Test almost all of your most important ECG rhythm interpretation skills with this case.

Sent by Anonymous, written by Meyers, edits by Smith:

A female in her 70s with history of HTN woke up around 2am with severe shortness of breath. EMS found the patient in moderate respiratory distress, hypoxemic on room air, with diffuse rales. CPAP was initiated. The prehospital ECG is unavailable but reportedly showed a wide complex regular tachycardia at around 150 bpm. 150mg amiodarone was given for presumed VT with no obvious effect.

She arrived at the ED at 2:52 AM. She had normal mental status, and was in moderate respiratory distress with diffuse rales, with respiratory rate 30/min, and initial blood pressure 129/60.  Her oxygen saturations were in the 90's. Bedside US showed severely reduced global LV function and bilateral diffuse B-lines. 

Here is her initial ECG (no prior for comparison, she's on vacation from out of town to visit family, with no other available history): 

What do you think?

At this point in the case you face some very interesting and difficult questions:

1) Is the patient stable or unstable? 

2) What do you think the ECGs show? What is the rhythm?

3) Do you think the rhythm is the cause of the symptoms? What is happening pathophysiologically with this patient?

4) Given the above, how will you proceed?


Stable or Unstable:
By the ACC/AHA definitions, the patient could be called "unstable" based upon the presence of acute heart failure (assuming you attribute the acute heart failure to the rhythm). 

Regardless, this patient has a normal mental status, is tolerating BiPAP, and is no longer hypoxic -- is she peri-arrest?? No. You have some time.

The ECG:
Regular wide complex tachycardia at ~140 bpm. The differential is then VT, SVT with abnormal conduction, Sinus tach with abnormal conduction, or any of these with or without the ever-important hyperkalemia. The QRS complex morphology is very similar to LBBB, with the only outliers being leads V5 and V6, which are negative instead of positive as would normally be seen in perfect lead placement in LBBB.  However, I and aVL do have monophasic R-waves typical of LBBB -- that V6 does not agree with I and aVL raises the suspicion of possible lead misplacement, as they normally share a common general axis.

The beginning of the QRS shows rapid depolarization, with the time from onset of QRS to the nadir of the S-wave in V1-V4 approximately 40ms (generally fast enough to suggest the use of specialized conduction system rather than the slowly creeping cell-to-cell myocardial propagation of a PVC; less than 50 ms is typical of true LBBB). With nearly perfect LBBB morphology and very fast initial QRS depolarization, this QRS complex is very likely to be created by depolarization anterogradely down the Right Bundle Branch, meaning it is either supraventricular with LBBB or originates within the Right Bundle itself (rare). 

In V1 between the QRS complexes there is a distinct large negative deflection which is likely atrial activity. Using the rhythm strip of V1 to trace this activity to other leads, you can see an "extra bump" in the T-waves in the corresponding location in leads V6 and II. This also prompts the question whether there is an extra set of P/flutter waves hidden in the QRS. It is difficult to tell. Lewis leads are an option that may help in this scenario by clarifying P-waves or revealing flutter waves.

Despite these characteristics, there is no way to exclude VT based on this ECG. Other than wide complex QRS, there are no particular features suggesting hyperK. There are no signs of ischemia superimposed onto this abnormal QRS complex with appropriately discordant ST-T segments.



The Pathophysiology:
There are at least two main competing explanations for this patient's overall clinical picture:

1) Primary acute onset SVT/VT, in the setting of unrecognized poor LV function -- acute heart failure with pulmonary edema

2) Primary acute hypertensive pulmonary edema ("SCAPE" -- Sympathetic Crashing Acute Pulmonary Edema), which is facilitated by history of hypertension with poor LV function; compensatory sinus tachycardia with baseline or rate-related aberrancy

Either explanation could also be caused by ischemia from ACS, or could result in demand-related ischemia.

Factors that may help differentiate:

• A 75-80 year old female should have a theoretical maximum sinus tachycardia around 140-150 bpm (220-75=145). This patient's rate of 139 bpm is not so fast that we should doubt sinus tach based on the rate.
• SVT is usually, but not always, faster than 140 bpm. The exception of course is atrial flutter, which is commonly 135-160 bpm. 
• A rate of 139 bpm is unlikely to cause hemodynamic compromise in a young structurally normal heart (which is not the case here)
• SCAPE usually presents with sinus tachycardia

Factors that don't help differentiate:

• Bedside US showing poor LV function and diffuse B-lines does not help differentiate these two, because poor LV fct and pulmonary edema may be associated with both. These findings are consistent with underlying heart disease that would predispose to "Sympathetic Crashing Acute Pulmonary Edema" ("SCAPE"), but they would also help explain why a primary arrhythmia with rate of 139 bpm could be so poorly tolerated.
• Blood pressure is "normal" or "pseudo-normal." Some will say she is not hypertensive enough to have SCAPE at 129/60. Of course, she has already been receiving NTG drip and BiPAP. External BP measurement is also unreliable, but even if it were the true arterial pressure, it still may not help differentiate here. When a patient with acute heart failure has "normal" or low BP, it may represent cardiogenic shock, especially in a patient who likely has HTN at baseline. 
• Cardiogenic shock may be the result of the rate, or the rate may be the appropriate expected response to the cardiogenic shock, pulmonary edema, and sympathetic response of SCAPE. 

How to Proceed with this Patient:
You have to either choose whether you think the rhythm is the cause, or proceed with management that is based on acknowledging both possibilities simultaneously. Options for this patient with wide complex regular tachycardia and some signs of hemodynamic compromise but not peri-arrest include: 

Immediate attempted intervention on the rhythm:
 - Synchronized electrical cardioversion
 - Adenosine and/or vagal maneuvers
 - Medical cardioversion (procainamide, amiodarone, etc)

These options all incur some small risk (sedation for cardioversion, very small risk of deterioration in rhythm with adenosine, hypotension or rhythm deterioration with amiodarone/procainamide), while having the potential benefits of cardioversion (if the rhythm is not Sinus Tach) and further diagnostic information for the rhythm. 

Observe the patient on NTG drip and BiPAP for a short time (~10 minutes at bedside):
Observe for improvement with the current ongoing interventions, more historical or EMR information, serial ECGs, and bedside features that help differentiate the rhythm including variation in rate, occasional dropped beats revealing flutter waves, etc. The risk of this strategy is prolonging hemodynamic insult and demand ischemia if the rhythm is the cause, and the benefit is potentially avoiding the risks of immediate interventions above if the rhythm is sinus tach and not the cause.


My (Meyers) personal belief given the information currently available in this case is that any of the above options above are reasonable if you are not able to prospectively determine that this is sinus rhythm. Electrical cardioversion in particular offers a rapid and effective diagnostic challenge in this scenario, and is very safe when performed by well-trained emergency physicians. On the other hand, the patient is not peri-arrest and the presentation sounds very much like the almost daily 3am wake-up SCAPErs that we all know so well, who improve rapidly in the first 10 minutes of arrival on NTG and NIV.

Smith comment: I think the P-waves in leads V1 and II are very clear, and that this is sinus tachycardia. I would not cardiovert. It is always tempting for emergency physicians to do something, but we must resist that temptation when doing something that makes the situation worse. Give the patient a bit of time and support, and you will see the rate slowly drift down, which does NOT happen in the other re-entrant etiologies of wide complex tachycardia, such as VT or SVT with aberrancy or atrial flutter. Only the automatic rhythm sinus tachycardia will have a slowly decreasing rate. If the patient worsens, it is time for endotracheal intubation.


Back to the Case:

BiPAP and low dose NTG drip were continued on arrival. The ED team was split on whether this represented VT or SVT with aberrancy, but nobody thought it was sinus tach and they agreed on their suspicion that the rhythm was the cause of the acute heart failure. 

The resident on the case states they watched the heart rate for approximately 15 minutes and it fluctuated only between 138 and 142 bpm. They then sedated with etomidate and attempted cardioversion, with BiPAP and NTG continued throughout. After these interventions, here is the next available ECG:

The QRS morphology is identical (confirming supraventricular origin), but the rate is now 118 bpm and the possible atrial activity seen on the initial ECG is clear and definitive now at the lower heart rate. It appears to be sinus tachycardia, and further raises the suspicion that the prior ECG also represented sinus tachycardia.

After sedation, BIPAP, and shock, the rate continued to drift down, leveled off around 105-110bpm and stayed there for the duration of the ED stay. BiPAP was weaned off about an hour later.

Here is a repeat ECG:

The QRS complex in V6 is now upright, while other leads remain identical to prior ECGs. This suggests a change in lead placement, and now the morphology is even more consistent with classic LBBB.

Unfortunately, the decrease in rate after shock also does not help differentiate SVT from SCAPE with compensatory sinus tach: If it was SVT, then the shock may have caused cardioversion with subsequent lowering of the rate; if it was SCAPE with compensatory sinus tach, then the decrease in rate could easily be explained by ongoing therapy with BiPAP, NTG drip, sedation with etomidate taking away the sympathetic surge that was feeding the positive feedback loop of SCAPE and compensatory sinus tach.

Retrospectively, I believe that SCAPE with compensatory sinus tachycardia is much more likely to have been the case here, based on the identical QRS and P-wave morphology seen later in definitive sinus rhythm.

Case Resolution, Part 1:

Troponin T rose from undetectable initially to around 0.17 ng/mL over the first couple hours then fell again. CXR showed severe pulmonary vascular congestion and pulmonary edema. A CT pulmonary embolism protocol failed to demonstrate any acute PE. She was admitted to the cardiac step down unit.

Cardiac catheterization revealed minimal CAD (10-30% stenoses in several small vessels, with no lesions deemed acute culprits) and severely reduced global systolic function with EF 29%.

During the first few days of her hospitalization she was observed to have flash pulmonary edema almost every night around 1-3am. She received escalating doses of lasix with improvement, and was put on 40mg lasix BID indefinitely. Outside records revealed only additional history of type 2 diabetes (already on metformin) which was also optimized and the patient's metformin dose was increased. She was discharged on hospital day 9. 


Case, Part II: Patient returns to ED:

But the patient apparently just won't quit teaching us about ECGs while on her vacation, and re-presented 1 week later complaining of an acute episode of chest pain with shortness of breath, with several days of preceding nausea and diarrhea. Vitals and exam were unremarkable, with no respiratory distress. Her pain had decreased just prior to her initial ECG:

What do you think? Are there signs of ischemia to explain her chest pain? Is is possible to have acute coronary occlusion with a recent "non obstructive" cath? Any non-ischemic abnormalities?

Of course it is possible to have acute coronary occlusion with a recent "non obstructive" cath. There are many etiologies, including simply a good old-fashioned plaque rupture of a lesion that was less than 30% stenotic. Not to mention the possibility of extra-luminal atherosclerosis, coronary spasm, or complications from the cath itself.

But there are no original or modified Sgarbossa criteria present. Sinus rhythm with (almost perfect) LBBB. The QRS is identical in its morphologic components compared to the prior discharge ECG, but there is still a very important difference in the QRS complex. Do you see it?

It's significantly wider. Prior QRS duration was 136-142 msec consistently during last admission. Today it's 168 msec. So that must trigger your hyperK cognitive hard stop alarm, which prompts you to then look for the other signs of hyperK. The T-waves are not dramatically more peaked than prior. The rhythm is sinus, not junctional or lower. But the PR interval is 200 msec, compared to 164 on the discharge ECG from 1 week ago. So we have a new wider QRS and new longer PR interval. This is strong but subtle evidence of hyperkalemia and must be acted upon, especially in any patient who complains of weakness. FYI, there is also new fragmented QRS, which suggests old infarction and is not associated with hyperK. This could be simply the way the QRS looks when it is stretched out, uncovering components of the QRS morphology that were not visible before. 

The hyperkalemic changes were not recognized, and no treatment was started yet.

Initial labs returned grossly abnormal:

Na = 114

K *unavailable*

Cl = 82

Bicarb = 9

Glucose = 209

Creatinine = 1.24 (baseline 0.80)

Anion Gap = 21

Troponin T = undetectable

Lactate 3.8

Another example of why you can't wait on the K level to diagnose and treat hyperK. Of course, the more important reason is that the patient may decompensate before the level comes back (if you're lucky enough for a true, non-erroneous level to ever come back). This is supported by the findings of Durfey et al in the newest retrospective cohort study of hyperkalemia which will be reviewed on this blog soon. 

Hyperkalemia was still not suspected, and there was concern that these very abnormal lab values were erroneous as the patient seemed extremely well appearing and was actually asymptomatic except for persistent vague weakness.

Repeat labs were sent for clarification, and returned at 1400 (approximately 3 hours after presentation):

Na = 118

K 7.2

Cl = 81

Bicarb = 12

Glucose = 209

Creatinine = 1.42

Anion Gap = 21

With the K now resulted, hyperkalemia was suspected and a repeat ECG was performed:

The QRS is slightly wider still, with QRS duration 178 msec. PR interval is still 200 msec. No obvious change in T-wave morphology. This is mildly worse than presentation.

At this point the patient received 2gm calcium gluconate, 500 mL lactated ringers, 40mg lasix IV, 10U insulin, and 10mg albuterol nebulizer. Kayexalate was also given later.

Repeat ECG several hours later:

QRS duration has decreased significantly, now 148 msec, which is near the baseline from last admission which was recorded with normal potassium level. PR interval has decreased 182 msec. 

Luckily she did not experience any rhythm or cardiovascular deterioration before hyperkalemia therapy, and the treatment was successful in lowering the K. Labs two hours after treatments showed K = 7.0, which is barely improved from 7.2, implying that the K would have risen even higher without such aggressive therapy. Two hours later the K was measured at 5.9, and continued to decrease from there.

She was transferred to the MICU where she continued to improve with supportive care, without the need of dialysis or other aggressive interventions. She was discharged on day 6. Her presentation and lab abnormalities were explained likely as multifactorial including:

1) initiation of lisinopril 5mg and spironolactone 25 daily (which had been titrated in tandem with lasix during last admission)

2) possible metformin-induced lactic acidosis in the setting of recently increased metformin dose, with possible inciting factors such as IV contrast loads given for CT PE scan and coronary catheterization; resulting in the high lactic acid level and associated nausea, vomiting, fatigue, dehydration with resultant decreased clearance of lisinipril/spironolactone, etc

3) possible euglycemic DKA (beta hydroxybutryate = 0.38 on initial labs)

ECG at discharge. QRS duration back down to 140msec, PR interval to 162 msec.

She did well, but this probably wasn't her idea of a relaxing vacation with her family. 

Learning Points:

1. "Stable vs unstable" per current guidelines is misleading; if the patient is not peri-arrest or in extremis, there may be more time or options than ACLS would have you believe.
2. Differentiating rhythm etiologies of wide complex tachycardias can be very difficult, but the approach to management can proceed safely without knowing the exact rhythm.
3. Make a habit of watching the leads being placed. Don't let lead misplacement make these cases even more difficult.
4. Shocking ST is better than missing VT, but in situations like this there may be a little more time to figure out all your options.
5. The importance of recognizing and treating hyperkalemia cannot be overstated.