Monday, September 7, 2020

Young Man with a Heart Rate of 257. What is it and how to manage?

A 30-something was in the ED for some minor trauma when he was noted to have a fast heart rate.  He acknowledged that he had palpitations. but only when asked.  He had a history heavy alcohol use.  Blood pressure was normal (109/83).

Here is his 12-lead:
There is a wide complex tachycardia with a rate of 257, with RBBB and LPFB (right axis deviation) morphology.


The Differential Diagnosis is: 
SVT with aberrancy(#) 
      [AVNRT vs. WPW (also called AVRT*)]
      Atrial flutter with 1:1 conduction, with aberrancy
      VT coming from the anterior fascicle (fascicular VT)@


*AVRT = AV Reciprocating Tachycardia (Tachycardic loop that uses both the AV node and an accessory pathway.  Depending on whether the accessory pathway is unidirectional or bidirectional, this can go down the AV node and up the accessory pathway (orthodromic), or down the pathway and up the AV node (antidromic).

#Aberrancy means that the impulse coming from (AVNRT) or through (Orthodromic AVRT) the AV node is too rapid to allow for repolarization of all the conducting fibers.   In this case, the right bundle and the posterior fascicle are unable to repolarize, but the anterior fascicle is. The impulse goes through the (left) anterior fascicle (which is superior) and then goes from this superior left location through non-conducting fibers to the inferior and right.  Hence the latter part of the QRS is to the right and inferior (RBBB morphology and right and inferior axis).

@Read about Fascicular VT here: 

Idiopathic Ventricular Tachycardias for the EM Physician


Case Continued

He was completely stable, so adenosine was administered.

This resulted in conversion to sinus rhythm:
Sinus rhythm

Aside: Now that we know the rhythm converts with adenosine, the differential diagnosis is narrowed.  See Learning point 1 below.

Case continued

The patient reverted to tachycardia.  This confirms SVT, either AVNRT or WPW.  Right ventricular outflow tract VT also converts with adenosine, and it also has an inferior axis, but it does not have a right bundle branch block morphology

He was given adenosine again.

What do you think of this management?















Comment on management: If adenosine converts, and then the patient reverts, there is no point in going to adenosine without some other therapy to prevent reversion.  Adenosine has a very short half life.  This patient proved that he will go back into SVT after the adenosine is gone.

Management options for continuously reverting SVT are of several kinds:

1) longer acting AV node blockade (most commonly calcium channel blockers, but could be a beta blocker)
2) suppression of the PACs that initiate SVT (beta blockers, which also block the AV node)
3) Also, a type 1a antidysrhythmic (such as procainamide) to slow depolarization might work.

First: try giving 2-4 g of Magnesium, then adenosine again.
Next: try verapamil, which will convert it as well as adenosine does, but has a much longer duration of action and so will maintain sinus rhythm.
Never give verapamil to someone with poor LV function.


Dosing: 

Verapamil 
Dosed at 2.5-5 mg IV over 2 min (over 3 min in elderly patients).
A follow-up dose of 5-10 mg (0.15 mg/kg) IV is administered 15-30 min later if the SVT persists and no adverse reaction occurs. The maximum dose is 20-30 mg. may be followed by an infusion of 0.005 mg/kg/min.

Diltiazem 
Dosed at 0.25 mg/kg IV over 2 min.
A subsequent dose of 0.35 mg/kg IV is administered if no response is seen and no significant drug-induced adverse event occurs.
Infusion is 5-15 mg/hr

Other options include beta blockers.

Case continued:

Adenosine was given again and the patient converted, then reverted.
The patient was cardioverted, then reverted.
The patient was cardioverted again, then reverted.
Magnesium and procainamide were given and the patient did not revert.  

Procainamide is another reasonable solution to the problem.  It does not block the AV node but does slow phase 0 of depolarization, which will also frequently break the re-entrant cycle.  In this pediatric study, it was 71% successful and better than amiodarone.  
https://www.ahajournals.org/doi/full/10.1161/CIRCEP.109.901629

Aside on Procainamide: it also has the very theoretical benefit of not blocking the AV node if this is WPW with an anterograde conducting pathway AND the patient converts to atrial fib.  The fact that we saw no delta wave in the 12-lead is good evidence that, if there is an accessory pathway, it does not conduct in the anterograde direction.]

Follow up

Later history revealed that he had been having palpitations with rapid ventricular rate for several years, about 2 episodes per year.  These episodes start with sudden onset tachycardia.  He is uncertain whether his rhythm is regular or not and he is uncertain about the rate but thinks it's "extremely fast and it is like the heart is beating in my neck". 
Most of the times he thought that these were panic attacks and he was trying to just relax for the episodes to go away.  They usually lasted anywhere between 1-2 hours.

The patient was found to have a "concealed" posteroseptal pathway (WPW without delta waves) confirmed to have SVT at EP study and was ablated.

Here is the Electrophysilogist's note:


"Only 1 pathway attachment could be ablated, the second one deep within the CS could not be ablated with high power.  Sustained SVT could not be induced after that."

"Due to some difficulty maneuvering the catheters, and with accessory pathway being noted on the EP study, it would be important to rule out any structural abnormalities that could be associated with accessory pathway like Ebstein's anomaly.  I have ordered an echocardiogram which will be done today, after that patient can be discharged to home with follow-up in 2 to 3 months." 

The echo was normal.


Learning points

1. In this regular wide complex tachycardia, since the rhythm converted w adenosine, it is almost certainly SVT w aberrancy, which can be either: 
            A. AVNRT w aberrancy, or 
            B. Orthodromic AV Reciprocating Tachycardia (WPW), also with aberrancy

You might also consider these, but they don't fit: 

     B. Antidromic AV Reciprocating Tachycardia (WPW) -- very unlikely given the morphology  
     C. RV outflow tract tachycardia (but this will have LBBB morphology -- so it is not RVOT)

2. If the rhythm converts and then reverts to tachycardia with either adenosine or electricity, Neither one of those modalities should be attempted until some longer acting pharmacological solution is given.

3.  WPW does not always have delta waves on the baseline ECG. This is called "Concealed conduction".  It may happen because the accessory pathway can only conduct in a retrograde direction (hence, orthodromic SVT).  It can also happen if the accessory pathway is so far away from the sinus node that the impulse goes through the AV node before it can pre-excite the bypass tract.

4.  Many people experience SVT as a "Panic Attack." (see below: SVT misdiagnosed as panic disorder)

5.  The AV node in young people can sometimes conduct at extremely fast rates.  In this case, it was able to conduct at a rate of 257 (down the AV node, then up the bypass tract)

6.  These tachydysrhythmias are so fast that they can degenerate into ventricular fibrillation. Admission and referral to electrophysiology is always indicated.


SVT misdiagnosed as panic disorder
Lessmeier TJ, Gamperling D, Johnson-Liddon V, et al. Unrecognized paroxysmal supraventricular tachycardia. Potential for misdiagnosis as panic disorder. Arch Intern Med. 1997;157(5):537–543.
Lessmeier et al. performed a retrospective survey in 107 patients with reentrant PSVT and found that 67% had symptoms fulfilling the DSM-IV criteria for panic disorder. Only 48 (45%) patients were correctly diagnosed upon initial evaluation; 55% were undiagnosed for a mean of 3.3 y following initial presentation, including 13 patients with apparent pre-excitation on resting ECG. Physicians initially attributed symptoms to “panic, anxiety or stress” in half of these patients, with women more likely than men to have their symptoms attributed to psychiatric causes (65% vs. 32%; <.04).



===================================
MY Comment by KEN GRAUER, MD (9/7/2020):
===================================
Interesting case with thorough discussion by Dr. Smith on arrhythmia management. As a result — I’ll limit my comments to a few additional points.
  • The patient in today’s case is a 30-something man admitted for minor trauma. The patient had a history of heavy alcohol use. He was mildly symptomatic with palpitations — but was felt to be completely stable at the time his initial ECG was obtained. For clarity — I have put the 2 ECGs in today’s case together in Figure-1.

Figure-1: The 2 ECGs in today’s case (See text).





Looking at ECG #1: As per Dr. Smith — the differential diagnosis of the extremely rapid SVT rhythm (at ~255/minute) seen in ECG #1, in which there is no clear sign of atrial activity — includes: i) A reentry SVT rhythm (ie, AVNRT vs orthodromic AVRT); ii) AFlutter with 1:1 AV conduction; andiii) VT.

IF the rhythm in ECG #1 was VT — it would almost certainly be a form of Idiopathic VT — since there is no indication from the history that this 30-something man has underlying ischemic heart disease. As a result — it’s worth briefly reviewing this entity of Idiopathic” VT.
  • Drs. Meyers, Smith; Weingart wrote an extensive review on Idiopathic VT in the September 14, 2018 post of Dr. Smith’s ECG Blog.
  • My Comment at the bottom of this Sept. 14, 2018 post adds a series of PEARLS on “My Take” regarding this subject.
  • I’ll add here 2 more reference links on the subject — by Brugada; Diez  and — by Tondo et al.

WHAT is Idiopathic VT?
  • The vast majority of VTs are associated with underlying structural heart disease.
  • PEARL #1: It is important to remember that ~10% of patients who present with VT do not have ischemic or underlying structural heart disease — nor do they have a metabolic or electrolyte disturbance — nor do they have QTc prolongation. The importance of recognizing these patients with Idiopathic VT who have a structurally normal heart — is that the presentation, clinical course, and both short- and long-term management differ greatly compared to the ~90% of patients with the “usual” ischemic or structural forms of VT.
  • Although exceptions exist — the “good news” regarding patients who present with idiopathic VT — is that this rhythm is generally seen in an otherwise healthy, younger adult population (often <40yo). Long-term prognosis tends to be surprisingly good! Suspect an idiopathic form of VT when a younger adult without known coronary or structural heart disease develops a regular WCT (Wide-Complex Tachycardia) rhythm during exercise or other strenuous effort — and despite this, seems to tolerate the WCT rhythm surprisingly well.
  • Not all forms of idiopathic VT are predictable based on their ECG appearance (Anderson et al, 2019). That said — many of them are, which is important for management considerations since (as per Dr. Smith above) — Adenosine and/or Verapamil may be treatments of choice for idiopathic VT. In contrast, Adenosine and Verapamil are ill-advised (if not, contraindicated) for treatment of ischemic VT.

By far, the most common form of idiopathic VT are the OT VTs ( = Outflow Tract VTs). The other frequently encountered form of idiopathic VT is Fascicular VT.
  • Among the Fascicular VTs — the most common type by far (over 90% of cases) is Left Posterior Fascicular VT — in which the ECG shows a RBBB/LAHB pattern (VT exit near the posterior hemifascicle). Much less commonly there may be Left Anterior Fascicular VT (RBBB/LPHB pattern) — and rarely Septal Fascicular VT (RBBB with a normal axis).
  • Among the OT VTs — Most attention is given to RVOT VT (Right-Ventricular Outflow Tract VT) — because RVOT VT makes up ~80-90% of all OT VTs.
  • But in ~10-20% of cases — there may be LVOT VT (Left-Ventricular Outflow Tract VT). This is important to appreciate, because initial management of OT VTs (ie, Adenosine, Verapamil) is similar for RVOT and LVOT VT — but ECG recognition of RVOT and LVOT is different!
  • RVOT VT is usually fairly easy to recognize on ECG — because chest leads show a LBBB pattern, with an inferior axis in the limb leads (ie, much greater positivity of the QRS complex in inferior leads compared to lead I).
  • LVOT VT may be more challenging to recognize on ECG. You may also see a LBBB pattern in the chest leads with LVOT VT (as well as the inferior axis in limb leads). Although many complicated variations in QRS morphology are possible (that extend way beyond our scope! — Anderson et al, 2019) — the chest lead LBBB pattern characteristic of LVOT (as distinguished from RVOT) — is that transition tends to occur earlier (ie, by V1-V2 for LVOT vs after V3 or V4 for RVOT).
  • The other reason recognition of LVOT VT is so challenging — is that it sometimes presents with a RBBB pattern in the chest leads (in the form of wide, prominent R waves in leads V1,V2) + the inferior axis in limb leads. This could resemble the Left Anterior form of Fascicular VT.

BOTTOM Line SIMPLIFICATION: Initial use of Adenosine for treatment of a previously healthy, hemodynamically stable patient who presents with presumed idiopathic VT is completely appropriate, and a treatment of choice. Adenosine is especially likely to work IF the patient has an OT VT (ie, either RVOT or LVOT). That said, the clinical reality is — that you will not always be able to recognize all forms of idiopathic VT that are likely to be Adenosine-responsive based on ECG appearance.
  • IV Verapamil (or Diltiazem) is an effective, alternative treatment for idiopathic VT. And, IF you know that the WCT rhythm is indeed Fascicular VT — then IV Verapamil is the drug of choice.
  • Be aware that there are case reports of Adenosine working for Fascicular VT. That said — most of the time Adenosine won’t work for this rhythm (Reviriego) — which is why IF you knew the WCT rhythm was Fascicular VT, then you might decide not to start treatment with Adenosine.
  • KEY Point: Do not use Adenosine or Verapamil/Diltiazem if you know that the WCT rhythm is ischemic VT. These drugs are not effective for this indication — and, risk of adverse effects significantly increases (with real risk of deterioration to VFib if Verapamil/Diltiazem is used to treat ischemic VT).





PEARL #2 — Did YOU see the Electrical Alternans in ECG #1? The fascinating but uncommon phenomenon of electrical alternans is frequently misunderstood — and, it is often overlooked when it does occur. Electrical alternans can be subtle.
  • Although most commonly associated with pericardial tamponade — electrical alternans has also been associated with an expanding array of other clinical conditions.
  • In its simplest form — electrical alternans is a beat-to-beat variation in any one or more parts of the ECG recording. It may occur with every-other-beat  or with some other recurring ratio (3:1; 4:1; etc.). Amplitude or direction of the P wave, QRS complex, ST segment and/or T wave may all be affected. Alternating interval duration (of PR, QRS or QT intervals) may also be seen.
  • NOTE: There are 3 of the 12 leads in ECG #1 that show clear evidence of electrical alternans. To facilitate identifying this — I have enclosed these 3 leads within a RED rectangle in Figure-2. Isn’t the every-other-beat alternation of R wave amplitude now obvious in leads V3V4 and V5? More subtle, but still readily identifiable — is the every-other-beat alternation in T wave amplitude seen in leads V3 and V4 in Figure-2.
  • In addition to pericardial tamponade — one of the most helpful insights that recognition of electrical alternans provides, is that it suggests a reentry mechanism for a regular SVT rhythm. In this setting — QRS alternans during a regular SVT rhythm (as we see in Figure-2) often indicates retrograde conduction over an AP (Accessory Pathway). That said — because QRS alternans can occasionally also be seen with simple AVNRT (in which the reentry pathway is contained entirely within the AV node) — recognizing this form of electrical alternans does not prove the existence of a participating AP — but it is suggestive. (And, a reentry SVT with a participating AP was found in today’s case!).

BOTTOM Line SIMPLIFICATION: Even if recognizing electrical alternans in a regular SVT does not prove the existence of a participating AP — knowing that the mechanism of this SVT is almost certain to be reentry may help in clinical decision-making regarding optimal management. In Today’s Case — recognition of electrical alternans provides yet one more reason in support of initially trying Adenosine.
  • NOTE #1: Although not common — Be aware that electrical alternans may occasionally be seen with monomorphic VT.
  • NOTE #2: Among the list of other Clinical Conditions in which electrical alternans has been described include the following: — long QT syndrome — severe electrolyte disturbance (low Ca++; low K+/Mg++) — alcoholic or hypertrophic cardiomyopathy — acute PE — subarachnoid hemorrhage — cardiac arrest or the post-resuscitation period — and various forms of ischemia (spontaneous or induced by exercise; severe LV dysfunction).
  • NOTE #3: In the context of a long QTc or ischemia — the finding of ST segment and/or T wave alternans may predict the occurrence of malignant ventricular arrhythmias.
  • For MORE on Electrical Alternans — CLICK HERE.

P.S.: The BEST way not to overlook electrical alternans — is to remember to LOOK for it whenever you have a regular narrow or wide tachycardia of uncertain etiology. Doing so may provide an important clue to the etiology of the rhythm.

Figure-2: I’ve enclosed within a RED rectangle the 3 leads in ECG #1 in which there is clear evidence of electrical alternans. (See text).






10 comments:

  1. Thank you for the great case as usual.

    My doubt is quite basic, where do you mark the end of the QRS complex so as to determine the width of the QRS. Often I find that it is difficult to clearly make out the end point of the QRS complex in tachyarrhythmia ECGs.

    I was taught to look at the widest precordial lead which had a clear beginning & end for the QRS complex. So do we have to calculate the width of the QRS till the point where the S wave touches the baseline of the ECG?

    My question is more of a general question & not specifically for this ECG. The QRS width in this case is relatively straighforward.

    Thank you once again for the excellent discussion.

    ReplyDelete
    Replies
    1. Thanks for the kind words. I have always taught others to measure intervals (PR, QRS, QT) in whichever of the 12 leads you can clearly see the onset and offset of the interval — and in which the interval looks longest. With the PR interval — lead II will usually give the “best view” when the rhythm is sinus. But I’ve used any of the 12 leads for measurement of the QRS and QT. I’ll often check myself — by looking at 2 or 3 leads, to make sure I’m getting a similar interval duration. The KEY with the QRS — is to be aware of how common it is for part of the QRS to lie on the baseline — and therefore giving false indication of the QRS being narrower than it really is. As we’ve shown many times on this blog — when there is a long lead simultaneously-obtained rhythm strip at the bottom of the tracing — drawing a vertical line up from that rhythm strip allows easy correlation between interval onset and offset in the various other leads. Final CAVEAT — In my experience, bedside monitors/defibrillators often are “off” (either over- or under-measuring QRS width) — so whenever possible when treating at the bedside a patient in a tachyarrhythmia — I like to obtain a hard-copy recording of the rhythm in order to be more certain if I’m dealing with a wide or narrow QRS tachycardia. And YES — I like the S to cross the baseline (but a picture is worth 1,000 words in this determination — :)

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  2. A Great case. So much to learn! . I do recognize I had not seen the electrical alternance, so I am very grateful for Dr Grauer´s pearl #2. THANKS to you and Dr Smith. We do not have procainamide, nor adenosine. We get amiodarone and have seen it used in patients that have AVNT or AVRT so as to avoid recurrence of arrhythmia while EPs can see them. Is there a niche for its use in this cases?

    H Muñoz, MD Caracas, Venezuela.

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    Replies
    1. @ Hector — THANKS so much for your nice words! Different medications are available in different parts of the world. I’ve often thought that much of “preferred antiarrhythmic therapy” depends on the experiences and comfort level of the provider at the bedside. Amiodarone has potential advantages that include: i) familiarity by many providers and ease of administration protocol; ii) ability to use in patients with heart failure; iii) low incidence of Torsades (even though the QT may lengthen with use of this drug); and iv) efficacy in treating WCT rhythms (may convert VT as well as various SVTs including WPW with very rapid AFib). As with any medication given for a tachyarrhythmia — adverse effects can occur, so the provider needs to be ready to cardiovert as needed if things don’t go as planned. So although I would have preferred starting with Adenosine in today’s case — one uses what is available, and Amiodarone might be effective.

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  3. Great post and explanation. I LOVE it. I would like to write some words about the ECG#1 and some questions. I like to use your 5 key parameters in any arrhythmia, watch your Ps, QS and the 3 Rs. This approach is useful for me. Anyway, there appears to be slight STD in a number of leads on this tracing, because tachycardia which is a common cause of STD, isn't correct?AND I really want to know how can I distinguish the different tachycardia( Sinus Tachycardia, Reentry SVT, Atrial Tachycardia and Atrial Flutter) based on rate? Thanks a lot, my teachers!
    Anderson Santos from Brazil.

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    Replies
    1. Oi Anderson! Obrigado (thanks) for the nice words — and I’m glad you like my, “Ps, Qs & 3R Approach” for systematic arrhythmia interpretation. YES — there most definitely is ST depression in many leads in ECG #1 — but this is common with tachycardia — and especially given the excessively rapid rate here — I would ignore the ST depression, and focus instead on treating the arrhythmia. As we can see in ECG #2 — the ST depression has resolved after conversion to sinus rhythm with return to a normal heart rate.

      As to distinguishing the various forms of SVT (supraventricular tachycardia) by heart rate — NOTHING is perfect. Different authors cite different limits. The guidelines I generally go by suggest that in adults (rates are different in children!) — in adults the atrial rate of “untreated” ( = NO meds) AFlutter is generally ~300/minute, with a range between ~250-350/minute. Since the most common conduction ratio in AFlutter is 2:1 — this means the usual ventricular rate in untreated AFlutter is ~150/minute (usual range ~140-160/minute). All bets are off if the patient is on an antiarrhythmic medication — which may slow the atrial rate. 1:1 AV conduction with AFlutter is unusal unless the patient has WPW — and in the case of AFlutter with WPW, conduction preferentially goes down the AP (Accessory Pathway) — so the QRS will be wide. So it is possible for AFlutter to conduct 1:1 in anyone … (even if they don’t have WPW and are not on antiarrhythmic meds) — but this is rare.

      Common limits for ectopic ATach tend to be ~240/minute in adults. This might attain ~260/minute for the Reentry SVTs, though usually AVNRT and AVRT do not go this fast. The rate of 257/minute in today’s AVRT case is “within the range”, though clearly faster than is usually seen.

      As to sinus tachycardia — in a “supine” adult (ie, an adult who has not just finished exercising) — the rate usually does not exceed ~160-170/minute. That said — you CAN have exceptions to this if there is a “sympathetic surge” for whatever reason — and sinus tach can on occasion in a younger, healthy adult with sympathetic surge reach ~200/minute (thought this is rare). However, children (depending on age) can have sinus tach at such faster rates.

      When doing stress testing — we use a formula to predict “maximal exercise sinus tach heart rate” = 220 - Age. Therefore, under normal circumstance, for a 50yo — the theoretical maximal exercise rate = 220 - 50 ~170/minute.

      BOTTOM LINE: Exceptions exist. The above are just general “rate guidelines” — but I never use heart rate as the sole determinant of an arrhythmia. Hope that helps! — :)

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  4. 257 BPM and he is stable for more than 1 hour? How?

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    Replies
    1. I wasn’t there — so I can only comment from my computer … IF I’m reading this case correctly — the amount of time the patient was in AVRT at 257/minute in today’s case was not documented. The patient merely described episodes which “usually lasted between 1-2 hours” — but as we know, unless these are timed by clock and a heart rate this fast is documented for that amount of time — we just do not know for certain … (ie, patient estimation of time when not based on looking at the clock is subject to much error).

      That said — the patient in today’s case is young (30-something) — and presumably has a normal heart and well-functioning AV node + some excess sympathetic tone from his trauma. Some patients (amazingly) tolerate exceedingly fast heart rates for surprisingly long periods of time. I’ve seen this with rapid AFib in WPW — in which you wouldn’t think that fast a rhythm could be tolerated for so long. So it IS possible to tolerate a reentry SVT at 260/minute for a surprising amount of time. Clearly if you were in the ED with this patient — you would not want to wait this long to cardiovert if initial trial of medication was ineffective.

      As a corollary — I’ll comment on the surprisingly long duration that certain sustained VTs can maintain. Cases of VT have been documented, in which the patient remained alert and stable literally for DAYS — not at a rate of 250/minute, but nevertheless in a fast VT. Bottom Line — “Ya gotta be there” — And you have to be ready to immediately cardiovert when there is any question of hemodynamic instability — but some adult patients CAN tolerate exceedingly fast tachyarrhythmias for surprisingly long periods of time.

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  5. thank you so much for your great explanation , very instructive
    is the negative deflection in II a retrograde conducted p wave and would this allow or support the diagnosis of AVRT ?
    thank you for your comment
    Christian

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    Replies
    1. @ Christian — Excellent question you ask! — though I don’t have a definitive answer. As you indicate — retrograde P waves generally manifest as a negative deflection in the inferior leads, and as a positive deflection in right-sided leads like aVR and V1. The problem in ECG #1 — is that the heart rate is so very fast (!) at ~255/minute — so this leaves me uncertain as to the meaning of the “extra deflections” that I see. There is a terminal S wave (seen at the very end of the QRS) in lead II — but I also see an terminal s wave (albeit smaller) in ECG #2 in lead II after Adenosine converted the rhythm. So this negative deflection is not a “new” deflection seen only during the SVT rhythm (as it should be if it represented retrograde atrial activity). Then in lead II during ECG #1 (at ~255/minute) — the ST segment also has a “negative dip” that I do not see in ECG #2 (after conversion to sinus) — but this “negative dip” looks wider than I’d expect if it was a retrograde P wave, and I suspect it is just ST segment depression. The overly fast rate in my opinion just makes it difficult to be sure of what the deflections mean. In theory — when there is orthodromic AVRT, then retrograde atrial activity due to AVRT (in which the reentry circuit lies OUTSIDE of the AV node, therefore taking longer to complete than for AVNRT in which the circuit is entirely contained WITHIN the AV node) — so with AVRT, there should be a relatively longer RP’ interval, which is another reason why that negative deflection at the end of the QRS complex in lead II of ECG #1 is unlikely to represent a retrograde P wave. I hope the above makes sense — :)

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