Saturday, February 9, 2019

Right sided heart failure and tachycardia.

A middle-aged male presented with tachycardia, dyspnea, and 4+ bilateral leg edema.
What is the rhythm?

There had been an ice storm, and it was the busiest day in the history of our emergency department because of falls.  I reduced 12 fractures that evening and was in constant motion.   I looked at this and saw the negative component of the P-wave in V1, and immediately diagnosed sinus tachycardia.

I did a bedside echo:
There was good LV function
You can see a very large RV (closest to probe) and RA (on far right).
Lungs were clear to auscultation and there were no B-lines.

Volume overload was confirmed with this:
This shows the distended inferior vena cava (IVC), further supporting high right sided pressures and right heart failure.

So he clinically had right heart failure, subacute in onset.  If I had simply looked carefully through his chart, I would have found that this was not all new, but rather an exacerbation of a chronic problem.

Not having done that, pulmonary embolism was on the differential and we obtained a CT pulmonary angiogram:
This shows a massive right atrium and dilated right ventricle

Another slice of the CT showing the same thing:
A massively dilated right atrium

Later, I looked back at the first ECG; Here it is again:
It was suddenly clear to me from lead II across the bottom that this was atrial flutter.

Why is there a negative component to the atrial wave in V1?

Normally, one of the rapid ways to differentiate sinus from flutter is too look for a biphasic up-down atrial wave (sinus) vs. an upright atrial wave (flutter).

It turns out that there was a previous ECG to compare to:
This is clearly sinus, but with a mostly upright P-wave.
It is biphasic as usual, but the "up" component is (which is the right atrial component) is far larger than the subsequent negative deflection (representing the left atrium)

The answer has to do with the massive right atrial hypertrophy.  Normally, the P-wave in V1 is biphasic.  The initial upright part is the right atrium and the latter part, inverted, is the left atrium.  In this case, the right atrium is massively enlarged and results in almost all of the P-wave being upright.

Further complicating the problem, when the patient goes into atrial flutter, as with this presentation, the flutter wave has a large negative component due to the right atrial enlargement.

Thus, the atrial morphology is reversed in this patient, deceiving the physician (this physician) into believing it was sinus when it was really flutter.

And atrial flutter was the precipitating etiology of the patient's worsening right heart failure.

He required furosemide and ablation of the atrial flutter.

Formal Echo:

The estimated left ventricular ejection fraction is 50-55 %.
There is no left ventricular wall motion abnormality identified.
Mitral valve insufficiency mild.
The estimated pulmonary artery systolic pressure is 20 mmHg + RA pressure.
Right ventricular enlargement .
Paradoxical septal motion severe.
Decreased right ventricular systolic performance.
Tricuspid valve insufficiency severe.
Right atrial enlargement.
Based on the appearance of the IVC, the RA pressure is elevated.


RV function is probably worse than on the study of 2016. This is reflected
by more pronounced paradoxical septal motion, a lower PA pressure and
probably more TR.

Learning Point:

Atrial Flutter may have a mostly negative atrial wave on the ECG, mimicking sinus tachycardia, when there is marked right atrial enlargement.

Comment by KEN GRAUER, MD (2/9/2019):
Illustrative case by Dr. Smith — regarding acute arrhythmia interpretation. It’s so helpful to have clinical and echocardiographic correlation, with availability of a prior tracing for comparison. I focus my comments on the 2 ECGs shown in this case (Figure-1).

Figure-1: The initial ECG (= ECG #1at the time the patient presented to the ED, with comparison to a prior ECG (= ECG #2on this patient (See text).

ECG #1 (= the initial ECG in the ED)The approach to arrhythmia interpretation that I favor — is to: iFirst assess the patient hemodynamic status; and, iito use a Systematic Approach to Arrhythmia Interpretation.
  • The patient in this case presented in acute right-sided heart failure. That said, from what I surmise — immediate cardioversion was not needed — which meant there was at least “a moment” to better assess clinical parameters, including the cardiac rhythm.
  • I favor the following memory aid for recalling the 5 KEY parameters for arrhythmia interpretation: “Watch your Ps & Qand the 3 Rs”. Thus, we look for the presence of waves (or for sign of atrial activity if clear sinus rhythm is not present— QRS width — and the Rs (Rate and Regularity of the rhythm — and IF atrial activity is present, whether atrial activity is Related to neighboring QRS complexes).
  • PEARL #1: The reason I favor a systematic approach to rhythm interpretation (ie, NOT jumping to a single diagnosis — but first assessing each of the 5 KEY parameters cited above) — is that otherwise you risk premature fixation on a single rhythm diagnosis without considering other possibilities.
  • The 5 KEY Parameters: Although at first glance, it looks like sinus P waves may be present in ECG #1 — the PR interval in sinus mechanism rhythms usually shortens when heart rate increases — and, it looks like the PR interval for the upright deflection in lead II, as well as for the negative deflection in lead V1 is relatively longer-than-expected for a sinus mechanism rhythm in view of how fast the heart rate is. In addition, several leads (ie, all inferior leads, aVR, V5,V6) suggest that there may be 2:1 atrial-to-ventricular conduction. I was therefore not-at-all certain in my initial impression of ECG #1 that the rhythm was sinus.
  • It is difficult to accurately assess QRS duration for the rhythm in ECG #1. This is because of baseline artifact — and, as we’ll see in a minute — because of the underlying rhythm. So although I thought the QRS appeared to be at least of borderline duration (ie, ~0.11 second) — QRS morphology to me suggested a supraventricular rhythm.
  • The rhythm in ECG #1 is regular. I estimate the ventricular rate to be ~135/minute.
  • I’ll defer the 5th parameter (ie, Is atrial activity related to the QRS?) for a moment.
ASSESSMENT — What we have described in ECG #1, is that there is a Regular SVT at ~135/minute, without clear sign of sinus P waves. Recognition of a regular SVT with uncertain atrial activity should prompt the following Differential Diagnosis — iSinus Tachycardia (perhaps the deflections we see are sinus P waves after all …?); iia Reentry SVT (ie, AVNRT, AVRT); iiiAtrial Tachycardia; and, ivAtrial Flutter. Although other entities are possible (ie, SA nodal reentry tachycardia) — these 4 entities make up the overwhelming majority of regular SVTs that the emergency provider will see.
  • PEARL #2: By far (!!!) — the most commonly overlooked diagnosis in all of arrhythmias is atrial flutter. This is because flutter waves may be atypical in morphology, and because flutter waves may be hidden within the QRS complex and/or ST-T wave. In adults, the rate of flutter circulating within the atria in patients who have not yet been treated with an antiarrhythmic agent (that may slow the rate) is ~300/minute (usual range ~250-350/minute). By far, the most common conduction ratio in untreated AFlutter = 2:1. As a result, the ventricular rate in untreated AFlutter is almost always ~150/minute (within a range of ~135-165/minute). Therefore, the BEST way not-to-overlook the diagnosis of AFlutter is to always suspect it whenever you see a regular SVT with uncertain atrial activity at a rate of ~150/minute (ie, at a rate between ~135-165/minute). This is precisely the situation we have in ECG #1.
  • PEARL #3: Using CALIPERS facilitates diagnosis. The way I “look” for AFlutter — is to search all 12 leads for sign of atrial activity. We know lead II is the best lead for assessing sinus rhythm. The next best lead for assessing sinus rhythm is lead V1. When searching for possible 2:1 flutter activity — the best leads in my experience are leads II, IIIaVF; aVR; and V1. I generally look at these 5 leads first. After that — I then look at each of the remaining 7 leads for possible atrial activity. Set your calipers to precisely ONE HALF the R-R interval. Then see if there is any lead in which you can precisely walk out 2 deflections for each QRS complex.
  • In ECG #1  Lead aVF shows 2:1 deflections best (RED arrows). These deflections march out precisely with my calipers. There is a constant PR interval in front of each QRS complex. Since there are 2 deflections for each QRS — this means that the atrial rate = 135 X 2 = 270/minute. It would be rare indeed for ATach to go this fast (and neither sinus rhythm now reentry SVTs go this fast) — therefore the rhythm in ECG #1 is almost certainly AFlutter. And, if you step back a little bit from this tracing — there does appear to be a sawtooth pattern in each of the inferior leads.
  • In support that the RED arrows in ECG #1 truly indicate atrial activity — I’ve drawn in some vertical RED LINES that show similar 2:1 deflections in simultaneously-obtained lead aVR and lead II. Other leads that seem to show the same 2:1 activity include leads III, and possibly V5 and V6.
  • IF needed — one could confirm diagnosis of AFlutter with either a vagal maneuver or a “chemical” vagal maneuver (ie, use of Adenosine) — but using calipers has virtually already confirmed your diagnosis!
  • As per Dr. Smith — abrupt onset of the tachyarrhythmia, with resultant reduction in hemodynamically effective atrial contraction appears to be the reason for exacerbation of this patient’s condition. Management should focus on conversion to sinus rhythm.
  • P.S.: The vertical PURPLE lines in ECG #1 show that the prominent negative deflection before each QRS complex in lead V1 is not a sinus P wave. Instead it appears to be part of the flutter wave.

ECG #2 ( = the prior ECG on this patient)There are a number of interesting findings on this patient's baseline ECG:
  • Clear indication of sinus rhythm (ie, an upright P wave with fixed and normal PR interval in lead II ).
  • QRS widening in a pattern consistent with RBBB. Vertical BLUE lines in lead V1 of ECG #2 show QRS duration to be ~0.11-0.12 second, which is long enough to satisfy criteria for RBBB. Note the rSR’ pattern in lead V1 + wide terminal S waves in lateral leads I and V6 (within the BLUE circles) — which solidifies the diagnosis of RBBB.
  • There is RAE in ECG #2! Most often RAA is diagnosed by the finding of tall, peaked and pointed P waves in the inferior leads. On occasion however, you will only see a prominent pointed P wave in leads V1 or V2 — which given the clinical history here, is diagnostic of RAE in this case.
  • Note T wave inversion in leads V1 and V2 in ECG #2 (BLUE arrows). This could reflect RV “strain” — or — it could simple reflect commonly seen secondary ST-T wave changes in association with RBBB — or — it could represent both a reflection of RBBB + RV “strain”.
  • Now go back to ECG #1, and take another look at the QRS complex in lead V1. I suspect there was also RBBB in ECG #1, albeit much more difficult to see in ECG #1 due to the baseline artifact and flutter activity.
  • The Echo in this patient showed significant RAE and RVH. Note how difficult it is to diagnose RVH from the 2 ECGs in this case. This is common — as the ECG diagnosis of RVH is typically difficult, and often not apparent until late in the process. Signs consistent with RVH that we do see include relatively low voltage, lots of S waves, RBBB, T inversion on ECG #2 in leads V1 and V2 — and RAE. Keep in mind that there is only one condition in medicine that produces right atrial enlargement without also producing RVH ( = tricuspid stenosis) — so clear ECG diagnosis of RAE (as was done in ECG #2 by the prominent, peaked P waves in leads V1,V2) is an indirect clue that RVH is likely to be present (supported by the above noted ECG findings) — albeit definitive diagnosis of RVH required Echo.

  • Regarding "My Take" on a Systematic Approach to ECG Interpretation — CLICK HERE. For the part regarding systematic Rhythm Interpretation — Scroll down to Figure 4 on this web page, for the “First 2 Parameters = Rate & Rhythm).
  • For “My Take” on the ECG diagnosis of RVH  CLICK HERE.
  • For “My Take” on the ECG diagnosis of LAE & RAE  CLICK HERE.


  1. Doubt
    I can see notched P waves in Lead 2
    and exaggerated Negative component in V1... isn't that indicative of Left Atrial Enlargement?
    Right Atrial Enlargement would cause an exaggerated positive comp in V1.

    1. Right atrial enlargement enlarges the positive component only in sinus rhythm. Opposite in flutter. See the baseline ECG above in sinus: the positive component is indeed enlarged.

    2. Please see this blog post — — which reviews in detail "My Take" on how to diagnose RAA and LAA by ECG. It's not always straightforward, though I believe I present a practical, user-friendly approach that is easy to apply — :)

  2. HI DR GRAUER. Thank you very much for your invaluable comments and discussion.
    I wander if you have Any comment on QRS axis?, seems to be abnormal LAD during tachycardia.
    Thanks from Caracas Venezuela
    H Munoz, MD

    1. Thanks for your excellent question. YES, there clearly is a leftward axis in ECG #1 — although in ECG #2 (which was the baseline tracing), this is less marked (ie, the QRS complex in lead II of ECG #2 is not as negative as it was in ECG #1). Potential reasons are actually more complex than may at first be apparent — which is the reason I decided “not to go there” in my initial commentary. As per My Comments (above) — there is complete RBBB in ECG #2. Although more difficult to see in ECG #1 — I believe there was also RBBB in ECG #1. The concept of “axis” makes less sense in RBBB — because the DIRECTION of electrical activity goes initially L-to-R (left-to-right) due to normal septal depolarization — then R-to-L (as the LV depolarizes) — and finally L-to-R (and the RV depolarizes with delay due to the rbbb) — and HOW do you determine the “average direction” of electrical activity when depolarization vectors do a “zig-zag”? (ie, L-to-R, then R-to-L, then L-to-R)? Therefore, I’d say in ECG #1 that there is RBBB/LAHB. This raises the question as to WHY there is less left axis deviation in ECG #2? Could it be that the tachycardia was not present? Could it be that development of the hemiblock (LAHB) is new? Could it be new marked left axis deviation due to increase in RV forces (from exacerbation of right heart failure — and YES, you CAN get marked LAD on occasion as a response to severe pulmonary disease!)? — or could it be some combination of each of these? BOTTOM LINE: Yes, there an increase in LAD during tachycardia, though the specific reason for this in my opinion is not clear cut. Hope that helps to answer your question — :)

    2. Thanks again. great discussion.
      H Munoz, MD

  3. Awesome case dr. Smith. . Well i have few questions. 1)How to decide the P wave conducted to ventricles by just seeing PR interval.

    1. If there is a QRS for every P-wave (or every flutter wave, or every other flutter wave) and there is a fixed PR interval (or flutter-ventricle interval), then it is conducted.

    2. I agree completely with Answer by Dr. Smith! The interesting thing, is that with AFlutter, it is RARELY the P (flutter) wave closest to the QRS that conducts. This is because of "concealed conduction" (ie, the AV node being "bombarded" by ~300 atrial impulses/minute — so there is some delay until conduction occurs) — but recognition of a FIXED PR interval (as you can easily see in ECG #1 in my Figure-1) confirms that there IS conduction! — :)

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