Saturday, January 28, 2012

Chest pain and hypotension in a patient who is 3 weeks post STEMI

A middle aged patient who was 3 weeks s/p STEMI came from cardiac rehab where he developed some chest pain, dyspnea and weakness on the treadmill.  In the ED he had some continued chest pain and hypotension. Here was his ECG:
There are inferior and lateral Q-waves with T-wave inversion in the corresponding leads.  There is minimal ST elevation.  There is no acute STEMI.  This is diagnostic of recent, reperfused STEMI.  The T-inversions are "reperfusion T-waves." 

This looks like the typical ECG of someone who had a recent Q-wave MI.  The small amount of ST elevation is persistent, not acute.  Acute STEMI would have upright T-waves.  With re-occlusion, the T-waves become upright (pseudonormalize, as in these cases).  The patient might be having cardiac ischemia, but if he is, it is unstable angina or non-STEMI, or perhaps he has not YET pseudonormalized, so serial ECGs may be important.

Below are his presenting STEMI ECG and his post-PCI ECG from 3 weeks prior:

Because of the hypotension, chest pain, and T-wave inversions, the physicians were worried about MI, took the patient to the critical care room, and called the cardiologists.  However, these T-wave inversions should be expected at one month after MI.  This is normal for these patients.

They also did an ED bedside ultrasound, shown here:

This shows a large amount of pericardial fluid, with some echogenic structures that appear to be thrombi or fibrinous exudate. The RV free wall collapses, indicating tamponade.  If you are uncertain where the pericardial fluid is, I have annotated still images with arrows at the bottom of the post.

The differential includes hemopericardium from myocardial rupture, or from coronary artery rupture from PCI, or Dressler's syndrome of post-MI pericardial effusion. 

After pericardiocentesis was unsuccessful, he was taken to the OR for a pericardial window.  300-450 ml of serosanguinous fluid was drained.  The patient was given a probable diagnosis of Dressler's syndrome.

Differential of peri-infarct pericardial fluid
The differential includes 1) pericarditis with effusion or 2) hemopericardium.
1) Pericarditis with effusion:
   a) If 3 weeks after MI, then Dressler's syndrome (Dressler's syndrome is also known as post-myocardial infarction syndrome, post-cardiac injury syndrome and postpericardiotomy syndrome), which is a late post-MI autoimmune pericarditis occurring about 3-4 weeks after the MI.  Dressler's syndrome appears to be quite rare, according to Shahar and Lichstein
   b) Nonspecific pericarditis
2) Hemopericardium would be due to myocardial rupture, which could be due to:
   a) Rupture of a coronary artery due to PCI or
   b) Free wall Myocardial rupture (see below, next paragraph).  

Myocardial rupture is not uncommon. It is found on 1% to 3.5% of autopsies of patients who died of MI. It is associated with transmural MI; since most STEMI are aborted with reperfusion therapy, it is not as common as it once was. It is more common in women, and in patients who have a first MI and have a good EF, as it requires a pump force from the healthy myocardium to produce high pressure which ruptures the infarcted myocardium. The "rupture" is not an explosion, rather a small tract through the myocardium which leaks blood into the pericardium, and kills by tamponade.
Myocardial rupture is usually preceded by postinfarction regional pericarditis (PIRP). PIRP is indicated on the ECG by 2 findings: 1) persistently positive (upright) T-waves at 48 hours, or 2) premature reversal of inverted T-waves to positive deflection by 48 to 72 hours after STEMI. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual. There should be QS-waves indicative of completed transmural MI.
Patients who present with chest pain or cardiac arrest and have an ECG diagnostic of STEMI could have myocardial rupture. Obviously, administration of heparin and/or lytics is hazardous. These patients may survive. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. 5 of 6 presented with chest pain and an ECG indicating reperfusion therapy, but were detected by bedside ultrasound.
Plummer D et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of EM 23(6):1333-1342; June 1994.
For more information, see chapter 28 of Smith's "The ECG in Acute MI."

Below are still images of the ultrasounds.  White arrows point to pericardial fluid.


  1. Detailed report and analysis with images. Thank you for sharing this sir.

  2. Not the specific defination but in the ED settings, the way I learnt low voltage was less than 30 in V1-V3.That combined with SOB &CP in the initial ecg in Post MI did hint to a differential among others of pericardial effusion.

    1. Low-voltage ECG is usually defined as a QRS amplitude of 5 mm (0.5 mV) or less in all of the frontal plane leads and 10 mm (1.0 mV) or less in all of the precordial leads. You don’t always see low voltage in both limb and precordial leads. Sorry, but I’m not sure which ECG you are referring to here … but regardlessless — NONE of the 3 tracings shown in this case show low voltage (≤5mm) in ALL 6 limb leads. I’d hesitate to make a diagnosis of pericardial effusion solely on the basis of chest leads with the amount of voltage we see here … It’s good to keep in mind other potential causes of low voltage = pneumothorax — hypothyroidism — pleural effusion — large body habitus — chronic pulmonary disease … So while I AGREE that in certain situations, significant reduction in QRS amplitude might suggest the possibility of pericardial effusion — bedside echo will be the way the diagnosis is made.


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