Saturday, November 30, 2019

Severe shock, obtunded, and a diagnostic prehospital ECG. Also: How did this happen?

A middle-aged woman was found down in her apartment unconscious. She was in shock with thready pulses.

A prehospital ECG was recorded:
Limb leads:

Precordial Leads
What is the therapy?

This is pathognomonic of hyperkalemia (I suppose it could be due to a massive overdose of a sodium channel blocking drug, maybe).

Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? 
---I don't think that it is possible to say for certain, and it does not matter.  The rate is not fast enough to be causing shock, so if it is VT, the priority is still to treat hyperK and secondarily to cardiovert.

The patient should receive immediate IV calcium (and also treatment to shift the potassium into the cells).

The medics did not recognize hyperkalemia. They thought it was VT, but did not shock.  They later told me that even if they had diagnosed hyperK, the only calcium they have is Calcium chloride, not gluconate.   ....However, it is perfectly fine to give Calcium chloride!!  Just have a reliable IV so that it will not extravasate.  The morbidity of extravasated CaCl is minimal compared to the mortality of life threatening hyperkalemia.  Important: It takes 3 grams of calcium gluconate to equal the amount of calcium in 1 gram of Ca Cl. 

They transported to the ED.  On arrival, the patient was in shock, was intubated, and had an immediate cardiac ultrasound.

What does a heart look like on ultrasound when the EKG looks like that?

Here you go:

It's not the world's greatest cardiac ultrasound video, but it does appear to show poor function and low volume.

She was treated with:

5 g Ca gluconate, 100 mEq bicarb, 7.5 mg nebulized albuterol, 160 mg furosemide, 10 units insulin,
50 mL 50% dextrose.

The K returned at 7.4 mEq/L.

The followup ECG is here:
Now the QRS is only slightly prolonged. There is some ST depression and peaked T-waves.

The history, obtained subsequently, is interesting:

The patient had been seen at an outside ED 2 days prior and the K was 2.5 mEq/L and a creatinine 1.5 mg/dL.  Hospital admission had been recommended, but she left that ED against medical advice.

At that discharge, she was prescribed KCl 40 mEq tabs to take 3 times daily.  She had home health nurse visits, and a BMP was sent the next day (the day prior to admission, presumably after 120 mEq of KCl replacement -- if she was taking as directed).  At that time, her potassium had risen to 4.7 mEq/L. 

Apparently, her prescription was for yet more doses, so by the next day she was dangerously hyperkalemic.

This patient weighed only 51 kg.

Comment on this K replacement

A 70 kg patient with a K of 2.5 is probably in a deficit of at least 200 mEq, but one at a weight of 50 kg is in a significantly lower deficit.

This brings up the topic of how much K to give someone who is dangerously hypokalemic.

I address K replenishment is a couple posts and repost that commentary below.

Here are other posts on hyperK, large calcium doses for hyperK, and ventricular tachycardia in hyperK

Weakness, prolonged PR interval, wide complex, ventricular tachycardia

Very Wide and Very Fast, What is it? How would you treat?

This patient with VT in the context of hyperK required both defibrillation and 13 g of Calcium Chloride (CaCl):

A middle aged man with unwitnessed cardiac arrest

See this amazing case in which hyperK was not initially diagnosed:

This shows on serial ECGs the effect of Calcium:

Replenishing K in hypokalemia

This comes from this post:
Could the dysrhythmias have been prevented?

I could find very little literature on the treatment of severe life-threatening hypokalemia.  There is particularly little on how to treat when the K is less than 2, and/or in the presence of acute MI.  Here are the American Heart Association Guidelines: 

Part 10.1: Life-Threatening Electrolyte Abnormalities

Treatment of Hypokalemia

"The treatment of hypokalemia consists of minimizing further potassium loss and providing potassium replacement.  IV administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of less than 2.5 mEq/L).  Gradual correction of hypokalemia is preferable to rapid correction unless the patient is clinically unstable.

"Administration of potassium may be empirical in emergent conditions.  When indicated, the maximum amount of IV potassium replacement should be 10 to 20 mEq/h with continuous ECG monitoring during infustion  A more concentrated solution of potassium may be infused if a central line is used, but the tip of the catheter used for the infusion should not extend into the right atrium.

"If cardiac arrest from hypokalemia is imminent (i.e., malignant ventricular arrhythmias are present), rapid replacement of potassium is required.  Give an initial infusion of 10 mEq IV over 5 minutes; repeat once if needed.  Document in the patient's chart that rapid infusion is intentional in response to life-threatening hypokalemia."

This last section is appropriate for this case.  Everyone is appropriately worried about giving K too fast.  How much does rapid infustion increase the K?  There is, again, little empirical data on this topic that I can find (see 2 studies below, which do not really answer the question).  Perhaps there are studies in animals that I have not found?  
Total Body Potassium: a 70 kg person has about 7500 mEq of total body K, but the extracellular fluid has only about 48 mEq!   Of course the difficulty with K replenishment is that the total body stores may be depleted by far more than can possibly be quickly repleted.  The estimated deficit associated with a serum decrease from 4.0 to 3.0 mEq/L is 100-200 mEq of total body K, and from 3.0 to 2.0, the associated loss is double, at 200-400 mEq.* [Sterns RH, et al. Internal potassium balance and the control of the plasma potassium concentration. Medicine (Baltimore) 1981;60:339-54].  

But 100 mEq given all at once would raise the serum K by 30 mEq/L (and be immediately fatal)!!

*The NEJM review referenced below (and ACLS, for what that is worth), states that, on average, in a "typical" 70 kg person, the serum K falls by 0.3 mEq/L for every 100 mEq total body deficit.  However, this review references the Sterns article above, which by my reading does not state this.

Here are some calculations for a safe rapid dose:
A 70 kg person has about 5 liters of blood, and 3 liters are serum (2 liters are RBCs).  If 10 mEq is given very rapidly, leaving no time for intracellular shift, then it will raise serum K by about 3.3 mEq/L.  If the patient is at 1.8, that will raise it to 5.1 mEq/L.  One need only get the K above 3.0 to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 mEq/L).  5 mEq rapid bolus would raise this patient's K from by 1.6, from 1.8 to 3.4 mEq/L.   The difficulty is in estimating the ongoing shift.  As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly.  Thus, it is critical  in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed.

In the case presented, it is not clear to me that the 10 mEq of K was given rapidly.  I suspect it was set to go over 1 hours on a pump, which is the usual practice.  It would be difficult to get a nurse to give it faster!  However, in this case, it would be appropriate to give it over 5-10 minutes, with monitoring, then immediately measure the K again and be ready to give more.

Further complicating the issue is that severe hypokalemia can result in rhabdomyolysis and subsequent K release, with resulting hyperkalemia!
Here is another post on hypoK: 

Patient with severe DKA, look at the ECG

In this post, I discussed another patient I took care of: 

Prehospital Cardiac Arrest due to Hypokalemia

I recently had a case of prehospital cardiac arrest that turned out to be due to hypokalemia.
We could not resuscitate her, but we did have excellent perfusion with LUCAS CPR, such that pulse oximetry had excellent waveform and 100% saturations, end tidal CO2 was 35, and cerebral perfusion monitoring was near normal throughout the attempted resuscitation.  This was before we started doing ECMO for refractory V Fib.

During the resuscitation, I ordered 10 mEq KCl push, but the patient received 40 mEq of KCl, push (far more than recommended)  The resident had ordered 40 mEq and that is what the nurses heard.

Is 40 mEq too much? Or the right amount?

Contrary to my expectations, after pushing 40 mEq, the K only went up to 4.2 mEq/L.

What is the right amount of K to push in life-threatening hypoK?
In a 70 kg person, there are 5 liters of blood and 3 liters of serum.  Since it takes some time (how long?) for K to shift out of the intravascular space into the interstitial space and then into the intracellular space, 3.0 mEq of K pushed fast and circulated theoretically would raise serum K immediately by 1.0 mEq/L, and 10 mEq would increase it by 3.3 mEq/L, from 1.9 to 5.2.   Thus, 40 mEq should raise it by 13 mEq/L!! 

But this is before redistribution to the interstitial space.

As I indicated above, in our cardiac arrest case, after pushing 40 mEq, the K only went up to 4.2 mEq/L.   
There are about 13 liters of extracellular fluid in a 70 kg person (10 liters interstitial fluid + 3 liters serum).  So if K redistributes very quickly to this extracellular space, then 40 mEq is appropriate.

The difficulty is in estimating the ongoing shift.  As you infuse K, it will start to shift into depleted cells and the serum K will fall again rapidly.  Thus, it is critical in patients like this to repeatedly and rapidly, after each bolus, measure the K, and supplement as needed.

Friday, November 29, 2019

Coronary Disease and Chest pain: Is it acute inferior OMI or old inferior MI?

An elderly woman with a h/o myocardial infarction presented with 2 hours of burning substernal chest pain.

Here is her ECG:

Is there an OMI?
What is the best next strategy to assess for OMI?

ECG description:

There is sinus rhythm.  There are well-formed Q-waves in inferior leads, with some minimal ST Elevation, and reciprocal ST depression in aVL.  The STE with STD in aVL is typical of inferior OMI, right?

Except for the well-formed Q-waves, which suggest an old inferior MI.

There is also an early R/S transition in precordial leads, with a large R-wave in V2.  This suggests previous posterior MI as well.  (Bayes de Luna would say "lateral MI")

There are also Q-waves (qR-waves) in V3-V6 of old anterior MI.

This ECG is classic for old inferior MI with persistent ST elevation.  Why? Because of very well formed Q-waves, and h/o MI.

Differentiate acute inferior MI from old inferior MI
There is no very good way to differentiate inferior acute OMI with Q-waves from old inferior MI with persistent ST Elevation.  They can look remarkably similar, and so looking for old ECGs and other historical information is key.

On the other hand, anterior aneurysm (persistent STE after old MI) can be fairly reliably distinguished by the T/QRS ratio.
See this case: 

Subtle Anterior STEMI Superimposed on Anterior LV Aneurysm Morphology

And many more: 

So what is the Plan?? 

Look for an old ECG and previous echocardiogram.

Indeed, previous ECGs looked the same and the patient had inferoposterior akinesis on previous echo.

The pain resolved on its own and the patient ruled out for MI by troponin.

It is still possible that the patient had unstable angina.  However, the point is that if she did have acute ischemia, it is not manifesting on the ECG.  Only old infarction is manifesting.

Anyone with coronary disease and substernal chest pain, even with a normal ECG, has a high likelihood of ACS (MI or unstable angina) and should be managed as such.

Look what happens when you do not take clinical unstable angina seriously:

Beware crescendo angina in patient with known CAD

Here is another inferoposterior true aneurysm, reprinted from my book:
Notice it looks like an acute inferoposterior OMI, except for the well formed inferior Q-waves.
There are no large R-waves in V1-V3 (which would be expected with old posterior MI).  This is because there was also an old anterior MI with anterior Q-waves.
This was proven on echo (diastolic dyskinesis) and the patient ruled out for MI by troponins.

Here are 3 previous posts on the topic of inferior aneurysm:

Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?

MY Comment by KEN GRAUER, MD (11/29/2019):
Straightforward, but very important case by Dr. Smith regarding making distinction between acute vs old infarction. This task was especially challenging in this case — because this elderly woman with a history of prior MI presented with new-onset (began 2 hours earlier) substernal chest pain. I’ll add the following thoughts to commentary by Dr. Smith.
  • For clarity — I’ve reproduced and labeled the ECG in this case in Figure-1.

Figure-1: The initial ED ECG in this case (See text).

My Thoughts on ECG #1:
  • Dating an infarction by ECG is an imperfect science — with heavy dependence on History (ie, When did your chest pain begin?” ). That said — not all patients with acute MI have chest pain — and even when they do, there is often not a reliable history as to when the symptoms began. And then, many patients who present with chest discomfort — end up not having acute infarction ...
  • Realistically, often the “best” we can do from interpreting an ECG is to say that ECG changes look ACUTE” (ie, just happened, or probably happened no more than a few hours earlier) — vs OLD” (happened at some point in the past = more than a few days ago, up until months or years previously) — vs SUBACUTE” or "RECENT" (ie, happened at some point in time between our definition of “acute” or “old” ). That said, there is an additional category — which is, that there may have been prior infarction and then superimposed on an old MI, is a new acute event. That is the situation suggested by the ECG in this case.
  • Independent of this patient's history — We KNOW there has been previous inferior MI in ECG #1. Not only are each of the inferior Q waves deep (especially considering the modest height of R waves in these leads— but in addition, these Q waves are wide (especially in leads III and aVF) — and, there is marked fragmentation (notching) in each of these 3 inferior leads. While any of these 3 features alone (ie, increased depth of Q waves — or — increased width of Q waves — or — definite fragmentation of the QRS), if seen in one or more of the 3 inferior leads, increases the likelihood that inferior Q waves represent prior infarction — seeing all 3 of these features in each of the 3 inferior leads (as we do in this case) — makes it a virtual certainty that there has been prior inferior MI.
  • There are Q waves in leads V3-thru-V6 (Be sure you note that the initial deflection in lead V3 is a small-but-definitely-present q wave). These Q waves in the anterolateral chest leads are not normal because: i) Depth of the Q wave in lead V6 is clearly disproportionately deeper-than-should-be-expected for a “normal septal q wave”, especially given the modest R wave amplitude in this lead; ii) While possible for “normal septal q waves” to extend as far over as lead V4 — they should not be seen in lead V3 — especially given the relatively tall R wave that we see in lead V3; andiii) There is marked fragmentation of the QRS complex in leads V4, V5 and V6. These points taken together suggest that the precordial Q waves we see in leads V4-V6 are the result of prior lateral (or antero-lateral) infarction.
  • As per Dr. Smith, the finding of early transition (ie, R=S already by lead V2, with persistence of surprisingly tall R wave amplitude in neighboring lead V3) strongly suggests prior posterior MI, especially given the virtual certainty of prior inferior MI (ie, there is usually a common blood supply to the inferior and posterior walls).

Findings in ECG #1 that suggest an acute event may be occurring include:
  • Slight-but-real ST elevation in the inferior and lateral precordial leads.
  • Extra peaking (almost pointed) T waves in each of the 3 inferior leads.
  • Mirror-image oppositely directed T wave inversion in lead aVL (with lead I also showing a smaller amount of similarly-shaped T wave inversion).

On the other hand — ECG findings suggesting that ECG #1 does not represent an ongoing acute event include:
  • Well-established Q waves in the inferior and lateral precordial leads, in association with marked fragmentation in multiple QRS complexes (ie, fragmentation is often a longterm sign that indicates infarction or scarring has occurred at some point in the past).
  • Distinct straightening of the ST segment (prior to the onset of the T wave) that is seen in multiple leads (See straightened horizontal, or almost horizontal RED lines in ECG #1).
  • Lack of ST segment depression in those leads with T wave inversion (which are leads I and aVL).
  • Lack of any ST depression at all in leads V1, V2 and V3 (ST depression in at least 2 of these leads is almost invariably present when posterior infarction is recent).

BOTTOM LINE: I would have guessed that the findings in ECG #1 were not acute — but as per Dr. Smith, I was not at all certain. The inferior lead T wave peaking (with oppositely-directed T wave inversion in lead aVL) could have been an acute change superimposed on prior inferior MI ...
  • Finding a prior ECG on this patient, as well as a prior Echo report turned out to be invaluable for confirming that ECG #1 showed no acute changes.
  • FINAL POINT: Ideally, you will be able to find not only a prior ECG on your patient — but also enough clinical information to ensure that the previous ECG you located reflects a true “baseline” tracing (and that this previous ECG was not obtained at the time of a prior recurrence of an acute event)!

Our THANKS to Dr. Smith for presenting this case!

Wednesday, November 27, 2019

A 50-something Australian with sudden severe epigastric and chest pain presented looking extremely ill.

A 50-something with sudden severe epigastric and chest pain presented looking extremely ill.

Here is her ECG:
What do you think?

There is ST Elevation in V2-V6, worrisome for ischemia.

Or is it?

Notice the very large R-waves and the very prominent J-point notching, with small S-waves.

This is typical of Benign T-wave Inversion, which is commonly seen in black patients of African heritage.

This case was sent from Australia and the patient was aboriginal.   I have never heard of or seen benign T-wave inversion in Australian aboriginal blacks.

The cath lab was activated and the patient was taken for angiogram, which was normal.

The lipase returned at 16,000.  The patient had pancreatitis.

One other tip: Pancreatitis often causes chest pain, but usually has severe epigastric tenderness; acute MI, though it may cause epigastric pain, usually does not have severe epigastric tenderness.

If the patient did have severe tenderness, and you recognize this benign pattern on the ECG, then you would be dissuaded from activating the cath lab.

If there was no other etiology of pain found, and you are not certain about the ECG, it is of course not wrong to activate the cath lab.

In either pathology, the patient may appear very ill.

The link above has 11 cases, one of which is this one (if you only want to read one):

15 yo AAM with ST Elevation and T-wave Inversion. Hypertrophic Cardiomyopathy or Normal ("Variant")?

MY Comment by KEN GRAUER, MD (11/28/2019):
Interesting case, that at least in part reflects a repolarization variant — since acute cardiac catheterization was done, and was found to be normal. That said — I’ll offer a somewhat different perspective on this case, in that I’m not entirely convinced ( = my opinion) that all ECG findings are solely the result of a repolarization pattern.
  • For clarity — I’ve reproduced and labeled the ECG in Figure-1.
Figure-1: The ECG in this case (See text).

The patient in this case was a 50-something black aboriginal woman, who presented with sudden severe epigastric and chest pain. She looked extremely ill, and was found to have a markedly increased serum lipase consistent with acute pancreatitis.

As per Dr. Smith — ECG findings of concern in Figure-1 for a possible acute cardiac event include:
  • ST segment coving with slight elevation in the chest leads.
  • Fairly deep and symmetric T wave inversion in multiple leads.

On the other hand — ECG findings suggestive of a repolarization variant include:
  • Prominent J-point notching — which is especially marked in lead V3, and also well seen in lead V2 (PURPLE arrows in Figure-1).
  • A typical upsloping shape to the ST segments in leads V2 and V3, leading to T wave inversion — in a pattern similar to a number of the repolarization variants shown in the link provided by Dr. Smith at the end of his comment.

Additional ECG findings against this being acute OMI include:
  • Voltage for LVH in lead aVL (that clearly surpasses the R wave amplitude criterion in this lead, which is 12 mm). Generous R wave amplitude in other chest leads. There is also T wave inversion in high lateral leads I and aVL (as well as in the lateral chest leads) — although the slowly downsloping ST depression typical of LV “strain” is lacking ...
  • The unusual finding of small-but-definite q waves in 5 of the 6 chest leads (BLUE arrows). Most of the time when small q waves of similar size are seen across multiple chest leads (as in Figure-1) — it is not the result of infarction.
  • PEARL: Awareness of the fact that diffuse ST-T wave abnormalities are surprisingly common with cases of severe acute pancreatitis (See HERE).

MTHOUGHTS: This is clearly a difficult case — and I completely agree with Dr. Smith that the providers cannot be faulted for activating the cath lab. I thought the ECG findings in Figure-1 were most likely the result of a combination of factors:
  • I suspect this patient has J-point notching and a component of ST-T wave abnormalities consistent with benign T wave inversion in black patients of African heritage.
  • In Addition — this ECG suggests LVH (marked increase in QRS amplitude in lead aVL in a 50-something black patient). At least some of the lateral T wave inversion we see may be the result of LV “strain”.
  • To me — the ST segments (before they transition to T wave inversion) — just look “different” from most repolarization variants I’m used to seeing, in that the ST segment is not as coved, and not as upsloping.
  • MTHEORY  I think this patient has LVH + a component of non-ischemic T wave inversion as a result of her severe acute case of pancreatitis (which is known to cause ST-T wave abnormalities) — both of which are superimposed on top of a baseline repolarization variant.
  • The Way tFind Out  Without additional information — I don’t believe we can fully attribute the ECG findings in Figure-1 to a benign repolarization variant. We Need: i) more history (Is this patient hypertensive?); ii) an Echo (Is there significant LVH?); and, iii) either a baseline ECG for comparison and/or a follow-up ECG on this patient after her acute illness has resolved. Until then — the most I’d be comfortable saying is that this ECG most probably does not reflect acute OMI.

Our THANKS to Dr. Smith for presenting this interesting case!

Tuesday, November 26, 2019

Global ST depression with ST elevation in aVR - what is the cause?

Written by Pendell Meyers

An elderly patient with cardiac history presented with shortness of breath. This ECG was brought to me with concern for diffuse ST depression and STE elevation in aVR.

What is your response?

Flutter waves are simulating diffuse ST depression, and therefore there must be the reciprocal finding of apparent STE in aVR.

The ventricular rate is slightly greater than 100 bpm, with 2:1 block. This means an atrial flutter rate of 200 bpm, which is somewhat unusual unless the patient has a very large, dilated left atrium and/or antidysrhythmic medications which slow the speed of action potential conduction (typically class 1, Na channel blocking agents).

AV nodal blocking agents were given and the rhythm changed to atrial flutter with slower, variable block (strip not available unfortunately).

The patient did not have ACS. Three troponins were negative. The patient was treated for atrial flutter and did well.

Learning Point:

Atrial flutter can mimic diffuse ST depression, which always must cause reciprocal ST elevation in lead aVR. It can also mimic ST elevation, or conceal true underlying ST deviations. See these other cases for examples:

Is this inferor STEMI?

MY Comment by KEN GRAUER, MD (11/26/2019):
I will add to the Learning Points on this important Teaching Case presented by Dr. Meyers.
  • For clarity — I’ve reproduced and labeled the ECG in this case in Figure-1 (See text).
Figure-1: The 1st ECG shown in this case (See text).

POINT #1: The clinicians who initially interpreted this tracing, and voiced concern about “diffuse ST depression with ST elevation in aVR” — were not systematic in their interpretation. Instead, they jumped to assessment of ST-T waves. The 1st STEP in the systematic approach for interpreting any ECG — is to start with assessment of the rhythm — which was clearly not done.
  • In my experience, the biggest mistake (by far! ) that I see even experienced interpreters make — is the failure to LOOK FIRST at the long lead II rhythm strip at the bottom of the 12-lead tracing. It literally should take NO more than 2-3 seconds for your “educated eye” to scan this long lead II. If you do not see an upright P wave preceding each QRS complex with constant PR interval in this long lead II — then you do not have sinus rhythm.
  • The only exceptions to this rule (when the rhythm could still be sinus despite lack of an upright P wave in lead 2) — are if you have: i) lead misplacement (most commonly, mixing up the left and right arm electrodes)orii) dextrocardia. Therefore, the rhythm in Figure-1 is clearly not sinus rhythm — because the P wave in lead II is not upright (RED arrow in lead 2).
  • Bottom Line: IF you don’t begin your assessment of each and every ECG you interpret with a 2-3 second “educated look” at the long lead II rhythm strip — then you are GUARANTEED to miss a lot of non-sinus rhythms.

POINT #2: Once you have ensured that the patient is hemodynamically stable — there are 5 Parameters to assess in the Systematic Interpretation of any cardiac rhythm. These 5 parameters are easily remembered by the saying, "Watch your Ps, Qs and the 3Rs". (CLICK HERE for detailed discussion on how I apply this systematic approach to rhythm interpretation).
  • NOTE  It does not matter in what sequence you assess these 5 parameters, as long as you always assess each one. I often change the sequence I use, depending on the arrhythmia I’m looking at (ie, Start with those parameters that are easiest to identify for the particular rhythm in front of you! ).
Applying this Systematic Approach to the rhythm in Figure-1:
  • P waves (or if definite P waves are not seen ... Is there evidence of atrial activity?) — As already stated, the RED arrow in lead II shows there is no upright P wave in lead II. That said, the consistent negative deflection that precedes each QRS complex in lead II (as well as in other leads) — suggests that there is atrial activity.
  • Is the QRS complex wide or narrow? It should be apparent in Figure-1 that the QRS complex is narrow in all 12 leads. Therefore — the rhythm is supraventricular!
The Rs: iRate of the rhythm; ii) Is the rhythm Regular?andiii) If P waves (or atrial activity) is present — is this atrial activity Related to neighboring QRS complexes?
  • In Figure-1 — the ventricular Rate of the rhythm is ~110/minute (ie, as shown in lead II — the R-R interval is just under 3 large boxes in duration — so the ventricular rate is a bit faster than 300/3 ~110/minute).
  • Unfortunately — there is some curving and distortion of Figure-1. That said, the ventricular rhythm appears to be Regular.
  • Atrial activity (in the form of the negative deflection that precedes each QRS complex in each of the inferior leads) — does appear to be Related by a constant PR interval with the QRS complex that immediately follows it.

POINT #3: As I have often emphasized — the fastest and easiest way to instantly become MUCH “smarter” in rhythm interpretation — is to regularly use CALIPERS.
  • In Figure-1 — it should be easy to see IF you are using calipers, that there are 2 negative deflections for each QRS complex — and that these negative deflections are precisely regular (BLUE arrows in the long lead II rhythm strip). Thus, there is 2:1 AV conduction.
  • Further confirmation of precise 2:1 atrial activity can be seen by the regular positive deflections in leads aVR and V1 (PURPLE arrows in these leads).

POINT #4: When the ventricular rhythm is regular, and there is 2:1 AV conduction — the best way to calculate the atrial rate is to double the ventricular rate. In this case — 110/minute ( = the ventricular rateX ~220/minute for the atrial rate.
  • Therefore — By the Ps, Qs, 3R Approach, the rhythm in Figure-1 is a regular SVT (SupraVentricular Tachycardia) at ~110/minute, with 2:1 AV conduction (atrial rate ~220/minute).

POINT #5: To remember that there is a Differential Diagnosis for any regular SVT rhythm, as well as for a regular SVT rhythm with 2:1 AV conduction (CLICK HERE for My Review of a similar case on the November 12, 2019 post in Dr. Smith’s ECG Blog).
  • Since in this case, there is 2:1 AV conduction in Figure-1 — we can for practical purposes, rule out sinus tachycardia and a reentry SVT (such as AVNRT or AVRT). This essentially leaves us with distinguishing between AFlutter vs ATach (Atrial Tachycardia).
  • Untreated AFlutter in adults is most often associated with an atrial rate of ~300/minute (250-350/minute range). Since the most common conduction ratio for new AFlutter is 2:1 — the ventricular rate of untreated AFlutter is most often close to ~150/minute (ie, 300/2 ~150/min.). The KEY to these generalities regarding the rates with AFlutter, is the word “untreated”. IF this elderly patient is on any antiarrhythmic (or antihypertensive) medication that might slow the rate — then AFlutter might present with a ventricular rate that is significantly slower than 150/minute. Missing from the history of this patient is mention of what drugs this elderly patient is taking!
  • It is not always possible by ECG to distinguish between ATach vs AFlutter, especially if the rate of AFlutter is slower-than-usual (See HERE). That said — the presence of typical sawtooth” atrial activity (slanted RED lines in the latter portion of the long lead II rhythm strip) — strongly suggests that despite the slower-than-usual atrial rate, the rhythm in Figure-1 is AFlutter and not ATach.

POINT #6: A semantic point that I feel is important to make — is that the rhythm in Figure-1 is AFlutter with 2:Aconduction (and not 2:1 AV “block”).
  • Use of the term, “block” implies pathology. Instead, it is physiologic that in the presence of the very rapid atrial rates seen with flutter, that only 1 out of every 2 impulses arriving at the AV node is conducted to the ventricles.

POINT #7: Finally — I doubt there would be significant ST deviation (elevation or depresson) if the AFlutter in this case resolved. With practice — one gets pretty good at “mentally subtracting” flutter waves from the ST segments — and to my eye, doing so would result in ST-T waves suggesting no acute changes in this patient.

Our THANKS to Dr. Meyers for presenting this instructive case!

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