"How could I convince my interventionalist to come do a cath in the middle of the night?"

I just received this email today.  I receive these fairly frequently:

Dear Dr. Smith:

I am an Emergency physician working in an outlying hospital in _________. We have an interventional hospital to which we refer cath lab patients.  I had a 31 year old with typical chest pain and vomiting and the attached ECG. I was sure he was infarcting but couldn’t convince the interventionalist to take him (after emailing him the ECG).

I treated the patient aggressively with medical management and transfered him to the tertiary center.  They did not take him to the cath lab emergently.  When he went to the cath lab the next morning he had a 99% proximal LAD lesion and a massive troponin rise.

I found the experience a little frustrating and was wondering if there was any specific ECG criteria or feature that I could have used to convince the cardiologist to get out of his bed at midnight.

Thanks for your help on this.

Kind regards,

Dr. _________

Here is the ECG:

There is minimal ST depression at the J-point in lead V3, and much more in V4-V6.  In precordial leads, there should be some J-point elevation, especially in a young male (that is why the guidelines for STEMI require more than 2.5 mm for a male under age 40, although this is not very sensitive).
There is a hyperacute T-wave in aVL, with reciprocal ST depression in II, III, aVF.
--This ECG is diagnostic of severe ischemia.
--Precordial T-waves are similar to de Winter's T-waves, but not quite as large.
--(de Winter's T-waves are hyperacute T-waves preceded by ST depression and diagnostic of LAD occlusion or subtotal occlusion).

Dear Reader,

My talk at SMACC-Chicago this year directly addresses this: the FALSE STEMI NonSTEMI Dichotomy.  The lecture will be posted online some time this year.

This ECG clearly shows ischemia, but not STEMI.  There is diffuse ischemic ST depression.  

In this case, there is no reason for demand ischemia (type 2 MI).  So this ischemia is due to thrombus causing subtotal occlusion, though not 100% occlusion (usually of LAD, but could be the Left Main).   Thrombus propagates and can fully occlude at any moment.

Thrombus often lyses, then propagates, then lyses back and forth in a very dynamic process.

Both the American College of Cardiology/American Heart Association guidelines (ACC/AHA) (Circulation 130:2354-2394; Dec 23/30, 2014 p. 2367 or p. e368), and the European Society of Cardiology guidelines, recommend emergent angiogram and PCI for patients without STEMI who have:

1. Refractory ischemia

2. Hemodynamic instability

3. Pulmonary edema

4. Electrical instability

This may include patients without specific ECG findings or positive troponins, but only due to high clinical suspicion.

Here is the quote from the ACC/AHA: 

4.4.4. Early Invasive and Ischemia-Guided Strategies:

Recommendations

Class I

4.4.1. An urgent/immediate invasive strategy (diagnosticangiography with intent to perform revascularization if appropriate based on coronary anatomy) is indicated in patients (men and women¶) with NSTE-ACS who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures).42,44,138,338 (Level

of Evidence: A)

This patient has refractory ischemia.  If you have managed his BP, given nitro, given aspirin and heparin and clopidogrel or ticagrelor, and beta blockers if not contraindicated (low stroke volume, bradycardia, AV block), and there is still ischemia, then the major societies recommend emergent angiogram.

Here is a quote from the European Society of Cardiology

“Optimal timing of PCI in Non ST Elevation-ACS has been studied extensively.” (see all studies outlined below)

However:

•“Patients at very high risk”

•   Refractory angina

•   Severe heart failure

•   Life-threatening ventricular arrhythmias

•   Haemodynamic instability

•“Were not included in RCTs, in order not to withhold potentially life-saving treatment.”

•“Such patients may have evolving MI and should be taken to an immediate (less than 2 hours) invasive evaluation, regardless of ECG or biomarker findings.”

Finally, the ACC/AHA now recommends thrombolytics for some ACS with ST depression:

2013 STEMI guidelines approve lytics for ST depression with STE in aVR!!  

Quote: "Fibrinolytic therapy should not be administered to patients with ST depression except when a true posterior (inferobasal) MI is suspected or when associated with ST elevation in lead aVR." 16,117–120 (Level of Evidence: B)

Circulation. 2013;127:529-555.  this is on p. 537.

I'm attaching some critical slides from my talk.

You can send this to him/her.

Steve

This is my slide summarizing all trials of emergent vs. delayed PCI for NonSTEMI:

•ABOARD* trial (n=360), Montalescot, JAMA 302:947; 2009

–1 vs. 20 hours, no diff., LMWH mostly, No sophisticated ECG analysis

–Refractory symptoms excluded

•TIMACS,* Mehta, NEJM 360:2165; 2009, 3000 patients

–No diff except for patients with in-hospital GRACE score greater than 140 (Early is better)

–Early was not very early (14 vs. 50 hours)

–Excluded refractory ischemia (personal communication, Mehta.  Even though the methods do not state it, Dr. Mehta wrote to me in an email: "I cannot imagine that anyone would have enrolled a patient with ongoing refractory ischemia")

•ISAR-COOL,* JAMA 290:1593, 2003; n = 410

–Better early (but 2.4 hours vs. 86 hours); included tirofiban and clopidogrel 600

–Death or Large MI: 11.6% vs. 5.9%;

–Before PCI: 3 death and 10 large MI in later group vs. 0 deaths and 1 small MI in early group; After PCI: 11 MI in both groups

•LIPSIA-NSTEMI, Thiele, Eur Ht. Journal 2011, n = 400

–1.1 vs 18.6 hours.  Death or MI: 21% (delayed) vs. 16% (Immediate), p = 0.17, low statistical power to detect a difference

–Excluded refractory ischemia

•ELISA PCI, van’t Hof, Eur Ht J 24:1401; 2003.  N= 220. Delayed always got GP IIb IIIa inhibitor (tirofiban). All received enoxaparin.

–6 vs. 50 hours.  Patent vessel: 66% (late) vs. 82% (p = 0.05)

•Meta-analysis.  Katritsis Eur Ht. J 32:32; 2011 (excludes LIPSIA-NSTEMI)

–In non-urgent cases, early PCI reduces recurrent ischemia and shortens length of stay

•Summary:

–Rapid/Urgent Cath for high risk, unstable, or refractory ischemia due to ACS.

Sudden Severe SOB and ST Segment Elevation: What is the Diagnosis and Treatment?

A middle aged man with history of MI presented by EMS for the sudden onset of difficulty breathing. 

Prehospital, he was in respiratory distress and tachypneic, and was tachycardic to 130.  SpO­­­­­­_­­2 was 85% on high flow oxygen.  Prehospital ECG (not available) was read as  ***ACUTE MI***  and the cath lab was activated by EMS.  

He was agitated upon arrival.  Lung exam revealed good air movement but no rales or wheezes (clear).  [Think: what does this mean?]  Heart rate was 140 bpm.  Extremities were cool. His left leg was mildly swollen compared to the right.  He was in severe shock.

The patient was intubated immediately upon arrival.  The end-tidal CO2 was low (~18 mm Hg).

The physician requested tPA to be prepared due to concern that this represented a massive PE.  It was withheld pending confirmation of the diagnosis and partially due to the uncertainty about whether he could go to the cath lab for STEMI if he received tPA. 

An ECG was recorded while a bedside ultrasound was also done:

There is sinus tachycardia.  There is inferior ST elevation with reciprocal ST depression in aVL and  in lead I, very suggestive of STEMI.  There is RV conduction delay (R'-wave in V1) with ST elevation in V1-V3 that is not suggestive of STEMI.  
Another possibility to consider is inferior and RV MI (STE in V1), with acute severe right sided failure.

Thus, the initial EKG was concerning for STEMI.

The bedside cardiac ultrasound was revealing: 

There is LV hypertrophy and a low volume LV with adequate systolic function.  The RV is hypokinetic and dilated (high volume RV).

The providers were concerned that the generous RV in the setting of respiratory distress, hypoxia, tachycardia, and unilateral leg swelling was very concerning for PE, but they felt that it did not fully explain the EKG findings.

Here is a view of the inferior vena cava:

It is dilated.  This is very suggestive of high right sided pressures.  But that by itself does not help in the diagnosis, because shock from both LV STEMI and PE would increase right sided pressures.

There was a discussion about whether this represented PE or STEMI. Treatment options were considered including TPA or cath lab activation. A second EKG was recorded:

Comment: What is going on?

Salient facts: The patient had sudden SOB with severe hypoxia and shock, but with clear lungs.  Ultrasound further confirmed this with absence of B-lines (not recorded).

Furthermore, a low end tidal CO2, though also associated with cardiac arrest, is common in patients with massive pulmonary embolism.  Because the lungs are ventilated but not perfused, the CO2 cannot be excreted through the airways and the etCO2 is low.

One might be tempted to attribute right sided failure to inferior MI with right ventricular MI and RV failure, but RV failure from RV MI does not cause hypoxia.

Acute STEMI only causes hypoxia if it results in pulmonary edema.  This patient had clear lungs.  When patients have severe pulmonary edema, the gas exchange is poor, and areas of the lung that are ventilated are OVER-perfused (causing pulmonary edema) and the end tidal CO2 (and arterial and venous pCO2) are high because the alveoli are filled with fluid.

A chest X-ray, taken 5 minutes after the ECG was recorded, confirmed clear lungs:

There is no pulmonary edema

Acute hypoxia with clear lungs and clear chest X-ray is pulmonary embolism until proven otherwise!

But another ECG showed even larger STEMI:

Sinus tach with PACs.  Now there is additional ST elevation in lateral leads, also diagnostic of STEMI.

STEMI on an ECG only tells you there is transmural ischemia.  The STE does not tell you the etiology.

In other words, the ECG may diagnose ischemia; it does not diagnose ACS.  

Rather, in less than 5% of STEMI cases, the ischemic ST elevation is caused by severe demand ischemia such as that caused by massive pulmonary embolism. 

The ECG findings were more pronounced now with ST elevation in II, III, aVF, and V4-V6. The cath lab activation was confirmed.

The patient became bradycardic and hypotensive.  tPA was given.

Another echo was done:


There is now worsening function of both ventricles.


There was no response to norepinephrine infusion nor to external pacing. He soon became pulseless and compressions were started. The resuscitation was continued for a prolonged period but the patient remained in PEA and never achieved ROSC. No autopsy was performed.


Learning Points:
1. Hypoxia with clear lungs is pulmonary embolism until proven otherwise (see other etiologies below)
2. STEMI only causes hypoxia by causing pulmonary edema
3. Massive Pulmonary Embolism can result in a STEMI ECG, identical to ACS STEMI.  (I have seen this numerous times but this is the first time I've posted one)
4. Low end tidal CO2 is typical of massive PE.  High end tidal CO2 is typical of severe pulmonary edema.
5. Shock from STEMI has unmistakably poor LV function and on bedside echo
6. RV failure from RV MI does not cause hypoxia.
7. Perhaps most important: if the differential is STEMI vs. massive PE, just give the tPA, front loaded (100 mg).  There is no contraindication to angiography and PCI for a patient who has received thrombolytics and remains in shock.  In fact, it is the therapy that is recommended therapy for patients who are in shock and need to be transferred to a PCI capable institution.

(Certainly if you know without doubt that STEMI is the diagnosis, then do not give tPA if you are at a PCI capable institution and rapid PCI can be done.)


Hypoxia with clear chest X-ray
1. Pulmonary Embolism.
2. Asthma
3. Hypoventilation (high pCO2)
4. Sepsis (pulmonary vasodilation and shunting)
5. Anatomic right to left shunt (VSD etc.)
6. Vasodilators such as nitroprusside (cause pulmonary vasodilation and shunting)



2013 STEMI Guidelines.  JACC 61(4):p. e97

5.3. Transfer to a PCI-Capable Hospital After Fibrinolytic Therapy

5.3.1. Transfer of Patients With STEMI to a PCI-Capable Hospital for Coronary Angiography After Fibrinolytic Therapy: Recommendations.  

CLASS I

1. Immediate transfer to a PCI-capable hospital for coronary angiography is recommended for suitable patients with STEMI who develop cardiogenic shock or acute severe HF, irrespective of the time delay from MI onset (354). (Level of Evidence: B)

Also in this section:

Angiography and PCI may be done also for:

2.  Patients with STEMI who receive thrombolytics at an outside hosptial and do not have reperfusion (as determined by EKG) should go immediately for PCI.

3.  Patients who have successful reperfusion with thrombolytics should wait 2-3 hours for their PCI.

Pediatric Drug Dosing Book - Indispensable! Far better than any App. Nearly FOMAed: only $25.00.

I don't usually deviate from ECGs and Cardiology, but I must for this.

My partner, Albert Tsai, our director of pediatrics, has written what we all here at Hennepin believe is the best resource for use of drugs and devices in Pediatric Critical Care.

This 4th Edition is available for only $25.00 (includes printing and handling costs, no matter where you live, no profit).  

So it is not completely FOAMed, but almost.

You can only pay by check and snail mail (no credit card or PayPal) using the following order form:
Order Form (print it, fill it out, send with check)

This book has every possible device, tube, airway, IV, infusion etc. and the sizes/doses divided by age/size in kg, including premies, newborn, etc.

With only the size or age of the patient, down to weeks (for premies) or months (or, if over 1 year old, by year), then you open to that page and have all the drugs and device sizes and doses listed.

Sample pages are below.

The drugs are listed by:
--Concentration
--Dose of drug per kg
--Amount of drug (mg or g) per dose for that size patient
--Milliliters per dose (given the concentration and dose) for that size patient
--special comments such as dose alterations if given down the endotracheal tube.

We have used this for 25 years at HCMC and we have found it indispensable.  Dr. Tsai has never promoted it or published it through a national publishing company.  If he had, it would be sold everywhere.

As it is, you have to get it from our hospital for a nominal fee.

Here are some example pages to give you an idea how comprehensive and easy to use this book is.

It is far better than an App because once you open it to the correct page, you can see all drugs/devices and their doses/sizes at a glance, and also hands free.

There are "many boxes" of 4th Edition books remaining, each with 25 books.  First come, first serve.

Dr. Tsai is working on the 5th Edition, but I have no idea when this will be done, and it will cost somewhat more.

The Cover

Organized by tabs with Age, Weight and whether you need infusions or just doses. 

Upper Part of the Table of Contents.  Each age group is associated with two facing pages so that you never have to turn a page once you have it open to the correct age/weight

Lower Part of the Table of Contents

Some important details

Example Layout for a Premie who is 23-32 weeks gestation and weighs ~1 Kg.
Notice that all information is visible on the two facing pages.  
It is hands-free: you never have to touch it or turn a page.  
If you have sterile gloves on, you need not contaminate them.

Just the left facing page of the above layout for the 23-32 week premie age group

Closeup of the Upper Left Part of the Layout shown above for 23-32 weeks premie, 1 Kg.

Just the right facing page of the above 23-32 week premie, 1 Kg layout.

2 weeks of chest pain, weakness. Presents with tachycardia.

A middle-aged male with no significant past history complained of chest pain for 2 weeks.  He stated that it was intermittent and there were no identifiable triggers. The pain was located at upper left chest without radiation and was "sharp" and aggravated by deep inspiration.  He endorses some SOB.

On exam he appeared somewhat lethargic, with a normal body habitus, and had the following vital signs:  BP 116/77 mmHg | Pulse 117 | Temp(Src) 36.4 °C (97.5 °F) | Resp 16 | SpO2 95%.

Cardiac exam was normal.  There was bilateral mild pitting edema.

An ECG was recorded:

What do you think and what do you want to do?
See below.

There is diffuse low voltage.  The ECG is otherwise nonspecific.

General guideline for low voltage: less than 5 mm in all limb leads and less than 10 mm in all precordial leads.

This low voltage should call to mind pericardial effusion.  There is no electrical alternans, which would be specific for tampondade.

You should do an immediate bedside echocardiogram.  Some would say all chest pain patients in the ED should get a bedside echo.

A bedside echo was done.

Here is the parasternal view:


Huge effusion with collapse of right ventricle.


Here is the subxiphoid view:


More evidence of collapse of the RV.  You can also see echogenic fibrinous strands.

Here is the apical view:


More fibrinous strands.


The patient underwent emergent pericardiocentesis.  His creatinine returned at 5.42 mg/dL and BUN at 66 mg/dL.  No other etiology of effusion was found and a diagnosis of uremic pericarditis was presumed, although the BUN was not extremely high.  Dialysis was sufficient to prevent recurrence.

Further details which are unnecessary for the learning points are withheld in the interest of privacy.

Learning Point:

1. Low Voltage has many etiologies, but the most dangerous in emergency and critical care, especially when associated with tachycardia, is pericardial effusion.  Electrical alternans is not always present.
2. Consider a bedside ultrasound for all patients with chest pain, especially if it is worrisome and unexplained.
       Look what else you might find.
       And if you look at the valves with Doppler, look what else you might find.
3.  Pericarditis does not consistently manifest with ST elevation on the ECG.

Low voltage is caused by:

1.  Impedance due to fluid, fat, or air between the heart and the recording leads.
2.  Loss of viable myocardium (usually infarction)
3.  Myocardial infiltrative diseases such as amyloidosis or myxedema

Specific examples include:
Pericardial effusion
Pleural effusion
Obesity
Emphysema
Pneumothorax
Pneumomediastinum and Pneumopericardium (see this case)
Previous MI
Severe Dilated Cardiomyopathy
Amyloidosis
Hemochromatosis
Hypothyroidism

A very elderly woman with a pacemaker and minimal symptoms

This was a very elderly woman with a pacemaker and minimal symptoms:

What are these broad complexes superimposed on the native QRS?  Are they paced?

These cannot be anything other than artifact.

Although they are regular, and appear in every lead, they occur during the ventricular refractory period during beats 1, 2, 3, and 4, and these ones also are identical to those which are between ventricular beats.

I do not know what was causing this.

Right Bundle Branch Block. What else?

This is complementary to a recent previous post.

A dialysis patient presented with pedal edema.  As a screen for hyperkalemia, an ECG was recorded:

QRS duration is 183 ms.  What do you think?

A previous ECG was immediately found at a time when the K was 6.1 mEq/L:

QRS duration is 167 ms, but a previous ECG with a normal K had a QRS of 184 ms.
What do you think?

This shows how subtle hyperkalemia can be, and yet still be diagnostic.

See the two side-by-side here:

                        Previous, with K 6.0 mEq/L                                            This Visit

Notice how the ST segment is flatter on the right than on the left (see especially lead V4).  Such a flat ST segment is part of what makes the T-wave peaked, as the rise of the T-wave from a flat ST segment is very steep.

My previous post showed the failure to recognize such a subtle sign of hyperkalemia and the subsequent v fib arrest.

In RBBB, a QRS duration greater than 175 ms should make you strongly suspect hyperK (see this link!).  In this case, in the past, there actually had been such a long QRS in the presence of a normal K, so this case was an exception.

The patient's K was 7.1 mEq/L.

A young healthy male with epigastric pain and tachycardia

A young previously healthy man with no past medical history presented with a complaint of epigastric pain for a few days.  He had no other complaints.   He appeared well.  Vitals were HR 107, BP 140/70, sats 98%, RR 20, Temp 36.7.

He had a normal exam except for the mild tachycardia.

The physician was planning on discharging the patient except for the tachycardia, which prompted him to obtain an ECG.  He was startled by the result.  He showed it to me:

QRS 105 ms.  Sinus tach.  RV conduction delay (R'-wave in V1)
Diffuse ST depression, diagnostic of ischemia.

Not knowing anything else about the patient, I just said, "This is ischemic ST depression.  He is seriously ill."

He denied any chest pain, shortness of breath, vision changes, numbness, tingling, weakness in upper or lower extremities, neck pain or stiffness, or urinary symptoms.  He had no personal or family cardiac history.   He had no calf pain or swelling, no recent surgery or travel, no history of clot or hemoptysis.  He stated he was working too hard and not drinking enough water.

They did more workup.

He started to complain of a mild sore throat and headache.   A test for group A Strep was positive.  A troponin I returned at 0.454 ng/mL.  Perhaps myocarditis?

Fluids were given for presumed dehydration.

The patient then became very SOB.  He spiked a fever.  He went into respiratory failure.  He was intubated.  Here is his chest X-ray:

Pulmonary Edema without cardiomegaly

A bedside echo was done:



There is hyperdynamic function.  There is no evidence of myocardial dysfunction or decreased contractility.  There is no apparent reason for cardiogenic pulmonary edema.

Here is another view:



There is a finding here that could make the diagnosis if you are looking for it and are good at reading ultrasounds.

It may be seen on this still capture of the video below:

The image captures the aortic outflow tract and you can see a very irregular aortic valve (circled).  Watch the video again.

This was not seen and Doppler was not done (until a much later formal echo).  What is the probable diagnosis?
























The diagnosis was aortic valve endocarditis with severe aortic regurgitation.  Blood cultures were positive for a common organism.

I cannot give more information without compromising patient confidentiality, but no more is needed to make the point.

Learning points:

1.  An ECG can often find serious cardiac pathology when none is suspected.
2.  ST depression is most often due to demand ischemia, less often due to acute coronary syndrome
3.  "Positive" troponins have many etiologies

4.  Most important: A hyperdynamic heart on cardiac echo does not rule out heart failure or cardiogenic shock: acute valvular failure is too often forgotten as the etiology.

See this case.
And this case.

And don't forget tricuspid regurgitation as an etiology of right heart failure.  We have seen two cases of acute tricuspid insufficiency from trauma (sudden compression of heart during systole rupturing chordae to tricuspid).

What is the culprit vessel?

A patient presented with chest pain and had this ECG:

There is obvious ischemic ST elevation with reciprocal ST depression.
What is the culprit artery?

A high lateral STEMI was diagnosed and the patient was taken to the cath lab.  

The interventionalist was surprised to find that the infarct artery was the RCA.

This was sent to me for explanation.  What is the explanation?


If you look at the QRS, you see that there are well formed R-waves in V5 and V6, but a Q-wave in aVL and very low voltage R-wave in lead I.  All are lateral leads and usually have similar QRS findings (though not always because V5 and V6 are more inferior than I and aVL).  The difference in this case is too large to be due to this normal variation.

So I stated that the leads were misplaced and to send me an ECG with the leads properly placed, if one was available.

Fortunately, there had been a second ECG recorded slightly later.   It was available and sent:

Now the R-wave is clearly positive in all lateral leads.  Thus, in this ECG, leads were properly placed.  And the ST elevation is inferior, with reciprocal ST depression in I and aVL.

Learning Point:

1. Try to assess the QRS before assessing the ST segments and T-waves.  Our eyes are always drawn to the ST segments first.

This is similar to proper technique of reading an X-Ray.  One is always drawn to the pathology, or the pathology one is seeking.  If you look elsewhere first to find any incidental or related findings, you will not forget to look for pathology.  But if you look for pathology first, you will forget to scrutinize the remainder of the exam and will miss important findings.

This behavior also leads to the misdiagnosis of PseudoSTEMI patterns as STEMI patterns: many PseudoSTEMI patterns are abnormal repolarization (ST-T abnormalities) that are due to abnormal depolarization (abnormal QRS).  If you look at the QRS first, you will not miss the LVH or RVH or bundle branch block or Brugada or hyperK.  Then when you see the ST elevation you will be prepared to know that it could be secondary to an abnormal QRS (not primary due to ischemia).

This ECG is NOT Pathognomonic of Brugada Syndrome

This was contributed by a friend and colleague from a Yale affiliated hospital, Brooks Walsh.

Here is Brooks' case

I had a great opportunity to co-manage a patient with one of my partners, Dr. Charles Mize. He is not only an avid resuscitationist, but also a devoted reader of Dr Smith’s ECG Blog.

A 30-something adult with type 1 DM, but no cardiac disease, presented to the ED with nausea, vomiting, and abdominal pain. They had a history of multiple visits to the ED for gastroparesis (with or without DKA), and their symptoms were stereotypic for prior visits. Analgesia, fluid, and antiemetics were provided, and a basic metabolic panel was sent.

The patient’s symptoms improved, the labs returned, and an ECG was obtained. It was handed to my partner Dr. Mize (since I was at lunch). He activated the cath lab, moved the patient to the resus room, and asked that I finish my soup sooner rather than later.

The computer interpretation read “** ** ACUTE MI / STEMI ** **.”  What does it show?

The ST-segment elevations in V1 and V2 are dramatic, and along with the ST-segment depressions in the inferior and lateral leads could suggest a STEMI. The down-sloping ST-segments with T-wave inversion also could represent a Brugada pattern. However, the QRS is modestly prolonged (about 120 ms in V3), and the ST-segment depressions in the inferior and lateral leads are followed by symmetric, narrow-based, and “peaked” T-waves. This all points to hyperkalemia.

The patient continued to deny chest pain, or that their abdominal pain was different from past episodes. His prior ECG was unremarkable. The potassium was 6.6 mEq/L.

We agreed to provisional activation of the cath lab, although we suspected that we would soon be canceling it. I then performed a point-of-care echocardiogram to assess for gross systolic dysfunction.

A point of care echocardiogram is not an appropriate test to rule-out acute ischemia. However, there was no large wall motion abnormality in the apex (correlating with the ST elevation in V1 and V2). If we had found overt akinesis in that region, we would not have proceeded to our next step.

Dr. Mize administered one gram of calcium chloride IV, and obtained numerous repeat ECGs:

First, right before the CaCl push:

Right before CaCl push

Then during push:

Next, during the CaCl push (note the heart rate increase and jumpy baseline – CaCl burns! Next time I’ll have a running NS line to dilute it):

One minute later:

I texted the ECG and echo clip to the interventionalist, and canceled the activation. Serial troponin levels were undetectable.

Two important lessons from this case

1. Push calcium first!

Our sequence of ECGs demonstrates the rapidity with which calcium can normalize the ECG manifestations of hyperkalemia, reducing the risk of fatal ventricular arrhythmias. There still exists confusion about the optimal approach to treating severe hyperkalemia, with many clinicians still turning to sodium bicarbonate or sodium polystyrene (Kayexalate) as first-line agents, despite the evidence that these agents work very slowly, if at all!

Case reports of hyperkalemia producing “pseudo-STEMI” and/or “pseudo-Brugada” are legion, over decades of the medical literature.  Prior examples can be found on this blog (here, here, and here). 

Two cases on this blog of pseudo-inferior-posterior STEMI due to hyper-K are particularly vexing.  Here is the second one.


But there are also many reports in the formal medical literature:

A case report from the NEJM is typical; ECGs were obtained at K=7.9 and K=5.1, with marked improvement in the ECG:

2. Even a K < 7 can produce dramatic ECG changes.

Our patient’s level of only 6.6 demonstrates that even “moderate” levels of potassium can produce severe ECG abnormalities. 

By contrast, the following examples from the literature all had initial potassium levels ranging from 7.0 to over 9!

K = 7.53

Recasens, Lluis, Oona Meroño, and Nuria Ribas. “Hyperkalemia Mimicking a Pattern of Brugada Syndrome.” Revista Española de Cardiología (English Edition) 66, no. 4 (April 2013): 309. doi:10.1016/j.rec.2011.04.021.

K = 9.4

Sims, Daniel B., and Laurence S. Sperling. “ST-Segment Elevation Resulting From Hyperkalemia.” Circulation 111, no. 19 (May 17, 2005): e295–96. doi:10.1161/01.CIR.0000165127.41028.D1.

​

K = 7.0

Irani, Farzan, Rahil Kasmani, and Yousuf Kanjwal. “Hyperkalemia and Cocaine Induced Dynamic Brugada-Type Electrocardiogram:” European Journal of Emergency Medicine 17, no. 2 (April 2010): 113–15. doi:10.1097/MEJ.0b013e32832e46d1. 

​

K = 7.0

Littmann, Laszlo, Michael H. Monroe, Lee Taylor III, and William D. Brearley Jr. “The Hyperkalemic Brugada Sign.” Journal of Electrocardiology 40, no. 1 (January 2007): 53–59. doi:10.1016/j.jelectrocard.2006.10.057.

​

K = 7.7

Kurisu, Satoshi, Ichiro Inoue, and Takuji Kawagoe. “Brugada-like Electrocardiographic Pattern Due to Hyperkalemia.” Clinical Cardiology 32, no. 7 (July 1, 2009): E23–E23. doi:10.1002/clc.20274. 

​

K = 8.3

Bellazzini, Marc A., and Tom Meyer. “Pseudo-Myocardial Infarction in Diabetic Ketoacidosis with Hyperkalemia.” The Journal of Emergency Medicine 39, no. 4 (October 2010): e139–41. doi:10.1016/j.jemermed.2007.04.024.

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