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ST elevation

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.

 

Myocardial Infarction With Non-obstructive Coronary Arteries

Wed, 03/14/2018 - 14:36 -- Dawn

This ECG was obtained from a 37-year-old male who was complaining of non-radiating substernal chest pain.  He offered no significant medical history.  He denied taking any medications.  He was hypertensive and bradycardic on arrival in the Emergency Dept. He was alert and ambulatory.  Approximately 20 minutes after first being seen by paramedics, he suffered an episode of ventricular fibrillation in the E.D.  He was resuscitated and sent to the cath lab.  His coronary arteries were without lesions.  We do not know the results of any lab tests, including troponins.

What does the ECG show?  The rhythm is sinus bradycardia at a rate of 48 bpm. The PR, QTc, intervals and QRS duration are normal.  The QRS frontal plane axis is normal and there is good R wave progression in the precordial leads.  There is ST segment elevation in Leads I, aVL, V2, and V3, with reciprocal ST depression in Leads III and aVF.  The ST segments that are elevated retain a relatively “normal” shape, being concave upward. There are no abnormal T wave inversions or pathological Q waves.

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.

Takotsubo Cardiomyopathy

Mon, 01/01/2018 - 14:13 -- Dawn

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.

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”.

Brugada Pattern

Tue, 06/06/2017 - 14:41 -- Dawn

This patient is a 50-year-old man with a history of epilepsy and early dementia. He had a VP shunt placed in the hospital and was then discharged home.  He became extremely weak, which was not characteristic of him, and 911 was called.  He was transported to the hospital uneventfully. He was found to be afebrile.

This ECG shows a “classic” Brugada pattern. Brugada Syndrome is a hereditary disease that is associated with a high risk of sudden cardiac death. It is due to a mutation in the sodium channel gene (channelopathy). The ECG characteristics are:

·         ST elevation in V1 through V3 of at least 2 mm at the J point in the right precordial leads (V1-V3).

·         Coved upward ST segments with  negative T waves in the affected leads.

Brugada Syndrome is diagnosed when the ECG pattern exists with one of the following:

·             Polymorphic ventricular tachycardia (VT).

·             Documented ventricular fibrillation.

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.

Subtle ST Changes

Mon, 04/11/2016 - 19:18 -- Dawn

This ECG is from a 65-year-old woman who presented to the Emergency Department with a complaint of chest pain.  We have no other clinical information. 

There are several subtle, but real, abnormalities on the ECG that should be evaluated in conjuction with her clinical situation.  This is a good ECG to discuss with your more advanced students who have mastered recognition of blatant ST elevation M.I. (STEMI).  But, let’s start with what is NORMAL here. 

NORMAL FEATURES        The normal findings are:  normal sinus rhythm at about 68 bpm.  The rhythm is regular without ectopy. The intervals are within normal limits.  The frontal plane axis is normal. The T waves are all upright. 

ABNORMAL FEATURES         There is subtle ST segment elevation in Leads V1 through V3, and in I and aVL.  The shape of the ST segments is concave upward, or normal.  In a young, asymptomatic patient, we probably would not be at all concerned about this amount of ST elevation.  However, this is an older patient with chest pain. In the chest leads, the R wave progression is interrupted, as the QRS goes abruptly from negative to positive in Lead V3.  This could be due to loss of r waves ( pathological Q waves forming) in V1 and V2 lead placement, or something else. 

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