The 4 Physiologic Etiologies of Shock, and the 3 Etiologies of Cardiogenic Shock

A 60-something presented with hypotension, bradycardia, chest pain and back pain.

She had a h/o aortic aneurysm, aortic insufficiency, peripheral vascular disease, and hypertension.  She had a mechanical aortic valve.  She was on anti-hypertensives including atenolol, and on coumadin, with an INR of 2.3. 

She was ill appearing.  BP was 70/49, pulse 60.

A bedside echo showed good ejection fraction and normal right ventricle and no pericardial fluid.

Here is the initial ECG:

What do you think?

This ECG actually looks like a left main occlusion (which rarely presents to the ED alive):  ST Elevation in aVR, but also in V1, and what appears to be "coving" of the ST segment in aVL, which suggests ST Elevation in that lead as well.

There is bradycardia, which is ominous in such a sick patient.  This may be due to atenolol, but could simply be a sign of severe illness.

Whereas ST elevation in aVR is usually reciprocal to the the ST depression of subendocardial ischemia, with a negative ST vector towards leads II and V5, and may be accompanied by STE in V1 (which is in the same direction as aVR), when there is also STE in aVL it implies a more directly superior ST axis (supported by ST depression in all of II, III, aVF).

When the ST axis is directly superior, there may actually be transmural ischemia of the "base" of the heart (the base is actually the top of the heart, which really does not have a wall -- the ventricles have openings to the atria at the base, and so no complete wall).  However, the anterior, lateral, posterior, and septal walls all have a superior portion that may result in ST elevation in a superior direction if all walls have subepicardial ischemia, as in left main occlusion.

It is important to remember that an ECG like this represents possible left main occlusion only if it is a result of ACS!! 

Knotts et al. found that such ECG findings only represented left main ACS in 14% of such ECGs: 
Only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as ≥ 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).  It was a baseline finding in 62% of patients, usually due to LVH. 

Reference: Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.    

Case continued:

The chest X-ray was consistent with pulmonary edema, and the ultrasound showed a "plump" inferior vena cava.  (This data is all consistent with high right and left sided filling pressures, which is the hallmark of cardiogenic shock -- not obstructive, distributive, or hypovolemic)

Aortic dissection was considered (with involvement of the coronary arteries and aortic outflow obstruction), but a CT scan was negative for dissection.

The cath lab was activated.

It is a very long story, but I will make it brief:

The angiogram could not be done because of inability to access the arterial system (unexplained).

The interventionalist listened to the heart and heard both a systolic flow murmur across the valve and a diastolic murmur.

A formal echo showed aortic insufficiency, then TEE showed a mass on the aortic valve, and surgical exploration showed aortic valve thrombosis.  

This was not ACS.  This was not Left Main occlusion.

Comment:

Shock has 4 basic etiologies:

1. Obstructive (pulm embolism, tension pneumothorax, tamponade, atrial myxoma, etc.)
These were all ruled out
2. Distributive (sepsis, neurogenic, beriberi, etc.).  The patient showed no signs of high output
3. Hypovolemic (dehydration, hemorrhage, third spacing)  The IVC was plump

4. Cardiogenic -- the likely culprit

Cardiogenic shock has 3 basic physiologic etiologies:

1. Poor pump function (diastolic or systolic)  The bedside echo showed good pump function, though that does not completely rule out diastolic dysfunction.
2. Dysrhythmia (too fast or too slow to adequately fill and pump)  There was only some mild bradycardia
3. Valvular.  The pump works but the blood goes the wrong way.  This is what we are left with: Valvular etiology is frequently forgotten.  Any valve dysfunction can result in shock, especially aortic, mitral, or tricuspid (I have never seen a case of acute pulmonic valve dysfunction and cursory search found nothing)

Aortic valve thrombosis should be considered in any patient who has a prosthetic aortic valve, especially a mechanical one.  It is a catastrophic complication, which is why we are so careful to maintain a high therapeutic INR on these patients.

One could say that this case is a hybrid of cardiogenic and obstructive shock, but since it is all valvular, let's call it cardiogenic.

Suffice it to say that one should suspect valvular thrombosis in patients with artificial valves who have:

1. Dyspnea
2. New or worsening heart failure
3. Hypotension or shock

One should listen for muffled heart sounds or a new murmur, but this is not sensitive.

One should be suspicious especially if the INR is not at the goal of:

2.5  - for bi-leaflet or current-generation single tilting disk mechanical aortic valves is 2.5 if they have no risk factors for thromboembolism 

3.0  - if they have a ball-cage mechanical valve (because of the associated higher risk of thrombosis) or risk factors for thromboembolism such as atrial fibrillation, left ventricular systolic dysfunction, prior thromboembolism or hypercoagulable state.

3.0  - (range, 2.5 to 3.5) for patients with mechanical mitral valves 

3.5 to 4.0 -  for patients with mechanical tricuspid valves. 

Transesophageal echo may be necessary for diagnosis.

Always think about doing Doppler on the valves during POCUS.  It is not that difficult to see regurgitation.  Had that been seen, the diagnosis would have been made much earlier.

Complications of aortic thrombosis include, of course, severe obstruction of aortic outflow (with shock), aortic insufficiency and regurgitation, and embolism to any artery in the tree, resulting in stroke, myocardial infarction, or other catastrophic infarction.

The combination of outflow obstruction (decreased cardiac output) and regurgitation (low diastolic pressure) results in severe coronary ischemia.  The coronaries are perfused during diastole when the myocardium is not contracting.

There is no reason to write more about this complication, as there are many good articles on the topic.  See this one:
https://www.mayoclinic.org/medical-professionals/cardiovascular-diseases/news/prosthetic-valve-thrombosis-time-is-critical/mac-20430866

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Comment by KEN GRAUER, MD (11/30/2018):

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Interesting case with an excellent discussion and timely reminder by Dr. Smith of the principal etiologies of shock and cardiogenic shock. I limit my comments to the initial ECG, which I’ve reproduced for clarity in Figure-1.

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Figure-1: Initial ECG on a woman in her 60s, presenting with shock (See text). 

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My interpretation of the ECG in Figure-1 was as follows:

• Baseline artifact. This is most marked in leads I and III, suggesting the cause might be the right upper extremity.
• Sinus bradycardia at a rate just over 50/minute. All intervals (PR, QRS, QT) are normal. Slight leftward axis, though not quite leftward enough to qualify for LAHB (since the QRS complex is still predominantly positive in lead II).
• Probable LVH (See below).
• Diffuse ST-T wave depression, with especially deep T wave inversion in leads V4-thru-6 — and biphasic T waves in leads III, aVF and V3. Significant ST elevation in leads aVR and V1, with fatter-than-they-should-be T wave peaks in these leads, and a pattern for the ST-T waves in leads aVR and V1 that looks “reciprocal” to the ST-T wave depression in many of the other leads.

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IMPRESSION: Sinus bradycardia with probable LVH + ST-T wave changes suggestive of LV “strain” + diffuse subendocardial ischemia. Urge clinical correlation.

• Why “probable” LVH? The ECG is an imperfect tool for assessment of LVH. At best — sensitivity of the ECG for picking up LVH is no more than 55%. Echo is far superior to the ECG for assessment of chamber enlargement. That said, when the clinical situation is “right” — and, voltage criteria for LVH are met — and, ST-T wave repolarization changes of LV “strain” are present — then specificity of the ECG for detecting LVH may be more than 90-95%! Admittedly, voltage criteria for LVH are not met in Figure-1 (ie, the R wave in lead V6 falls shy of the 18-20 mm needed in this lead). But, given the high prevalence clinical situation (ie, this patient has known hypertension plus aortic insufficiency) + nearly enough R wave amplitude in lead V6 (16mm) + ST-T wave changes consistent with LV “strain” in all lateral leads (ie, leads I, aVL, V4-6) — true chamber LVH is likely (CLICK HERE — for more on the ECG diagnosis of LVH).
• It would be extremely interesting to see a baseline ECG on this patient, taken at a time when she is not in acute cardiogenic shock! My GUESS as to what such a “baseline” ECG on this patient would show is: i) ST-T wave changes of LV “strain” in the same 5 lateral leads with similar shape for the ST-T waves, but with less J-point depression than the 2-4mm seen in leads V4-thru-V6 in Figure-1; ii) much less (if any) ST elevation in leads aVR and V1; iii) possibly an upright T wave in lead V2, with a shape reciprocal to the ST-T wave depression seen in the lateral chest leads in Figure-1 (ie, LV “strain” often results in mirror-image upright ST-T waves in anterior leads, compared to the ST-T depression seen in lateral chest leads); iv) much less (if any) ST depression in leads II, III, aVF and V3 (with loss of biphasic T waves); and, v) possibly greater R wave amplitude in lateral chest leads (sometimes ischemia reduces R wave amplitude ... ).
• Without the luxury of seeing this patient’s “baseline ECG” — we are reduced to educated guessing about which ECG findings in Figure-1 are “new” vs “old” vs “new on-top-of old”. My hunch is that what we are seeing in Figure-1, is a combination of longstanding LVH with LV “strain” + superimposed diffuse subendocardial ischemia in this patient with acute cardiogenic shock from complications of her valvular heart disease. Cardiac catheterization would have told us if significant underlying coronary disease was also contributing to the subendocardial ischemia.

Our THANKS to Dr. Smith for presentation of this interesting case.

Saddleback ST Elevation. Is it STEMI? Is it type II Brugada?

A 50-something presented with epigastric and chest pain.

Here is his ECG:

What do you think?  QTc 388 ms.

Computer interpretation:

SINUS RHYTHM
INCOMPLETE RIGHT BUNDLE BRANCH BLOCK
ST ELEVATION, CONSIDER SEPTAL INJURY
***ACUTE MI***








There is a saddleback, which is rarely due to MI.  V2 has the morphology of type II Brugada, as there is a relatively large beta angle, described here:

Explanation
1. Draw a horizontal line from top of r' wave (black line 1)
2. Draw a horizontal line 5 mm below this (green line 2)
3. Extend the downsloping r'-ST segment (black line 3) until it intersects the green line
4. Measure the base.  
If greater than 3.5 mm, then meets criteria (this is equivalent to a 35 degree beta angle)

However, whenever you see an rSR', especially with a saddleback, think of lead placement.

Then look at the P-wave in V2.  Is it fully upright?  If not, then there is probable high placement of lead V2.

I went back to look and, indeed, V1 and V2 were placed too high.

I put them in the correct position and we recorded another ECG:

Now the P-wave in V2 is upright.  The lead is placed correctly.
Looks like typical normal variant ST elevation (otherwise known as early repolarization)
QTc 384

You can use the LAD-Early Repol Formula to differentiate this from LAD occlusion:

ST elevation at 60 ms after the J-point, relative to PQ junction (STE60V3), = 2.5mm
QTc by computer = 384
R-wave amplitude in V4 (RAV4) = 19mm
Total QRS amplitude in V2 (QRSV2) = 17.5mm

Any of these calculators work:
Use the iPhone app: SubtleSTEMI
Use the Android app: ECG SMITH
Use the link at the top of the blog.
Use MDcalc.com: https://www.mdcalc.com/subtle-anterior-stemi-calculator-4-variable

4-variable formula: 15.1 (A value less than 18.2 favors early repol.  This value is very low.)

The patient was diagnosed with reflux

Learning Points:

1. Saddleback ST Elevation is almost never STEMI
2. Saddleback STE may be type II Brugada syndrome
3. A Type II mimic may result from leads V1 and V2 placed too high
4.  An inverted P-wave in lead V2 implies lead misplacement too high


Saddleback in STEMI:

Here are the only 2 ECGs with V2 "saddleback" that I have ever seen which really represented an LAD Occlusion:

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

A Very Subtle LAD Occlusion....T-wave in V1??

Here are other cases of saddleback STE:

Is this Saddleback a STEMI??

Epigastric pain, Syncope, and Saddleback ST Elevation

A 65 Year Old Man with Chest pain and Precordial ST Elevation

Non-Vagal Syncope and Saddleback Morphology in V2

Is this STEMI? Pattern Recognition is Key

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My Comment, by KEN GRAUER, MD (11/28/2018):

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Great case for illustrating a number of important concepts — albeit it raises a series of questions without definite answer. For clarity — I put both tracings together in Figure-1. For the purpose of fostering discussion — I’ll play “Devil’s Advocate” with my comments below:

Figure-1: TOP ( = ECG #1) — Initial ECG in this case. BOTTOM ( = ECG #2) — Repeat ECG after verifying correct lead placement. The lead V1 and V2 electrodes had been placed too high on the chest in ECG #1 (See text). 

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ECG #1: ( = the Initial Tracing):

The initial concern at the time ECG #1 was obtained was whether the ST elevation in leads V1 and V2 was indicative of acute OMI. As it turned out — leads V1 and V2 were placed too high on the chest, so that ECG #1 was not a valid tracing for such assessment. That said — I think it worthwhile to specify reasons why even if lead placement had been correct, acute OMI would still be unlikely on the basis of this initial ECG:

• The shape of the ST elevation in leads V1 and V2 in ECG #1 is concave up, which is usually a benign morphology. As per Dr. Smith — the “saddleback” configuration (seen best here in lead V2) is rarely due to acute MI.
• Apart from leads V1 and V2 — there really is no abnormal ST segment deviation. The slight ST elevation seen in lead V3 does not exceed the 1-2 mm of concave-up ST elevation commonly seen in leads V2 and/or V3 with normal repolarization variants. No other lead shows any ST elevation. There is no reciprocal ST depression. So, even if all leads had been correctly placed in ECG #1 — I would not have suspected acute OMI.

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Assessing for a Brugada-2 ECG Pattern:

A “saddleback” (ie, Brugada-2) ECG pattern is assessed for by applying the criteria in the Figure explained by Dr. Smith above. I illustrate application of these measurements in the magnified insert of the middle complex in lead V2.

• In ECG #1 — the base of the triangle (horizontal PINK line) formed by drawing lines from the peak of the r’ in lead V2 looks to be extremely close to 3.5 mm, which is right at the upper limit qualifying for a Brugada-2 pattern.
• Criteria for a Brugada-2 ECG pattern disappeared once the V1 and V2 electrodes were correctly positioned (See ECG #2 in Figure-1). While disappearance of the saddleback pattern in lead V2 after repositioning of the V1, V2 electrodes is comforting — it should be appreciated that in some patients with Brugada patterns, the ECG abnormality may only be seen with higher-than-usual electrode lead positioning (ie, in the 2nd or 3rd interspaces). This is because the abnormal electrical activity leading to a Brugada ECG pattern arises from a very limited zone located in the RVOT — and in some patients this electrical zone requires higher lead placement for detection. This raises the difficult-to-answer clinical question of when to do additional ECGs on a patient with placement of leads V1,V2 in the 2nd and/or 3rd interspaces?
• When associated with appropriate clinical features (ie, personal history of cardiac arrest, polymorphic VT, non-vagal syncope, positive family history of sudden death at an early age, etc.) — then spontaneous occurrence of a Brugada-1 ECG pattern is diagnostic of Brugada Syndrome. On the other hand — isolated occurrence of a Brugada-2 pattern is non-diagnostic, although when associated with other features, it may raise clinical suspicion and warrant pharmacologic challenge and/or referral to EP cardiology.

For More on Brugada ECG Patterns:

• Dr. Smith’s March 26, 2015 post has great illustrations reviewing assessment for a Brugada-2 ECG pattern.
• My 29-minute ECG Video on the topic reviews the basics of recognizing Brugada-1 and Brugada-2 patterns, with detailed discussion of Brugada Syndrome.

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Regarding Malposition of Leads V1 & V2:

Dr. Smith’s suspicion of lead malposition in this case was invaluable for accurate diagnosis. He then confirmed his suspicion by checking the patient himself to see where the V1, V2 electrodes had been placed — and followed this up by repeat ECG that revealed the patient’s “true” ECG.

• We’ve previously reviewed clues to quickly Recognize V1, V2 Misplacement (Click HERE).
• I was admittedly less suspicious about lead V1,V2 misplacement in this case — because: i) The negative component of the P wave in lead V2 is relatively modest; ii) The P wave and QRST morphology in leads V1 and V2 looks quite different from the all-negative P wave and QRST complex appearance in lead aVR; and, iii) The distinct terminal S waves in both leads I and V6 suggested to me that the r’ in leads V1 and V2 might simply be explained by the presence of incomplete RBBB. That said, Dr. Smith’s suspicion was correct — and the saddleback pattern disappeared on the repeat ECG.

ECG #2: Some Unusual Findings:

As discussed by Dr. Smith — this patient’s “true ECG” ( = ECG #2) no longer manifests a saddleback pattern, and does not show any acute changes. Nevertheless — there are some additional ECG findings worthy of mention.

• There is a surprising amount of fragmentation of the QRS complex in ECG #2. For example, the QRS complex shows a 4-component (rSr’S’ ) QRS deflection in lead III. Multi-fragmented complexes are also evident in leads aVL and aVF. S waves are present in 11 of the 12 leads on this tracing. Clinically — the significance of these unusual findings is uncertain — though “fragmentation” often indicates “scar”, and might reflect underlying cardiac disease. Whether to explore this possibility further would depend on clinical correlation.

Arrhythmia? Ischemia? Both? Electricity, drugs, lytics, cath lab? You decide.

Written by Pendell Meyers with edits by Steve Smith

A male in his 60s presented with off and on shortness of breath and chest pressure over the past few days. He was hypertensive and tachycardic, with mildly increased work of breathing. Here is his initial ECG:

What do you think? What will you do for this patient? How many problems does he have?

When the team saw this ECG, we obviously noticed the large STE in the inferior leads, with STD in V1-V5, I, and aVL, and STE in V6. However we also noticed that the rhythm is rapid, regular, and narrow, with no P-waves, at a rate of approximately 200 bpm, and therefore not sinus rhythm in this patient in his 60s. The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. The rhythm differential for narrow, regular, and tachycardic is sinus rhythm, SVT (encompassing AVNRT, AVRT, atrial tach, etc), and atrial flutter (another supraventricular rhythm which is usually considered separately from SVTs). Therefore this patient is either in some form of SVT or atrial flutter. 

Atrial flutter, when regular, must be conducting at 1:1, 2:1, 3:1, etc. 

If 1:1, a regular ventricular rate of 200 as the result of atrial flutter would require a flutter rate of 200, and that is too slow for flutter (unless the patient is taking a type I antidysrhythmic such as flecainide, which slows atrial conduction and flutter rate). Atrial flutter in the absence of modifying medications is generally from 240-360 bpm. Furthermore, most old adult AV nodes cannot conduct at 200 bpm.

If 2:1, this would require a flutter rate of 400 bpm. This is far too fast for flutter. 

The most common case of atrial flutter results in a ventricular rate of approximately 150 bpm, due to the average size of the atria and the normal rate of atrial conduction (resulting in an atrial rate of approximately 300 bpm), combined with the typical capacity of the AV node to conduct (usually 2:1 block in the setting of an atrial rhythm going 300 bpm).

So we asked the patient if he had any new medications recently. 

He said, "I just started taking flecainide last week." Chart review confirmed that he had been started on flecainide for atrial fibrillation.

This new information makes the diagnosis of atrial flutter far more likely: first, atrial fibrillation and flutter are closely associated and, second, this makes a flutter rate of 200 bpm (with 1:1 conduction) quite likely.

Back to the interpretation of the ECG: Does the rhythm matter to you in this case? If so, why?

The rhythm does matter! For many reasons, including these:

1) The flutter waves of atrial flutter are well known to mimic ST deviations, as well as hide true ischemic ST deviations from the reviewer. In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished.

2) Tachycardia to this degree can cause ST segment changes in several ways. First, there can simply be diffuse ST depressions (which obligates reciprocal STE in aVR) associated with tachycardia which are not indicative of ischemia. Second, the increased demand created by extreme tachycardia may exceed the ability of the coronary arteries to supply sufficient blood (due to preexisting three vessel or left main disease, with or without ACS). In this case, there is diffuse ischemic ST depression of subendocardial ischemia, of course with accompanying reciprocal STE in aVR. Finally, if a region of the myocardium supplied by a severely flow limiting (but not necessarilly fully occluded) lesion suddenly undergoes massively increased demand due to acute tachycardia, the supply/demand mismatch may be so great that the tissue undergoes acute transmural ischemia, both subendocardial and subepicardial, which may result in infarction (just as in the case of classic thrombotic Occlusion MI). This case represents the same physiologic event as OMI in terms of the result on the myocardium, therefore with identical ECG features, however there may not be ACS!

So you do care what the rhythm is, and you should be wondering:

Am I being fooled into seeing ST elevations due to possible flutter waves?

Is that an obvious STEMI underneath that rhythm?

If I fix the rhythm will the ST changes resolve?

Is he even stable enough to attempt changing his rhythm? Is he unstable enough to warrant cardioversion? Do ischemic changes on ECG mean unequivocally that the rhythm is "unstable" and therefore mandate electrical cardioversion?

His vitals were: 

BP 176/92

HR 202

SpO2 98%

RR 20

Exam: Mild increased work of breathing. Mildly sweaty. Fatigued-appearing but mentating perfectly. Clear lungs. Perfused extremities.

What would you do and in what order?

Our bedside assessment of the situation was this: 

The patient did not appear critically ill or acutely unstable to us. He did not appear to be actively decompensating in front of us. We felt that we had a few seconds to think about our next move. During this time, we activated the cath lab. We believed that the ST deviations on the presentation ECG were far out of proportion and not morphologically consistent with only flutter waves mimicking STE - we thought there was truly a visible current of injury present. But we recognized that the injury pattern may be either due to OMI, or secondary to the extreme rate combined with a preexisting lesion (type II STEMI). Either way, the rhythm must be dealt with first, because it is exacerbating either form of ischemia and can be treated more rapidly than an occlusion. In the best case scenario, all ST segment deviations may cease after a few minutes of normal heart rate, making Occlusion MI less likely. Conversely, if there truly is OMI underlying the rhythm, normalization of the rhythm will expedite its discovery and management.

We discussed several pharmacologic and electrical options. We first gave adenosine 6mg. There was a temporary break in the rhythm, but artifact prevented seeing any uncovered flutter waves at this moment, then the rate immediately jumped back up to 202 bpm. 

Next we gave 15mg diltiazem IV push, which should slow AV conduction and clearly reveal the flutter waves (or, if PSVT, which is unlikely, it will convert it). Diltiazem is not terribly effective for conversion of atrial flutter to sinus, so this should not be an expected result. Approximately 1 minute later, the rhythm broke from 202 bpm into this:

The rhythm has converted to sinus! (Again, not an expected outcome with diltiazem). There is still a clear signal of focal transmural ischemia in the inferior and posterior walls. Despite the fact that the magnitude/proportionality of the ST segment changes has improved, it is difficult to distinguish the relative component of decreased rate. If you're having an OMI of the inferior and posterior walls, it makes sense that the ECG changes would be more pronounced at higher heart rates because there is even more mismatch between supply and demand. Not to mention that tachycardia makes essentially all ECG findings more dramatic, regardless of whether there is ischemia or not. 

It also takes a while for ischemia and ST segments to resolve - wait a while and repeat it, just like you would post-ROSC! 

Here is his baseline on file for comparison:

Normal ECG, complete with some normal STE in V4-V6.

The lower heart rate was maintained, as were the ST segment changes above, over the next 10 minutes in the resuscitation room. His symptoms improved with decreased heart rate, but did not fully go away.

He was taken to the cath lab.

They found the following CAD:

LAD prox 70%
LAD mid 80%
LAD distal 90%
Circumflex mid 95%
RCA prox 70%
RCA mid 90%

It seems that the angiographers identified two culprit lesions:

1) mid LCX: TIMI 3 flow initially, still 3 after intervention, thrombus present

2) mid RCA, TIMI 3 flow initially, still 3 after intervention, thrombus present

Both lesions were stented. 

Serial troponin T measurements rose from zero to 2.80 ng/mL over the next 10 hours. 

Here is the ECG after intervention:

Persistent STE in III and aVF, with persistent STD in V2-V5. However, there is terminal T-wave inversion in the inferior leads and large upright T-wave morphology in the anterior leads, signifying the changes of successful reperfusion rather than ongoing transmural ischemia.

Flecainide was discontinued. The patient did well. Although we are not electrophysiologists, we are under the impression that it is standard, or at least common,  when a patient starts flecainide to also start the patient on oral diltiazem in case the patient develops atrial flutter. We asked the patient about this, and he stated that his doctor told him to start taking flecainide in place of his atenolol. He was not instructed to take any calcium channel blocker or beta blocker with the flecainide. Perhaps this event could have been avoided. We also asked one of our electrophysiologists who states that patients should not be started on flecainide without first ruling out CAD, to prevent situations like this. 

With the report of thrombotic lesions and the magnitude of troponin rise, as well as classic ECG changes that persisted beyond correction of the tachycardia, it is possible that this patient did indeed suffer Occlusion MI or its equivalent, simultaneously with his 1:1 atrial flutter. But this is not definite because the angiogram was not done at the same time as the ECG changes suggesting OMI. 

On the other hand, it is still possible that there was actually no ACS at all. Anyone with severe preexisting stenoses with a heart rate of 200 bpm will have the same ECG and troponin findings from start to finish. Sometimes what appears to be thrombus on angiogram is not actually thrombus.

Learning Points:

Acute arrhythmias such as SVT, rapid AF, and atrial flutter may coexist and/or be caused by ischemia, or vice versa.

The ECG cannot differentiate the various etiologies of acute transmural ischemia - the myocardial cells do not know the reason for their acute lack of blood supply, they simply report that they are dying imminently. The same is true for diffuse subendocardial ischemia. You must figure this out clinically.

Flecainide slows the rate of conduction, sometimes causing an atrial rate of 200 bpm and therefore allowing 1:1 conduction with adverse results.

Sometimes you must correct the rhythm to see what lies underneath.

See these other cases:

Atrial fibrillation with rapid ventricular response with ECG injury pattern

Tachycardia and ST Elevation.

Is this inferor STEMI?

Atrial Flutter with Inferior STEMI?

What is the Diagnosis?

Atrial Flutter Mimicking ST Depression

Inferolateral ST elevation, vomiting, and elevated troponin

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My Comment by KEN GRAUER, MD (11/26/2018):

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Excellent discussion by Drs. Meyers and Smith — in which they have covered numerous aspects of this case in superb detail! I limit my comments to a number of academic and semantic concepts relating to the arrhythmia in this case:

What is an “SVT”?

There are some semantics to the term, “SVT” = SupraVentricular Tachycardia. Supraventricular rhythms are defined as arising at or above the AV node, ergo “supra” (or above) the ventricles. When the rate of such rhythms is ≥100/minute — the rhythm qualifies as an “SVT”.

• SVT is a generic, all-encompassing term that includes any rhythm arising at or above the AV node, with an average rate of ≥100/minute. This technically includes not only reentry SVT rhythms (ie, AVNRT, AVRT) and atrial tachycardia — but also atrial fibrillation (if the average rate is fast enough) — atrial flutter — MAT — junctional tachycardia — and even sinus tachycardia, among others.
• Awareness of this semantic distinction is important in communication — since clinicians all-to-often associate the term “SVT” with different meanings. Just as we need to specify what we mean when we say a patient is “lethargic” — we should clarify what we mean when we use the term SVT.
• One instance in which the generic term, “SVT” is uniquely suited — is when the rhythm in question is an, “SVT of Uncertain Etiology”. This is the situation for the initial tracing in this case (ECG #1 = TOP tracing in Figure-1). The rhythm is an “SVT” — because the QRS complex is narrow and the rate is fast. Since the rhythm is regular — the differential includes sinus tachycardia, atrial flutter, atrial tachycardia, and reentry forms of SVT.

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Figure-1: TOP ( = ECG #1) — Initial ECG in this case. BOTTOM ( = ECG #2) — The resultant rhythm after IV Diltiazem (See text). 

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What is the Rhythm in ECG #1?

As per Dr. Meyers, awareness that this patient had just been started on Flecainide for treatment of AFib, but without concomitant use of an AV nodal blocking agent — greatly increases the likelihood that the SVT rhythm in ECG #1 is the result of a proarrhythmic effect of Flecainide (ie, conversion of AFib to AFlutter with 1:1 AV conduction).

• Without the knowledge that Flecainide was started — I would have guessed the rhythm in ECG #1 was AVNRT.
• As emphasized by Dr. Meyers — administration of IV Diltiazem usually does not result in prompt conversion of AFlutter. Instead — this drug typically slows the ventricular response, which generally reveals flutter waves if AFlutter is the underlying rhythm. In those instances in which Diltiazem does convert AFlutter to sinus rhythm — it tends not to do so abruptly. Unfortunately — the KEY rhythm strip in this case (ie, moment-to-moment monitoring immediately on administering IV Diltiazem) is missing. I suspect availability of this telemetry information would have confirmed the diagnosis of AFlutter with 1:1 AV conduction. That said, without such monitoring — we can only presume the diagnosis is Flecainide-induced AFlutter with 1:1 AV conduction.

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What is the Rhythm in ECG #2?

As per Dr. Meyers — administration of IV Diltiazem converts the SVT rhythm seen in ECG #1 to a supraventricular rhythm, albeit the rate is still tachycardic at ~115/minute.

• Rather than sinus rhythm — I suspect the rhythm in ECG #2 is a low atrial rhythm. That’s because we do not see an upright P wave in lead II. Although difficult to assess due to baseline artifact — positive P waves are seen in both leads I and aVL of ECG #2, and it appears that a tiny-amplitude negative P wave is seen in lead III. Clinically, this still counts as “chemical conversion” from AFlutter to an atrial mechanism — although persistence of tachycardia in ECG #2 (at a rate of ~115/minute) raises of the question of whether this could be an ectopic atrial tachycardia ... Restoration of sinus rhythm after PCI (the 4th ECG shown above in this case) resolves the issue of what the rhythm in ECG #2 might have been.
• Assuming there is no dextrocardia or lead misplacement — sinus rhythm is defined by the presence of a conducting upright P wave in lead II. Note that an upright P wave is seen in lead II of this patient’s baseline tracing, as well as in the post-intervention tracing ( = the 3rd and 4th ECGs shown above in this case).

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Final Semantic Point:

As has been emphasized — the most common ventricular rate for untreated AFlutter is ~150/minute (usual rate range ~140-160/minute). This is because under normal circumstances, there will be 2:1 AV conduction when the AV node is confronted with 300 atrial impulses/minute.

• Rather than 2:1 AV “block” — the term, 2:1 AV “conduction” is preferred. Use of the term, “block” implies pathology. Instead, it is a physiologic function of the AV node to limit the number of flutter impulses conducted to the ventricles, since perfusion will be better with a ventricular response of ~150/minute compared to 1:1 conduction with a ventricular rate of 300/minute.

Our THANKS again to Drs. Meyers and Smith for this superb discussion!