Discerning STEMI Mimics in the Field

Five cases that look and sound like a STEMI, but may not be

 

 
 
 

Ashley Brown, MD | Corey Slovis, MD | Jared McKinney, MD | Jeremy Brywczynski, MD | From the December 2013 Issue | Friday, December 13, 2013


Chest pain is a common emergency that prehospital providers must be expert at diagnosing and treating. Chest pain patients who have ST elevation usually are having an ST elevation myocardial infarction (STEMI). There are, however, other types of chest pain patients EMS providers need to be familiar with whose signs, symptoms, and ECGs may mimic a STEMI.

In this article we discuss five potential causes of chest pain with ST elevation where patients are not having a STEMI: cocaine chest pain, aortic dissection, pericarditis, pneumomediastinum and pneumothorax.

1. Cocaine & Chest Pain
Cocaine use is widespread and more than half a million patients are seen in EDs for cocaine-related medical problems each year, many arriving via EMS.1 Cocaine-related chest pain is the single most common complication cocaine users experience that requires emergency care, and chest pain or other cardiac complications are seen in about 60% of patients who present to the ED.2

Although cocaine use should always be considered in younger patients with chest pain, cocaine use has dramatically increased in those over age 50 and should now be considered in all new onset chest pain patients regardless of age.1

Although only a small percent of cocaine-related chest pain patients have a myocardial infarction (MI), almost all patients have the typical anginal symptoms of substernal chest pain that’s described as squeezing or pressure commonly associated with dyspnea, diaphoresis, palpitation, nausea and anxiety.2,3

Making matters worse, normal ECGs in patients who have chest pain after cocaine use are uncommon, and most cocaine-using patients seeking medical attention for cardiopulmonary complaints have ECG changes that can easily be confused with ischemia or infarction.

In one study, only 32% of cocaine using patients had a normal ECG while 42% had ST elevation; the remainder had other abnormalities including T wave inversions and/or nonspecific findings.4 Of note, none of the patients with ST elevation ultimately had evidence of MI. Other studies have shown similar findings.5

EMS providers should understand that most cocaine-related chest pain patients will have abnormal ECGs, and that, surprisingly, most ST elevation in this patient group does not represent a STEMI. Cocaine-related MIs do occur however, and somewhere between 0–6% of cocaine chest pain patients will have a STEMI or non-ST elevation MI.1–5

Cocaine causes chest pain, ischemia and infarction via multiple mechanisms based on its pharmacological properties. It’s also a very potent alpha agonist resulting in intense vasoconstriction and a marked increase in total peripheral resistance, or afterload. This can result in dramatic blood pressure elevation in the brain, aorta and systemic circulation.

This same vasoconstriction can result in profound decreases in coronary blood flow. Cocaine is also a very powerful beta agonist, which results in increased heart rate, increased force of myocardial contractility and a dramatic increase in oxygen consumption. Thus, at a time when the heart needs the most blood flow and oxygen delivery due to beta-induced rate and contractility increases, it has decreased blood flow due to alpha induced vasoconstriction.

These ischemic-causing effects are magnified by cocaine’s ability to increase platelet aggregation, its acceleration of atherosclerosis and stimulation of thrombus formation.3 Besides causing myocardial ischemia and infarction, cocaine’s pharmacological properties can also cause hypertensive emergencies, intracranial hemorrhage, pulmonary edema and aortic dissection.6

Cocaine MI may occur immediately after cocaine use or over the next 12–18 hours. The risk of MI increases up to 24 times within the first hour of cocaine use and then tapers off over time.6

Because it’s usually impossible clinically to differentiate cocaine induced chest pain from true ischemia and MI, all patients should be treated as if they might be having acute ischemia and/or a true MI. They should initially be treated with oxygen, have an O2 saturation probe placed, IV access secured, continuous ECG monitoring and a 12-lead ECG rapidly performed and transmitted if possible. (See Table A.)

Table A:
The “Opening Gambit” in Chest Pain

Oxygen

O2 saturation monitor

IV access

ECG monitoring

12-lead ECG

Chest pain patients should receive four chewable 81mg aspirin or one 325mg tablet. Although chest pain in non-cocaine users is usually treated by nitroglycerin, we, along with others, recommend starting with a benzodiazepine such as Valium (diazepam), Versed (midazolam) or Ativan (lorazepam) for cocaine-induced chest pain.5,6

The benzodiazepine should be titrated to the relief of the patient’s chest pain and to lower their pulse and blood pressure. If the chest pain is not relieved by the benzodiazepine, then nitroglycerin should be added. It should be pointed out that experts don’t agree whether benzodiazepine or nitroglycerin is the best drug for cocaine users with chest pain or whether the two complement each other and provide better chest pain relief when used together.7,8

Although beta blockers are used in tachycardic and hypertensive patients with increased sympathetic tone due to extreme anxiety, hyperthyroidism or withdrawal, they are contraindicated in treating acute cocaine ingestion. Beta blockade may allow unopposed alpha stimulation and cause hypertensive emergencies or other adverse effects.9

Summary: Cocaine use commonly causes substernal chest pain that is classic for angina and does so in patients who may also have ST elevation mimicking a STEMI. Although most patients with cocaine-associated chest pain don’t progress to MI, they’re at significant risk, and regardless of age, should be considered potential STEMI patients and treated with aspirin and benzodiazepines. Chest pain that doesn’t respond to a benzodiazepine should also be treated with nitroglycerin.

2. Aortic Dissection
Another potential mimic of acute myocardial infarction (AMI) is aortic dissection. Although aortic dissection is uncommon, the treatment is vastly different from that of AMI. This difference in therapies is very important as the treatments used in caring for a STEMI can dramatically increase morbidity and mortality in patients suffering from aortic dissection.13

Because symptoms of dissection can be very similar to that of an MI, providers must remain vigilant in considering the diagnosis when caring for a patient with chest pain. Unfortunately, the initial presentation of aortic dissection is commonly missed by providers both in the field and in the ED.

Aortic dissection occurs when there’s a tear in the inner lining of the aorta (the intima) which allows blood to dissect into this false lumen. (See Figure 1.) The ascending and descending aorta can be involved, and men are more commonly affected than women.

The most common risk factor identified for the development of aortic dissection is chronic hypertension. Some other predisposing factors include connective tissue disease such as Marfan’s syndrome, cocaine ingestion, aortic disorders, aortic valve disease and cardiac surgery.10,11

Like patients with AMI, patients with aortic dissection often don’t present with “classic” dissection symptoms, and presentation will depend on what part of the aorta is involved. However, the most common presenting symptom is chest pain that is acute and maximal at onset, described as sharp or tearing/ripping, with radiation to the back.10,11 (See Table B.)

Table B: Classic Symptom Triad of Aortic Dissection

1. Tearing or ripping pain

2. Pain that is maximal at onset

3. Pain that moves to back,
up neck or into stomach

Other presenting signs/symptoms may include back pain, abdominal pain, syncope and acute paralysis. Chest pain associated with dissection doesn’t often radiate to the arm or jaw as is more common in AMI. Most patients will be hypertensive at onset and hypotension may be an important clue for cardiac tamponade and impending cardiac arrest.

Another clue to the diagnosis of aortic dissection is a significant discrepancy in blood pressure between the right and left arm or diminished pulses in the lower extremities as compared to the upper.

ECG changes are common in the setting of acute aortic dissection and can involve ST elevation, ST depression or T wave inversions. Studies have shown that about 50% of patients will have acute ECG changes on their first ECG while only about 30% will have a normal ECG with no abnormalities.10,12,14

ST elevation can occur as result of hypotension, dissection into the coronary artery wall, ostial occlusion or coronary occlusion secondary to bulging of the false lumen. The ECG findings are very similar to those seen in patients with an acute coronary syndrome or AMI. The most likely artery involved will be the right coronary artery, which would lead to a classic inferior MI pattern on the ECG with ST elevation in leads II, III and aVF. (See Figure 2.)

This can often lead to a misdiagnosis and result in standard AMI therapy with treatments such as antiplatelet and thrombolytic therapy, which in turn can lead to disastrous complications such as propagation of the dissection, cardiac tamponade or aortic rupture.

Patients with dissections who have ST-T changes are also at higher risk of death and are more likely to have complications such as shock, cardiac tamponade and significant aortic regurgitation.14

As with any patient with chest pain, patients suspected of having an aortic dissection should receive the “Opening Gambit.” If there’s a high index of suspicion for a dissection, aspirin should be withheld until discussion with medical control.

Caution should also be given to the administration of nitroglycerin. While nitroglycerin will lower blood pressure, it may also cause a reflex tachycardia and increased contractility that will worsen the shear forces on the already-torn aorta, thus propagating the dissection. Finally, antiplatelet and thrombolytic agents should be avoided at all cost.

Summary: Aortic dissections are relatively rare but are often fatal. Only early diagnosis and therapy can improve the possibility of survival. EMS providers should always ask patients with chest pain if: 1) it came on suddenly; 2) was maximal at onset; and 3) if it felt like tearing or ripping. If any of these characteristics are present, suspect dissection and talk with medical control before aspirin and nitroglycerin are given.

3. Pericarditis
Chest pain secondary to acute pericarditis is yet another challenging chief complaint to assess for any responding EMT or paramedic. This is because the presentation, symptoms and ECG manifestations of pericarditis often closely mimic those of acute myocardial ischemia or infarction. Pericarditis is the inflammation or infection of the “sac” that covers the heart and usually provides a painless and sterile lubricating cover in which the heart in enclosed.

Chest pain due to pericarditis accounts for 5% of all ED visits for chest pain in the absence of MI.15 In the U.S. and Canada, pericarditis is usually caused by infection (viral, bacterial, fungal or parasitic), immunological (rheumatic fever, systemic lupus erythematosis or polyarteritis), malignancy, drug-induced or related to uremia.15

As with all patients who request EMS assistance, any chest pain call must be taken very seriously, and myocardial ischemia or infarction must be on the top of any differential diagnosis. There are, however, several characteristics of the pain associated with pericarditis that may help distinguish from the typical presentation of AMI.

The patient with pericardial inflammation usually describes a current or recent fever and the pain is usually made worse by inspiration or leaning forward. The pain may improve with leaning backward, and one may hear a friction rub, which is the sound of the pericardial irritation against a beating heart.16 In general, the patient with acute pericarditis tends to be younger, but never let age rule in or rule out any diagnosis.

The importance of the prehospital 12-lead ECG is paramount to the care of any patient with chest pain, as STEMI identification and early percutaneous coronary intervention (PCI) activation has saved many lives. The ECG associated with pericarditis may mimic that of a STEMI, and it’s of utmost importance paramedics understand the key differences in order to avoid a false PCI activation and potential harm to the patient.

The ECG typically demonstrated an early repolarization pattern as seen in many young, healthy patients, but classically will show diffuse concave upward ST segments in the anterior and lateral leads not necessarily in an anatomic distribution, which would be very uncommon in a STEMI. For example, ST elevation in the inferior leads (II, III, aVF) along with anterior (V1-V4) and anterior-lateral leads (V5, V6, I, L). There will also be diffuse PR segment depression as well as PR elevation in lead aVR.17

Findings of ST elevation in multiple leads that aren’t typically associated with one coronary artery as well as a history of fever and positional pain should lead one to a possible diagnosis of pericarditis.

Occasionally, the patient with pericarditis will develop a collection of transudative or exudative fluid secondary to the inflammatory process itself, resulting in a cardiac tamponade physiology. These patients will present with symptoms of pericarditis in addition to shortness of breath, muffled heart tones and possibly jugular venous distention.

This complication of pericarditis is important for the paramedic to be aware of, as giving nitroglycerin for chest pain in this situation may result in severe hypotension from loss of preload and resultant PEA arrest.18

In addition, if pericarditis is suspected, services that carry advanced antiplatelet agents such as clopidogrel (Plavix) or heparin products should be avoided as a small pericardial effusion may be transformed into a large and potentially devastating hemorrhagic pericardial tamponade.

Summary: Pericarditis is a cause of chest pain that every prehospital provider must be skilled at recognizing via both clinical cues and by its ECG manifestation. Patients with fever, chest pain, pleurisy and positional discomfort, in addition to typical ECG findings of diffuse non-anatomical ST elevation and PR depression, should be considered to have this medical condition. It should also be considered when one sees a “massive MI” by ECG yet the patient looks well and has stable vital signs. Nitroglycerin and advanced antiplatelet agent avoidance is suggested during transport.

4. Pneumomediastinum
Pneumomediastinum is air in the mediastinum, not including air inside of the esophagus or tracheobronchial tree. It can be due to the rupture of alveoli in the lungs that results in air dissecting along the bronchus into the mediastinum. It’s also caused by direct trauma to the esophagus, trachea or mainstem bronchi that could occur during medical procedures.

In children, pneumomediasatinum may occur due to foreign body aspiration. Causes in adults include blunt chest trauma, asthma exacerbations, Valsalva maneuver and forceful inhalation against resistance, especially in patients smoking illicit drugs such as crack cocaine.

Borhaave’s syndrome is a full-thickness rupture of the esophagus caused by forceful vomiting or a complication of recent esophogoscopy, and will cause pneumomediastinum. It has also been reported due to dissection from ruptured structures in the abdomen or retroperitoneum, such as a ruptured diverticulitis.25

Patients with pnemomediastinum generally present with severe substernal chest pain. It may be associated with a crunching sound heard over the heart during systole, called “Hamman’s sign” or “Hamman’s crunch.” Additionally, crepitus may be felt along the suprasternal notch. Patients may complain of cough, stridor or changes in voice along with chest pain. Patients may feel like they’re having a heart attack, can’t breathe correctly or have difficulty swallowing.24,25

Pneumomediastinum has been associated with a variety of ECG findings, including electrical alternans, T-wave inversion, loss of R-wave progression, low voltage QRS and even STEMI.20,21,24 (See Figure 3.) Only one case report of a STEMI mimic has been reported with pneumomediastinum;20 more commonly reported ECG changes are T-wave inversions and loss of R-wave progression in the anterior leads.

Proposed mechanisms for these changes include cardiac displacement due to air in the pericardium, ventricular enlargement and interference of the electrical signals due to air insulating the heart. Cocaine users often have abnormal ECGs, many with ST elevation;4,5 cocaine users with pneumomediastinum may have suspicious looking ECGs even without a STEMI.21

Prehospital treatment should begin with high-flow O2, which may help to begin the resorption of the mediastinal air. Further treatment should be directed at the underlying cause of pneumomediastinum, such as asthma exacerbation, as well as treating the patient’s chest pain.

While many cases of pneumomediastinum ultimately don’t require specific treatment, conditions such as Borhaave’s syndrome, where contents of the gastrointestinal tract enter the mediastinum, can be fatal without urgent surgical debridement to prevent infection.25

5. Pneumothorax
Pneumothorax occurs when there is air in the pleural space. Patients commonly present with acute onset of chest pain and dyspnea. Depending on the size of the pneumothorax, physical exam may reveal decreased or absent breath sounds on the side of the pneumothorax; patients with tension physiology may also demonstrate jugular venous distension, tracheal deviation, tachycardia and hypotension.

Patients who are young and otherwise healthy may remain asymptomatic until the pneumothorax grows to about 40% or develops tension physiology. Patients with underlying cardiac or pulmonary disease will develop symptoms at an earlier stage than those young, healthy patients with a spontaneous pneumothorax due to less physiologic reserve.25

Pneumothorax is commonly a result of chest trauma with accompanying rib fractures. However, pneumothoraces may also occur iatrogenically or spontaneously. Tall male smokers between the ages of 20-40 are at highest risk for a primary spontaneous pneumothorax, defined as one that occurs in the absence of lung disease. Secondary spontaneous pneumothoraces are those that occur in patients with underlying lung disease such as chronic obstructive pulmonary disease, asthma or congestive heart failure.25

ECG changes may also accompany pneumothoraces. In one case series, up to 23% of patients had significant ECG changes including ST elevation, ST depression, T-wave inversions, rightward axis deviation and low-voltage QRS complexes.22

Proposed mechanisms for these changes are similar to those for pneumomediastinum and include the insulating effects of air, alterations in the pendular motion of the heart and rotation of the heart. Additionally, the increased intrapleural pressure may actually restrict cardiac contractility and compress the coronary vessels, decrease venous return and stroke volume, leading to tachycardia.22,23

Although pneumothorax can cause ECG changes that mimic AMI, providers should also be aware that the acute stress of a pneumothorax can actually cause an MI.23

Ultimate treatment of pneumothorax depends on size, underlying cause and comorbidities. Patients with small pneumothoraces who are otherwise healthy and hemodynamically stable may not require any intervention. Prehospitally, all patients should be placed on high-flow O2 as this can aid in beginning the resorption of the pneumothorax and improve oxygenation.

Providers should maintain a high level of vigilance for the development of tension physiology. Tension physiology develops when there is a “one-way valve” that continues to allow air to enter the pleural space but not exit, causing air to build up between the lung and the chest wall, eventually compressing the structures in the mediastinum and contralateral chest. This leads to tachycardia, hypotension and increasing dyspnea. This is a medical emergency and requires rapid decompression through needle thoracostomy, finger thoracostomy or tube thoracostomy depending on the situation.

Needle decompression in the second intercostal space in the midclavicular line should be immediately performed, per protocol or after base station consent, in patients who become hypotensive and can’t keep their oxygen satuations above 90% and/or in those who can no longer adequately ventilate spontaneously. If unsuccessful, a second decompression should be attempted in the fifth intercostal space in the anterior axillary line.25

Summary: Both pneumomedisitinum and pneumothorax may present with acute chest pain and ECG findings that mimic, to some degree, that of a STEMI. Each should be included in the differential, especially in those patients at risk.

In Closing
Diagnosing and treating a STEMI expertly is one of the hallmarks of prehospital expertise. In order to be an expert at treating a STEMI, one needs to be sure the patient isn’t suffering from another cause of chest pain with ST changes such as cocaine use, an aortic dissection, pericarditis, pneumomediastinum or pneumothorax. We hope this article adds to prehospital provider’s ability to difference STEMI from its most common mimics.

References

1. Finkel J, Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011;86(12):1198–1207.

2. Brody S, Slovis C, Wrenn K. Cocaine-related medical problems: Consecutive series of 233 patients. Am J Med. 1990;88(4):325–331.

3. Hollander J, Hoffman R, Gennis P, et al. Prospective multicenter evaluation of cocaine-associated chest pain. Acad Emerg Med. 1994;1(4):330–339.

4. Gitter MJ, Goldsmith SR, Dunbar DN. Cocaine and chest pain: Clinical features and outcome of patients hospitalized to rule out myocardial infarction. Annal Int Med. 1991;115(4):277–282.

5. McCord J, Jneid H, Hollander JE, et al. Management of cocaine-associated chest pain and myocardial infarction. A scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation. 2008;117(14):1897–1907.

6. Schwartz BG, Rezkalla S, Kloner R. Cardiovascular effects of cocaine. Circulation. 2010;122(24):2558–2569.

7. Baumann B, Perrone J, Hornig S, et al. Randomized, double-blind, placebo-controlled trial of diazepam, nitroglycerin, or both for treatment of patients with potential cocaine-associated acute coronary syndromes. Acad Emerg Med. 2000;7(8):878–885.

8. Honderick T, Williams D, Seaberg D, et al. A prospective, randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes. Am J Emerg Med. 2003;21(1):39–42.

9. Sand IC, Brody S, Wrenn, K, et al. Experience with esmolol for the treatment of cocaine-associated cardiovascular complications. Am J Emerg Med. 1991;9(2):161–163.

10. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA. 2000;283(7):897–903.

11. Khan IA, Nair CK. Clinical, diagnostic, and management perspectives of aortic dissection. Chest. 2002;122(1):311–328.

12. Hirata K, Wake M, Kyushima M, et al. Electrocardiographic changes in patients with type A acute aortic dissection: Incidence, patterns and underlying mechanisms in 159 cases.
J Cardiol. 2010;56(2):147–153.

13. Hansson EC, Dellborg M, Lepore V, et al. Prevalence, indications and appropriateness of antiplatelet therapy in patients operated for acute aortic dissection: Associations with bleeding complications and mortality. Heart. 2013;99(32):116–121.

14. Kosuge M, Uchida K, Imoto K, et al. Frequency and implication of ST-T abnormalities on hospital admission electrocardiograms in patients with type A acute dissection. Am J Cardiol. 2013;112(3):424–429.

15. Lilly LS. Treatment of acute and recurrent idiopathic pericarditis. Circulation. 2013;127(16):1723–1726.

16. Wang K, Asinger R, Marriott H. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med. 2003;349(22):2128–2135.

17. Spodick D. Acute pericarditis: Current concepts and clinical practice. JAMA. 2003;289(9):1150–1153.

18. Oakley C. Myocarditis, pericarditis, and other pericardial diseases. Heart. 2000;84(4):449–454.

19. McConaghy J, Oza R. Outpatient diagnosis of acute chest pain in adults. Am Fam Physician. 2013;87(3):177–182.

20. Brearley WD Jr., Taylor L, Haley MW, et al. Pneumomediastinum mimicking acute ST-segment elevation myocardial infarction. Int J Cardiol. 2007;117(2):e73–e75.

21. Sakabe K, Fukuda N, Wakayama K, et al. Spontaneous pneumomediastium: A cause of T-wave inversion in electrocardiogram. Int J Cardiol. 2004;94(1):123–126.

22. Senthilkumaran S, Meenakshisundaram R, Michaels AD, et al. Electrocardiographic changes in spontaneous pneumothorax. Int J Cardiol. 2011;153(1):78–80.

23. Shiyovich A, Vladimir Z, Nesher L. Left spontaneous pneumothorax presenting with ST-segment elevations: A case report and review of the literature. Heart Lung. 2011;40(1):88–91.

24. Tse TK, Tsui KL, Yam LY, et al. Occult pneumomediastinum in a SARS patient presenting as recurrent chest pain and acute ECG changes mimicking acute coronary syndrome. Respirology. 2004;9(2):271–273.

25. Johnson NN, Toledo A, Endom EE. Pneumothorax, pneumomediastinum and pulmonary embolism. Pediatr Clin N Am. 2010;57(6):1357–1383.

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Related Topics: STEMI mimics, STEMI, pneumothorax, pneumomediastinum, pericarditis, ECG, cocaine, chest pain, aortic dissection, 12-lead ECG, Jems Features

 

Ashley Brown, MD

Ashley Brown, MD, is an EMS fellow and instructor of emergency medicine at Vanderbilt University School of Medicine and a MedFlight fellow at the University of Wisconsin-Madison.

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Corey Slovis, MD

is professor and chair of emergency medicine at Vanderbilt and serves as the medical director for Nashville Fire Department and Nashville International Airport. Slovis is also a member of the JEMS editorial board.

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Jared McKinney, MDis an assistant professor of emergency medicine and is assistant medical director for the Nashville Fire Department.

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Jeremy Brywczynski, MD

Jeremy Brywczynski, MD, FAAEM, is an assistant professor of emergency medicine at Vanderbilt University School of Medicine in Nashville, Tenn. He is medical director of Vanderbilt’s aeromedical LifeFlight program and also serves as an assistant medical director for the Nashville Fire Department.

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