Physical Examination as a Helpful Aid in Decision-Making in Challenging ECGs

This was contributed by Co-editor Emre Aslanger, an interventional cardiologist in Turkey. @AslangerE

A 65-year-old gentleman presented to the emergency department after experiencing two recent ICD shocks in the preceding hours.

His medical history includes hypertension, a decade-long battle with diabetes, ischemic heart disease, a coronary bypass graft surgery ten years ago, a diagnosis of congestive heart failure for the last five years, and a prior ICD implantation five years ago. 

A recent angiogram report indicated a totally occluded left anterior descending artery (LAD) and right coronary artery (RCA), with 30-40% narrowings in the left circumflex artery (LCx). The report also noted totally occluded left internal mammary artery (LIMA)-LAD and aorto-RCA grafts. Further investigation into viability revealed complete scar tissue in the LAD territory but viable tissue in the RCA territory.

His current medication regimen includes apixaban, carvedilol, perindopril, spironolactone, torasemide, dapagliflozin, amiodarone, and ivabradine.

The patient was promptly admitted to the hospital for further evaluation.

An initial electrocardiogram (ECG) is provided below. What do you think?

What is the rhythm?

The rate is 132 bpm. 

There is some ST-segment elevation in DII, DIII, aVF, V4-6. 

Due to the observed ST-segment elevation, the medical team expressed immediate concern. Although the patient reported experiencing mild pressure-like chest pain, there was suspicion among clinicians that this might be indicative of an older change. A rapid echocardiogram was performed, revealing an ejection fraction of 20% with thinning of the anterior-apical walls. 

The initial troponin T level was measured at 30 ng/L. A subsequent ECG was taken:

There is persistent ST elevation, especially being concordant in inferolateral leads.

This raised considerable concern among the medical team. 

However, there remained uncertainty among clinicians regarding the significance of this finding.

What is the rhythm?

While the initial impression might not immediately suggest ventricular tachycardia (VT), a closer examination raises suspicion.

Notably, there are deflections which look like P-waves, easily seen in lead II (see Ken Grauer's annotated ECGs below).

Smith: Are they P-waves? They look like P-waves in lead II, but if you go up to lead V1, you should expect to see a biphasic up-down P-wave at the same time as the deflection in lead II. And such biphasic waves are not there. So probably not P-waves!

What are they if they are not P-waves?

QRS complexes are wide, but how wide?

Are the apparent P-waves (which now we suspect might not be P-waves) actually part of the QRS, in which case the QRS is even wider than it appears?

Where does the QRS begin? (Again, see Ken's discussion below)

Discussion continued

The absence of pace spikes suggests this is not a pacemaker/ICD-related rhythm in this patient with an ICD.

The presence of thinned myocardium and known large amount of scar tissue makes for a nidus for VT. Thus VT is very probable.

A wide native QRS can be expected in a patient with a dilated heart and a history of heart failure, even if it is sinus rhythm. so the question of whether those are P-waves is critical.

Additionally, the qR morphology, particularly in a patient with right bundle branch block (RBBB) type wide QRS complex tachycardia (WQCT), lends further support for VT.

Furthermore, a pertinent physical examination finding to consider is:

Intermittent cannon waves, indicative of atrioventricular dissociation, emerged during the assessment, further supporting the diagnosis of ventricular tachycardia (VT). This finding, while reliable and sensitive, requires a focused search for its identification.

Simultaneously, a programmer device was employed, and the programmer ECGs revealed notable distinctions between the atrial and ventricular channels. The atrial channel displayed considerably less activity (atrial sense, AS) compared to the ventricular channel (ventricular sense, VS), reinforcing the diagnostic likelihood of VT. 

Following administration of midazolam for sedation, the patient underwent successful cardioversion with an internal energy of 15J.

The subsequent ECG, taken 5-10 minutes post-shock, depicted a soothing of ST deviation. The patient rapidly regained consciousness, reporting no residual pain. A peak troponin level of 70 ng/L was observed.

Learning Point: Concordant ST segment elevation can arise from profound ischemia triggered by ventricular tachycardia (VT), or it may represent an exaggerated basal ST change accompanying tachycardia. While a cautious approach involves considering the worst-case scenario, the clinical context should always guide decision-making. In this particular case, prioritizing rhythm control as the initial step, and subsequently assessing whether the symptoms and signs of ischemia abate, proved to be a prudent strategy. This approach facilitated stabilization of the patient without encountering significant challenges during the angiographic procedure.

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MY Comment, by KEN GRAUER, MD (1/1/2024):

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Today's case by Dr. Aslanger is challenging with an important message. This 65-year old male patient with severe underlying coronary disease presented to the ED after receiving several ICD shocks. Because of concern for an acute MI — the fact that he was in hemodynamically stable VT (Ventricular Tachycardia) went unnoticed for some time — until intermittent cannon waves, use of a programmer device and reassessment of QRS morphology on ECG revealed the correct diagnosis of VT.

• I thought it EASY to be confused by this patient's first 2 ECGs! For clarity in Figure-1 — I've labeled his initial tracing.

Why is ECG #1 So Challenging?

There are several reasons with the initial ECG in today's case is so challenging:

• The QRS complex in ECG #1 is extremely wide. As per Dr. Aslanger — a number of medical providers were confused by what initially appears as marked ST elevation with reciprocal ST depression, indicative of an acute STEMI. That was also my first impression.
• It looks like the rhythm in Figure-1 is sinus (Don't the RED arrows in lead II look like upright, conducting sinus P waves?).
• No "baseline" ECG is available for comparison. This is especially problematic given the wide QRS in Figure-1 that resembles RBBB/LPHB morphology.
• The post-cardioversion tracing is paced — such that we still do not have any idea of what native (conducted) QRS complexes might look like in this patient expected to have an abnormal baseline ECG due to extensive underlying disease.
• With most attention directed at the potential new ST elevation — it becomes EASY to forget about how fast the heart rate is! (ie, ~130-135/minute in Figure-1).

Looking Closer: Using the "Shark Fin" Technique:

The biggest problem I had with today's fascinating tracing — was determining the limits of the QRS complex. Use of a similar technique to that which we've often described for assessing patient's with "Shark Fin" ST elevation can be invaluable! (See My Comment at the bottom of the page in the May 19, 2020 post in Dr. Smith's Blog).

• The challenge in interpreting a tracing with Shark Fin morphology — is to define the J-point that separates the end of the QRS complex with the beginning of the ST segment.
• The "extra challenge" in today's tracing — is to also define the onset of the QRS complex — so as to distinguish this from the "pseudo-P waves" highlighted by the RED arrows in Figure-1.
• To paraphrase Drs. Smith and Meyers — "When the QRS is wide, the J-point will hide. So your next step is to Trace it down, and Copy it over." In today's case — we need to do the same to determine the onset of the QRS complex.

I illustrate this process in Figure-1.

• The long, thin, downward BLUE arrow provides a vertical line from the point I believe marks the onset of the QRS (which I have based on the short BLUE arrows in leads V3,V4,V5 placed at the very onset of the wide Q waves in these leads).
• Note that the bottom of this long, thin, downward BLUE arrow — passes through the middle of the small, upright deflection before the wide QRS in the long lead II rhythm strip. Rather than a "sinus P wave" — this point marks the onset of the QRS!
• 
  
• Copying this point over — I then drew long, thin upward RED arrows starting from the middle of this small, upright deflection before the QRS in the long lead II — to convincingly show that what one might easily think represents a sinus P wave, is in fact the initial part of the QRS complex!
• 
  
• For interest — I've also drawn a long, thin downward YELLOW arrow defining my impression of the end limit of the QRS. This makes for a very long QRS complex!

Figure-1: I've labeled the initial ECG in today's case (See text).

Recognition of Cannon Waves:

An important PEARL in Dr. Aslanger's discussion relates to the recognition of intermittent Cannon waves. This physical exam sign is seen with AV dissociation — and results from right atrial contraction against a closed tricuspid valve. Cannon waves are associated with reduced RV compliance or elevated RV end-diastolic pressure (Ali et al — Ann Noninvasic Electrocard 22:e12423, 2017 — and — Chen and Pel-Ying Pai — Circulation 119:e381, 2009).

• In addition to various forms of AV block — intermittent cannon waves may be seen with premature beats (PACs, PJCs, PVCs) — selected SVT rhythms with AV dissociation — and VT. 
• The above said, when a regular WCT is seen on ECG — as per Dr. Aslanger, this confirms VT!
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• As an additional modality for assessing a rhythm such as the one in today's case (assuming the patient is hemodynamically stable) — Use of a Lewis Lead may faciltate recognition of independent atrial activity unrelated to ventricular contraction (See My Comment in the November 12, 2019 post in Dr. Smith's ECG Blog).