ECG Blog #139 (Atrial Flutter – AV Block – Artifact – Sinus Rhythm)

The rhythm in Figure-1 was diagnosed as AFlutter (Atrial Flutter) with 4:1 AV conduction. Do you agree?

• What could be done to confirm your answer?

Figure-1: Lead II rhythm strip. Is this AFlutter? 

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Interpretation: As emphasized in ECG Blog #137 — the most common ventricular response to untreated atrial flutter is with 2:1 AV conduction. But the next most common ventricular response is with 4:1 AV conduction. At first glance, the rhythm in Figure-1 appears to be atrial flutter with this latter conduction ratio. However, close inspection reveals this is not the case!

• Use of calipers demonstrates that the small upright deflections on the baseline between QRS complexes are definitely not regular. This makes it extremely unlikely that these deflections represent flutter activity, since flutter waves (by definition) should be extremely regular.
• There is also a changing relationship between these small vertical deflections (that are seen throughout the baseline on this rhythm strip) — and neighboring QRS complexes. In contrast, with atrial flutter — there is usually a constant relationship between atrial deflections and neighboring QRS complexes. This is because with the exception of the variable conduction variant of flutter — there will usually be a readily identifiable repetitive pattern of atrial activity with respect to each QRS complex that results in a predictable conduction ratio.
• Finally, if one steps back a bit from this tracing — underlying upright (sinus) P waves can be seen to precede each QRS complex with a fixed (and normal) PR interval (red arrows in Figure-2). The fact that these sinus P waves are unaffected by the smaller, irregularly occurring upright deflections proves that these smaller pointed deflections are the result of artifact.

Figure-2: We have labeled Figure-1 by adding red arrows to highlight underlying regularly-occurring sinus P waves (See text).

Comment: The best way to prove artifact — is to go to the bedside to observe the patient as the ECG is being recorded. Tapping, scratching, coughing, shaking, shivering, seizing and tremor are but a few of the common causes of artifactual arrhythmias. The patient in this case had Parkinson’s disease, which characteristically produces a tremor at a frequency that approximates the rate of atrial flutter. Bottom Line: It is easy to be fooled by artifact. It is well to develop a healthy respect for the gamut of “real appearing” arrhythmias that artifact distortion may produce.

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For More on this Subject:

• See also ECG Blog #132 — for another example of artifact ...

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ECG Blog #138 (SVT – AV Block – Atrial Flutter – Atrial Tachycardia – Digoxin)

How would you interpret the rhythm in Figure-1? What is your differential diagnosis? Can you be sure of your answer from looking at this lead MCL-1 rhythm strip?

• Why is it important to know if this patient is on Digoxin?

Figure-1: Lead MCL1 rhythm strip. Is this AFlutter or ATach? 

Interpretation: The rhythm in Figure-1 is regular with a ventricular rate of ~115/minute. P waves outnumber QRS complexes by two to one (Figure-2) — making the atrial rate ~230/minute. The QRS complex is narrow, implying a supraventricular mechanism — and each QRS complex is preceded by a P wave with a constant PR interval. Thus P waves are related to the QRS complexes, albeit only one of every two P waves is conducted to the ventricles. Therefore, this is an SVT (SupraVentricular Tachycardia) rhythm with 2:1 AV conduction. The differential diagnosis is between AFlutter (Atrial Flutter) vs ATach (Atrial Tachycardia).

Figure-2: We have labeled Figure-1 by adding red arrows for the regular atrial activity. There are 2 P waves for each QRS complex (See text).

Diagnostic Considerations:

• In favor of AFlutter — is regular and rapid atrial activity with a peaked upward deflection in this right-sided MCL-1 monitoring lead. That said, the atrial rate of 230/minute is a bit below the usual atrial rate range for untreated atrial flutter (of 250-350/minute) — and, the expected “sawtooth” pattern of atrial flutter is missing in this lead.
• In favor of ATach — is the atrial rate (below 250/minute) and, the isoelectric baseline (rather than sawtooth) in this lead.
• Note: We are not told if this patient is taking an antiarrhythmic agent (such as flecainide, amiodarone, sotalol, etc.) that might slow the atrial rate of flutter. We are also not told if this patient is taking Digoxin. This is important because SVT with 2:1 conduction in a patient taking Digoxin should strongly suggest the possibility of digitalis toxicity. Given greatly reduced use of this drug at the current time — atrial tachycardia with block due to digitalis toxicity is no longer commonly seen — but it remains important to inquire about this medication since you may occasionally encounter patients who are still taking Digoxin.

Bottom Line: It is impossible to be certain of the rhythm diagnosis in Figure-2 from this single rhythm strip without the benefit of additional information (ie, previous clinical history; knowing what medications the patient is taking, etc.). Seeing a full 12-lead ECG might help by revealing a typical sawtooth pattern in other leads. That said, the clinical reality is that neither rate nor baseline appearance (sawtooth vs isoelectric baseline) have been shown to reliably distinguish between ATach vs AFlutter. Fortunately, from a non-cardiologist’s perspective — both initial and long-term management of these two SVT rhythms is similar (once you have ruled out the possibility of digitalis toxicity).  Initial efforts entail slowing the ventricular response, with consideration of EP = electrophysiology referral if the arrhythmia is persistent or recurs.

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Clinical Note: Assuming this patient is not on Digoxin — the terminology used to describe the arrhythmia seen in Figure-1 is far less important than the overall clinical concepts involved. This is because what used to be classified as “atrial tachycardia” in non-Digoxin toxic patients is now often referred to as an “atypical” form of AFlutter.

• Included within the broad category of “atypical” AFlutter rhythms are various types of atrial tachycardias that may arise from anywhere within the atria or neighboring pulmonary veins.
• Some atrial tachycardias may be “focal” or automatic (often recognizable by non-sinus P wave appearance — “warm up” phenomenon until the ectopic tachycardia is established — relatively slower rate — and on occasion slightly variable P-P intervals).
• Other atrial tachycardias may be much faster, perfectly regular, lack an isoelectric baseline — and be clinically indistinguishable from AFlutter based on ECG appearance. That said, since practically speaking both persistent ATach as well as persistent AFlutter are indications for EP referral — definitive diagnosis from the initial ECG is not essential.

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For More on this Subject:

• See also ECG Blog #40 — for review of a relevant SVT case.

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ECG Blog #137 (SVT – AV Block – Atrial Flutter – Atrial Tachycardia – Atrial Fibrillation)

The rhythm in Figure-1 was diagnosed as AFlutter (Atrial Flutter). Do you agree? If so — Is there anything unusual about this rhythm strip?

Figure-1: Lead MCL1 rhythm strip. Is this typical atrial flutter? NOTE — Enlarge by clicking on the Figure.

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Interpretation: Atrial flutter is characterized by a special pattern of regular atrial activity that in adults almost always occurs at a rate of 300/minute (250-to-350/minute range). The most common ventricular response to atrial flutter (by far! ) — is with 2:1 AV conduction. As a result, the ventricular rate with untreated atrial flutter will usually be close to 150/minute (ie, 300÷2) — although the ventricular rate may be slower if the patient is taking antiarrhythmic drugs.

• Less commonly with atrial flutter — there is 4:1 AV conduction (ventricular rate ~75/minute) — or a variable ventricular response.
• Odd conduction ratios (ie, 1:1: 3:1; 5:1) are possible, but extremely uncommon unless the patient is on antiarrhythmic medication or has WPW (Wolff-Parkinson-White) Syndrome.
• Atrial flutter typically manifests a sawtooth appearance that is usually best seen in the inferior leads. That said, flutter waves may sometimes be subtle and only seen in a handful of leads (if at all).
• Distinction between ATach (Atrial Tachycardia) and AFlutter may be difficult. This is especially true when the characteristic sawtooth appearance of flutter is missing, and the rate of atrial activity is at least slightly below the usual range for flutter.
• NOTE — Practically speaking, distinction between ATach and AFlutter matters little in the acute setting — since initial treatment of these 2 entities is similar (ie, use of AV nodal rate-slowing medication). There is also an area of "overlap" between atypical forms of AFlutter and ATach — for which distinction lies in the realm of the EP cardiologist.

The ventricular response in Figure-1 is regular at a rate of ~85/minute. Regular atrial activity is seen — but instead of 2 P waves for each QRS, there are 3 P waves for each QRS complex (Figure-2). Note that the PR interval preceding each QRS complex is the same! This tells us that there is conduction — in this case with a 3:1 ratio (ie, only one out of every 3 P waves seen within each R-R interval is being conducted to the ventricles).

• Since we know that there are 3 times as many P waves as QRS complexes in this example — the easiest way to accurately calculate the atrial rate is to multiply the ventricular rate (85/minute) by 3. This yields an atrial rate of ~255/minute, which is above the usual range rate for atrial tachycardia (which generally doesn’t exceed 240/minute). As a result, the rhythm in Figure-2 most probably represents the unusual case of AFlutter with an odd conduction ratio (here with 3:1 AV conduction).

Figure-2: We have labeled Figure-1 by adding red arrows for the regular atrial activity. There are 3 P waves for each QRS complex (See text).

PEARL: There will usually be “something else” going on medically with the patient when you encounter AFlutter with an odd conduction ratio. Many such patients will be receiving one or more antiarrhythmic drugs (that may slow the flutter rate and affect the AV conduction ratio) — or perhaps the patient has already undergone ablation for one or more previous episodes of AFlutter.

• The unusual situation of AFlutter with 1:1 AV conduction (ventricular rate close to 300/minute) — should lead one to inquire IF the tracing is from a child who may have congenital heart disease and/or a patient of any age with WPW. Bottom Line: Non-cardiologists will probably only rarely see AFlutter with an odd conduction ratio, if at all.

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For More on this Subject:

• See also Section 14.4 (from our ACLS-2013-ePub) — on Atrial Flutter.

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ECG Blog #136 — Run of Narrow, then Wide Beats

The rhythm in Figure-1 was observed as a previously healthy young adult was being treated for his “palpitations”. He was hemodynamically stable at the time. Interpret the rhythm.

• What happened? Should what we see be cause for alarm?

Figure-1: Lead II rhythm strip during treatment (obtained from a patient with palpitations). Should what you see be cause for alarm? 

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Note: Discussion of this tracing is far easier if beats are labeled (Figure-2).

Figure-2: We have labeled all beats in Figure-1.

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Interpretation: The patient is hemodynamically stable. The first 9 beats show a regular SVT rhythm (SupraVentricular Tachycardia) at a rate between 185-190/minute. No atrial activity is seen during this run. The rhythm changes beginning with beat #10.

• After the run of SVT — it is easiest to look next at beats #11,12. Both beats are clearly ventricular in etiology — since the QRS complex is wider and completely different in appearance from QRS complexes during the SVT run at the beginning of the tracing.
• Beat #10 manifests an intermediate morphology between the narrow beats before it — and the ventricular couplet that follows. Beat #10 is a fusion beat — which means it is due to simultaneous occurrence of a supraventricular and ventricular beat. Therefore, beats #10-through-12 constitute a 3-beat salvo of ventricular tachycardia. PEARL: Recognition of fusion beats can be facilitated by looking not only to see if QRS appearance is intermediate between beats occurring before and beats that come after — but also by looking to see if ST-T wave appearance is intermediate! This clearly is the case here — as T wave shape and amplitude of beat #10 is indeed intermediate between T wave shape and amplitude of beats #9 and #11.
• Note that there is conversion to sinus rhythm beginning with beat #13. Another ventricular couplet follows (beats #14,15) — with the tracing ending in a regular sinus rhythm at a normal rate.

IMPRESSION: The rhythm in Figure-2 begins with a 9-beat run of AVNRT (AV Nodal Reentry Tachycardia). The rate of this SVT rhythm is too fast for atrial flutter with 2:1 conduction. It is also must faster than the usual rate range of sinus tachycardia. Abrupt conversion to sinus rhythm (beat #13) supports the diagnosis of AVNRT, which is a common cause of “palpitations” in the young adult age group.

• We do not know if conversion to sinus rhythm was achieved by a vagal maneuver, by medication — or by a combination of the two. Regardless — the point to emphasize is that it is a common and normal phenomenon to see PVCs (including ventricular couplets or salvos) at the time of conversion from a reentry tachycardia to sinus rhythm. Therefore, there is no cause for alarm from the rhythm in Figure-2, and assuming no other concerning features, additional workup would not be indicated at this time.

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For More on this Subject:

• See ECG Blog #128 and Blog #129 that review Fusion Beats in detail.
• See also these Sections from our ACLS-2013-ePub — Section 13.0 on SVTs of Uncertain Etiology — and Section 14.3 on SVT/PSVT/AVNRT.

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ECG Blog #135 (Regular WCT – Fascicular VT – RBBB – LPHB – SVT)

The ECG in Figure-1 was obtained from a 55-year old man who presented for emergency care with palpitations and fatigue. Blood pressure was 80/50 mmHg at the time this tracing was recorded.

• Is this VT (Ventricular Tachycardia)?
• How certain are you of your answer?

Figure-1: 12-lead ECG obtained from a 55-year old man with palpitations. Is this VT? 

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Interpretation: The rhythm is a regular WCT (Wide-Complex Tachycardia) at 180-190/minute without clear sign atrial activity. Although QRS appearance resembles RBBB (Right Bundle Branch Block) with LPHB (Left Posterior HemiBlock) — QRS morphology is not completely typical for this conduction defect because:

• Instead of a discrete rsR’ pattern in lead V1 — there is a double notch to the initial deflection in this lead, and — we do not see a clear s wave that descends below the baseline.
• The initial slender positive deflection (r wave) in lead I, followed by a predominant deep negative deflection is consistent with LPHB — but lack of a predominant R wave in lead II is not.

IMPRESSION: As emphasized in ECG Blog #134 — statistically, more than 80-90% of all regular WCT rhythms that lack sinus P waves will turn out to be VT. As a result — VT should always be assumed until proven otherwise! And, in view of slightly atypical features for RBBB/LPHB (as described above) — the likelihood that this rhythm represents fascicular VT would seem to be at least 90%. That said, given the presence of symptoms plus low blood pressure at the time this tracing was recorded — immediate cardioversion was indicated regardless of whether the etiology of this rhythm turned out to be VT or SVT (SupraVentricular Tachycardia) with either preexisting bundle branch block or aberrant conduction.

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Follow-Up: The patient received an electrical shock. This resulted in conversion of the rhythm to that seen in Figure-2.

• What happened? Does the post-conversion 12-lead ECG shown in Figure-2 prove what the etiology of the initial rhythm in Figure-1 was?

Figure-2: Post-conversion ECG after electrical shock. Is the etiology of the initial rhythm seen in Figure-1 now clear?

Discussion of Figure-2: The post-conversion 12-lead ECG seen in Figure-2 now shows sinus rhythm with QRS widening consistent with RBBB/LPHB. The KEY diagnostic observation is that QRS morphology in Figure-2 is virtually identical to QRS morphology during the tachycardia (that was seen in Figure-1). This proves that the initial rhythm was not VT — but rather SVT with preexisting bifascicular block.

• Note fragmentation of the widened QRS complex in several leads of both tracings. This is especially well seen in lead V2 (in which there is distinct angular notching of the S wave) — but it is also seen in the irregularity of the S wave in lead I, the R wave in leads III and aVF, and the notched initial r wave in lead V1. Fragmentation was also seen in Figure-1 during the tachycardia. During the WCT rhythm — such fragmentation contributed to our impression of a somewhat atypical RBBB appearance that made VT more likely. But its persistence after conversion to sinus rhythm suggests that in addition to the underlying conduction defect — the patient has underlying heart disease (ie, scarring from prior infarction and/or cardiomyopathy).
• QRS morphology can only go so far in predicting the etiology of a regular wide tachycardia. When ECG features of simple RBBB are completely characteristic (ie, distinct tri-phasic rsR’ complex in lead V1, with s wave descending below the baseline, and taller right rabbit ear) with smooth, wide terminal S waves in leads I and V6 — this appearance tends to be highly specific in predicting a supraventricular etiology. But the reverse is not true, such that atypical RBBB features are far less specific in their predictive value (See ECG Blog #42 for additional details).
• Sometimes one is surprised by the ultimate etiology of an arrhythmia. The ECG during a wide tachycardia is not a perfect predictive tool. That said, the correct diagnostic procedure was followed in this case. As always — Treat the patient, NOT the monitor. Since the patient was hemodynamically unstable because of the rapid rate of the presenting rhythm — immediate cardioversion was the intervention of choice regardless of the etiology of the arrhythmia!

Final Semantic Point — The reason for QRS widening in Figure-1 was not aberrant conduction! Instead, there was preexisting bifascicular block (RBBB/LPHB). If the reason for QRS widening would have been “aberrant conduction” — then the QRS widening would have resolved once the heart rate slowed.

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Acknowledgment: — My thanks to Darren Butcher (from London, UK) for his permission allowing me to use this case and ECG.

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For More on this Subject:

• See ECG Blog #38 — for review of Fascicular VT.
• See ECG Blog #42 — for my user-friendly approach to assessing the regular wide tachycardia.
• See ECG Blog #134 — for recent review of a WCT rhythm that we can definitively say is VT from the initial ECG.

ECG Blog #134 — Is there AV Dissociation?

The 12-lead ECG in the Figure was obtained from a hemodynamically stable older adult with new-onset “palpitations”. 

• Is this VT (Ventricular Tachycardia)? 
• How certain are you of your answer?

Figure-1: 12-lead ECG obtained from an older adult with palpitations. 

Interpretation: Although we are told that this patient was hemodynamically stable at the time this ECG was recorded — knowing this does not help in determining the etiology of the arrhythmia. That’s because some patients with VT may remain alert and hemodynamically stable for surprisingly long periods of time (ie, for hours or longer). That said, knowing this patient is stable does provide an extra moment of time to contemplate your differential diagnosis and management.

• Unfortunately — there is no simultaneously-obtained long lead rhythm strip. That said, it should be clear that the rhythm is a regular WCT (Wide-Complex Tachycardia) at a rate of ~110/minute without clear sign of sinus-conducting P waves (ie, there is no consistent upright P wave with constant PR interval in lead II). As a result — a ventricular etiology should be assumed until proven otherwise. Statistically, more than 80-90% of all regular WCT rhythms that lack sinus P waves will turn out to be VT.
• Features that increase the likelihood of a ventricular etiology for this tracing even more include: i) Extreme axis deviation (ie, all negative QRS in each of the inferior leads); ii) marked QRS widening (to at least 0.14 second); iii) all positive QRS in lead aVR; iv) all negative QRS in lead V6; and, v) QRS morphology not resembling any known form of bundle branch block or hemiblock. Based on these ECG features, predicted likelihood of a ventricular etiology increases to well over 95% (See our ECG Blog #42 for more details).
• There is one additional clue that allows 100% certainty of a ventricular etiology in this case (Figure-2). Although subtle — note the presence of unmistakable P waves periodically punctuating the baseline in a number of leads. These are best seen in lead III (before the 2nd QRS complex in this lead, and then notching the end of the QRS of the 3rd beat) — and, in lead aVF (notching the ST segment of the 1st beat in aVF, as well as appearing before and after the last beat in this lead’s recording). These P waves are regular and unrelated to neighboring QRS complexes — which defines this finding as AV Dissociation.

Figure-2: We highlight the presence of subtle-but-regular P waves that are unrelated to neighboring QRS complexes (red arrows). This defines AV dissociation — which proves our presumption of a ventricular etiology for this tracing. 
NOTE — Using calipers is essential if you hope to identify AV dissociation when it is present.

Final Comment: The rate of the ventricular rhythm in the Figure-1 is relatively slow for VT (ie, well under 130/minute). As a result, this rhythm is best classified as AIVR (Accelerated IdioVentricular Rhythm). AIVR is most commonly seen as an “escape” rhythm that occurs in association with acute or recent infarction — or following reperfusion of a major coronary artery. Immediate cardioversion of AIVR is rarely needed, and the rhythm often spontaneously resolves. Clinical correlation is essential for optimal management.

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For More on this Subject:

• See ECG Blog #42 — for my user-friendly approach to assessing the regular wide tachycardia.
• See ECG Blog #108 re recognition and clinical significance of AIVR.
• See ECG Blog #133 re utility of AV dissociation for proving VT.

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ECG Blog #133 — Is there AV Dissociation?

The lead II rhythm strip shown in Figure-1 begins with 3 sinus-conducted beats. There follows a run of a WCT (Wide-Complex Tachycardia). How certain are you that the run of WCT that begins with beat #4 is VT (Ventricular Tachycardia)?

Figure-1: Lead II rhythm strip. How certain are you that the run of wide beats beginning with beat #4 is VT? 

Interpretation: As stated, the first 3 beats in Figure-1 are sinus-conducted. The PR interval is upper normal at 0.20 second. The P-P interval changes slightly — so there is underlying sinus arrhythmia. QRS morphology then abruptly changes beginning with beat #4. The QRS widens, and is oppositely directed (all positive) compared to the narrow rS complexes of the first 3 beats. There is no reason for aberrant conduction to occur beginning with beat #4. This is because beat #4 occurs late in the cycle at a time by which conduction properties that lead to aberrancy should have long ago resolved. Instead we can state with 100% certainty that the run of wide beats beginning with beat #4 is VT:

• The first principle is that abrupt onset of a regular (or at least fairly regular) wide rhythm of different morphology than sinus-conducted beats predicts VT with greater than 90% likelihood. Consideration of clinical details (ie, history of underlying heart disease and/or prior documented VT episodes) — together with morphologic ECG features can often increase certainty of our diagnosis beyond this level (See Below for MORE on this Subject).
• Beat #4 is a Fusion Beat. Note that the PR interval preceding beat #4 is shorter than the PR interval preceding each of the 3 sinus-conducted beats at the beginning of this tracing. This means that something else must have happened to produce the oppositely-directed upright QRS complex of beat #4 — because the on-time sinus P wave preceding beat #4 simply did not have enough time to complete its conduction through the ventricles.
• Fusion beats manifest QRS and ST-T wave morphology intermediate between the QRS and ST-T wave morphology of sinus-conducted beats and ventricular beats. Depending on how deep in the ventricles the sinus P wave is able to penetrate — the resulting QRS and ST-T wave will look more like sinus beats or ventricular beats. Beat #4 is an upright QRS complex (like the wide run of beats that follow) — but beat #4 is not quite as wide, nor is its negative T wave as deep as the beats that follow because there is fusion (simultaneous occurrence) of supraventricular and ventricular activation.
• AV Dissociation is also seen on this tracing, at least at the beginning of the run of wide beats. The P wave preceding beat #4 is on time. Note that another on-time P wave is seen to notch the ST-T wave just after beat #5 (Figure-2). But since these last two P waves do not conduct normally — there is AV dissociation. The abrupt onset of a different-looking WCT rhythm with fusion beats and AV dissociation provides indisputable proof that the rhythm in the last part of Figure-2 is VT.

Figure-2: Use of calipers allows us to easily establish that 2 additional on-time P waves are seen after the first 3 sinus-conducted beats. The RED arrow highlights the 2nd of these last two on-time P waves, which notches the ST segment of beat #5. Since this final P wave is not conducting — there is (by definition) at least transient AV dissociation. Together with the fusion beat (beat #4) that manifests a QRS complex and ST-T wave intermediate between that of the preceding sinus beat (beat #3) and subsequent wide beats (beat #6 and thereafter) — we can say with 100% certainty that the run of wide beats beginning with beat #4 is VT.

PEARL: The clinical utility of recognizing fusion beats and/or AV dissociation that occurs in association with a WCT (Wide-Complex Tachycardia) rhythm — is that either of these findings proves that the rhythm must be VT. That said, neither finding is commonly seen with faster forms of VT — because the rapid rate of the tachycardia often obscures atrial activity that is hidden within QRS complexes or the ST-T wave. This case illustrates an exception in that we can clearly identify both a fusion beat and transient AV dissociation at the onset of the WCT — and this allows us to be 100% certain of our diagnosis!

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For More on this Subject:

• See ECG Blog #42 for full discussion on assessment of the wide tachycardia.
• See ECG Blog #128 and Blog #129 that review Fusion Beats in detail.
• See ECG Blog #134  and Blog #151 for additional examples of AV Dissociation in the diagnosis of a regular wide tachycardia.

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ECG Blog #132 (Ventricular Tachycardia - VT - Vfib - Artifact - Cardioversion)

The lead II rhythm strip shown in Figure-1 was obtained from an older adult patient on telemetry. Should the patient be immediately cardioverted?

Figure-1: Lead II rhythm strip obtained from a patient on telemetry. 

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Interpretation: Although at first glance, this tracing prompted much concern on the telemetry unit — prompt cardioversion is not the optimal initial intervention. Instead, there is much baseline aberration with spurious-looking complexes that occur at a rate over 300/minute in parts of the tracing. No real tachyarrhythmia has a ventricular rate this fast in adults.

• The first thing to do when confronted with a potentially worrisome tracing such as this one is to check on the patient. Doing so revealed that the patient was vigorously coughing at the time this tracing was recorded. The artifact totally disappeared as soon as the patient stopped coughing.

Comment: Artifact is common in clinical practice. At times, it may be extremely difficult to distinguish artifact from a real tracing. The consequences of mistaking artifact for ventricular tachycardia (as was almost done for the tracing in Figure-1) are not trivial. Patients have been shocked, and investigative procedures (such as cardiac catheterization) have been ordered. Remember the following:

• Check on the patient first. If the patient is alert and hemodynamically stable — then the rhythm is far less likely to be ventricular tachycardia. This means you have at least some time to investigate further.
• The most likely causes of artifact simulating ventricular tachycardia are inconsistent skin-electrode contact and body movement (scratching, tremor, shivering, coughing, hiccups, brushing teeth, writhing in bed, interference from a mechanical device, etc.).
• ECG features that suggest artifact as the cause include geometric appearance (unphysiologic vertical deflections) that are unpredictably irregular, often at exceedingly rapid rates. On a 12-lead tracing, one often inexplicably sees highly unusual deflections in some leads, but not in others.
• Being able to identify an underlying regular rhythm that is undisturbed by artifactual deflections provides proof that the phenomenon is not real. We illustrate this in Figure-2.

Figure-2: Identification of an underlying rhythm undisturbed by artifact proves that the phenomenon is not real (See text).

Discussion of Figure-2: It often helps to step back a bit from the tracing. Doing so suggests the several deflections near the middle of Figure-2 (marked by a red X) might represent underlying QRS complexes. Set you calipers to the interval between these complexes. Doing so allows you to march out regularly-occurring deflections at a rate of ~130/minute throughout the tracing (red arrows). This proves the much smaller, highly variable and overly rapid vertical deflections are artifact.

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For More on this Subject:

• See Knight et al: Clinical Consequences of ECG Artifact Mimicking VT (NEJM 341: 1270-1274 — 1999).
• See also ECG Blog #44 —

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