Heart rate of 230 beats per minute

What can you say about this ECG at a rate of 230 beats per minute?

Answer below













The QRS is very narrow (about 70 ms?), so it must be a pediatric ECG. 

Thus, the fact that the rate is 230 bpm does not necessarily mean that it is SVT because infants can have very fast sinus rhythm.  Thus, what appear to be p-waves are indeed p-waves (see leads II and V1).  This is from a febrile 3 month old infant.  The ECG was done because the heart rate was 230 and the differential included SVT vs. sinus tachycardia.  This ECG, and the fact that the heart rate was variable (not constant) confirmed sinus tach.  Note also how the PR interval is very short.  Again, this because all intervals in infants are short. 

Notice also that there is right ventricular hypertrophy.  There is an S-wave in lead I, tall R-waves in leads V1-V3, with late transition to S-waves in precordial leads, and T-wave inversion in right precordial leads.  This is typical of pediatric ECGs because the fetal circulation depends on the right ventricle.  So these are normal findings in the ECG of an infant.


With management of fever and dehydration, the heart rate normalized.

Reminder:
Never trust the computer read.  The computer read is usually very good at determining pacemakers and intervals, but it was way off in this case:  it said: "electronic ventricular pacemaker" and measured the QRS at 202 ms!

Young African American Male with Atypical Stabbing Chest Pain

An thin, athletic African American of age under 30 had some chest trauma and stabbing pain that was positional.  He had this ECG recorded:

There is sinus rhythm with high voltage.  The QTc is 392.  There is T-wave inversion in V2-V6.

Click here for the answer and discussion and more cases.

Inferior MI with positive troponin: Acute STEMI or Old MI with new NonSTEMI?

A 40 year old male without cardiac risk factors and with no h/o CAD presented with a few days of intermittent typical chest pain.  He has a history of "reflux" and asthma.  He seemed to be pain free during this first ED ECG, but he was unclear about it:

Sinus rhythm with a nonspecific intraventricular conduction delay of 138 ms.  There are significant Q-waves in inferior and lateral leads diagnostic of MI, and there is ST elevation in leads III and aVF (less than 1 mm), with T-wave inversion (suggestive of old MI or reperfused MI) with a bit of reciprocal ST depression in aVL.  Prominent R-waves in V1-V3 also suggest posterior extension.

This ECG is typical not of acute inferior STEMI, but of old, or at least subacute STEMI: the T-waves are inverted and there are well-formed Q-waves.  What about reciprocal ST depression in aVL?  This is seen both in acute inferior STEMI and in "old inferior MI with persistent ST elevation," also known as "LV aneurysm morphology."    For this reason, these two entities can be very difficult to differentiate.  We have discussed anterior LV aneurysm frequently in the past.  Though both have ST elevation, Anterior STEMI and anterior aneurysm are much easier to differentiate.

The initial troponin I returned at 0.075 (+), complicating the issue.  Is it a NonSTEMI superimposed on old MI?  If it were subacute STEMI, there would be a much higher troponin.  So a bedside echo was done by the emergency physician.  Here we see the parasternal short axis view, which gives a cross section of the LV, with the anterior wall closest to the transducer and the inferior/posterior wall farthest:

Still picture at end systole: Narrow arrows show thin and akinetic inferior wall, compared to thick arrows which show a normal wall thickness in an area with good myocardial shortening (normal anterior wall motion).

Wall motion abnormalities are seen in both acute and old MI.  However, only old MI has a thin wall (scarred myocardium).  This echo shows a thin and akinetic inferior wall, confirming old inferior MI.  There is very poor LV function.

The patient was treated medically and admitted.   The troponins peaked at a level consistent with NonSTEMI.  Angiogram revealed severe 3 vessel disease with a chronically occluded right coronary artery.  The patient went for bypass surgery.  There was no evolution of ECG changes, nor resolution of ST elevation, confirming these were old findings.

Male in his 40's with chest pain.

A male in his 40's was in his usual state of health until 3 hours prior when he developed L-sided chest pressure, radiating to the neck, while walking.  He called 911.   His prehospital ECG is identical to the first ED ECG shown below.  Based on this, the paramedics activated the cath lab, administered nitroglycerin, and the pain resolved. 

This ECG was then recorded in the ED:

There is at least 2 mm STE at the J-point in leads V2 and V3, but the morphology of the T-wave is typical of early repolarization (slow upstroke, fast downstroke).  There is minimal ST elevation in I, aVL, V5 and V6.  There are not exclusions to using the formula: no inferior ST depression, no upward convexity, no precordial T-wave inversion, no Q-waves, and no terminal QRS distortion.  Thus, the Early Repolarization vs. LAD occlusion equation can be applied (see sidebar for Excel applet that can be use to make this calculation): STE60V3 is 4 mm, QTc was 416ms, and RA-V4 is 15mm.  Thus, the equation value is [1.196 x STE60V3]+[0.059 x QTc]–[0.326 x RA-V4] = 23.753, which is greater than 23.4 and would indicate STEMI.   The specificity of the rule is not perfect, but a value above 23.4 should at least prompt you to aggressively evaluate the patient.

Legend

--STE60V3 = ST elevation at 60 ms after the J-point, relative to the PR segment, in lead V3
--QTc is Bazett corrected QT interval
--RA-V4 is the R-wave amplitude in lead V4

This was not recognized, and the ECG was interpreted as early repolarization.  A bedside echocardiogram reportedly showed no wall motion abnormality. 
A repeat ECG was recorded:

Here, V2-V5 have less ST elevation and the T-waves are smaller.  It appears normal, and different from the presenting ECG.  An application of the equation has equivocal results depending on whether the STE60V3 is measured at 1.5 or 2.0 mm.

Nevertheless, the change shows that the previous ECG was indeed due to acute coronary syndrome (ACS).  

This was not seen and the cath lab was de-activated.  The patient was admitted and ruled out for Acute MI with serial troponin I less than 0.04 ng/ml (using a sensitive troponin assay).  

Not all ACS has a positive troponin.  When negative, it is of course called “unstable angina.”  Unstable angina (see more such cases here) usually presents with a normal or nonspecific ECG, or with ST depression or T-wave inversion, but it may present with transient ST-segment elevation.  And, surprisingly, transient ST elevation does not always result in a positive troponin.  The ischemia may resolve so quickly that there is both no wall motion abnormality and the troponin is negative!

With the advent of high sensitivity troponin in the future, perhaps such cases will become more rare.  But this increased sensitivity may come at the expense of worse specificity, or more false positive troponins. 

The patient was discharged, and 13 days later presented with identical chest pain, which again resolved, and had the following ECG after resolution of pain:

There is new T-wave inversion in I, aVL, V4-V6.  There is terminal T-wave inversion (biphasic) in V2 and V3, but complicated by the U-waves seen in these leads.  This T-wave inversion represents a form of Wellens’ syndrome, indicating spontaneous reperfusion of a brief left anterior descending coronary occlusion.

   

Outcome: This time, the troponin was positive [which one would expect when there is not just resolution of STE, but also T-wave inversion (Wellens')].   The patient underwent coronary angiography, which showed severe subtotal LAD disease and 70% left main disease.  He underwent coronary artery bypass surgery. 

This case illustrates the importance of paying close attention to the ECG and its evolution.  Using the formula may help.

Lessons:

1.  Coronary occlusion may be brief, with spontaneous reperfusion.

2.  Serial troponins may be negative even in ACS with transient ST elevation (unstable angina may have transient ST elevation)

3. Though early repolarization may change over months, if it changes from one ECG to the next on the same day, it is probably not early repol.

4.  Use the equation to help you differentiate early repol from LAD occlusion.

Bradycardia

A 60'ish male presented with 2 weeks of intermittent chest pain.  He has a history of MI and renal insufficiency.  Now he feels weak.  His pulse is 42 with a BP of 140/35.  Here is his initial ECG:

What is the rhythm, and what the etiology?

His charts showed he had presented to a clinic 2 months prior with chest pain and had an identical ECG  which was read as "no change from old".  The ECG prior to that one, however, did not have bradycardia (so there really was a change from old).  The patient had been sent home from clinic.





Rhythm analysis: there is a regular rhythm with a QRS that is borderline prolonged at 110 ms (QRS on the previous truly normal ECG was 105 ms).  Are there p-waves?  Yes, but they are after the QRS, and they are inverted.  And the R-P interval is very prolonged at about 440 ms.  So there is either sinus arrest or severe sinus bradycardia (such that the junction or bundle of HIS escapes before the sinus node can fire).  There is atrial activity (the p-wave); it is inverted because it is being activated from below.

Diagnosis: Sinus arrest or extreme bradycardia with junctional escape and retrograde p-waves with prolonged VA conduction.

One might also say there is a severe 1st degree AV block because of the long R-P (not P-R) interval, but our electrophysiologist, Rehan Karim, states that:

"One cannot infer that VA conduction tells you what AV conduction would be.  It is well known that patients who have complete AV block may have intact VA conduction.  That is, a ventricular beat gives rise to retrograde p waves, but the P-waves or atrial pacing does not conduct to the ventricles.  Same is true with adenosine: there can be few times when adenosine will affect AV conduction but may or may not affect VA conduction."

What are the common causes:

1. hyperkalemia
2. Ischemia (no evidence of ischemia on this ECG)
3. Drugs (he was not on any that woul do this): digitalis, beta blockers, calcium channel blockers, Na channel modulators
4. Sick sinus
5. Increased vagal tone, but this would also slow the escape.
5. Variety of other less common etiologies, such as Lyme, infiltrative diseases

Atropine 1 mg was given without change.  Potassium returned at 6.2 mEq/L.  3g of Calcium gluconate were given and the rate immediately went to 60.  Here is the subsequent ECG:

Sinus rhythm with a PR interval of approximately 200 ms.  The QRS is acttually slightly longer, at 113 ms.

The patient ruled out for MI by serial troponins.

When a patient has bradycardia, always think of hyperkalemia among other etiologies. 

Right Bundle Branch Block with New Anterior ST elevation

An elderly female with no known history of CAD presented to the ED as a walk-in with vomiting and upper abdominal discomfort.  The following ECG was recorded at t = 0:

There is sinus rhythm with Right Bundle Branch Block and ST elevation in leads V1 and V2, suspicious for STEMI. The computerized QRS duration is 138 ms. 

 A previous ECG was found:

There is an RSR' with right ventricular conduction delay and downsloping ST depression in V1 that is reminiscent of Brugada pattern.  The computerized QRS duration is 84 ms.  The ST elevation is confirmed to be new.

The cath lab was activated but the interventionalist was busy with another case.  In the interim, more data was found:  The first troponin returned elevated slightly.  A stat echo was ordered.  Heparin, Plavix and Nitroglycerine were ordered.  After ondansetron, the nausea subsided.  Further history revealed that the patient had undergone ablation for atrial fibrillation 7 days prior.  She had been on propafenone but was changed to flecainide following her ablation.  She was also on dabigatran (Pradaxa).  Her Na returned at 124 mEq/L.  Echo was completed and there was EF of 65% with no wall motion abnormality.  Repeat ECGs are below:

2nd ECG, t = 50 minutes

3rd ECG, t = 100 minutes

 There is little evolution of ST elevation.  The absence of a wall motion abnormality makes anterior STEMI very unlikely.


It was decided that the changes were due to Brugada-like pattern due to Na channel blockaid from flecanide in the setting of recent poor PO intake, nausea and vomiting.  Elevated troponin was due to recent ablation. The nausea and vomiting were attributed to dabigatran, which the patient had not tolerated well in the past (she had previously had such GI symptoms).  The patient was admitted to telemetry, her Na was replaced with IV fluids, flecainide was discontinued.  Metoprolol was started, dabigatran discontinued, and rivaroxaban was started.  ECG returned to baseline - incomplete RBBB was still present.  Serial troponins remained stable at a low but elevated level.  The patient had an uneventful hospital stay.

Flecainide, a sodium channel blocker, prolongs the QRS by at least 25%.  Dehydration, with lowered glomerular filtration, may elevate levels of flecainide.  Hyponatremia exacerbates the effects of sodium channel blockers (and treatment with hypertonic sodium, usually in the form of sodium bicarbonate, improves its effects and shortens the QRS).

This shows how sodium channel blockade can also elevate the ST segment, mimicking Brugada syndrome.

Lessons?

1. First, non-specific symptoms have a much lower pretest probability for MI.  We are all told that many MIs present with atypical symptoms (which is true).  But more important is to remember that, because so many illnesses present with atypical symptoms (abd pain, nausea/vomiting, dyspnea), such symptoms are much more likely to have a different etiology than MI.
2. A brief look at a patient's medical history can shed a lot of light on the present situation.
3. When in doubt, do an immediate echocardiogram
4.  The ECG itself is suspect: A friend sent me this case without any history, and asked me to interpret the ECGs.  My immediate response was "no STEMI".  How did I know this?  There is something slightly bizarre about the RBBB in these ECGs, though this I find difficult to put into words.  However, another feature is usually present in RBBB with LAD occlusion that I can put into words: there is usually at least 1 right precordial T-wave that is upright. See these cases:

Case 1 of RBBB with LAD occlusion
Case 2 of RBBB with LAD occlusion
Case 3 of RBBB with LAD occlusion
Case 4 of RBBB with LAD occlusion

Precordial ST depression. What is the diagnosis?

A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG:

Here is the patient's previous ECG:

Here is the patient's presenting ED ECG:

There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6.  There is no ST elevation.  Precordial ST depression may be subendocardial ischemia or posterior STEMI.  How can we tell the difference?  See the list below.



If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)].  This was indeed done:

Notice the limb leads have been reversed (axes of every lead are inverted!).  But we are now concerned with the precordial leads.  V7-V9 (labelled V4-V6) have no ST elevation. 

Notice there is tachycardia.  I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia.  In this case, the patient had failed to take his atenolol in the AM and was having reflex tachycardia in addition to ACS.  BP was 160/100.  He was given metoprolol IV which succuessfully brought his heart rate and BP down.  His chest pain resolved completely, but his ECG continued to show profound ST depression.  We performed a bedside echo and found a posterior wall motion abnormality.

The cath lab was activated and the patient went for immediate angiography, which showed a 95% hazy thrombotic lesion with TIMI III flow in a large first obtuse marginal (OM-1) off the circumflex.  Therefore, the angiographer had time to visualized the other arteries.  The RCA was chronically occluded but supplied a small area.  The LAD had a 75% proximal lesion that by fractional flow reserve was hemodynamically significant.  So there was 3-vessel disease, but with an acute posterior STEMI.  The OM-1 was opened and stented, then the LAD was stented 3 days later.

The acute infarct-related artery was off the circumflex and the affected wall was posterior (STEMI).  The posterior leads were falsely negative.  See far below for data on posterior leads.

Does this matter that the posterior ECG was a false negative?  If there is ST depression (as there is here), it is ACS.  Whether it is subendocardial ischemia or posterior STEMI, if you cannot get it to resolve, you must activate the cath lab.  And even if it is STEMI, if you get it to resolved with medical therapy, then you have opened the artery without intervention and a delay is acceptable.


This is very popular post from almost 4 years ago on posterior MI.  At the bottom are 7 ways to help differentiate the ST depression of posterior STEMI from subendocardial ischemia.  I have copied them here:

Some ways to differentiate subendocardial ischemia from posterior STEMI

First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved.
Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia.
Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs. younger smoker).
Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs.
Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations).
Sixth, placement of posterior leads (take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in just one lead is very sensitive and specific for posterior MI.
Seventh, an immediate echocardiogram can make the distinction.  These are very difficult and it is very hard to detect a posterior wall motion abnormality unless you are very experienced.  I recommend a formal study with Definity before concluding there is no posterior wall motion abnormality.
Eighth, see above.  Whether or not it is STEMI, the cath lab should be activated if the ischemia cannot be controlled medically: aspirin, nitro, beta blockers, clopidogrel, heparin/enoxaparin, GP IIb/IIIa inhibitor. 


Here is a short summary of data on posterior leads, from: 

Critical Decisions in Emergency and Acute Care Electrocardiography.  William Brady and JD Truwit, editors.  Blackwell Publishing 2009. (Smith SW as editor of section on Acute Coronary Syndromes).  This is a quoted excerpt from a chapter that was written by Daniel T. O’laughlin, MD, and edited by me.

Posterior Lead Orientation and Diagnostic Criterion

The posterior precordial leads are positioned in the 5^th intercostal space at the same horizontal line as V6.  Lead V7 is placed at the posterior axillary line, V8 just below the tip of the scapula and V9 at the paravertebral border.¹  STE up to 0.5mm measured at the J point relative to the PR segment in all three leads can be normal.²  Wung and Drew evaluated the posterior ST segment changes during PTCA of the LCX and determined that utilizing a criterion of STE of greater than or equal to 0.5mm, rather than greater than or equal to 1mm, demonstrated a sensitivity of 94% for detecting LCX occlusion related STE.³  This is compared to a sensitivity of 49% when the criterion was greater than or equal to 1mm STE.  Conversely, Matetzky et al. showed 100% specificity for posterior MI of STE greater than or equal to 0.5mm in at least one posterior lead.  In Wung’s study, 81% of patients with greater than or equal to 1mm STE in posterior leads also had other significant STE on the 12-lead ECG, and 96% had some ST deviation.³ However, 22-39% of patients experiencing posterior MI who have greater than or equal to 0.5mm STE in the posterior leads do not demonstrate STD in V1-V3.^3-5

1.         Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the Standardization and Interpretation of the Electrocardiogram: Part I: The Electrocardiogram and Its Technology: A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology. Circulation 2007;115(10):1306-24.

2.         Taha B, Reddy S, Agarwal J, Khaw K. Normal limits of ST segment measurements in posterior ECG leads. J Electrocardiol 1998;31 Suppl:178-9.

3.         Wung SF, Drew BJ. New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction. Am J Cardiol 2001;87(8):970-4.

4.         Matetzky S, Friemark D, Feinberg MS, et al. Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-V9: "hidden" ST-segment elevations revealing acute posterior infarction. J Am Coll Card 1999;34(3):748-53.

5.         Matetzky S, Freimark D, Chouraqui P, et al. Significance of ST segment elevations in posterior chest leads (V7-V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J Am Coll Card 1998;31(3):506-11.