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

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

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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.

Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer.

I was handed this ECG of a patient with dyspnea:

What do you think?

Computer interpretation: Normal EKG
Physician Overread (Final interpretation): Normal EKG

The ST segment is very flat, with a sudden rise to the peak of the T-wave.  This makes the base of the T-wave look very narrow.  A narrow-based T-wave is nearly pathognomonic for hyperkalemia.  My diagnosis was hyperkalemia.

The resident I showed it to saw nothing.  I explained all this to the resident, then went to see the patient.

Turns out he is a dialysis patient.

Later, the ECG computer interpretation was overread by another physician, and that physician thought it was normal, but took the step to compare with the most recent previous ECG.  There was no change, so that physician concluded that it was indeed normal and entered "Normal EKG" as the final diagnosis.

However, I looked a bit more in depth, and the previous ECG had also been recorded during hyperkalemia.

The K returned at 6.3 mEq/L.

Let's look at a couple previous ones from 2 years prior:

This was recorded when this patient presented with diaphoresis and muscle cramps:

The formal read was normal except for "possible old lateral MI"
QTc was measured at 484 ms which appears to be accurate, but the statement did not say "long QT"

There are definitely peaked T waves, and a long flat ST segment with an abrupt rise to the peak of the T-waves.

The K was 6.6 mEq/L

What else do you suspect?

This ECG was recorded a few hours later after bringing down the K to 4.8 mEq/L.:

These are now normal T-waves.
Can you see the difference between these and the T-waves in the 1st 2 ECGs?

Computer interpretation AND physician overread:
Normal except for long QT (486 ms)

The other thing you might have suspected is hypocalcemia, as the long QT is long because of a long ST segment (not because of a wide T-wave). 
The (not ionized) Ca on these 2 ECGs was 6.4 mg/dL (very low)
On the first ECG above, the QTc was 402 ms and the Calcium was normal.

The diagnosis was fluid overload and hyperkalemia.  Dialysis fixed both.

Learning Points:

1. Peaking of T-waves can be very subtle
2. Comparison with previous must be done with a previous that is recorded in the presence of a normal K.
3.  Peaked Ts are not necessarily large or tall.  They have a narrow base, and a sharp upstroke.  Often they look as though they would puncture you if you sat on them.
4.  Early repolarization and even LVH can have T-waves that mimic hyperK.
5. Having the physician read every EKG, whether the computer calls it normal or not, is of course only useful if the physician can recognize the abnormality

If you miss hyperK T-waves, your patient may have an unexpected cardiac arrest:

Here is a really interesting post, in which a patient with very subtly peaked T-waves, which are misinterpreted as early repolarization, has a ventricular fibrillation arrest before the K returns high:

HyperKalemia with Cardiac Arrest. 

Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia

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Comment by KEN GRAUER, MD (6/15/2019):

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Instructive case! I focus My Comments on ECG #1 = the initial ECG obtained in the ED (Figure-1). In my opinion, rather than calling this ECG “normal” (as did 2 clinicians and the computer) — there are 4 ECG findings that should be noted: i) Prolonged QTc; ii) LVH, clearly by voltage; iii) ST segment straightening in multiple leads; and, iv) Tall, peaked (and pointed) T waves with a narrow base in at least 4 of the 6 chest leads. 

• While I fully acknowledge that some of these ECG findings are subtle — I submit that recognition that this ECG is not “normal” would not have been overlooked IF interpreters had used a Systematic Approach (For “My Take” on how routine use of a Systematic Approach not only improves accuracy, but also speeds you up — See Dr. Smith’s May 7, 2019 Blog).

Figure-1: The initial ECG done in the ED (See text).

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Beginning with Descriptive Analysis:

• There is baseline artifact in ECG #1 — which is most marked in the limb leads. That said, this does not prevent accurate interpretation of the key findings.
• Rate & Rhythm — The rhythm is sinus at ~85/minute. Intervals — The PR interval is normal. The QRS complex is not wide. However, the QTc is somewhat prolonged. I measure the QT = 400 msec (See markings in lead V3). Correcting for the heart rate of 85/minute — I estimate a QTc ~470-480 msec (which is clearly above the upper expected range ~440 msec).
• Axis — The frontal plane QRS axis is normal (about +30 degrees).
• Chamber Enlargement — There is no atrial abnormality, and no RVH. But voltage criteria for LVH are definitely satisfied! I have reviewed “My Take” on a user-friendly approach to ECG diagnosis of LVH in Dr. Smith’s April 27, 2019 Blog. For ease of recall — I’ve excerpted the user-friendly criteria I favor in Figure-2. ECG #1 is an example in which the most commonly helpful criteria (35 & 12 — as per Figure-2) are negative — but both Cornell Criteria (R in aVL + S in V3 ≥28 for a man) and especially Peguero Criteria (deepest S + S in V4 ≥28mm for a man) are met. NOTE: Short, horizontal BLUE lines in leads V4 and V5 indicate the limits for R wave and S wave amplitude in these leads, in which overlap of complexes makes assessment a bit challenging.
• Q-R-S-T Changes — There are small, narrow Q waves in leads V5 and V6 (most probably normal septal q waves). R Wave Progression — shows slightly delayed transition (the R becomes taller than the S wave is deep between lead V4-to-V5). ST-T Waves — show ST segment straightening (short PURPLE lines in leads V4,V5,V6) and frank ST flattening (PURPLE lines) in leads V2 and V3. This is not normal — as the ST segment should normally be gently upsloping (Please see My Comment in Dr. Smith’s June 9, 2019 Blog). And, there is even a hint of ST depression in leads V5 and V6.
• As noted by Dr. Smith — it is because of this ST segment straightening and flattening in multiple chest leads — that the abnormal shape of the T waves in leads V2-thru-V6 should be noted. As a memory aid — the shape of the Eiffel Tower (= tall and rising to a point at the top, but with a surprisingly narrow base) — should recall the shape of typical hyerkalemic T waves (See Figure-1).

Putting this Together to formulate your Clinical Impression:

• After looking at the ECG in Figure-1 — my thoughts were that we needed to know more about this patient! I saw sinus rhythm — a prolonged QTc — definite LVH by voltage — and, ST segment straightening + flattening (and slight ST depression) + T waves in multiple leads that strongly suggested hyperkalemia.
• The fact that the QTc is prolonged in association with hyperkalemia should suggest that there may also be hypocalcemia (these 2 electrolyte abnormalities in patients with renal disease so often go hand-in-hand). Although sensitivity and specificity of the ECG is far from optimal for detection of hypocalcemia — the morphologic picture we see here (ie, with fairly straightened but not elevated ST segments, at the end of which appears a hyperkalemia-looking T wave) should strongly suggest this possibility, especially in a patient with severe renal disease.
• NOTE — Marked LVH is very common in chronic dialysis patients. The reason why T waves in ECG #1 are not all that tall in multiple leads — and why ST-T wave changes typical for LV “strain” are not seen — might be that these 2 conditions are each attenuating ST-T wave effects of the other (ie, IF on a “baseline” of marked LVH + “strain”, serum K+ then becomes markedly elevated — then you might see exactly the ST-T wave pattern we see here in Figure-1, in which there is diffuse ST straightening with slight lateral ST depression + relatively modest T wave height in most leads given the high K+ value = 6.3 mEq/L).
• P.S. — Very important point emphasized by Dr. Smith! — when going back in the patient’s chart to look for prior tracings — BE SURE (as best you can) to determine the patient’s clinical status at the time the “baseline” tracing was done. This is why peaked and pointed T waves looked “unchanged” from the first prior tracing in this case — when the patient’s serum K+ was also high ( = 6.6 mEq/L) at that time.

Figure-2: The user-friendly criteria I favor for ECG diagnosisof LVH (For my source —  CLICK HERE).

A Pathognomonic ECG. What is it?

This patient presented with weakness, decreased urine output, and vomiting:

What is the ECG diagnosis?

There is a very long QT (computer says the QTc is 525 ms) due to a long ST segment.  This is pathognomonic for hypocalcemia.  The ionized Ca was 2.34 mg/dL (normal is 4.4-5.2)

The Cr was 12.1 indicating (new onset) of renal failure.

Calcium was given without much change.

The next AM the non-ionized Ca was 5.7 mg/dL (normal: 8.6-12.0).

Here was a repeat ECG:

QTc 523.  Long ST segment remains.

Although the QT is very long, long QT due to hypocalcemia is rarely associated with Torsades de Pointes.

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Comment by KEN GRAUER, MD (3/19/2019):

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There are a number of ECG patterns that should immediately suggest a clinical diagnosis. This is one of them! The value of recognizing this particular ECG pattern — is that it may expedite your clinical diagnosis even before laboratory results return.

• To my reading — both of the ECGs in this case looked similar. I chose the 1st ECG — and for clarity, I’ve put it together with a user-friendly method I devised many years ago to rapidly estimate the QTc (Figure-1).

Figure-1: The initial ECG in this case — and a rapid method for estimating the QTc (See text).

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COMMENT: I wanted to discuss a number of interesting aspects regarding the ECG in Figure-1. As per Dr. Smith — our attention is immediately captured by the very long QTc interval in ECG #1. Measurement of intervals is one of the tasks that the computerized ECG interpretation is usually very accurate with. The computer calculated a QTc = 525 ms for the ECG #1.

• I like the “eyeball method” to tell at a glance if the QTc is likely to be prolonged. Assuming the heart rate is not too rapid (this method works less well with heart rates >90-100/minute) — one may suspect that the QTc will be long if the longest QT interval that you can clearly see on the tracing is more than half the R-R interval.
• To quickly estimate a numerical value for the QTc — I developed a Correction Factor that has been surprisingly accurate for me in assessing too-numerous-to-count QTc values that I’ve estimated over the past 3+ decades.  As per the text under the ECG in Figure-1 — you only need to remember 3 values (ie, 1.1 for a rate ~75/min; 1.2 for ~85/min; and 1.3 for ~100/minute). With a little practice using this method — you can estimate the QTc within seconds.
• Applying my method to the case at hand — the rhythm in ECG #1 is regular, with an R-R interval just under 4 large boxes. Thus, the heart rate is just a bit over 75/minute (ie, 300÷4). I selected lead V3 as one of the leads where we can clearly define the onset and offset of the QT interval. I measure the QT in this lead to be ~2.4 large boxes = 480 msec. Using a correction factor of 1.1 (since the heart rate ~75/minute) — I estimate the QTc = 480 + [480 X .1 = 48) = 480 + 48 ~528 msec. For speed and ease of calculation — I usually round off values (it’s all an estimate anyway! ) — but I’ve enjoyed being able to get very close to computer-calculated QTc values by this simple correction factor method.

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When the QTc is Prolonged:  Assuming there is no bundle branch block, ischemia or infarction — I suggest remembering the following short LIST whenever you recognize QTc Prolongation. Think of: i) Drugs (many drugs prolong the QT interval — and combinations of drugs may result in marked prolongation); ii) “Lytes” (ie, Think of low K+ — low Mg++ — and/or — low Ca++); and, iii) a CNS Catastrophe (ie, stroke, bleed, coma, seizure, trauma, brain tumor).

• Clinical correlation will typically suggest which one or more of these 3 causes of a prolonged QTc is operative for the case at hand. The patient in the case presented here had new-onset renal failure — so, assuming normal mentation and no potentially QT-altering drugs — electrolyte disturbance should be strongly suspected.

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ECG Findings of HypoCalcemia:  Hypocalcemia generally prolongs the QT interval. It is therefore one of the entities on our short LIST to immediately think of whenever you recognize QT prolongation.

• PEARL #1: In theory — pure hypocalcemia does not affect the T wave! As a result — the characteristic ECG picture of hypocalcemia is that of a flat and prolonged ST segment, at the end of which occurs a surprisingly normal-looking T wave.
• PEARL #2: Hypocalcemia and hyperkalemia may occur together in patients with renal failure. Clinically — this combined electrolyte disorder may occasionally be suspected by the ECG finding of peaked T waves with narrow base that occur at the end of a long and flat ST segment that produces a prolonged QT interval.

Final THOUGHT: We were not told what the serum K+ value was in this case. Given the very long QT interval in ECG #1 + the remarkably flat ST segment in most leads + the peaked and relatively narrow base for many T waves that look taller-than-they-should-be in leads II, III, aVF, and V2-V4 — I suspect combined Hypocalcemia and Hyperkalemia in this case.