A Middle-Aged man had a single vehicle motor vehicle collision with significant energy.
He was hypotensive upon arrival.
A bedside ultrasound was done immediately. Here are 3 clips.
There is pericardial fluid with echogenic material, diagnostic of hemopericardium with thrombus.
An ECG was recorded:
Sinus tachycardia. There are Q-waves in II, III, aVF, and V3-V6. There is ST elevation in the same leads. The T-waves are inverted in V4-V6, and are beginning to invert in II, III, aVF. This is diagnostic of subacute MI.
What do you conclude?
This explains everything. There was subacute MI with myocardial rupture and hemopericardium that resulted in the patient becoming hypotensive and losing control of the vehicle.
The initial troponin returned at 74 ng/mL. This is very high and cannot occur acutely. In other words, this cannot be due to trauma. The ECG cannot occur with trauma either (Q-waves, ST Elevation, T-wave inversion). This confirms your diagnosis of non-traumatic myocardial rupture.
The patient was taken to the operating room where he could not be saved.
You might think that death is inevitable from myocardial rupture, but it is not!
In 1994, from our institution (Hennepin), Plummer et al. published this case series:
In it, Dr. Plummer describes 6 cases of an apparent acute STEMI who presented with chest pain (3), SOB and weakness, and one with profound hypotension. Rather than immediately receiving reperfusion therapy (which, at the time, was tPA), all underwent bedside ultrasound which uncovered hemopericardium. One presented very hypotensive, 4 with Systolic BP 80-90, and one with SBP of 140. All ECGs showed subacute MI. All went to the operating room emergently. 2 survived neurologically intact.
Non-traumatic Myocardial Rupture
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--see this case), 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).
Also, not all rupture is of the free wall:
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) persistenly 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.
For more information, and several cases, see chapter 28 of Smith's "The ECG in Acute MI," starting on page 273, at this link.
For more cases related to myocardial rupture, go to this link.
He was hypotensive upon arrival.
A bedside ultrasound was done immediately. Here are 3 clips.
There is pericardial fluid with echogenic material, diagnostic of hemopericardium with thrombus.
An ECG was recorded:
 |
| What do you think? |
Sinus tachycardia. There are Q-waves in II, III, aVF, and V3-V6. There is ST elevation in the same leads. The T-waves are inverted in V4-V6, and are beginning to invert in II, III, aVF. This is diagnostic of subacute MI.
What do you conclude?
This explains everything. There was subacute MI with myocardial rupture and hemopericardium that resulted in the patient becoming hypotensive and losing control of the vehicle.
The initial troponin returned at 74 ng/mL. This is very high and cannot occur acutely. In other words, this cannot be due to trauma. The ECG cannot occur with trauma either (Q-waves, ST Elevation, T-wave inversion). This confirms your diagnosis of non-traumatic myocardial rupture.
The patient was taken to the operating room where he could not be saved.
You might think that death is inevitable from myocardial rupture, but it is not!
In 1994, from our institution (Hennepin), Plummer et al. published this case series:
Emergency department two-dimensional echocardiography in the diagnosis of nontraumatic cardiac rupture. 23(6):1333-1342; June 1994.
In it, Dr. Plummer describes 6 cases of an apparent acute STEMI who presented with chest pain (3), SOB and weakness, and one with profound hypotension. Rather than immediately receiving reperfusion therapy (which, at the time, was tPA), all underwent bedside ultrasound which uncovered hemopericardium. One presented very hypotensive, 4 with Systolic BP 80-90, and one with SBP of 140. All ECGs showed subacute MI. All went to the operating room emergently. 2 survived neurologically intact.
Non-traumatic Myocardial Rupture
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--see this case), 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).
Also, not all rupture is of the free wall:
Large Transmural STEMI with Myocardial "Rupture" of Ventricular Septum
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) persistenly 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.
For more information, and several cases, see chapter 28 of Smith's "The ECG in Acute MI," starting on page 273, at this link.
For more cases related to myocardial rupture, go to this link.
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