A Middle-Aged Man with Chest pain, Hypotension and Tachycardia

In the evening, a middle-aged man complained of chest pain at the nursing home.  Nurses found him with a BP of 50/30 and heart rate of 130 and called EMS.

He was awake, with a pulse of 130 and BP of 50/30.  Fluids were started. 

The patient arrived alert but cool and clammy.  His chest pain was vague.  He complained of chronic dyspnea.  He mentioned "cancer" and "chest".

Here was his prehospital ECG, which I viewed immediately while the resident performed cardiac ultrasound:

What do you think?

There is a narrow complex tachycardia at a rate of 130.  Is is sinus?  I could not see P-waves.  There is low voltage.

The BP rose to 70/40 after some fluid was infused.

Here is the cardiac ultrasound which the resident performed as I viewed the ECG:


This shows a huge pericardial effusion.

The IVC was very distended and there were no B lines.

We could not get a very good view of the RV to assess for collapse.

An ED ECG was recorded:

What do you think?

What do you want to do next?














ECGs: there is a regular narrow complex tachycardia still at a rate of exactly 130, with no P-waves and also no change since the prehospital ECG.  Re-entrant tachycardias (atrial flutter, PSVT, AVRT, VT) have constant regular heart rates, whereas sinus tachycardia will usually gradually change rate with differing conditions (for instance, after infusion of fluid and BP increase, sinus tach rate might decrease from 130 to 125, for instance).   It is also possibly PSVT, but much less likely, especially at a rate of 130 (slow for PSVT).

So there is a re-entrant rhythm.  Leads II and aVF appear to have flutter waves.  I diagnosed atrial flutter with 2:1 conduction.

We knew he probably had a malignant effusion.  We knew he would need the effusion drained.  and that it may ultimately require a more sustained solution than pericardiocentesis with a pigtail catheter could provide.  That is to say, that he would probably would need a surgical pericardial window.  If the surgeon would want to do that this evening, we would simply stabilize the patient for transfer to the OR.

How would we do that?

We continued fluids, with improvement in BP.

What do you want to do next?













Our plan was first to convert to sinus rhythm.  A slower rate, with atrial contribution to ventricular filling, would improve cardiac output and BP.

One could drain the pericardial fluid first.  The reason we did not is that there was a discussion of taking the patient to the OR instead for a more permanent solution of a pericardial window.

Considerations in converting to sinus:
1. Adenosine in order to confirm atrial flutter (slow AV conduction and reveal flutter waves), or to convert if this is re-entrant SVT.
Example:

What happens when you give adenosine to a patient with this rhythm?

But this is unlikely to be PSVT, so we did not use adenosine.

2. Electrical cardioversion.  There is some risk of stroke when converting atrial flutter.  We had no medical records.  We did know he was on a beta blocker, so it could have been the case that he is in chronic atrial fib/flutter.   However, he was in shock and we had to take the risk of cardioversion.

3. Chemical cardioversion.  Without first giving an AV nodal blocker, chemical cardioversion with agents such as procainamide can paradoxically increase the ventricular rate by slowing the atrial flutter rate enough for the AV node to conduct every beat; 1:1 conduction would result in a much faster ventricular rate.  Electricity is far easier anyway.

Clinical course:

We gave 0.15 mg/kg of etomidate and undertook synchronized cardioversion at 100 J.  We used etomidate because it is unlikely to affect hemodynamics.

The patient converted to atrial fibrillation.  We then used 200J to cardiovert to sinus rhythm:

Sinus rhythm, rate ~100

The patient's condition improved significantly, but remained tenuous.

Therefore, we performed ultrasound-guided pericardiocentesis.  Ultrasound showed the most fluid at the apex, so that is the approach we used.  We removed 400 mL of bloody fluid and the BP rose to 140 systolic.

Next day, the patient was again in atrial flutter with a rapid ventricular response.

It was converted with ibutilide.

Comment from K. Wang:

"A difficult case very well handled. During tachycardia, in this case, the baseline continuously undulates especially in leads II, aVR and V1; very good for atrial flutter.  Sometimes, atrial flutter waves are better described as "dome, dome, dome..." rather than "sawtooth" as in this case. The last tracing shows a long QT interval which most likely is the effect of drug(s) given."

K. Wang.

Learning Point

Hypotension may be multifactorial.  In pericardial tamponade, preload of the RV is critical, and this is impaired by atrial flutter, in which the atrial contribution to ventricular filling ("atrial kick") is impaired.  Fluids may help, but restoring sinus rhythm is even more important. 

In this case, the patient was not in extremis (he was awake, without pulmonary edema or cardiac ischemia), so we could proceed to treat it in stepwise fashion with fluids, then cardioversion, then pericardiocentesis.  Each step improved the patient's condition.  Had the patient been in extremis, we would have still done all these, but much more quickly or simultaneously.

ECG Learning Points: 

Atrial flutter rate is constant, sinus is varying
PSVT rate is usually faster than 130 (normal: 140-280)
Pericardial effusion results in low voltage

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My Comment, by KEN GRAUER, MD (8/3/2018):

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Superb discussion by Dr. Smith about a fascinating case with numerous teaching points about clinical diagnosis and management. I’ll focus my comments on arrhythmia diagnosis. For ease of discussion — I’ve put the 3 of the 5 ECGs shown in this case together in Figure-1 — which for convenience, I’ve labeled ECG A; ECG B; and ECG C.

Figure-1: Comparison of 3 of the 5 ECGs shown in this case. ECG A — is the 1st ECG done in the ED (which looked virtually the same as the prehospital ECG). ECG B — done the next day, showing a faster ventricular rate than was seen on ECG A. ECG C — after conversion with Ibutilide to sinus rhythm  (See text).

• ECG A (TOP tracing in Figure-1) — is the 1st ECG done in the ED (which looked virtually the same as the prehospital ECG). The BEST way to describe the rhythm in this tracing is as a regular SVT at ~130/minute without clear sign of sinus P waves — plus, there is hemodynamic compromise in association with this rhythm (ie, the patient was symptomatic and markedly hypotensive). As is often the case with tachyarrhythmias — precise diagnosis of the rhythm may not be possible at the time one needs to initiate treatment. The point to emphasize is that precise diagnosis of this SVT rhythm was not essential — since regardless of etiology, synchronized cardioversion was deemed necessary at the time the patient was being seen.
• NOTE: Description of this rhythm is facilitated by recall of this phrase: “Watch your Ps and Qs — and the 3Rs.” This phrase reminds us of the 5 KEY Parameters for rhythm assessment: i) Are there P waves? (or better stated, Is there atrial activity?); ii) Is the QRS wide or narrow? (ie, wide means clearly more than half a large box in duration = >0.10 second); iii) What is the Rate of the rhythm? (atrial & ventricular rates); iv) Is the rhythm Regular?; and, if there is atrial activity — v) Are P waves Related to the QRS? It does not matter in what sequence you ask yourself these 5 questions — as long as you always asses each of these 5 parameters!
• Regarding P waves — It almost looks as if an upright sinus P wave is seen in lead II of ECG A (See the 3 RED arrows in the long lead II rhythm strip). The problem is, that the PR interval of the upright deflection in lead II (under the RED arrows) is relatively long — and if anything, the PR interval should shorten when there is tachycardia. The “Bix Rule” (named after the famous Viennese cardiologist) — states that if, with an SVT of uncertain etiology, you see a P wave occur near the middle of the R-R interval — that there probably is another P wave hidden within the QRS complex! Therefore — I initially suspected that there is atrial activity in ECG A — but that there may be 2:1 AV conduction … That said, what we can say about this atrial activity — is that it is Related to neighboring QRS complexes (ie, this upright deflection occurs at a constant distance from the next QRS) — which means that even if there are 2 P waves for each QRS — one of these P waves is conducting!
• As to the other Key Rhythm Parameters — The QRS complex is obviously narrow in ECG A (it is narrow in all 12 leads!). The rhythm is perfectly Regular. This leaves us with the last of the 5 Key Parameters = estimation of the ventricular Rate. It is worth spending an extra moment on how to quickly and accurately estimate rate. I favor the Every-Other-Beat Method. Find a QRS complex that begins or ends on a heavy grid line (I took the complex in lead II of ECG A that is under the 1st BLACK vertical line). Note that it takes a little bit less than 5 large boxes to record 2 beats. Therefore, the R-R interval of HALF of the ventricular rate ~ 4.6 large boxes. If the R-R interval of half the ventricular rate would have been 5 large boxes — then half of the rate would be 300÷5 = 60/minute. Half of the rate here is therefore a little faster than this, or ~65/minute X 2 = 130/minute as the approximate ventricular rate in ECG A. As we’ll see in a moment — precise estimation of rate is very helpful in distinguishing between the various supraventricular tachycardias.
• PEARL #1: There is a short Differential Diagnosis LIST to remember for the Common Causes of a Regular SVT without clear sign of sinus P waves: i) Sinus tachycardia (sometimes sinus P waves may be hidden in the ST segment); ii) a Reentry SVT (such as AVNRT or AVRT); iii) Atrial flutter; and, iv) Atrial tachycardia. It has tremendously helped me over the years to recall this short List — since doing so quickly narrows the diagnostic possibilities. As we have already stated — the Bix Rule makes sinus tachycardia highly unlikely in this case, since the PR interval is much longer than is usually seen when the rate is this fast. Any of the other 3 entities on this List is possible … BUT ...
• PEARL #2: In my experience — the most commonly overlooked arrhythmia (by far!) is AFlutter. That’s because flutter waves may often be hidden within the QRS complex or within ST-T waves. Therefore, the BEST way not to overlook the possibility of AFlutter is the following: Always Suspect AFlutter with 2:1 AV conduction until proven otherwise — whenever you see a regular SVT at a rate close to 150/minute. That’s because the atrial rate with untreated AFlutter in adults is most often ~300/minute (range ~250-350/minute) — and the most common conduction ratio of AFlutter is 2:1. Since the ventricular rate in this case ~130/minute — this still could be within the lower rate range for atrial flutter (ie, 130 X 2 = 260/minute) — so we definitely need to consider this possibility.
• PEARL #3: The BEST way to instantly increase your ability at complex arrhythmia detection is to use Calipers. They instantly make you “smarter”. The cardiologist that fails to use calipers will overlook the diagnosis of certain complex arrhythmias. To “look” for flutter waves — I set my calipers at precisely HALF the R-R interval. Although I always look in all 12 leads — leads II, III, aVF, aVR and V1 are the most helpful leads for detecting occult atrial activity in my experience. That said, thin vertical RED lines in ECG A show why we cannot see a 2nd P wave — because if present, it would fall precisely within the QRS complex ...
• PEARL #4: Sometimes it helps to step back a little bit from the tracing. As per Dr. Smith — doing so for ECG A does suggest a subtle sawtooth pattern in each of the inferior leads — so I too suspected the rhythm for ECG A was AFlutter. That said — we would not be able to prove this diagnosis without doing more (ie, use of Lewis Leads — application of a vagal maneuver — use of Adenosine — or additional monitoring) — NONE of which is indicated, since immediate cardioversion is the therapeutic intervention of choice in this unstable patient. NOTE: The appearance of atrial activity in ECG A is not that of “typical” AFlutter — in which there is CCW rotation around the cavotricuspid isthmus (CTI), that characteristically produces a much more obvious sawtooth pattern with prominent negative deflections in each of the inferior leads. Whether the rhythm in ECG A is one of the 10-20% of “atypical” atrial flutters — or — atrial tachycardia (which is often indistinguishable on the surface ECG from atypical forms of AFlutter), is impossible to be sure of from this single tracing.
• ECG B (MIDDLE tracing in Figure-1) — was done the next day. By the “Ps, Qs, 3R” Approach — there once again is a regular SVT, this time at a faster rate of ~150/minute. Clear sign of sinus P waves is lacking — as there is no distinct upright P wave deflection in lead II. Once again, using calipers — we look in all 12 leads in search of regularly occurring deflections at precisely half the R-R interval (which if present, would strongly suggest 2:1 atrial activity). Thin vertical RED lines in lead I of ECG B show regular notching with this 2:1 ratio. In addition, a regular sawtooth pattern is suggested in the long lead II rhythm strip of ECG B (thin vertical RED lines in the long lead II). Detection here of atrial activity at ~300/minute is virtually diagnostic of AFlutter (ATach only very rarely goes that fast …).
• NOTE: The reason flutter waves are so difficult to recognize in ECG B — is that we are dealing with one of the “atypical” AFlutter types. But we KNOW the notches in lead I of ECG B are real — because these notches are no longer seen in lead I of ECG C after conversion to sinus rhythm! (GREEN arrows show return of sinus rhythm).

BOTTOM LINE: The best way not to miss the diagnosis of AFlutter — is first, to think of it — to use calipers — and then to look for it, keeping in mind the pointers suggested above.