Massive Transfusion for Motorcycle Collision with Hemorrhage, Troponin Elevated.

This ECG was done in a middle aged woman who was in a motor vehicle collision in which her vehicle "T-boned" another, so there was trauma to the anterior chest.  She had multiple rib fractures as well as serious hemorrhage and underwent massive transfusion.

Her initial troponin I, part of a critical care order set, returned at 0.55 ng/mL, and an ECG was recorded:

There are no P-waves visible. --Sinoventricular rhythm

RBBB and LAFB morphology. Rate 114.

This could be a junctional rhythm with RBBB and LAFB.

Or, much less likely, it could be a very accelerated escape rhythm from the posterior fascicle.

Either could be a result of myocardial contusion

There is some minimal ST depression -- this could represent ischemia

What else is there that could use therapy immediately?

There is a very long ST segment resulting in a very long QT.

I measure the QT as 410 ms, with a Hodges QTc of 515 and a Bazett of 580 ms.  It is important to remember that the QT with BBB is always longer because the QRS is longer.

To Correct the QT for Bundle Branch Block, one can:
1) measure the JT interval and correct it for rate.
2) measure the Tpeak to Tend interval which should be less than 85 ms, but is also rate-related.
3) subtract the excess QRS duration of the BBB from the total and use that as the raw QT, then correct for rate.
These can be complex and I refer you to a paper we wrote on the topic:
https://www.sciencedirect.com/science/article/abs/pii/S0167527316324445

If we use 3), the QRS duration is 133 ms, for 33 excess ms.  Subtract 33 ms from the QT of 410 and the result is 377 ms.  The QTc of 377 at a heart rate of 120 = 482 for Hodges and 533 for Bazett, both long.

So however you measure, the QT is long and this is because of hypocalcemia.

Case continued:

The initial ionized Calcium, before any transfusion, was 3.83 mg/dL.  Based on this ECG, we drew another sample for Ca measurement and gave 3 g Ca gluconate empirically.  The ionized Ca (drawn before replenishment) returned at 2.93 mg/dL.  A subsequent value returned at 4.26 mg/dL.

Ken Grauer below thought that there was evidence of Hyperkalemia, perhaps transient.
There were 2 K values measured in the ED: 3.7 mEq/L and 3.8 mEq/L

A subsequent ECG was recorded several hours later, after the hemorrhage was controlled and the blood pressure stabilized:

Sinus rhythm with normal intervals, no RBBB, no LAFB, no long ST segment.
It is possible that the myocardial contusion caused a transitory BBB, or it could have been rate related.
Bundle Branch Block has been reported in association with myocardial contusion.

FYI: when blood is donated, citrate is added to chelate the calcium to prevent clotting.  So massive transfusion leads to hypocalcemia.

Echo:

Technically difficult study.

The estimated left ventricular ejection fraction is 76 %.

There is no left ventricular wall motion abnormality identified.

The estimated pulmonary artery systolic pressure is 49 mmHg + RA pressure.

Normal left ventricular cavity size.

Hyperdynamic systolic performance .

No wall motion abnormality

No evidence for pericardial effusion.

Right ventricular enlargement (probably due to hypoxemic resp failure).

Decreased right ventricular systolic performance.

The troponin peaked at 1.38 ng/mL and the patient was diagnosed with myocardial contusion.

Learning Points

1. Bundle Branch Block and fascicular block could be due to myocardial contusion.
2. Beware Hypocalcemia after massive transfusion.  It presents on the ECG as a long ST segment with resultant long QT

===================================

MY Comment by KEN GRAUER, MD (7/3/2020):

===================================

The patient in today’s case is a middle-aged woman who was brought to the ED following a motor vehicle accident. She sustained chest wall trauma, including rib fractures with serious bleeding. The patient was in shock on arrival in the ED — and multiple blood transfusions were needed. Her initial ECG is the top tracing shown in Figure-1:

QUESTIONS:

• HOW would you interpret ECG #1?
• WHAT is the rhythm in this tracing?
• WHY is the QRS complex wide?
• What are YOUR thoughts on ECG #2, obtained following initial management?

Figure-1: The initial ECG in this case (TOP) — with the repeat ECG (BOTTOM) obtained several hours later, after stabilization in the ED (See text).

ANSWERS regarding ECG #1:

Severe trauma requiring blood transfusions is a common emergency presentation. Cases like this bring up a series of important considerations regarding ECG assessment and initial management in the ED. I’d add the following thoughts to the excellent discussion by Dr. Smith.

• The reason I numbered the beats in ECG #1 — is to highlight that beats #8, 14 and 15 are distorted by artifact. We know that the upright deflection preceding the QRS complex of beat #8 in the long lead II rhythm strip (BLUE arrow) is not a P wave — because this deflection is only seen in front of beat #8 — and because a glance above beat #8 at simultaneously-obtained leads aVR, aVL, aVF shows bizarre, physiologically-impossible distortion within the T wave of beat #7, without the slightest change in the R-R interval compared to other beats. Similarly, the ST depression in beat #14 in the long lead II rhythm strip, and the bizarre appearance of the QRST complex of beat #15 in leads V1 and V2 are impossible in the face of the lack of such changes in other beats on this tracing. Bottom Line: There are no P waves in ECG #1.

As per Dr. Smith — this leaves us with a regular WCT ( = Wide-Complex Tachycardia) at ~120/minute, without P waves as the rhythm in ECG #1. The upright QRS in lead V1, with predominantly negative QRS in each of the inferior leads — is consistent with RBBB/LAHB morphology. But, WHAT is the cause of the wide QRS in ECG #1? And, WHAT is the rhythm in ECG #1?

• Dr. Smith suggested that the wide QRS and lack of P waves could reflect either a junctional rhythm with RBBB/LAHB — OR — a very accelerated escape rhythm arising from the posterior hemifascicle.
• The QRS widening with bifascicular conduction block could be the result of myocardial contusion, given the severe chest trauma suffered by the patient.
• Additional findings noted by Dr. Smith in ECG #1 included a long QT interval. This was consistent with the patient’s significantly reduced ionized serum Ca++ level.

Some Additional THOUGHTS:

• I interpreted ECG #1 as suggestive of 2 electrolyte disorders = Hypocalcemia and Hyperkalemia. Both of these electrolyte disorders are common and often seen together following trauma that necessitates multiple blood transfusions.
• As I discussed in My Comment at the bottom of the July 1, 2020 post — combined low Ca++/high K+ should be suspected in the setting of a potentially predisposing clinical setting WHEN you see an ECG showing: i) Peaked T waves (especially if these T waves are taller-than-expected); and, ii) A prolonged QT interval with a “tent sign” (ie, a peaked T wave appearing at the end of a prolonged QT interval, in association with a fairly normal/straight ST segment preceding the peaked T wave). This is precisely what we see for the T wave appearance in no less than 6 of the 12 leads in ECG #1. The size and degree of peaking seen for the T waves in leads II,III,aVF; and V4,V5,V6 (if not also V3) — is disproportionately increased compared to what should-be-expected given the underlying tracing.
• PEARL #1 — Virtually all emergency care providers are thoroughly familiar with the hyperkalemic T wave picture of tall, peaked T waves seen in multiple leads (with these T waves typically showing symmetric ascending and descending limbs of the T wave — together with a relatively narrow T wave base).  However, many providers are unaware that you may also see inverted T waves with hyperkalemia — and that when you do, the deepest part of these inverted T waves also tends to be pointed when serum K+ is elevated (as is seen for the inverted T waves in leads aVL, V1 and V2 in ECG #1).
• There are a number of reasons why the patient in this case may have elevated serum K+ levels. These include: i) Severe trauma with bleeding; ii) Multiple blood transfusions; iii) Hypovolemia from shock (following severe blood loss); and, iv) Acidosis from shock, a result of sustained hypotension with poor tissue perfusion (with acidosis resulting in an increase extracellular K+ levels).
• PEARL #2 — I interpreted ECG #1 in this case without knowing serum electrolyte levels. But regardless of whether the 1st laboratory serum K+ level were to come back normal or high — the appearance of the ST-T waves in ECG #1 tells me that at the moment ECG #1 was obtained — there almost certainly was Hyperkalemia. That hyperkalemia could be transient — as a result of extracellular cation shift. Consider that the patient in this case was promptly resuscitated in the ED. Blood and fluid volume was rapidly restored, and acidosis was probably quickly corrected. As a result — the duration of hyperkalemia may have been short-lived. That transient hyperkalemia following multiple blood transfusions is often the result of extracellular K+ shift from acidosis (rather than an increase in body K+ stores) — is supported in this study by Wilson et al (Am Surg 58[9]:535-545,1992) — in which a majority of multiple transfusion (and presumably acidotic) patients in the study group were no longer hyperkalemic after correction of acidosis.
• NOTE: In the follow-up ECG of today’s case, done just hours later ( = ECG #2) — 5 ECG findings are noted that are consistent with treatment of the hypocalcemia and hyperkalemia that was present at the time ECG #1 was obtained. These include: i) Return of sinus P waves; ii) Narrowing of the QRS complex (ie, complete RBBB has regressed to an incomplete form of RBBB); iii) Resolution of LAHB; iv) The QTc has normalized; and, v) There is no longer even the slightest hint of T wave peaking.

Regarding the RHYTHM in ECG #1:

I’ve previously reviewed sequential ECG changes of Hyperkalemia (For Review — SEE My Comment at the bottom of the January 26, 2020 post).

• The mechanism for these ECG changes of hyperkalemia is interesting (Webster et al: Emerg Med J 19:74-77, 2002). The characteristic T wave peaking of hyperkalemia is seen early in the process — due to an acceleration by elevated K+ levels of terminal repolarization. With more severe K+ elevation — there is depression of conduction between adjacent cardiac cells, eventually with depression of SA and AV nodal conduction. This may result in a series of conduction defects, including PR and QRS interval prolongation — frontal plane axis shift — fascicular and/or bundle branch block — and/or AV block with escape beats and rhythms. Ultimately, QRS widening may lead to a sine-wave appearance (fusion of the widened QRS with the ST-T wave — such that distinction between the two is no longer possible). If this severe hyperkalemia remains untreated — VT, VFib or asystole are likely to result as the terminal event.
• PEARL #3 — As serum K+ increases — P wave amplitude decreases. Ultimately, P waves may disappear. This is because atrial myocytes are exquisitely sensitive to the extracellular effects of hyperkalemia (much more so than the SA node, AV node, the His, and ventricles). As a result — despite lack of atrial contraction (ie, loss of P waves on ECG) — there may still be transmission of the electrical signal from the SA node over the conduction system and to the ventricles. Thus, rather than a junctional rhythm or fascicular escape rhythm — it is at least equally likely that the rhythm in ECG #1 is a Sino-Ventricular Rhythm (in which despite lack of P waves on ECG — the rhythm IS still initiated in the SA node, with electrical transmission through to the ventricles). But because P waves disappear and the QRS is often wide with a hyperkalemic sino-ventricular rhythm — it is EASY to mistake this rhythm as either AIVR (Accelerated IdioVentricular Rhythm) or VT.

Regarding QRS WIDENING in ECG #1:

• Several factors may account for the QRS widening we see in ECG #1. As per Dr. Smith — this patient sustained significant chest trauma — so cardiac contusion is a definite possibility.
• Although an escape rhythm arising from the left posterior hemifascicle is another possibility — I thought QRS morphology in ECG #1 and ECG #2 argued against this. Fascicular rhythms often resemble known conduction defects, but with some less typical features. In contrast — QRS morphology in ECG #1 is perfectly typical for RBBB, in that it shows a definite rsR’ morphology (with taller right rabbit ear) in right-sided lead V1 — and, not only terminal S waves in lateral leads I and V6, but also initial q waves in lateral leads I and aVL (ie, the qRs morphology in lead I of ECG #1 is the mirror-image opposite picture of the rsR’ RBBB morphology that we see in lead V1 — and this is strongly in favor of a supraventricular rather than fascicular escape etiology).
• Another possibility for QRS widening is Hyperkalemia itself. ECG #2 (which I imagine was obtained not long after correction of presumed hyperkalemia) — still shows incomplete RBBB, with preservation of the qRS morphology in lead I, and of the rSR’ morphology in lead V1. So, while the chest trauma may clearly have contributed to the conduction defect with QRS widening — Hyperkalemia itself may precipitate almost any type of conduction disorder (including LAHB and RBBB). The fact that the QRS complex narrowed significantly in ECG #2 so soon after K+ correction — is sooner than I’d anticipate if chest trauma and cardiac contusion was the sole cause of QRS widening.

Regarding the TREATMENT with Calcium Gluconate:

• The “good news” in this case — is that initial treatment with Calcium Gluconate was indicated regardless of whether the sole electrolyte disturbance was hypocalcemia from multiple transfusions — OR — if there was combined hypocalcemia with transient hyperkalemia. In addition to correcting hypocalcemia — IV calcium gluconate works within minutes to minimize the adverse effect of elevated extracellular K+ on myocytes, by restoring a more normal electrical gradient across cardiac cell membranes (in so doing, reducing the risk of malignant ventricular arrhythmias).
• PEARL #4 — A “tincture of time” + serial ECG tracings will often reveal the true etiology of the rhythm and cause of conduction disturbances. The KEY is to correlate serial ECGs with what is happening to the patient.  IV Calcium usually works fast. Resolution of ECG findings consistent with hyperkalemia (with prompt return of P waves) that corresponds in timing to correction of blood loss, hypotension, acidosis, and electrolyte disturbance — would support an important contributing effect in this case from hyperkalemia.