Tuesday, October 26, 2010

Tachycardia must make you doubt an ACS or STEMI diagnosis; put it all in clinical context

This 54 year old patient with a history of kidney transplant with poor transplant function had been vomiting all day when at 10 PM he developed severe substernal crushing chest pain. He presented to the Emergency Department with a blood pressure of 111/66 and a pulse of 117. He had this ECG recorded. He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG:

There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. There is reciprocal ST depression in I and aVL. At first glance, it seems the patient is having a STEMI.
But, remember, we do not evaluate and treat ECGs, we evaluate and treat patients. Even if this ECG is the first thing one sees (as it was for me), one should stop and think: "This is an unusual STEMI." Why?
ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock. Are the lungs clear? Is the patient cool and pale? Then ACS (STEMI) might be primary; this might be cardiogenic shock.
More often, tachycardia with ST segment abnormalities (elevation or depression) is due to an underlying illness (PE, sepsis, hemorrhage, dehydration, hypoxia, respiratory failure, etc.). One must clearly rule out these processes before jumping on the ACS diagnosis.
Furthermore, notice the well-formed Q-waves in inferior leads. These must raise suspicion of old MI with persistent ST elevation.
One very useful adjunct is ultrasound: Echo of his heart can distinguish aneurysm from acute MI by presence of diastolic dyskinesis, but it cannot distinguish demand ischemia from ACS.  In this case, bedside echo did not reveal a no wall motion abnormality, but there was hyperdynamic function, which is not consistent with cardiogenic shock but rather with sepsis or volume deficit.

Large volume fluid resuscitation was undertaken. The K returned at 6.9 mEq/L. The HCO3 was 8. Cr was 13.4. Even after 3 liters of fluid, his CVP was very low.
Troponins peaked at 0.275 ng/ml. An angiogram showed no acute coronary lesions. The patient was suffering from severe dehydration, possibly with sepsis.
After stabilization, old EKGs and an old echocardiogram were found, with the ECGs demonstrating old inferior MI with persistent ST elevation (LV aneurysm morphology) and the echo showing diastolic dyskinesis.

Monday, October 11, 2010

Pseudoinfarction patterns: there are many and this is one: what is it?

This is courtesy of Mohammed S. Alo, who kindly let me reproduce a case from his blog (Mohammed Alo's blog).

This is a 40 year old male with chest pain. The cardiologist was called for management of a STEMI:

It is sinus rhythm, and there is slightly wide and abnormal appearing QRS, with an rSR' (though I don't think the duration is long enough to be RBBB, but that is a bit hard to read). There is significant ST elevation in V2 and some in V3.  There is "saddleback" ST elevation.  However, it just does not have the appearance of anterior STEMI.

First, when assessing any ST-T abnormalities, one must determine if they are "primary" (due to pathology such as ischemia or hypokalemia, etc.) or "secondary" to an abnormal QRS. And here the QRS is abnormal. Then, think if it conforms to any known pathologic morphology. If you do, and you are aware of the 3 forms of Brugada syndrome, you will see that this is very similar to Type II Brugada.

Here is another case with "saddleback" ST elevation.

Here are the 3 types:
Type I: ("Coved type") V1 has an incomplete RBBB, a wide R' wave, a downsloping ST segment, and in inverted T-wave, like this:

Types II and III) These have a saddle back ST-T wave, as in the case presented. The ST segment is at least 1 mm in Type II and less than 1 mm in Type III

There are also variants of early repolarization that can mimic Brugada. Here is one that mimics type III Brugada (again, sorry it cannot be enlarged):

Case conclusion: the man did indeed have Type II Brugada ECG, not Anterior MI.

Brugada pattern ECG does not necessarily mean the patient has Brugada syndrome.  Here are the 2002 consensus diagnostic criteria for Brugada syndrome.

Type I Brugada
Appearance of type 1 Brugada pattern in more than one right precordial lead (V1-V3) in the presence or absence of a sodium channel blocker, and at least one of the following:
1) Documented ventricular fibrillation
2) self-terminating polymorphic ventricular tachycardia (VT)
3) Family history of sudden cardiac death at <45 years
4) Type 1 ST segment elevation in family members
5) Electrophysiologic inducibility of VT
6) Unexplained syncope suggestive of a tachyarrhythmia
7) Nocturnal agonal respiration

Type 2 and type 3 Brugada syndrome — a type 2 or type 3 Brugada ECG who meet both of the following criteria [7]:

1) Appearance of type 2 or type 3 ST segment elevation (saddle-back type) in more than one right precordial lead under baseline conditions, with conversion to type 1 following challenge with a sodium channel blocker.
2) One of (a-g) above.

•Appearance of type 1 ST segment elevation (coved type) (figure 2) in more than one right precordial lead (V1 - V3) in the presence or absence of a sodium channel blocker, plus at least one of the following:

a) Documented ventricular fibrillation
b) Self-terminating polymorphic ventricular tachycardia (VT)
c) Family history of sudden cardiac death at <45 years
d) Type 1 ST segment elevation in family members
e) Electrophysiologic inducibility of VT
f) Unexplained syncope suggestive of a tachyarrhythmia
g) Nocturnal agonal respiration

Monday, October 4, 2010

Inferior STEMI: can we predict the infarct related artery?

Inferior STEMI may be due to RCA or circumflex occlusion (and occasionally due to a "Type III" or "wraparound" LAD, with concomitant anterior MI). If inferior STEMI is due to RCA occlusion, then the right ventricle may be involved, and a right sided ECG is indicated. If due to circumflex, then one need not worry about RV MI. In addition, the interventionalists like to know which artery is involved before the angiogram, if possible.

Here is the ECG of a previously healthy 35 year old male with one hour of chest pain:

There is obviously an inferior STEMI.


1. There is no reciprocal ST depression in lead I
2. There is ST elevation in leads V5 and V6.
3. ST elevation in lead II is at least as high as that in lead III

These are 3 criteria which are highly correlated with circumflex occlusion.

Kontos MC et al. Am J Cardiol 1997;79:182
Chia BL et al. Am J Cardiol 2000;86:341
Bairey CN et al. Am J Cardiol 1987;60:456

DeVerna et al. (including Kurz MC and Smith SW) has more recently developed a decision rule (see diagram), presented at ACEP Research Forum in 2008 [DeVerna CJ et al. Ann Emerg Med2008;52(4 Suppl):S117.]. We are in the process of validating this tool. A score greater than or equal to 5 diagnosed circumflex occlusion with very high specificity.

Cardiac Arrest, acute ST elevation and depression superimposed on LVH, but NOT due to ACS

This young male had ventricular fibrillation during a triathlon. He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. On his bib it stated that he had a congenital heart disorder. He arrived in the emergency department hemodynamically stable. His initial ECG is shown here.

There is profound LVH with anterolateral ST elevation and reciprocal ST depression in II, III, aVF, and ST depression in V5 and V6 that could all be secondary to LVH or could represent ischemia superimposed on the  repolarization abnormalities of LVH: note that wherever there is ST depression, it is associated with a very high voltage R-wave.  The ST elevation in V1-V3 is typical of LVH (high voltage S-waves), but the ST elevation in aVL is concordant to (in the same direction as) the high voltage and thus very suggestive of injury pattern.

ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS.

 A bedside echo performed by the emergency physician showed no wall motion abnormality and confirmed LVH. A repeat ECG after a few minutes of cool down is shown.

Now there is much less ST segment deviation, less elevation and less depression.

The troponin returned positive, and the maximum troponin was 3.8 ng/ml. The next day, and angiogram showed normal coronary arteries. An echocardiogram confirmed aortic stenosis with a large pressure gradient. The stress of the triathlon cause demand ischemia and ventricular fibrillation.  He awoke and did  well.

Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI.

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