECG pattern, which is not surprising given the extensive septal damage.  Normally, the criteria for RBBB on the ECG includes an rSR' pattern in V1 (seen here) and a small, wide s wave in Leads I and V6.  This s wave is not seen here, presumably due to the effects of the ST elevation in those leads.

What matters clinically in a patient like this is not whether there is RBBB or another type of interventricular conduction delay. This patient needs immediate restoration of blood flow through the LCA and intensive medical/nursing care.  As mentioned before, this patient did not survive, in spite of being brought to a hospital.  We do not know the exact mechanism of death or treatment course in this case.

If you are teaching students to use multiple leads in assessing rhythm, this is a great example of how one or two leads can be very misleading.  I have used this ECG's V4 in an excercise illustrating this concept.  Shown V4, many people would call this "AIVR" or "V Tach".  Seen in context with the other leads, it is obvious that we are looking at ST elevation that is as high as the R wave.  Two leads are better than one, and twelve are better than two.

 

 

Dawn's picture

Extensive Anterior Wall M.I. With Recent Inferior Wall M.I.

This 88-year-old woman was brought to the Emergency Department in cardiogenic shock.  Very little is known of her past medical history, but it was relayed to the EMS responders that she had been ill for about four days, when she became much worse.

This ECG shows a large, acute anterio-lateral wall M.I., as evidenced by the ST ELEVATIONS in V2 through V6, Leads I and aVL.  To make matters worse, there are PATHOLOGICAL Q WAVES in Leads V2 through V6.  Pathological Q waves indicate areas of necrosis.  Because the myocardium facing the positive electrode is not electrically active, we "see through" the dead tissue to the myocardium on the opposite side of the heart.  Pathological Q waves could be thought of as "reciprocal R waves".  This represents a great deal of dead myocardium, which will be akinetic - not moving.

To make matters worse, she has pathological Q waves in the INFERIOR WALL as well, in Leads II, III, and aVF.  Her ST segments in those leads are flattened and possibly slightly elevated, but not much.  There are no reciprocal ST depressions in I and aVL, because they are affected by the anterior - lateral wall M.I., and are elevated.

The accompanying photos show her left coronary artery angiogram indicating severe coronary artery disease and a "missing" left anterior descending artery.  This is due to a proximal lesion that occurred around the area of the first diagonal artery, cutting off blood flow to a very large part of her anterior-lateral wall.  The photo of the right coronary artery shows a very tight lesion which is allowing some blood to pass.  The Interventionalist felt that this represented a resolving 100% occlusion (remember, she had been sick for four days).  As the blood clot broke up, blood flowed again, lowering the ST segments.  Unfortunately, permanent damage had already been done, and she had Q waves in the inferior wall also.  This leaves very little of her heart beating, and it is easy to understand why she presented in shock.  She suffered cardiac arrests several times during the procedure, and was managed with a balloon pump and ventilator.

Unfortunately, this type of injury is not survivable, and she died in the CVICU a few hours after her procedure. She contributes to our education by demonstrating the cumulative effects of M.I., especially when permanent damage occurs.  For a look at her ventriculogram, to understand the devastating effects of these injuries, go to our You Tube channel.

Dawn's picture

Acute Anterior-lateral M.I. With Right Bundle Branch Block and Left Posterior Fascicular Block

This ECG was obtained from a patient who suffered an occlusion of the left main coronary artery.  ST elevation is seen in Leads V1 through V6, as well as I and aVL.  This is an indicator that the circumflex artery is included in this M.I., and the occlusion is above the bifurcation of the LM and the circ.  The patient also has a right bundle branch block and a left posterior fascicular block.  This bi-fascicular block can be a dangerous complication of acute M.I., as two of the three main bundle branches are no longer functional.

The ECG shows typical ST depression, probably reciprocal to the elevation, in the inferior leads.

The right bundle branch block is diagnosed by the following criteria:  1) Wide QRS;  2) Supraventricular rhythm; and 3) rSR' pattern in V1 with Rs with a wide little s wave in Leads I and V6.

The left posterior fascicular block is diagnosed by right axis deviation and by ruling out other causes of right axis deviation.  In RAD, Lead III will have a taller positive ( R ) wave than Lead II, and a negative Lead I.

This type of occlusion is often called the "Widow Maker", and requires very rapid intervention to restore blood flow and prevent complicatons.  If there is good news, it is that there are no pathological Q waves, which would indicate necrosis, and this patient was taken quickly to a full-service cardiac center with interventional cath labs and open heart surgery available.

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ECG Teaching Series: ST Elevation M.I. With Hyperacute T waves

This series shows the evolution of ECG changes in anterior wall M.I. secondary to occlusion of the proximal left anterior descending artery.  The patient is an 88-year-old woman with chest pain.  She was designated a "cardiac alert" from the field by paramedics.  Her proximal LAD was opened and stented in the cath lab.  We do not have follow-up information on her.

The first ECG in the series, titled "12-Lead 3", shows ST elevation at the J point in V1 through V3.  In addition, the T waves are "hyperacute" - tall, broad, and asymmetrical. This can be an early, transient sign of myocardial injury.  Slight reciprocal depressions are seen in the inferior leads.  Lead V4 has a T wave inversion that is out of place with the progression of the T waves in V3 and V5.  Lead placement may be to blame.  Hyperacute T waves in a patient with chest pain should be taken very seriously.

The second ECG, titled "12-Lead 4", shows continued elevation at the J point in Leads V1 through V3, with a lessening of T wave amplitude.  In addition, Lead aVL is showing some T wave changes. The T wave is biphasic, and may be about to become inverted.  This is not an improvement!  V1 through V3 show us the anterior-septal wall, and an M.I. here indicates occlusion in the LAD.  Leads I and aVL show the high lateral area of the anterior wall, and damage here is an indicator that the occlusion is proximal.

The third ECG, titled "12-Lead 5", shows a "maturing" of the ST segment elevation.  Even though there is some significant artifact, we can see that the ST segment in V1 is coved upward, and the ST segment in V2 is flat.  Both shapes are abnormal, and a sign of CAD.  The T waves have become less pronounced, but V2 looks as if the T wave may become inverted in the near future.  V3 looks improved in this image.

The patient's clinical symptoms did not improve during these ECG changes.  Hyperacute T waves are not a definitive sign of STEMI, but they provide a highly visible warning that may catch attention.  They definitely are an indication to run serial ECGs, as these paramedics did.

 

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