Saturday, December 10, 2016

Acute Chest Pain: Computer reads "Nonspecific ST-T abnormalities"

A male in his 60's had a history of previously stented infero-posterior-lateral STEMI due to an occluded dominant circumflex, which had been opened and stented.

He called 911 for acute chest pain.

Here is the first prehospital ECG at time zero.  The computer read "Nonspecific ST-T abnormalities."

Time zero:
The computerized QTc was 431 ms.
The computer read "nonspecific ST-T abnormalities"
What do you think?

There is minimal ST elevation in V2 and V3.
T-waves are large in V2 and V3.
There are minimal down-up T-waves in III and aVF.

This is LAD occlusion until proven otherwise.  One must explain the minimal ST elevation in V2 and V3.  It is not due to LVH, LV aneurysm, or pericarditis.

Thus, it must be either normal variant ST elevation (loosely called "early repolarization") or acute LAD occlusion.  To me it is clearly LAD occlusion.

One can use the LAD occlusion/early repol formula to differentiate.  There is an iPhone app for it which really helps to be certain you are applying the formula correctly.

It is critical to use this formula only when the differential is subtle LAD occlusion vs. early repol (normal variant ST elevation). There must be ST Elevation of at least 1 mm. If there is LVH, it may not apply. If there are features that make LAD occlusion obvious (inferior or anterior ST depression, convexity, terminal QRS distortion, Q-waves), then the equation MAY NOT apply. These kinds of cases were excluded from the study as obvious anterior STEMI.

If you use these values:
Computerized QTc = 431 ms
ST elevation at 60 ms after the J-point in lead V3 (STE60V3) = 1.5 mm
R-wave amplitude in V4 (RAV4) = 6.5 mm

The resulting value = 25.1.  Any value greater than 23.4 is very likely to be LAD occlusion.

Case continued

This was recorded 22 minutes later: Again, nonspecific ST-T abnormalities
What do you see here?
The computer still reads "nonspecific ST-T abnormalities"
Note the computer reads the ST segment:
For V2, it is 1.03 mm
For V3, it is 1.58 mm
"Normal" for a male over age 40 is up to 2.0 mm in V2 and V3.

Now there is straightening of the ST segment in V2.  A straight ST segment is very rare in normal variant ST elevation, and the change makes it diagnostic of LAD occlusion.  Inferior ST segments have also evolved.  aVL has suspicious coving; it is probably a proximal LAD occlusion.

The ST elevation "criteria" are incorrect.

The patient arrived in the ED and had this ECG recorded at 25 minutes after the 2nd ECG (t = 47 minutes)

So this is the first ED ECG:
The computer interpretation: "Possible old inferior myocardial infarction."
Very similar, but now with more ST depression in inferior leads and subtle ST elevation in aVL.
Again, diagnostic of LAD occlusion, with evolution of findings.

The cath lab was activated.

This ECG was recorded 26 minutes later, just before the patient was transported to the cath lab:
Very interesting:
1. The ST depression in the inferior leads is gone, as is the STE in aVL, suggestive of reperfusion of the high lateral wall.
2. There is T-wave inversion in aVL, also suggestive of reperfusion.
3. V3 has developed terminal QRS distortion (loss of S-wave), suggestive of evolution of injury to the anterior wall.
4. There are the beginnings of Q-waves in V2-V4
Thus, it appears as if there has been worsening of the anterior wall and reperfusion of the high lateral wall.

My interpretation when I saw this was that the LAD thrombosis was at the ostium of the first diagonal (D1) and that it had partly reperfused, leaving D1 open and the LAD still occluded.

A 100% proximal LAD occlusion was found, with left-to-left collaterals (from the circumflex) perfusing the 1st diagonal.  This explains the reperfusion of the high lateral wall.

Here is the next day ECG:
Reperfusion T-waves in I and aVL, and V2.  Some persistent, minimal, ST elevation.

Peak Troponin I: 99 ng/mL (very high)


The estimated left ventricular ejection fraction is 50%
The estimated pulmonary artery systolic pressure is 39 mmHg + RA pressure.

Regional wall motion abnormality-distal septum anterior and apex akinetic
Regional wall motion abnormality-inferolateral (from previous STEMI).
Normal estimated left ventricular ejection fraction lower limits of normal.

Note there is no lateral wall motion abnormality because of the reperfusion, through collaterals, of that wall

Wednesday, December 7, 2016

Syncope Several Times, Complete Heart Block, And a Surprise ECG in the ED!

This was sent by one of our graduates who will remain anonymous.

A 55 year old male with a history of DM and HTN had 2 syncopal episodes, then a third while in the presence of EMS.  There was no drug use.

ECG 1. He was put on the monitor and it showed this:
There is a slow, wide complex.  There are P-waves that are regular but completely dissociated from the QRS.  In fact, they don't ever conduct.
So it is third degree heart block with a ventricular escape.
ECG 2. Within minutes, his heart rate normalized:
Normal sinus rhythm, diffuse non-specific T-wave inversion

ECG 3. He had no complaints on arrival to the ED. This ECG was recorded at 0209:
No obvious abnormalities

ECG 4. At 0416 (2 hours later) he developed "chest burning."  Here is his ECG:
Obvious Inferior Posterior STEMI

ECG 5. His burning quickly resolved, and this ECG was recorded 20 seconds later:
Resolving ST Elevation (That was fast!!)

The patient was "rattled" by this experience, felt as if something very bad had just happened.

ECG 6. 7 minutes later, the burning returned.  Here was the ECG at 0424:
This was the doctor's (my ex-resident's) response:
"He now has ST elevations in a different distribution.  Was inferior before, now lateral What the heck?  I had been considering coronary vasospasm, but the changing distribution seems to make that less likely."

He thought it might be vasospasm of two different coronary arteries.

ECG 7. At 0428 the burning persisted and this was recorded:
Now they are inferior again!!

7 minutes later the burning was gone and this ECG was recorded at 0435:
All STE has resolved again.

The Cath Lab was activated.  Here is the last ECG before he left for the cath lab at 0449:
There are now inferior reperfusion T-waves (inferior Wellens' waves!)
This supports some degree of infarction.
The troponin will be elevated, but not by much as these occlusions were brief.


The cath did not show an occlusion or a definite culprit, but some diffuse non-occlusive disease.  No PCI was performed.

I do not have the subsequent troponin.

Subsequent Echo was showed LVH and evidence of hypertrophic cardiomyopathy, without a wall motion abnormality.  EF was 65%.

The caregivers (emergency physician and cardiologists) were perplexed about what happened.

What happened?

Why the change in location of ST Elevation??? (There are two explanations below)

Look closely at ECGs 4, 6, and 7:

This was my explanation, which Haim Katalan shows was incorrect (his is below mine)

In 4. and 7., which have inferior  ST elevation, the QRS is positive in II, III, and aVF, but negative in aVL (5. also has this QRS axis)

In 6. which has lateral ST elevation, the QRS is negative in lead III, isoelectric in aVF and positive in aVL.

Thus, the limb lead placement was inadvertantly reversed between ECG 5. and 6.  And it was inadvertantly reversed back for ECG 7.

So this was a transient inferior STEMI.

Haim Katalan explanation

I looked carefully at ECG 6-7 and the first ECG with inferior STE. I don't think limb leads was misplaced. i) the chest leads looks different in ECG 6 from 7.  That can not be accounted for by limb lead swap. ii) Also in ECG 6 the STE in I & aVL have an action potential shape completely different from the STD in ECG 7 . iii) also no P wave axis change as would expected in lead swap. 

So my impression is that it was multi vessel spasm.

Transient STEMI is usually due to brief thrombotic occlusion that then lyses.  This occlusion happened several times.  The first time it did not result in chest pain but did result in complete heart block.  In Acute Coronary Syndrome, a thrombotic event, a culprit is not always found.  And the coronary disease may be mild in such cases: the thrombosis just happens at a minimally stenotic, but vulnerable lesion.  It is even possible to have thrombosis with a completely normal angiogram, though in less than 1% of cases.  In such cases, all the the atherosclerosis is outside the lumen, in the wall of the vessel. So you cannot see it on an angiogram, which is a "lumenogram."  You can see this with intravascular ultrasound, which very well images the thickness of the vessel wall.

Of course vasospasm is usually blamed for these transient ST elevation events, but unseen thrombosis is more common.

The good news is that transient STEMI has a better prognosis than non-transient STEMI, AND ACS with a non-obstructive angiogram has a better prognosis than those with tight stenoses or large thrombus burden.

Learning Points:

1.  Always check lead placement when things do not seem right!
2.  Beware of Transient STEMI
3.  Beware that ACS may have minimal findings on angiogram.

Monday, December 5, 2016

Right Precordial T-wave Inversion

This was posted on Facebook EKG club by Massimo Bolognesi, from Italy.  He is a highly respected Sports Medicine Cardiologist.

He graciously allowed me to re-post it here.

"This ECG was recorded on an asymptomatic 50 year old marathon runner who presented for pre-participation screening."

(This ECG could easily be seen in an ED chest pain patient, and I have seen many)

What do you think?

Sinus bradycardia.
There is high voltage.
There is ST elevation in V2 and V3
There are inverted T-waves in V2 and V3
There are prominent U-waves in V2 and V3

Many responders were worried about ischemia or hypertrophic cardiomyopathy.

Here was Massimo's response:

"I'm very sure of Early Repolarization (ERP) diagnosis in this case. 
First because I have a good eye on ECGs of endurance athletes
Second because I see a lot of these tracings
Third because the stress test determines the disappearance of ECG abnormalities found at rest
Fourth because the echocardiogram is normal
Fifth and last, the clinical presentation speaks clearly."  


I (Smith) have seen many similar ECGs in ED chest pain patients.  I have always believed them to be benign for the reasons described below.  But I have never had any data to support my beliefs, so I've never posted them.

Notice also that the QTc is very short. First, one must realize that the last wave is a U-wave, which is common in ERP.  So the QT must not be measured in V2 or V3.  The QT as measured in other leads is about 420 ms, with a preceding RR of 1500ms, resulting in a Bazett corrected QT interval of 345 ms. This short QT at least makes ischemia all but impossible.  ERP is, of course, associated with an increased long term risk of sudden death, but only marginally and only if in inferior or lateral locations

In addition, many readers of this Facebook post were worried about ischemia, including Wellen's syndrome ("What if this patient had presented with chest pain?"): 

Even in the setting of ischemia, the ischemia would not be represented by this ECG. This is a classic pattern and the QT is so short as to make ischemia very unlikely.  This is a normal variant.  I have seen this innumerable times in chest pain patients in the Emergency Department. At first glance, it may appear to be similar to ischemic T-waves, but it is not. The large upright U-wave, this high voltage, and the short QT interval differentiate it from ischemia.  

It is important to remember that even a patient with a normal variant could have a myocardial infarction, just as patients with completely normal ECGs may have MI.  

It is only to say that the ischemia is not represented on this ECG.

See this post on Benign T-wave Inversion.

Here is a relevant post on the inverted T-waves of Persistent Juvenile T-wave Pattern with many other the normal variants of T-wave inversion.

Friday, December 2, 2016

ST Elevation in aVL. Reciprocal ST depression in III. Is it MI?

I was reading this ECG in the queue, with no clinical info.

What do you think?

My interpretation was LVH, no evidence of MI.   There was no previous ECG or echo for comparison.

My ECG diagnosis may surprise you, as I have long discussed "ST elevation in aVL with reciprocal ST depression in lead III" as due to high lateral MI.

This is different because:
1) There is saddleback morphology in aVL, and
2) There is also high voltage.

I have previously talked about ST elevation with saddleback morphology in lead V2 as rarely being due to anterior STEMI.  See this post (the only case I've seen in which it was STEMI): 

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

Voltage on this ECG does meet Estes criteria for LVH: 
1) At least one R- or S-wave greater than 20 mm (lead II) = 3 points.
2) ST-T abnormalities in the absence of digoxin = 3 points
Total = 6 points
5 points is definite
4 points is probable
This scoring system comes from this original article.

However, meeting LVH criteria is not critical, as they are not sensitive.  Many cases of LVH show themselves only by the typical repolarization abnormalities.  In this case, we see somewhat typical repolarization abnormalities in leads III and aVF.

Estes criteria are only 34% sensitive for LVH as diagnosed by echo.   

In this paper that used other criteria, the sensitivity for LVH by echo was less than 10%!
At least one of, with or without ST-T abnormalities:
1) R-wave 11 mm in aVL
2) R-wave at least 25 mm in left precordial leads
3) S-wave at least 25 mm in right precordial leads
4) Sum of precordial SV1 or SV2 plus RV5 or RV6 at least 35 mm
5) Sum of lead I plus lead II at least 25 mm.

In both studies, specificity of the criteria was nearly perfect.

Case Continued

This 30-something presented with headache and chest pain.  He had a history of hypertension, apparently completely untreated.  His chest pain had lasted 40 minutes and was now gone.

Blood pressure was 170/105.

Another ECG was recorded several hours later:
No significant change

The history of HTN, the elevated BP, the high voltage, and the saddelback make it very unlikely that this ST elevation is due to STEMI.

The patient ruled out for MI by negative delta troponins.

Here is a post on True Positive ST elevation in aVL vs. False Positive ST elevation in aVL
However, I do not discuss saddleback in aVL in this post.

Wednesday, November 30, 2016

A Young Man with Recurrent Chest Pain and Dyspnea with Exertion


This is a young man who has had chest pain and dyspnea with exertion for years.  He presented to the ED with these symptoms again.  On this occasion, the CP was associated with stress and accompanied by some SOB, 7/10 at it's worse and made worse with activity, with radiation up into the left side of his neck and face.

No h/o hypertension.

Here is the ECG:
Probable Diagnosis?
I was shown this ECG and gave my opinion, as below.

Here is an ED bedside echo, parasternal long axis:

Look at the small the end-systolic LV chamber size

Parasternal short axis:

Again, look at the end-systolic chamber size!

What is the Diagnosis?

The ECG shows profound LVH with secondary ST/T abnormalities.  There is deep ST depression and T-wave inversions that are discordant to (in the opposite direction of) large voltage R-waves.  These ST-T abnormalities do not represent ischemia, although they could certainly hide ischemia.  Instead, these repolarization (ST-T) abnormalities are entirely secondary to depolarization abnormalities (huge voltage).

The echo shows profound LVH.  Whether it is definitely concentric or assymetric (which is seen in HOCM with assymetric septal hypertrohy) is hard to tell for certain with these bedside echos.

Comment: In a young man with no history of hypertension, and with these typical symptoms of hypertrophic cardiomyopathy (HOCM), this is HOCM until proven otherwise.

Case continued

He refused hospital admission.  He was discharged with followup for a formal contrast ultrasound and cardiology clinic.

Comment: In someone like this who refuses to be admitted, it is wise to start a beta blocker.

Case continued

He returned about a week later with similar symptoms: Central CP and SOB that can last minutes or hours, but this time it lasted for less than an hour and was again worse with activity.  There was no nausea or diaphoresis.

Here is his ECG on this visit:
Slower sinus rate, but otherwise the same.

His serial troponin I (Abbott Architect contemporary troponin, 99% = 0.030 ng/mL):
0 hour: 0.034 ng/mL
3 hour: 0.024 ng/mL
6 hour: 0.011 ng/mL

Thus, he had symptoms compatible with myocardial infarction and a diagnostic fall of troponin with one level (the first) above the 99% cutoff.  This meets the definition of MI, but only if the troponin elevation is also thought to be due to ischemia.

A Formal stress echo was done:

Dynamic intraventricular gradient 15 mmHg at rest and increased to 26 mmHg post stress.
Normal estimated left ventricular ejection fraction at rest.
Normal estimated left ventricular ejection fraction improved with stress.
No wall motion abnormality at rest.
No wall motion abnormality with stress.
Left ventricular hypertrophy concentric .
Dynamic intraventricular gradient .
Hypertrophic cardiomyopathy .
Left ventricular hypertrophy concentric obstruction.

Comment: So he has HOCM and it is likely that stress induces some ischemia in this hypertrophic myocardium. Therefore, one would call this a type 2 myocardial infarction due to outflow obstruction in HOCM.

Case continued

He was started on metoprolol and discharged.

Comment: Explanation of outflow obstruction and use of beta blockade:  In obstructive HOCM, the end-systolic volume is very small due to the hypertrophic myocardium, and it thus obstructs aortic outflow at end systole.  This the source of the "gradient."  It is similar to mild aortic stenosis, but only at end systole.  Beta blockers: 1) diminish the contractility and thus result in a larger end-systolic volume and less outflow obstruction and 2) slow the heart rate, allowing for more time to fill, resulting in larger end-diastolic volume which also results in higher end-systolic volume.

Here are some other cases of HOCM:
Exertional Chest pain and Near Syncope in a Young Adolescent
In this case, the more typical large septal R-wave is present in V1, indicative of hypertrophy of the septum.

Here is a fascinating case in which dehydration leads to low end-systolic volume and shock in an HOCM patient.  Esmolol works to manage the patient:

History of Hypertrophic Cardiomyopathy (HOCM), with Tachycardia and High Lactate

Monday, November 28, 2016

What are these wide complexes?

A middle-age male arrived by private car with chest pain.  He immediately became unresponsive, before an ECG could be recorded.

He was resuscitated from ventricular fibrillation and this 12-lead was recorded:
What are the wide complexes in the precordial leads?

Same ECG with annotation:
One may perceive these as wide complexes, but they are deceptive.
The arrows in V5 and V6 point to narrow complex QRS's.  What appears to be a very wide complex tachycardia is really narrow complex with massive ST elevation and huge hyperacute T-waves.

The rate is about 160.

The rhythm strip across the bottom (lead II) shows that these relatively normal duration QRS complexes are regular, but with intervening premature ventricular beats (PVC's, one of which is highlighted by the arrow, complexes 5, 6, 11, 12, 19, 22).
Thus, it is a supraventricular rhythm with PVC's.

Although no P-waves are visible in this, I suspect that it is sinus with PVC's.  PSVT should be converted by a PVC.
The cath lab was activated and the patient was intubated and received ticagrelor and heparin.  There was no treatment of the rhythm, but it gradually slowed down (as one would expect from supportive care in sinus tachycardia).

This ECG was recorded just before transportation to the cath lab:
Sinus tachycardia at a rate of about 100.
Massive ST elevation continues.

A mid LAD 100% thrombotic occlusion was opened and stented.  Door to balloon time was less than 60 minutes.  Echo next day showed 57% EF.  Peak troponin I was 250 ng/mL.  

Saturday, November 19, 2016

Diffuse Subendocardial Ischemia on the ECG. Left main? 3-vessel disease? No!

This was contributed by some folks at Wake Forest:
Jason Stopyra, Shannon Mumma, Sean O'Rourke, and Brian Hiestand.
It was edited by Smith

A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chest pain, weakness and nausea. The paramedic’s initial impression of the patient was that he was critically ill. The patient’s mental status was altered and his skin was pale and dusky. The initial blood pressure was 80/palp with a heart rate of 104, respirations 20, oxygen saturations of 94% and a finger stick blood glucose of 268. Exam was otherwise notable for audible wheezes, sluggish cap refill, confusion, and difficulty following commands and answering questions.

An immediate 12-lead EKG was obtained:
There is ST elevation in leads aVR and V1, with marked ST depression in I, II, III, aVF, V3-V6.
What should be done?  
Should the cath lab be activated?

Smith comment:
This patient did not have a bedside ultrasound.    Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip):

This is recorded with the LV on the right.

Look at the aortic outflow tract.  What do you see?  Answer below in the still shot.

Clinical Course

The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. En route, EMS administered aspirin 325mg by mouth, but withheld nitroglycerin due to initial hypotension. In addition, the patient received 750 mL of fluid resuscitation with transient improvement of blood pressure.

The patient was brought directly to the cardiac catheterization lab for PCI, bypassing the ED. In the cath lab, the patient’s blood pressure remained low. The diagnostic coronary angiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Aortic angiogram did not reveal aortic dissection. During the procedure, the patient had an increasing oxygen requirement and was intubated for airway protection and oxygenation. A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis, severe LVH, and a small LV cavity. The patient was transported to the CCU for further medical optimization where a pulmonary artery catheter was placed.

Here is the still shot of the ultrasound above:
This still shot shows the area of interest:
There is a hyperechoic area at the aortic valve
This is aortic sclerosis and is highly associated with aortic stenosis.
If you see this, you should Doppler the valve.
The aortic valve in this example also had critical stenosis by Doppler

The patient continued to be hemodynamically unstable with poor cardiac output and very high LV filling pressures. Despite the use of multiple high dose vasopressors, he continued to be hypotensive. The following day, the patient underwent balloon aortic valvuloplasty for severe symptomatic aortic stenosis with hypotension and NYHA class IV symptoms. Post-valvuloplasty, the patient’s pressure gradient improved, but was still substantial. Patient was continued on maximal pressors, but remained hypotensive. Approximately seven hours after he returned from valvuloplasty he went into asystolic arrest.

The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.  Although this is considered a "STEMI equivalent" and the ACC/AHA guidelines even approve of thrombolytics for ACS with this ECG, the usual criteria used to alert the cath lab team of an inbound Code STEMI are not met by this ECG.

Smith comment:
Remember, ST depression does not localize to the area of ischemia, so "infero-lateral" does not tell you where the ischemia is - in fact, it is diffuse subendocardial ischemia.  ST elevation in lead aVR is reciprocal to this ST depression of diffuse subendocardial ischemia; the ST depression vector is towards II and V5 and thus the ST elevation vector is towards aVR.

Author continued:
STE in aVR is often due to left main coronary artery obstruction (OR 4.72), and is associated with in-hospital cardiovascular mortality (OR 5.58).1 ST elevation of 1 millimeter or greater has been shown to be 80% sensitive and 90% specific for severe left main coronary artery and/or 3-vessel disease that may require coronary artery bypass grafting, in some series.2 The astute paramedic recognized this possibility and announced a CODE STEMI.

Smith comment:
I would change the above statement to: "In the setting of ACS, STE in aVR is often due to left main or 3-vessel obstruction...."  The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.  Diffuse subendocardial ischemia is more often due to supply/demand mismatch in the absence of ACS than it is due to ACS.  Common etiologies of supply/demand mismatch are hypoxia, tachydysrhythmias,  hypotension (from whatever cause), anemia, coronary artery stenosis without ACS, or (intraventricular) hypertension.

--Oxygen supply is determined by: 1) oxygen carrying capacity, 2) O2 saturation, and 3) Coronary flow.   Thus, in the absence of athero-thrombotic mechanism (ACS), myocardial ischemia can be brought on by:
1) Hypotension (diastolic hypotension, as all coronary flow happens during diastole because intramyocardial pressure during systole stops blood flow).  Hypotension may of course be a result of a brady- or tachydysrhythmia.
2) Hypoxia, including poisons of oxidative phosphorylation such as HS, CO, CN.
3) Anemia, or poisons of hemoglobin such as methemoglobin or CO
4) Fixed coronary stenosis that limits flow.

--Oxygen demand is determined by:
1)  Afterload (high resistance to LV outflow), which is increased by elevated blood pressure or by aortic stenosis
2)  Heart rate: sinus tachycardia

--This patient has both decreased supply (hypotension) and increased demand from 1) high afterload (LV pressures are very high because of the aortic stenosis outflow resistance) and 2) high heart rate.

--This demonstrates that there may be some value to heart auscultation, to listen for an aortic murmur.  In fact, bedside ultrasound might even find severe aortic stenosis.  If you can use Doppler, then you can diagnose it.

Authors' commentary: Cardiogenic shock in the setting of severe aortic stenosis.
As I met the paramedics and cath team in the lab, I was ready to see severe coronary disease (CAD), but the vessels were non-obstructive. This patient’s severe aortic stenosis (AS) and associated severe cardiogenic shock likely created the ECG pattern, resulting in a very difficult challenge for our inpatient team.

Fundamentally, cardiogenic shock is an issue of decreased cardiac output. This may be secondary to multiple factors, including decreased cardiac contractility (ie. myocardial infarction), arrhythmias, valvular pathology, shunts, or outflow obstructions.

As with other cases of shock, initial fluid resuscitation may be considered. In cardiogenic shock, fluid may worsen the pulmonary edema associated with acute heart failure, but may still be required to support the hemodynamic status of the patient.

Guidelines from the American Heart Association have been unchanged for decades with recommendations for positive inotropes, such as dobutamine and dopamine, in cases of cardiogenic shock.3 There is evidence to show that using sub-maximal doses of both dobutamine and dopamine in conjunction, rather than using a single agent, provides benefit for the patient. Benefits include improvement in the patient’s MAP and cardiac output, while minimizing the amount of myocardial oxygen used with the increased cardiac output (CO).4 This is crucial, as these patients may have already had some degree of cardiac ischemia. This was particularly important for the patient presented above, given the baseline increase in oxygen consumption seen in AS due to the outflow obstruction.

Smith comment: 
In a large randomized trial of dopamine vs. norepinephrine (11) for shock which was published after the above-mentioned recommendations, dopamine had more adverse events (especially severe dysrhythmias, and especially atrial fibrillation).  In the subgroup of patients with cardiogenic shock, dopamine had a 33% statistically significant elevated mortality over norepinephrine.   Thus, norepinephrine is a better choice in cardiogenic shock (as in this patient) than dopamine or dobutamine.  Dobutamine may be preferred in patients without severe hypotension who have high vascular resistance.
--De Backer D et al.  Comparison of Dopamine and Norepinephrine in the Treatment of Shock.  NEJM 362(9):779; March 4, 2009. 

Author continued: 
Another positive inotrope to consider would be milrinone as it decreases SVR and increases cardiac output; however, one must proceed with caution as the pharmacological mechanism of milrinone can cause vasodilation and worsen hypotension.

When pressors are not able to sustain blood pressure, balloon valvuloplasty may be considered. This is a procedure whereby a catheter is introduced through the femoral artery, and advanced to the have the tip distal to the left subclavian artery. A balloon is then threaded over the catheter, and is inflated and deflated with diastole and systole, respectively. It has been recommended as a bridge to surgery in those that are not candidates for surgery.5 Unfortunately, availability is generally limited to major medical centers.6,7 Surgical repair of AS, by either TAVR or SAVR, is the definitive treatment for this condition. It should be noted, though, that emergent surgical intervention in unstable AS patients is associated with significant mortality, with rates between 30-50%.8

Vasodilator therapy for critical AS

Although not applicable to the case above given the patient’s hypotension, nitroprusside may be appropriate for patients with pulmonary edema in the setting of acute heart failure secondary to AS. Though long thought to be contraindicated in AS due to the condition’s preload-dependent state, there has been some evidence to indicate nitroprusside is beneficial to these patients. In one important uncontrolled study, nitroprusside used in patients with critical AS and heart failure with reduced ejection fraction (mean EF of 21%, mean MAP of 81 mm Hg) had significant improvement of cardiac index, without any episodes of hypotension, ischemic EKG changes, arrhythmias, or dyspnea.9  The only criterion for exclusion from this study was hypotension, defined as either the need for intravenous inotropic or pressor agents (dobutamine, dopamine, epinephrine, milrinone, norepinephrine, or phenylephrine) or a mean systemic arterial pressure below 60 mm Hg. The mean MAP for these patients was 81 +/- 13.

Furthermore, a study compared patients with AS to patients without AS in acute pulmonary edema who received nitrates. There was no significant difference between the percentage of patients in each group who developed hypotension after starting therapy. However, there was note that once these patients did develop hypotension, patients with moderate and severe AS were more likely to have sustained hypotension despite interventions.10

The 2014 ACC/AHA guidelines for the Management of Patients with Valvular Heart Disease, referencing this article, gives this recommendation:

"CLASS IIb 1. Vasodilator therapy may be reasonable if used with invasive hemodynamic monitoring in the acute management of patients with severe decompensated AS (stage D) with NYHA class IV HF symptoms. (Level of Evidence: C) In patients who present with severe AS and NYHA class IV HF, afterload reduction may be used in an effort to stabilize the patient before urgent AVR. Invasive monitoring of LV filling pressures, cardiac output, and systemic vascular resistance is essential because of the tenuous hemodynamic status of these patients, in whom a sudden decline in systemic vascular resistance might result in an acute decline in cardiac output across the obstructed aortic valve. However, some patients do benefit with an increase in cardiac output as systemic vascular resistance is slowly adjusted downward due to the reduction in total LV afterload. AVR should be performed as soon as feasible in these patients."

The variables that interplay in cases of severe aortic stenosis are what cause these patients to be so difficult to manage, and specific therapies targeted to fix one issue often worsen the effects of another issue. If someone is in respiratory distress, their airway and breathing needs to be secured, either through non-invasive or invasive means. Next, the patient’s blood pressure needs to be stabilized. Oftentimes the most appropriate agent will be a positive inotrope, with consideration of a vasoactive agent in persistent hypotension. Once a patient is stabilized, determining the extent of damage to their myocardium and a plan for definitive management can then be determined.

Smith comment:

Supportive care is often overlooked in the management of cardiogenic shock.  The work of breathing demands significant cardiac output and thus puts demands on the heart.  Mechanical ventilation with paralysis removes up to 50% oxygen demand and can put the heart to rest.  I would immediately intubate a patient who is this ill.

As for other invasive therapies, intra-aortic balloon counterpulsation (12, 13) appears to work well in non-randomized studies, and this would also make sense: the balloon in the aorta inflates in diastole, increasing diastolic pressure and thus coronary flow. It also deflates during systole, which normally would reduce afterload; however, in the setting of aortic stenosis, the afterload is determined mostly by the valve, not by post-valve resistance.

Smith Final Comment:It is uncertain what initiated this patient's instability.  Any alteration in physiology can change "compensated" AS to "decompensated" AS.  For instance: sepsis, bleeding, dehydration, hypoxia, and mild ACS.  This patient had a small LV cavity which is unusual for someone with AS, poor LV function, and high filling pressures, but is probably due to severe LVH.  As LV filling pressures were found to be high, this small LV cavity would not be a result of volume depletion.  In any case, once AS becomes decompensated, for whatever reason, it is extremely difficult to manage because of the low coronary perfusion pressure and high oxygen demand.

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Wednesday, November 16, 2016

Chest Pain and Cardiogenic Shock with Profound ST Depression & STE in aVR. Activate the Cath Lab?

A middle-aged woman with known severe coronary disease had onset of substernal chest pain while at dialysis.  911 was called.  A prehospital ECG was similar to the first ED ECG, which is shown below.  The patient arrived with a systolic blood pressure of 90 mm Hg, too low to administer nitroglycerine.  An initial lactate was elevated at 5.5.

She was given aspirin, heparin, and ticagrelor.

Here is her initial ED 12-lead ECG:
There is atrial fibrillation with a rate of approximately 114.
There is extreme ST depression in multiple leads and ST elevation in aVR, suggesting left main and/or 3 vessel disease ischemia.
There is some STE in V1 and aVL, further suggesting left main involvement.

Is this Acute Coronary Syndrome?
Do you want to activate the cath lab?
What else do you want to know?

It is important to note that these findings, if due to atherothrombotic acute coronary syndrome (ACS), are NOT due to occlusion of the left main, as is frequently stated in online postings and in literature.  Instead, it is far more commonly due to severe obstruction with continued flow (an open artery).  See this post:

ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion

There are many causes of diffuse ST depression, with reciprocal ST elevation in aVR.  It is most commonly due to demand ischemia, not due to ACS!  So it pays to do a few minutes of research prior to making any drastic management decisions.

First, there was an ECG from 3 months prior:
This shows sinus rhythm.
This information is critical, because it shows that the patient might respond to therapy to convert her to sinus rhythm.  Chronically ill cardiac patients who are in chronic atrial fibrillation are very difficult to convert, but this patient was recently in sinus and may readily convert back to sinus.

Further review of her chart showed her to have "no revascularization potential".  Review of the previous angiogram reports showed that all native vessels were occluded and that all coronary flow depended on a single CABG Y graft from the aorta to both left anterior descending artery and to a posterior branch of the circumflex artery.  She was completely dependent on this graft.

It was known to be diseased and at extremely high risk for any intervention.

Consider this question: If this patient needs reperfusion therapy, what option(s) is (are) available?

A bedside ultrasound (not shown) revealed a small but hypertrophic LV chamber with reasonably good LV function.  There were no B-lines of pulmonary edema.  
(Chart review also showed previous echocardiograms had concentric hypertrophy with normal LV function.)

What do the results of bedside ultrasound tell you?  What do you want to do?

Given the new atrial fibrillation, and in consultation with the cardiologist, we decided to cardiovert her.  We gave her a small dose of etomidate (to avoid hemodynamic deterioration) and electrically cardioverted her with 150 J biphasic.   She required bag-valve mask ventilation during sedation.  She converted temporarily, then reverted again to atrial fibrillation.   We shocked her again, and she again converted to sinus rhythm. After several minutes she reverted to atrial fibrillation again.

It was now clear that to keep her in sinus rhythm, we would need an antidysrhythmic.  We chose amiodarone in spite of its possible negative inotropic effect.  She tolerated 2 150 milligram loads of amiodarone well, and was started on a drip.

This is her repeat ECG at 2 hours after arrival, on amiodarone:
There is sinus rhythm with premature beats in a bigeminal pattern.
It is difficult for me to say for certain if the premature beats are PABs with abberancy or PVCs.
The ST depression in not nearly as profound as before.

Chest pain had decreased from 10/10 to 3/10.

At this point, we were pretty convinced that her ischemia was due to atrial fibrillation with rapid ventricular response and loss of the atrial contribution to ventricular filling.  There was probably a component of volume depletion from dialysis, and we probably should have given a fluid bolus.

She was admitted to the intensive care unit in a better condition than when she arrived. Her condition continued to improve, with decreased chest pain and improving hemodynamics.  She became hypotensive at one point, with collapsing IVC on ultrasound, and improved with IV fluids.

She was admitted to the ICU on an amiodarone drip and continued to improve.

Here is her ECG at 6 hours after arrival:
There is sinus rhythm.  The ST depression in nearly entirely gone.

Troponin I peaked at 55 (very high).

She did well, was started on oral amiodarone, and was discharged after a couple days in the hospital.

What happened?

Although ACS is not out of the question, this was my assessment: the patient had a bit too much fluid removed during dialysis and, at the same time, went into atrial fib with RVR.  This resulted in decreased oxygen supply (decreased cardiac output due to decreased stroke volume, leading to poor coronary perfusion pressure in a patient with fixed coronary stenosis) as well as increased oxygen demand from a rapid rate.   This assessment is supported by the bedside ultrasound: she was in shock but had no pulmonary edema, and her LV chamber size was small with good function.

When a patient is in shock due to primary ACS without dysrhythmia, it is due to poor LV function (if not due to valvular disorder) and results in a more fully filled (even sometimes dilated) chamber and high filling pressures, and often with pulmonary edema.

When a patient is in shock due to atrial fibrillation with RVR and poor atrial contribution to ventricular filling, one may see a small, poorly LV filling, as with this patient.  [A patient may certainly get high pulmonary vascular pressures, and pulmonary edema, when atrial fibrillation is the initiating factor, but in this case such evidence of high pulmonary vascular pressure was probably absent due to volume depletion.]

It is possible that this was ACS, but that would only demonstrate how ACS with severe ischemia is not always best treated in the cath lab. Medical therapy often works (antiplatelet, antithrombtic, and -- though not in this case - nitroglycerine).

If it were ACS, what reperfusion options were available?

1) Aspirin, heparin, and a P2Y12 inhibitor.  We know that the administration of just these antiplatelet and antithrombotic agents may result in diminution of thrombus burden.

2) Very high risk percutaneous coronary intervention

3) Fibinolytic therapy!  When managing this patient, I kept this option in mind.  Fibrinolytics have long been forbidden for ST depression, but this is based on very sketchy data from the thrombolytic era.  In a nutshell, in those randomized trials, the patients enrolled had 1) few lead with ST depression, 2) very minimal ST depression and 3) were treated, depending on the study, at 6-12 hours after onset, a time at which most myocardium at risk may already be irreversibly infarcted.  Thus, the ACC/AHA 2013 STEMI guidelines now list diffuse ST depression, with ST elevation in aVR, as an indication for thrombolytic therapy.  I discuss this more at this post:

ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion.

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