This recent case, which occurred within the past year, was sent to me by an unnamed 2nd year EM resident.
She says she is a believer in all things FOAM!
As this case could have been managed better, she will remain anonymous. But rather than being critical of the management, just try to learn from it.
This is a subxyphoid cardiac view demonstrating moderate pericardial fluid. The LV appears to have reasonable function, but is rather small, suggesting poor filling. I do not have an image of the IVC. The aortic root was not imaged.
In the setting of subacute MI, one must entertain the idea of myocardial free wall rupture. Aortic dissection with leakage into the pericardial sac is certainly a possibility, but this would require 2 unusual events:
1) a delayed presentation (dissection with pericardial blood is usually so acute that the patient would present immediately after onset of symptoms).
2) Focal Anterior STEMI. Though dissections can dissect down the left main, they are
a) less common that the RCA
b) more deadly (if there is Left main occlusion)
i) when not deadly (incomplete occlusion), they present with diffuse ST depression, not anterior ST elevation (this ECG is consistent with LAD occlusion).
Patient course
She says she is a believer in all things FOAM!
As this case could have been managed better, she will remain anonymous. But rather than being critical of the management, just try to learn from it.
Case presentation:
A middle-aged woman with a history of vascular disease presented to a community Emergency Department after an episode of syncope. She complained of 24 hours of severe chest pain radiating to her back, and epigastric abdominal pain. Initial vital signs were BP 128/85, HR 122, RR 22 and O2 saturation was 98% on room air. Physical exam was significant for diaphoresis and agitation, tachycardia without murmurs, epigastric abdominal tenderness without rebound or guarding, and equal peripheral pulses.
An ECG was recorded:
 |
| This ECG is notable for narrow-complex sinus tachycardia, ST segment elevation with Qr-waves (deep Q, small r-wave) in V1-V2 and T wave inversions in V1-V4. There are no reciprocal ST segment depressions. |
Is this an acute MI?
The presence of such well developed Q-waves in the anterior leads suggests that this is not an acute STEMI, but rather a subacute anterior MI.
What is your next step?
What is your next step?
A bedside ultrasound was performed:
This is a subxyphoid cardiac view demonstrating moderate pericardial fluid. The LV appears to have reasonable function, but is rather small, suggesting poor filling. I do not have an image of the IVC. The aortic root was not imaged.
Is this pericardial tamponade?
Upon close inspection of the right ventricle, you can see that there is no collapse during diastole. The RV appears to be both filling and squeezing well, which argues against pericardial tamponade.
On the other hand, the patient has tachycardia and probable poor LV filling, so a fluid challenge would be appropriate.
Comment: What is the pericardial fluid?
On the other hand, the patient has tachycardia and probable poor LV filling, so a fluid challenge would be appropriate.
Comment: What is the pericardial fluid?
In the setting of subacute MI, one must entertain the idea of myocardial free wall rupture. Aortic dissection with leakage into the pericardial sac is certainly a possibility, but this would require 2 unusual events:
1) a delayed presentation (dissection with pericardial blood is usually so acute that the patient would present immediately after onset of symptoms).
2) Focal Anterior STEMI. Though dissections can dissect down the left main, they are
a) less common that the RCA
b) more deadly (if there is Left main occlusion)
i) when not deadly (incomplete occlusion), they present with diffuse ST depression, not anterior ST elevation (this ECG is consistent with LAD occlusion).
Patient course
The resident wanted to do pericardiocentesis, but was not allowed by her faculty. Labs were significant for initial mild troponin elevation (2.8 ng/mL), consistent with subacute MI.
A CT scan was performed due to suspicion for aortic dissection and was negative. Unfortunately the patient became hemodynamically unstable shortly after returning from the CT scanner. Fluids were started. The hemoglobin returned very low and so blood was transfused. Mental status declined and she was intubated, then went into PEA arrest (comment: "pulseless" electrical activity means that pulses cannot be felt, not that there is no perfusion and certainly not that there is no cardiac activity). Chest compressions were begun and Cardiac surgery was called. She did regain pulses at times and would have spontaneous movements, but would lose pulses again.
Comments:
1) Chest compressions are probably not helpful. They can improve venous return to the chest if done in conjunction with an ITD, but the problem is that the LV cannot fill, NOT that it cannot pump. The resident recognized the futility of chest compressions.
2) In the setting of tamponade, positive pressure ventilation may be fatal. It decreases venous return. Poor cardiac filling is the problem. Positive pressure ventilation makes it worse. Ventilation will not help a patient who has no circulation. Intubation should be a last resort. The intrathoracic pressure regulator (CirQLator, see references far at bottom) is an FDA-approved device that sucks air out of the endotracheal tube starting at end-expiration, and this may be the solution for patients who have poor venous return but need intubation. Unfortunately, this device is not yet commercially available even though it is FDA approved.
Case continued:
At the time of the arrival of the chest surgeon much later, the patient no longer had reactive pupils and was undergoing chest compressions.
The diagnosis of myocardial rupture was considered. The surgeon performed a thoracotomy in the ED, which revealed blood and large clots within the pericardial sac and a small anterior wall perforation. Attempts to suture the defect failed due to friability of the surrounding tissue. Open cardiac massage and aggressive resuscitation with blood products failed to achieve ROSC and the patient was pronounced dead approximately four hours after initial presentation.
Final diagnosis: myocardial rupture
The resident presented this as an "M and M" at her institution and "the sentiment was that thoracotomy in the ED in this setting would be extreme and even frowned upon," and that the diagnosis of free wall rupture is perceived to be uniformly rapidly fatal.
A CT scan was performed due to suspicion for aortic dissection and was negative. Unfortunately the patient became hemodynamically unstable shortly after returning from the CT scanner. Fluids were started. The hemoglobin returned very low and so blood was transfused. Mental status declined and she was intubated, then went into PEA arrest (comment: "pulseless" electrical activity means that pulses cannot be felt, not that there is no perfusion and certainly not that there is no cardiac activity). Chest compressions were begun and Cardiac surgery was called. She did regain pulses at times and would have spontaneous movements, but would lose pulses again.
Comments:
1) Chest compressions are probably not helpful. They can improve venous return to the chest if done in conjunction with an ITD, but the problem is that the LV cannot fill, NOT that it cannot pump. The resident recognized the futility of chest compressions.
2) In the setting of tamponade, positive pressure ventilation may be fatal. It decreases venous return. Poor cardiac filling is the problem. Positive pressure ventilation makes it worse. Ventilation will not help a patient who has no circulation. Intubation should be a last resort. The intrathoracic pressure regulator (CirQLator, see references far at bottom) is an FDA-approved device that sucks air out of the endotracheal tube starting at end-expiration, and this may be the solution for patients who have poor venous return but need intubation. Unfortunately, this device is not yet commercially available even though it is FDA approved.
Case continued:
At the time of the arrival of the chest surgeon much later, the patient no longer had reactive pupils and was undergoing chest compressions.
The diagnosis of myocardial rupture was considered. The surgeon performed a thoracotomy in the ED, which revealed blood and large clots within the pericardial sac and a small anterior wall perforation. Attempts to suture the defect failed due to friability of the surrounding tissue. Open cardiac massage and aggressive resuscitation with blood products failed to achieve ROSC and the patient was pronounced dead approximately four hours after initial presentation.
Final diagnosis: myocardial rupture
The resident presented this as an "M and M" at her institution and "the sentiment was that thoracotomy in the ED in this setting would be extreme and even frowned upon," and that the diagnosis of free wall rupture is perceived to be uniformly rapidly fatal.
Comment:
Early recognition and thoracotomy, best done in the OR, or even earlier pericardiocentesis with subsequent rapid OR thoracotomy, could have been life saving in this patient who was relatively young.
This is a clear case in which one or both of pericardiocentesis or ED thoracotomy would be indicated and possibly life saving. Emergency physicians must take the lead. Myocardial rupture must be highest on the differential. Treatment should be simultaneous with consultation with a cardiac surgeon, and should be fluids first, pericardiocentesis if fluids do not stabilize, and thoracotomy if the patient is in a downward spiral (or if pericardiocentesis is inhibited by pericardial thrombus).
This is a good case for demonstrating that emergency medicine must make the decisions and take the lead. One cannot wait for cardiologists or cardiac surgeons, although of course the surgeon has to agree to take the patient to the OR. The best way to get the surgeon to agree to take the patient to the OR is if the emergency physician successfully resuscitates FIRST; then there is no choice!
Early recognition and thoracotomy, best done in the OR, or even earlier pericardiocentesis with subsequent rapid OR thoracotomy, could have been life saving in this patient who was relatively young.
This is a clear case in which one or both of pericardiocentesis or ED thoracotomy would be indicated and possibly life saving. Emergency physicians must take the lead. Myocardial rupture must be highest on the differential. Treatment should be simultaneous with consultation with a cardiac surgeon, and should be fluids first, pericardiocentesis if fluids do not stabilize, and thoracotomy if the patient is in a downward spiral (or if pericardiocentesis is inhibited by pericardial thrombus).
This is a good case for demonstrating that emergency medicine must make the decisions and take the lead. One cannot wait for cardiologists or cardiac surgeons, although of course the surgeon has to agree to take the patient to the OR. The best way to get the surgeon to agree to take the patient to the OR is if the emergency physician successfully resuscitates FIRST; then there is no choice!
Myocardial rupture:
Mechanical complications of complete transmural myocardial infarction (untreated persistent STEMI, or treated STEMI with No-Reflow phenomenon) include ventricular free wall rupture (VFWR), inter-ventricular septum rupture, papillary muscle rupture and atrial rupture. Among these diagnoses, VFWR is the most common, occurring in 1.7% of 849 patients in the Multicenter Investigation of the Limitation of Infarct Size, published in 1989.
Aortic dissection was appropriately considered in the differential, but the patient should only undergo CT if stable. This would be a great time to use ultrasound to look at the aorta. ED Transthoracic ultrasound is pretty sensitive and specific.
Transesophageal echo will be an important tool for the ED in the future.
Ventricular free-wall rupture (VFWR, commonly referred to as cardiac rupture) typically presents either as sudden cardiac death or, less commonly, with chest pain, hypotension, syncope, cardiogenic shock or obstructive shock due to pericardial tamponade. Myocardial rupture typically occurs between 1-5 days after infarct, but has been documented weeks after AMI. Rupture can also occur early. The “rupture” may actually be more like a slow leak developing over hours to days. Diagnosis can be made by ultrasound, which may demonstrate pericardial fluid or clot with or without tamponade and may even provide visualization of the defect in the myocardial wall. Like other mechanical complications, treatment is immediate surgical repair.
Risk factors for myocardial rupture include first MI, single vessel disease, lack of collateral flow, transmural infarct (STEMI), female gender, advanced age, anterior MI, and delayed or no reperfusion. Patients treated with thrombolytics have higher rates of rupture than those who undergo percutaneous intervention, especially when thrombolytics are given 12- 24 hours after symptoms.
ECG in Myocardial Rupture
Myocardial rupture is preceded by post-infarct regional pericarditis (PIRP) in the majority of cases. See this paper on myocardial rupture and this paper on postinfarction regional pericarditis, both by Oliva et al. (and both full text links).
Full-thickness infarct causes localized inflammation of the epicardium (PIRP). So PIRP is a sign of full thickness infarct, which is the harbinger of myocardial rupture. Persistently positive T-waves or premature (upright) reversal of previous T-wave inversions after STEMI is suspicious for PIRP and the patient may be at risk for rupture. (See a case of PIRP and interventricular septum rupture here: http://hqmeded-ecg.blogspot.com/2014/07/subacute-anteroseptal-stemi-with.html).
Myocardial rupture is preceded by post-infarct regional pericarditis (PIRP) in the majority of cases. See this paper on myocardial rupture and this paper on postinfarction regional pericarditis, both by Oliva et al. (and both full text links).
Full-thickness infarct causes localized inflammation of the epicardium (PIRP). So PIRP is a sign of full thickness infarct, which is the harbinger of myocardial rupture. Persistently positive T-waves or premature (upright) reversal of previous T-wave inversions after STEMI is suspicious for PIRP and the patient may be at risk for rupture. (See a case of PIRP and interventricular septum rupture here: http://hqmeded-ecg.blogspot.com/2014/07/subacute-anteroseptal-stemi-with.html).
This case of rupture is unusual in that T-waves remained inverted.
Temporizing measures may include pericardiocentesis and volume loading (for tamponade). Overall mortality is high, but not inevitable; there is also high intraoperative mortality. Survival is higher when there is witnessed event, early medical intervention, and receipt of care at a facility with cardiac surgery.
In a large study, twenty-five
(76%) of the 33 patients with subacute ventricular rapture survived the
surgical procedure and 16 (48.5%) were long-term survivors.
At our institution (Hennepin County Medical Center), Dr. David Plummer reported in 1994 on 6 cases of STEMI that were diagnosed as myocardial rupture by bedside ultrasound in the ED. 2 of the 6 survived surgery. This is not a uniformly fatal condition!
Transesophageal echo will be an important tool for the ED in the future.
Other mechanical complications of Acute STEMI
Interventricular septum rupture causes left-to-right shunting and symptoms include progressive dyspnea, heart failure, palpable thrill and a new holosystolic murmur (2). It occurs in an estimated 1-2% of all AMIs (2,3). (I think this is overstated as well.) Diagnosis is made by Doppler ultrasound, and treatment is surgical correction of the defect. See this case.
Papillary muscle rupture is a result of posterior MI (inferoposterior or posterolateral or isolated posterior), and occurs in 1-3% of patients with AMI within 3-5 days. This mechanical defect leads to sudden onset dyspnea and acute pulmonary edema, and may also present with a new systolic murmur characteristic of mitral regurgitation. However, the defective valve area is often so large that there is little turbulence and often no murmur. Diagnosis is made by suspicion and then ultrasound with Doppler. The ED treatment is intubation with mechanical ventilation and paralysis to decrease myocardial oxygen demand, nitroprusside to decrease afterload, intra-aortic balloon pump, and surgical repair. See these 2 cases.
Learning points:
1. Include myocardial rupture in the differential for anyone with subacute MI AND persistent ST elevation, especially with tachycardia or hypotension. Confirm with bedside ultrasound. If pericardial fluid is found, aortic dissection should be pursued in a very acute situation.
2. Findings consistent with PIRP on ECG, new murmur, pericardial fluid, hemodynamic instability, or acute pulmonary edema should make one suspicious of a mechanical compication to acute MI.
3. Perform bedside echo early if suspicious for these diagnoses and consult surgery immediately if echo shows pericardial fluid or clot.
4. Not all patients with mechanical complications of MI die suddenly; early recognition, stabilization and surgical repair can be life saving.
5. Positive pressure ventilation is detrimental in tamponade.
5. Positive pressure ventilation is detrimental in tamponade.
References (CirQLator references are at the bottom):
1. Plummer et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of Emergency Medicine. 1994 June 23;6: 1333-42.
2. Sinikka P-S et al. Ventiruclar septal and free wall rupture complicating acute myocardial infarction: Experience in the Multicenter Investigation of Limitation of Infarct Size. Am Ht J 117(4):809-818; April 1989.
3. Lopez-Sendon J et al. Diagnosis of subacute ventricular wall rupture after acute myocardial infarction: Sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria. JACC 19(6):1145-1153; 1992.
4. Sahibzada et al. Ventricular Free Wall Rupture. Journal of Ayub Medical College, Abbottabad. 2009 21;2.
5. Moreno et al. Primary angioplasty reduces the risk of left ventricular free wall rupture compared to thrombolysis in acute MI. Journal of the American College of Cardiology. 2002 Feb 20;39 (4):598-603
6. Smith et al. Myocardial Rupture and Postinfarction Pericarditis. In: The ECG in Acute MI. 2002 Lippincot Williams & Wilkins.
7. Predictive factors of cardiac rupture in patients with ST-elevation myocardial infarction. Journal of Zhejiang University Science B. 2014 Dec 15;12:1048-54
8. Wehrens et al. Cardiac rupture complicating myocardial infarction. American Journal of Cardiology. 2004 95:285-92
9. Large transmural STEMI with myocardial “rupture” of the ventricular septum. From: Dr. Smith’s ECG Blog. http://hqmeded-ecg.blogspot.com/2014/07/subacute-anteroseptal-stemi-with.html
10. Haddadin et al. Surgical treatment of postinfarction left ventricular free wall rupture. Journal of Cardiac Surgery. 2009 Nov 24;6: 624–31.
11. Oliva PB, Hammill SC, Edwards WD.
Cardiac rupture, a clinically predictable complication of acute myocardial
infarction: report of 70 cases with clinicopathologic correlations. J Am Coll
Cardiol 1993;22:720-6.
12. Oliva PB, Hammill SC, Edwards WD.
Electrocardiographic diagnosis of postinfarction regional pericarditis:
ancillary observations regarding the effect of reperfusion on the rapidity and
amplitude of T wave inversion after acute myocardial infarction. Circulation
1993;88:896-904.
13. Hollander and Diercks. Acute coronary syndromes: Acute myocardial infarction and unstable angina. In: Tintinalli et al. Tintinalli’s Emergency Medicine 6th Ed. New York: McGraw-Hill.
14. Ashfaq et al. Mechanical complications following acute myocardial infarction. Journal of Pakistan Medical Association. 2012 Aug 62;8:861-5.
CirQLator (intrathoracic pressure regulator)
https://clinicaltrials.gov/
http://www.
http://www.asaabstracts.com/
http://www.ncbi.nlm.nih.gov/
CirQLator (intrathoracic pressure regulator)
https://clinicaltrials.gov/
http://www.
http://www.asaabstracts.com/
http://www.ncbi.nlm.nih.gov/
This is a study I published in which we studied the use of an Impedance Threshold Device on awake, non-intubated, hypotensive patients:
http://www.sciencedirect.com/
http://www.sciencedirect.com/
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