VF arrest at home, no memory of chest pain. Angiography non-diagnostic. Does this patient need an ICD? You need all the ECGs to know for sure.

Written by Willy Frick

A man in his 50s was at home with his family when they heard a thud and rushed into the room to find him unconscious with agonal respirations. His daughter immediately started CPR and another family member called EMS. When EMS arrived the patient was in ventricular fibrillation. They shocked him twice before return of spontaneous circulation. He was intubated in the field and sedated upon arrival at the hospital. Here is his presenting ECG:

ECG 1, t = 0

What do you think?

This was interpreted by the treating clinicians as not showing any evidence of ischemia. At first glance, it is easy to dismiss leads V1-V3 due to baseline wander. But close inspection reveals subtle terminal TWI in V4. Once you notice this, that you can appreciate biphasic T waves in V2 and V3 beneath the artifact. In context of VF arrest, this is extremely suspicious for reperfused LAD OMI.

Initial hsTnI was 384 ng/L. The patient was treated as possible NSTEMI and underwent coronary angiography about 4 hours after presentation. The report describes a 60% proximal LAD lesion with TIMI 3 flow. (TIMI 3 means the rate of passage of dye through the coronary artery is normal by angiography.) Lesions less than 70% are generally considered to be non-flow limiting. Given the presentation, the cardiologist stented the vessel and the patient returned to the ICU for ongoing critical care. Two subsequent troponins were down trending. Echocardiogram showed LVEF 66% with normal wall motion and normal diastolic function.

Within a few days, the patient was extubated and was neurologically intact. However, he did not remember much from the day of the arrest. He did not remember whether he had experienced any chest pain. At his family's request, he was transferred to a hospital closer to his home to continue care. He was admitted to cardiology. His transfer packet included notes, labs, cath report, and ECG reports, but no actual ECG images. His ECG at the accepting facility is shown below:

Accepting facility ECG

The team reviewed his angiography films with an interventionalist and thought they were suspicious for plaque rupture in LAD, but they were not confident. Stated differently, the differential diagnosis for the presenting syndrome was either ventricular fibrillation due to acute coronary syndrome, or idiopathic ventricular fibrillation and bystander stable CAD. This is a critically important determination because of the 2017 AHA/ACC/HRS Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. See the following management algorithm:

In other words, if this arrest is determined to have been due to acute coronary syndrome, the patient can be monitored without the immediate need for ICD implantation. On the other hand, if this was idiopathic VF and the interventionalist stented a stable moderate LAD lesion (remember, 60% is considered non-obstructive), the patient should have ICD implantation prior to discharge. Remember that hsTnI was 384 ng/L on presentation and trended down, relatively unimpressive.

They consulted EP for evaluation for ICD. The electrophysiologist is a reader of Dr. Smith's ECG Blog. When he reviewed the case, he only had access to the accepting facility ECG. He did not have access to ECG 1. In context, he thought it was suspicious but not diagnostic for reperfused LAD OMI. He contacted the referring facility and asked for copies of all the ECGs they had obtained. Here they are in sequence:

ECG 1, t = 0

ECG 2, t + 4 h

ECG 3, t + 24 h

ECG 4, t + 48 h

ECG 5, t + 72 h

In sequence and in clinical context, the ECGs tell a convincing story. The patient suffered LAD OMI at home and secondary VF arrest. By the time he arrived at the hospital, he already had spontaneous reperfusion, evident in the subtle TWI in the anterior leads in ECG 1. Non-emergent angiography showed an underwhelming "non-obstructive" 60% LAD lesion due to robust spontaneous recanalization, and over the next few days he had progressive deepening of his T waves followed by the beginning of return to normal. The relatively low troponin value fits exactly with brief LAD OMI.

By themselves (not evaluating the progression), the Queen of Hearts AI system diagnosed ECG 2 as Not OMI, and ECGs 3-5 as OMI (she is unable to compare serial ECGs even though this would make it much easier for her.)

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The patient was discharged without an ICD, in accordance with guidelines.

Learning points:

• Chart review is an under-appreciated, extremely high value practice. The electrophysiologist in this case saved the patient from getting an ICD simply by taking the time to gather and review existing medical data.

• OMI can be extremely brief with spontaneous recanalization and only mild troponin elevation. Angiography tells you the state of the vessel at that moment in time. Putting ECG in clinical context can tell you what the vessel looked like before presentation!

• Angiography can be misleading and must always be understood in clinical context.

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MY Comment, by KEN GRAUER, MD (6/23/2024):

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The beauty of Dr. Frick's presentation in today's case is its simplicity in conveying a critically important finding affecting the outcome of this patient.

• Simply by correlating the history of cardiac arrest with serial ECGs recorded after the event — it became obvious that the 60% lesion on cardiac cath, despite its surprisingly good TIMI 3 flow — was indeed the "culprit" artery that had spontaneously reperfused after the event.
• As per Dr. Frick — "Angiography can be misleading — and must always be understood in clinical context".

The parallels between today's case and Wellens' Syndrome are important to recognize. The principal difference between these entities, is that instead of a cardiac arrest being the event that suggests transient LAD occlusion — with Wellens’ Syndrome, it is the history of a recent episode of chest pain that has now resolved at the time we see an ECG showing signs of LAD reperfusion that tells us the LAD has recently occluded, but has now reopened.

• Clinical deduction by correlation of history with serial ECGs in Wellens’ Syndrome is similar to the process described by Dr. Frick in today’s case. With Wellens’ Syndrome — recognition of this entity is essential for expediting cardiac cath with PCI because of an otherwise excessively high risk that the recently opened “culprit” vessel may at any time reocclude.
• Yet just as initially occurred in today’s case — failure to correlate serial ECGs with the history almost led to misinterpretation of cardiac cath findings — until the EP cardiologist was consulted, and knew to go back to the basics of gathering all tracings for serial review.

The above said — it may prove insightful to take another look at the Wellens' Syndrome case instantly recognized by Dr. Smith in the August 12, 2022 post in Dr. Smith’s ECG Blog.

• The merit of reviewing this August 12, 2022 case — is our need as emergency providers to immediately recognize signs of cardiac reperfusion — that by simply correlating ECG findings with the history — we can know within seconds the pathophysiology involved, and the current state of the “culprit” vessel.
• 
  
• I find it amazing how application of the simply stated Learning Points by Dr. Frick at the end of today’s case can tell so much — if we simply stop to look and listen.

Regular Wide Complex Tachycardia. What to do?

A patient in the ICU with significant underlying cardiac disease [HFrEF 30%, non-ischemic cardiomyopathy, LBBB s/p CRT-D (biventricular pacer), AVNRT s/p ablation a few yrs ago, hx sinus tachycardia while on max tolerated BB therapy] went into a regular wide-complex tachycardia after intubation for severe COPD exacerbation. 

Here is the ECG:

Regular Wide Complex Tachycardia at a rate of 166 bpm.  

What do you think?

If the patient is unstable, he should be immediately electrically cardioverted.  Even if he is stable, that is the best course of action.

The majority of regular wide complex tachycardia are due to ventricular tachycardia (VT), and if the patient has a h/o HFrEF with cardiomyopathy, the VAST MAJORITY are VT.

When I first posted this, I thought the initial part of the QRS was wider, and favored AVRT or VT. 

But after receiving a few comments, I looked more closely and magnified it, and measured  the QRS onset (the initial deflection, the first part) of the QRS at about 80 ms.  

This is best seen in V1-V3, where the initial r-wave is very narrow and the rS is about 80 ms.

So this is likely SVT with LBBB.

What is the differential?

1. If it were wider, then VT and antidromic AV reciprocating tachycardia (AVRT) would be likely.  AVRT is due to accessory pathway with the impulse going down the bypass tract and up the AV node.  This results in what is, in effect, a ventricular origin since the ventricle is pre-excited by the accessory pathway.

2. Pacemaker mediated tachycardia (also called endless loop tachycardia).  This is not such a case, as there are no pacer spikes.

What to do?

Electrically cardiovert is always an option.  Adenosine is easiest.  With wide complex and known poor LV function, I would avoid a calcium channel blocker.

The patient was electrically cardioverted several times with 200J without any change!!

So they gave adenosine and the patient cardioverted.

Here is the post cardioversion ECG:

Now there is a ventricular paced rhythm at a rate of 120.

The ventricular pacing makes it impossible to know if there would be delta waves, so we don't know if this was orthodromic AVRT or AVNRT.

It appears that there are P-waves which are triggering the Ventricular pacing, so this post conversion ECG is most likely sinus tach with ventricular paced rhythm. 

Adenosine is safe in regular wide complex tachycardia.  It will not harm VT.  It will likely convert AVRT.  It is absolutely contraindicated in atrial fib with WPW.  

Some say you should not use it is AVRT because the patient might convert to atrial fibrillation.  This seems extremely unlikely to occur during the 10 seconds that adenosine is active.  

See Ken's comment below: most AVRT is orthodromic and is identical in appearance to AVNRT.  You don't have any hesitation to give these patients adenosine, correct?  And yet they have the same probability of converting to atrial fibrillation.  Thus, the argument against using adenosine in antidromic AVRT is fallacious.

Therefore, I use adenosine in regular wide complex tachycardia.

Follow up:

The patient signed out AMA before he could get his pacer interrogated.  We will never know for certain.

Here is a case of antidromic AVRT:

A 30-something with palpitations and lightheadedness

Here is another very complex case of antidromic AVRT:

Young Man with Very Fast Regular Wide Complex Tachycardia

Adenosine will also convert Right Ventricular Outflow Tract Ventricular Tachycardia:

Toothache, incidental Wide Complex Tachycardia

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MY Comment, by KEN GRAUER, MD (6/21/2024):

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Optimal time-efficient management of a regular WCT (Wide-Complex Tachycardia) — is among the most challenging of situations encountered by emergency providers. Seconds count — with the initial KEY decision being "electricity" vs a trial medication deemed most-likely-to-work by the provider at the scene.

• As per Dr. Smith — today's initial tracing shows a regular WCT rhythm at ~170/minute without clear sign of sinus P waves.
• 
  
• Even before looking at this initial ECG — statistical odds in an unselected adult population that this rhythm will turn out to be VT are at least 80%. 
• Given this patient's history of significant underyling heart disease — these odds (even before looking at this ECG) approach at least 90% that this rhythm will turn out to be VT.
• 
  
• Potentially — We can refine our "likely probability" that a regular WCT rhythm is or is not VT after we look at the ECG, with attention to QRS morphology during the WCT (ie, Does QRS morphology resemble any known form of conduction defect — in which case an SVT rhythm becomes at least slightly more likely) — and by comparing QRS morphology during the WCT with prior baseline ECGs on the patient during sinus rhythm (ie, To see if an unusual QRS morphology during the WCT might be identical to the unusual QRS morphology of the patient during sinus rhythm, thereby confirming a supraventricular etiology).
• 
  
• Clinical Reality: In an acute patient in a regular WCT rhythm — it will be rare indeed that we have access at the time to a prior ECG. Instead — we almost always need quickly begin treatment!

Regarding Today's Case:

Dr. Smith's approach that is (that is succinctly detailed above) — conveys the ideal approach to today's case (NOTE: We have presented numerous decision-making cases regarding WCT rhythms on Dr. Smith's Blog. Among others — "My Take" is reviewed in the May 5, 2020 post).

• As per Dr. Smith — VT needs to be assumed as the etiology of todays' initial ECG until proven otherwise. The safest treatment is clearly immediate electrical cardioversion.
• It turns out that today's patient was cardioverted "several times with 200J without any change". At this point Adenosine was given — and the patient converted (with what appears to be sinus P waves, immediately followed by ventricular pacing — as shown above at ~120/minute).

MY Thoughts on Today's CASE:

The "good news" — is that the patient was successfully treated, with return to a paced rhythm. In the interest of providing some additional thoughts — I'll offer the following:

• Electrical cardioversion is almost always successful in converting regular tachycardias to sinus rhythm — at least immediately after the electrical discharge is released. What sometimes (often) happens — is within seconds of this electrical discharge, the WCT rhythm returns. This is especially common following administration of Adenosine for a reentry SVT rhythm, since the half-life of Adenosine is measured in seconds.
• KEY Point: Always record the initial short-term period during and after interventions such as cardioversion and Adenosine administration. Things happen quickly! It is extremely difficult to know if your intervention was initially successful — but that the WCT then quickly returned unless you have hard copy of the rhythm during and immediately after the cardioversion or Adenosine administration. 
• Clinically — a hard copy recording during this period is important — because the ANSWER as to what the etiology of the WCT rhythm was will often be revealed during those initial seconds after cardioversion (or Adenosine) — and your subsequent treatment may vary depending on whether your intervention did not work at all — or — was effective for a few seconds, before recurrence of the WCT. Unless you have hard copy to show — We can not know if those "several times" that today's patient was cardioverted worked for a few seconds, or did not work at all.
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• Returning to "probability assessment" of today's WCT rhythm — QRS morphology of today's initial ECG looks very much like LBBB conduction (ie, all upright in left-sided lead V6 — and predominantly negative in the first 4 chest leads). Admittedly — the rsR' in lead I, with predominantly negative QRS in lead aVL is not typical of LBBB conduction — although in a patient with severe underlying heart disease, LBBB conduction will often look different than the "textbook" picture — so I thought QRS morphology was not helpful in my assessment of today's WCT rhythm.
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• BUT — I did think that there probably was retrograde atrial activity in today's initial ECG (RED arrows in Figure-1). While fully acknowledging that I could not be 100% certain — I thought that small-but-consistent pointed deflections (negative in leads II and aVF — and positive in leads aVR and V1) — were likely to represent retrograde P waves with a relatively longer RP' interval. IF I was correct in this interpretation — then the rhythm was likely to be antidromic AVRT (which I believe is supported by the fact that the sinus P waves seen just before pacer spikes in the post-conversion tracing are indeed pointed).
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• Final POINT: I completely support Dr. Smith's approach of using Adenosine to treat AVRT. In fact — this is done all the time, despite most providers being unaware they are doing so! I say this — because a significant percentage of patients with reentry SVTs thought to be "AVNRT" actually have "concealed conduction" over an AP (Accessory Pathway) that can only conduct retrograde. As such — these narrow QRS reentry SVT rhythms are in fact orthodromic AVRT with the reentry circuit including passage outside of the AV node over an AP. And, adverse effects are so rarely encounted from Adenosine administered countless times to these unsuspected orthodromic AVRT rhythms with "concealed" conduction over an AP. BOTTOM Line: As per Dr. Smith — Adenosine almost always works to safely convert orthodromic AVRT.
• 
  
• P.S.: To confirm whether my supposition of retrograde P waves with a long RP' interval was correct — We'd need to see a repeat ECG in sinus rhythm with WPW conduction, perhaps showing a similar LBBB conduction pattern but without those notches that I highlight with RED arrows in Figure-1. Since today's patient signed out AMA — We'll never know. 
• P.P.S.: Alternatively (given what I think are retrograde P waves with a longer RP' interval) — this still could be orthodromic AVRT in which either the RBB (Right Bundle Branch) was participating in association with an AP to form a reentry circuit with lbbb-like conduction — or — the LBBB conduction was simply a rate-related aberrancy result due to the rapid rate during the wide SVT rhythm.
• 
  
• NOTE: I review clinical utility of assessment of the retrograde RP' interval in My Comment at the bottom of the page in the October 25, 2022 post of Dr. Smith's ECG Blog.

Figure-1: I’ve labeled the initial ECG in today's case.

What would you do with acute chest pain and this ECG? You might see what the Queen thinks.

This is another case sent by the undergraduate (who is applying to med school) who works as an EKG tech.

Case

An 82 year old man with a history of hypertension presented to the ED with chest pain at 1211. He described his chest pain as pleuritic and reported that it started the day prior while swinging a golf club. 

An EKG for chest pain was obtained right away:

For an 82 year old, this is a good looking EKG, with sinus rhythm at a rate of 70 BPM.   

It is really completely normal

On arrival, the patient’s vital signs were normal and he rated the chest pain 1/10. A troponin T was drawn at 1229 and resulted slightly elevated at 23 ng/L (URL for men in this assay is 15 ng/L).

Three months prior to this presentation, he received a pacemaker for severe bradycardia and syncope due to sinus node dysfunction. 

The ED provider ordered a coronary CT scan to assess the patient for CAD. 

At around 1430, as the patient was being prepared to leave for the scan, he developed severe chest pain, dizziness, and became diaphoretic. Another blood pressure was checked. He was severely hypotensive, with a systolic pressure in the 50s. 

Another EKG was obtained:

There is now an atrial paced rhythm.  And there is significantly more ST Elevation.

Here is the PM Cardio digitization:

There are some notable changes between this EKG and the last. Most strikingly, there is new ST elevation most prominent throughout the proximal LAD distribution.

However, there is also a problem with digitization: the atrial pacing spikes are omitted

In V3, the ST elevation has increased by about 1.5 mm to almost 2 mm. 

In lead I, about 1.5 mm of ST elevation has developed.

The two leads are compared below:

There is now increased STE in both lead V3 and lead I

Let’s look at the entire picture:

Our elderly patient presented with very slight chest pain and his EKG looked normal. His pain suddenly became much worse in the ED and he became acutely diaphoretic, dizzy, and hypotensive. His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. 

Surely, he should be given heparin and taken for an emergent angiogram, right?

We should take a closer look at the second EKG: 

--All leads with ST elevation have very concave ST-T complexes, with flat ST segments. 

--The ST elevation is diffuse. 

-- Leads III and V1 are isoelectric, but all other leads have some ST elevation.  In other words, STE in lead II is greater than STE in lead III. 

While the ST elevation may be deceiving, this EKG does not look like acute OMI.

The undergraduate continues:

This new EKG pattern is more suggestive of acute pericarditis.

Usually with pericarditis, some degree of PR segment depression is expected. This EKG seems to lack it.  This is becaue the rhythm is NOT sinus; it is paced.

The atrial lead of the patient’s newly implanted pacemaker has taken over the rhythm, as his native sinus rate has dropped below 60 BPM. Although no pacer spikes can be seen in this digitized EKG, the P wave morphology has changed. Pacer spikes were also visible on the paper copy. Just as with ventricular pacing, atrial pacing distorts atrial repolarization, and PR segment depression happens because of an exaggerated atrial repolarization (Ta) wave.

____________

Smith comments:

--If it were inferior OMI, lead III should have more STE than lead II, and there should be STD in aVL

--If it were high lateral OMI, or proximal LAD OMI, there should not be STE in lead II

In other words, the ST vector is towards leads II and V5 (towards the apex of the heart).  This is typical of pericarditis.  

But, as I always say, you diagnose pericarditis at your peril.  When the ECG suggests pericarditis, you don't just avoid activating the cath lab. Instead, you need to do more investigation to ascertain whether the patient is having OMI or pericarditis.

____________ 

The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”. 

The Queen of Hearts recognizes the false positive and sees no OMI with high confidence:

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The emergency provider agreed with the conventional computer algorithm and thought the Queen was missing OMI; he went ahead and activated the cath lab for the STEMI protocol. The patient started receiving medications for “STEMI” (including heparin!!!) when the ED provider took a bedside echo:

This echo shows a pericardial effusion with RV invagination and bowing of the septum into the LV.  There is pericardial tamponade.

 

The ED provider canceled the STEMI protocol and updated the cath lab on the finding. 

The patient was taken emergently to the cath lab for a pericardiocentesis instead of a coronary angiogram. In the cath lab, 150 CCs of bloody fluid were drained from the pericardium. The patient’s blood pressure and symptoms improved immediately after the fluid was drained.

The post pericardiocentesis impression and plan read:

1. Pericardial effusion / tamponade - hemorrhagic, fairly acute as hemodynamically significant w only 150cc. Possible pacemaker lead perforation after after golf swing yesterday

2. Morphologic cardiac CT to eval lead perforation

3. PM interrogation eval lead thresholds

At 1451, the second troponin T came back at 24 ng/L, ruling out acute MI.

Final comment by the undergraduate: Let me know what you think! Maybe you can comment more about potential dangers for giving anticoagulants in acute pericarditis. I don't know much about that, but it seems to me that giving heparin to a patient with acute hemopericardium would be extremely dangerous. Recognition of the EKG could have avoided that. Luckily, the patient did well. 

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MY Comment, by KEN GRAUER, MD (6/18/2024):

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Today's case is humbling — fascinating — and emphasizes a number of KEY clinical concepts, most important of which is, "Always be ready to 'Think OUT of the box' when pieces of the clinical puzzle don't all add up". As a result of astute clinical reasoning and time-efficient evaluation — life-saving pericardial drainage was implemented instead of life-threatening anticoagulation.

Regular readers of Dr. Smith's ECG Blog are well familiar with what is perhaps my favorite Stephen Smith Adage = "You diagnose acute pericarditis at your peril!"

• Statistically, among patients presenting for emergency care with new chest pain — the overwhelming majority of ECGs that are diagnosed as "acute pericarditis" will turn out not to be the result of acute pericarditis. Instead, the much more common final diagnosis of such patients will be acute OMI.
• But, even 95-98% likelihood is not 100% — and on occasion pericarditis with pericardial effusion will occur, as in today's case. Dr. Smith details why the ST-T wave changes in today's 2nd tracing were atypical enough for acute OMI, that consideration of "something else" other than acute OMI was prompted. STAT Echo and minimal troponin elevation then confirmed the diagnosis.
• We review many cases of the mistaken diagnosis of pericarditis on Dr. Smith's ECG Blog (See My Comments in the June 11, 2022 post — the June 8, 2022 post — and the December 13, 2019 post, among many other examples throughout Dr. Smith's Blog).

Smith: Ken wrote this BEFORE we were provided with the original ECG #2, which clearly shows pacer spikes.

I'd add the following points to today's discussion: 

• Pacemaker spikes are not seen on the 2 tracing shown in today's case. That said — we might not expect pacemaker spikes to show because: i) This ECG is a digitized tracing, and on occasion — details such as pacing spikes are not always reliably reproduced with digitalization if they were of small size on the original ECG; — and, ii) Filter settings are not shown on these digitized tracings (I pose the question as to whether the patient has a pacemaker? — in My Comment in the January 13, 2024 post in Dr. Smith's ECG Blog — in which I review the importance of considering filter settings when assessing if the rhythm in a given ECG is or is not paced?).
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• The question arises in today's 2nd ECG as to whether the presence or absence of PR depression rules in or out acute pericarditis. As a result of decades of my admittedly anecdotal observation regarding this question — my conclusion is NO. I have seen PR depression in several leads (with PR elevation in lead aVR) in both normal individuals and in patients with acute MI — and I have seen acute pericarditis without any PR depression at all. 
• MY Approach: I continue to look for PR depression in several leads (in association with PR elevation in lead aVR) — whenever I consider the diagnosis of acute pericarditis. When I see PR depression — I consider this a minor supportive factor of the diagnosis. But when I do not see any PR depression — I realize that this in no way rules out acute pericarditis.
• And then I remember that, "Most of the time the patient in front of us will not turn out to have pericarditis" — albeit exceptions do occur, as in today's case.

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P.S. — As per Dr. Smith, I did not see the original version of the 2nd ECG at the time that I wrote my comment. I only saw the digitized tracing. As I now am provided with this original version — I’ll add the following observations:

• The pacing spikes are obvious on the original ECG — but pacing spikes are totally absent on the digitized version. This highlights the point that as helpful as ECG digitalization has become for improving our visualization — the technique is not perfect. As a result — I always spend an extra brief moment comparing the digitized version to the original tracing to ensure all essential information is reliably transmitted.
• If you look carefully in the lower lefthand corner of the original version of the 2nd ECG – you will see, “150 Hz”. This is an optimal filter setting for viewing special deflections such as pacemaker spikes — and is the reason we can see these spikes so clearly on the original ECG.