Thursday, July 9, 2020

Chest pain and Inferior T-wave Inversion. Does this patient need emergent cath lab activation?

This ECG was texted to me, initially with no information:

What do you think?

There are QS-waves in III and aVF.  There is a qR in lead II.  There is minimal STE, upsloping, with T-wave inversion in lead II.  Leads III and aVF only have deep, fairly symmetric T-wave inversion.

My interpretation and reply (paraphrase): There is subacute inferior MI and there has probably been prolonged pain.  The initial troponin will be high.  With T-wave inversion, it is possible that the artery has opened, but with subacute MI, the T-wave may be inverted even with persistent occlusion.  If there is persistent pain, then it is persistent OMI and the patient should go to the cath lab.

Notice also:  the T-wave in aVL is large and upright.  Is this a hyperacute T-wave?  No!  It is reciprocal to the negative T-waves in inferior leads.  See explanation at bottom of case.

Here is the history:

A 50-something woman chest pain for the last week that acutely got worse in the last day and was associated with nausea, diaphoresis, vomiting.  This pain is been ongoing for many hours.

The first troponin I was very elevated at 9.13 ng/mL.

The interventionalist was not entirely on board with this and said "It is not a STEMI."  My very astute partner said, "No.  It is an OMI."

Angiogram showed a 100% subacutely occluded RCA. It was opened and stented.

The estimated left ventricular ejection fraction is 59 %.
Regional wall motion abnormality-inferior and lateral, akinetic.

The final diagnosis was "NonSTEMI."

Learning Points:
1. Q-waves may be old or new.  When associated with deep T-wave inversion, especially with any ST Elevation, and especially when upsloping, they are likely new (subacute MI).  --old MI also has T-wave inversions, but they are more shallow.  Old MI may also have some ST elevation ("Old MI with persistent STE, otherwise known as LV aneurysm morphology) shallow T-wave inversions may be present with old MI, and may also be associated

2. Inverted reperfusion T-waves may result in Pseudo hyperacute T-waves in opposite leads.  In this case, the large upright T-wave in aVL is reciprocal to the deeply inverted T-wave in III.  See case below.

3.  STEMI, NonSTEMI, OMI.  The ECG in the clinical scenario is diagnostic of OMI.  As you can see, the diagnosis of NonSTEMI is meaningless on an anatomic level.  It is correct that 1 mm of STE was never measured.  It is possible that, had an ECG been done earlier in the course of this MI that there would have been STE diagnostic of STEMI.  Or maybe not.  In any case, it is the presence of an occluded artery (OMI) that is important, not the presence of, extent of, or magnitude of any ST Elevation.

4. Reciprocal Pseudo Hyperacute T-waves can mimic real hyperacute T-waves.  See this ECG from this post:

How do you explain these inferior hyperacute T-waves?

This was a case of Wellens' syndrome of proximal LAD (I, aVL, V2, V3).  See the very large inferior T-waves, reciprocal to the large inverted reperfusion T-waves in I and aVL.

MY Comment by KEN GRAUER, MD (7/9/2020):
Today’s case is “an ECG read”. By this I mean — No clinical information was available to Dr. Smith at the time he was initially texted the ECG shown in Figure-1. The KEY clinical question is whether the patient with this ECG is in need of acute reperfusion?
  • Sometimes it is obvious from the initial ECG (even before you know the history) — that acute coronary occlusion is ongoing. At other times — the initial ECG will clearly show no acute changes. Today’s case is challenging — because ECG #1 is equivocal. I would interpret this tracing as showing inferior MI of uncertain age.

Figure-1: The ECG that was texted to Dr. Smith in this case (See text).

I’d add the following thoughts to the above discussion by Dr. Smith:
  • The rhythm in ECG#1 is sinus bradycardia at 50-55/minute.
  • The PR interval is slightly prolonged at ~0.23 second ( = 1st-degree AV block).
  • The QRS complex is narrow. The QTc is not prolonged. The frontal plane axis is slightly leftward — but not leftward enough to qualify as LAHB (ie, the QRS is not predominantly negative in lead II). There is no chamber enlargement.
  • Q waves are present in each of the inferior leads. This includes QS complexes with a notch on the S wave upstroke in leads III and aVF. This patient has at some point had an inferior MI.
  • Transition is normal (ie, the R wave becomes taller than the S wave is deep between leads V2-to-V3).

The most concerning findings in ECG #1 relate to ST-T wave changes:
  • As per Dr. Smith — there is ST segment coving in lead II (curved RED line) — with slight ST elevation followed by shallow T wave inversion in this lead. The ST segment is not elevated in the other 2 inferior leads — but the shape of these ST segments in leads III and aVF also hints at coving, and evolves into deep, symmetric T wave inversion.
  • Lead aVL is remarkable for showing a precise mirror-image reflection of both the QRS complex and T wave that is seen in lead III. This T wave in lead aVL is disproportionately tall given the modest R wave amplitude in this lead — as well as being wider-than-it-should-be at its base. To a lesser extent — lead I shows a similar picture. These high lateral lead ST-T wave changes raise concern for being an acute reciprocal change.
  • Finally — there has also been posterior involvement. Normally, leads V2 and V3 show a gently upsloping ST segment (often with 1-2 mm of ST elevation). As per the RED line over the ST segment in lead V2 — this ST segment is uncharacteristically straight without the slightest amount of elevation.

IMPRESSION: This patient has had infero-postero MI of uncertain age that could be recent or ongoing.
  • The inferior Q waves and QS complexes are large, suggesting the MI did not just happen. That said, as has been previously shown on Dr. Smith’s ECG Blog — it is possible for Q waves to develop surprisingly soon after acute coronary occlusion (ie, as soon as within the 1st hour after acute occlusion!) — so inferior lead Q wave size on ECG #1 does not rule out the possibility of a single recent event.
  • With the exception of the slight ST elevation in lead II — lack of ST elevation elsewhere is against recent acute coronary occlusion. And, although definitely abnormal — the flat (straight) ST segments in leads V2 and V3 suggest posterior infarction is not new.
  • On the Other Hand — Sinus bradycardia with 1st-degree AV block are consistent with enhanced parasympathetic tone often seen during the early hours of acute inferior MI. In addition — there is some ST elevation in lead II, together with inferior lead ST coving + very deep inferior lead T wave inversion with a mirror-image hyperacute-looking T wave appearance in the high lateral leads. These findings suggest that the MI could be recent, or even ongoing. Clinical correlation (and ideally finding a prior tracing for comparison) is needed to make sense of these findings.

Follow-Up: The history for the patient in today’s case — is that this 50-something woman had a 1-week history of chest pain that became much worse on the day of admission. Her chest pain was ongoing for many hours at the time ECG #1 was obtained.
  • The clinical course of acute infarction is not always explained by a single cardiac event. Acute coronary occlusion may occur either at the onset of symptoms, or some time thereafter. There may be spontaneous reopening of the occluded vessel — followed by reocclusion — and then, sometimes repeating this process a number of times over ensuing hour or days.
  • BOTTOM LINE: In view of this history — my guess would be that this patient had her initial event a number of days earlier (perhaps at the time her symptoms began). That said — there are enough potentially acute findings in ECG #1 in this patient with ongoing severe chest pain that prompt cardiac cath is indicated for clarification of the clinical picture. As per Dr. Smith — the inferior T wave inversion might reflect spontaneous reperfusion — but, the overall findings in ECG #1 might also reflect either persistent coronary occlusion or new reocclusion. Persistence of this patient’s chest pain facilitated decision-making — and cardiac cath confirmed 100% RCA occlusion.

Tuesday, July 7, 2020

An Very Elderly Male with Epigastric pain, "ischemic ECG" and Interesting Imaging.

A very elderly male presented with epigastric pain on and off for 36 hours.

His exam was unremarkable.

Here is his ED ECG:
There appears to be atrial fibrillation (no previous history).
Extreme Left Axis Deviation
There are inferior and anterior QS-waves suggestive of previous MI
There is inferior ST Elevation, with reciprocal ST depression in aVL, as well as in V1, suggestive of inferior and right ventricular MI
There is ST depression maximal in V2 and extending to V6.
What do you think?

Myocardial infarction was suspected.

An initial troponin returned at 0.058 ng/mL (URL = 0.030 ng/mL)

A chest X-ray was obtained:
This shows the stomach in the chest

A CT was obtained (here is a sagittal view):

This shows the stomach behind the heart and compressing the heart against the anterior chest wall.
Here are a couple coronal sections:

This is a section anterior to the posterior herniated stomach

Here is a section behind the heart showing the herniated stomach
This section is behind the heart, showing the very large, distended stomach

Clinical course:

A nasogastric tube was placed and the stomach emptied.

Another ECG was recorded:
There is now sinus tachycardia and all ST changes suggestive of ischemia are resolved.

Troponin peaked at 0.078 ng/mL and then decreased to undetectable.

Cardiac echo showed no wall motion abnormality.

Learning Point:

Anatomic pathology can alter the ECG.  In this case, the compressed heart resulted in an ischemic appearing ECG.

MY Comment by KEN GRAUER, MD (7/7/2020):
Today’s case serves as a welcome reminder that non-cardiac structural conditions may alter the ECG — sometimes in dramatic fashion! This case features an elderly patient who presented to the ED with a large hiatal hernia, in which the gas-filled stomach protruded well into the chest cavity. As shown on CT in Dr. Smith’s discussion (above) — marked gastric distention with anatomic position directly behind the heart resulted in cardiac compression against the anterior chest wall.
  • NOTE: HH (Hiatal Hernia) is not necessarily a benign condition. The patient in today’s case presented with a 36-hour history of epigastric pain severe enough to prompt a visit to the ED.
  • Additional symptoms reported with a large hiatal hernia (in which a significant portion of the stomach has entered the thoracic cavity) include — dyspnea (especially with activity) — difficulty feeding — and, precipitation of cardiac arrhythmias.
  • The mechanism for producing arrhythmias is thought to result from cardiac compression — which could be of the LA (Left Atrium), causing atrial arrhythmias (especially AFib)  and/or of the mitral annular region, including the adjacent basal inferior LV (Left Ventricular) wall. Autonomic influence may contribute to arrhythmogenesis by compression (therefore stimulation) of the vagal and sympathetic nerves. Gnanenthiran et al. postulated that one or both of these mechanisms may have been the cause in their Case Study Report of Ventricular Tachycardia that was felt to be caused by HH-induced cardiac compression (Heart Rhythm Case Reports 4:362-366, 2018).
  • In addition to arrhythmogenesis — large HH may also produce a variety of ECG abnormalities, including ST segment depression and/or elevation  T wave inversion in multiple leads — and/or alteration in QRS morphology.

“Take-Home” PEARLS from Today’s Case:
As per the Learning Point by Dr. Smith — Anatomic pathology can alter the ECG. Other potential examples of non-cardiac, chest cavity structural conditions that may result in significant ECG alterations include: ipneumothorax; ii) pleural effusion; iii) space-occupying lesions (including benign and malignant tumors); ivchest wall deformities; v) large body habitus; andvi) anatomic variants (including dextrocardia and the various types of situs inversus). Other than the well described conditions of pericardial effusion and the various types of situs inversus — I found literature on this subject was limited. Nevertheless, brief perusal of the literature I did find left me with the following impressions:
  • Each of the above conditions may be associated with ECG abnormalities similar to those I listed above for large HH = ST depression and/or elevation — T wave inversion — axis shift — poor R wave progression — Q waves and/or QS complexes. As a result — each of the above conditions is prone to producing a pseudo-infarct pattern, as occurred in today’s case.
  • Therefore — Don’t Forget to order (and look at) the patient’s Chest X-Ray. IF your patient’s primary symptom is chest discomfort — and, the ECG shows worrisome ST-T wave abnormalities — it is all too EASY to rush down the path toward acute cath lab activation, only to later discover some anatomic abnormality that was obvious on a simple chest X-ray.

Taking Another Look at the ECGs in Today’s Case:
For clarity — I’ve put both of the tracings from today’s case together in Figure-1. Consider the following questions:
  • HOW did YOU interpret ECG #1?
  • ECG #2 was obtained after nasogastric tube insertion that decompressed the stomach. Has this patient had prior infarction(s)?

Figure-1: The 2 ECGs in today’s case (See text).

MY Thoughts on ECG #1:
There is significant baseline artifact, with intermittently spaced small vertical spikes. These are not pacemaker spikes.
  • The overall rhythm is irregularly irregular. P waves are absent. Therefore — the rhythm is AFib, here with a controlled ventricular response.
  • The QRS complex appears to be minimally widened (between 0.10-0.11 second in duration). QRS morphology looks supraventricular.
  • There are deep QS complexes in each of the inferior leads. There appears to be a tiny, initial positive deflection in leads V1 and V2. Thereafter — QRS complexes vary between showing either a similar, small initial r wave vs a QS complex. The R wave in the chest leads never exceeds 2 mm in amplitude, such that transition never occurs.
  • As per Dr. Smith — there is slight-but-real ST elevation in each of the inferior leads (albeit with an upward-concavity ST segment shape) — with reciprocal ST depression in both high lateral leads (leads I, aVL).
  • In the chest leads — the ST elevation in lead V1 is clearly abnormal. The remaining chest leads all show ST depression, which (as per Dr. Smith) is most marked in lead V2. This chest lead J-point ST depression rises to disproportionately elevated and peaked T waves in leads V2-thru-V6.

My IMPRESSION: In a patient with new symptoms — ECG #1 is certainly consistent with ACS (Acute Coronary Syndrome) — and could reflect acute infarction in progress.
  • Additional Thoughts on ECG #1 — The slight QRS widening without manifestation of any specific conduction defect + the AFib rhythm suggest that this patient is likely to have some form of underlying heart disease. The deep QS complexes in each of the inferior leads — and remarkable lack of any R wave progression in the chest leads looks bizarre. Clearly this overall picture could reflect prior extensive infarction — though I was struck by the unusual and similar likeness of the QRS-ST/T wave appearance in leads V2-thru-V5. I would have LOVED to find a prior ECG on this patient to help sort out what was “new” vs “old” (vs “new + old” — although in the absence of any prior tracing, the above-described ST-T wave changes mandate assuming ACS until proven otherwise.

What Happened After NG Tube Decompression:
I found it especially interesting to compare lead-by-lead the appearance of ECG #2 with initial ECG #1:
  • As per Dr. Smith — AFib is no longer present in ECG #2. Resumption of sinus rhythm (sinus tachycardia at ~105/minute) is challenging to appreciate because: i) there is even more baseline artifact in ECG #2 compared to what was seen in ECG #1 (especially in leads II and V1, which typically are the best leads for spotting sinus P waves); ii) P wave amplitude is small; andiii) P wave morphology varies from one beat to the next. That said — Return to regularity of the rhythm and the RED arrows highlighting atrial activity in ECG #2 are consistent enough to confirm resumption of sinus rhythm after NG decompression.
  • Deep QS complexes remain in each of the 3 inferior leads.
  • Although there is slight increase in R wave amplitude in lateral chest leads V5 and V6 — R wave progression remains extremely poor in ECG #2.
  • Interestingly — there is some beat-to-beat variation in R wave and S wave amplitude in the chest leads of ECG #2. This is probably the resut of respiratory variation from movement of the diaphragm (which is contiguous to the portion of the stomach protruding into the chest cavity, and lying adjacent to the posterior surface of the heart).
  • The “good news” (as per Dr. Smith) — is that the acute-looking ST-T wave changes in leads V2-thru-V5 of ECG #2 have greatly improved. I’m not convinced that ST elevation in the inferior leads is less — but there clearly is less J-point ST depression in high lateral leads I and aVL — and the abnormal ST elevation in lead V1 has probably resolved (though this is hard to assess given all the artifact in V1).

My CONCLUSION: Prior to reviewing the literature for discussing this case — I had not fully appreciated the impact of the mechanism of cardiac compression as a causative factor in: i) altering QRS morphology; iiprecipitating supraventricular and/or ventricular arrhythmias (including VT, which can be sustained) — andiiiproducing ST-T wave changes (ST elevation and/or depression) that may mimic old or new infarction.

  • CT imaging (as shown by Dr. Smith) clearly suggests there was compression of cardiac structures in this case by the distended portion of the stomach protruding into the chest cavity. Presumably, the degree of cardiac compression was greatly reduced following NG decompression — which corresponded to resolution of AFib and marked reduction in acute-looking ST-T wave changes in ECG #2.
  • That said — this patient still has a large hiatal hernia (most likely with a large portion of the stomach still protruding into the thoracic cavity) — even though the component of ischemic- and arrhythmia-inducing cardiac compression appears to be relieved.
  • HOW MUCH of the inferior and anterior lead QS complexes might be a result of this patient’s large, protruding hiatal hernia? Was an ECG ever done before development of the hiatal hernia? I’d LOVE to know IF the unusual inferior QS complexes and persistently poor R wave progression would resolve if this patient’s large hiatal hernia was surgically corrected. Finally — Did this patient have prior infarction(s)? Unfortunately — I don’t think we can answer this question with only the information we have at hand ...
  • Clinically — the decision as to whether or not this elderly patient should undergo surgical correction of his large hiatal hernia may prove more difficult than I would have thought prior to researching this topic. Balancing this patient’s advanced age and underlying comorbidities — is convincing CT scan evidence of direct cardiac compression by the hiatal hernia + ECG evidence that recurrent gastric distension risks AFib recurrence with significant cardiac ischemia.
  • TO OUR READERS: Do YOU have cases of non-cardiac chest cavity structural abnormalities producing remarkable ECG changes that you’d like to share? If so — please SEND them to us at the CONTACT LINK for Interesting ECGs (in the righthand column of this blog, near the top of the page).

Friday, July 3, 2020

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. 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:

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.

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 (7/4/2020):
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:

  • 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; andv) 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.

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