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.  SpO­­­­­­­­2 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.  

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:
--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
Pneumomediastinum and Pneumopericardium (see this case)
Previous MI
Severe Dilated Cardiomyopathy

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).