CE Article: Common STEMI Imitators: Part 1

EMTs and paramedics are trained to evaluate for and identify patients experiencing acute coronary syndrome (ACS) and ST-elevation myocardial infarction (STEMI), and with good reason: Early identification of STEMI in the field and activation of and rapid transport to a STEMI center reduces patient morbidity and mortality. However, besides improving our ability to identify STEMIs in the field, the addition of the 12-lead ECG in the prehospital environment can also lead us to inadvertently misidentify a number of etiologies of ST-segment elevation that don’t result from ACS and STEMI.

These STEMI imitators (Table 1) are not insignificant. A STEMI imitator can place a patient under increased risk if they are administered unnecessary medications (nitroglycerin, aspirin, morphine or fibrinolytics), and the unnecessary activation of STEMI teams and catheterization labs leads to wasted resources. As such, it is important for the EMS provider to be familiar with STEMI imitators and how to identify them in the field.

This month’s CE article is uses a case-based approach to explore some STEMI imitators. A discussion of all imitators is beyond the scope of this article, so we will focus on four for close examination.

Case #1: Benign Early Repolarization

A 37-year-old female presents conscious, alert and oriented, complaining of chest pain. She says everyone in her office has been sick with the flu and describes a three-day history of low-grade fever, malaise and dyspnea with exertion. Today she developed chest pain described as sharp and right-sided, 5 on a scale of 0–10 and reproducible with cough and deep inspiration. She has no significant medical history, and she describes how she is a semiprofessional triathlete and “in very good shape.” There is no cardiovascular disease in her family, and she takes no medications and has no known drug allergies.

Your clinical exam reveals bronchi on auscultation of the mid and upper right lung fields; the left side is clear. Her skin is warm, normal color and slightly diaphoretic. Vital signs are: HR, 88/min.; BP, 122/70 mmHg; RR, 18/min. with good tidal volume; SpO2 = 96% on room air; temperature, 100.1°F (37.8°C) tympanic. Per your protocol you perform a 12-lead ECG, shown in Figure 1. What is your interpretation of this ECG? How would you treat this patient?

Benign early repolarization (BER) is an ECG pattern most commonly seen in young, healthy, athletic patients; it occurs in about 5%–13% of the general population. This makes it a relatively common, incidental ECG finding. Though historically it’s been thought that BER is associated with good, if not excellent, health, recent reports have suggested that persons with early repolarization may be at increased risk for cardiac dysrhythmia, idiopathic ventricular fibrillation and death.1–4

BER can be intermittent and not always present on ECG.5 Characteristic ECG findings include:6

J-point elevated 1 mm or more in two or more adjacent leads, often with notching or slurring (Figure 2);

Widespread concave ST-segment elevation, especially in V2–V5 (Figure 3);

Large, asymmetrical, concordant (points in same direction as QRS) T-waves in the same leads;

No reciprocal ST-segment depression (except in aVR);

No progression on serial ECGs.

There are no clinical exam findings that are specific or even suggestive for BER. BER is an ECG entity without any clinical manifestations.

Differentiating Between BER and STEMI

This is a great example of the typical patient we can expect to see with BER: a young patient with a seemingly noncritical presentation and a complaint of seemingly noncardiac chest pain in whom we do not expect to find ECG evidence of a STEMI. This patient presents with a history of present illness and clinical exam findings strongly suggestive of pneumonia or some other flulike illness. The evidence of ST-segment elevation on a 12-lead would probably come as a surprise to most providers. The fact that she is young, in good health and without a history of cardiovascular disease allows us to consider her low risk for AMI and STEMI and decide to not treat for ACS despite the ST-segment elevation.

While patients with STEMI can have elevation of the J-point with concave ST-segment elevation early in the progression of AMI, the ST-segment elevation typically becomes more pronounced and convex (rounded upward) as the infarction evolves. An evolving STEMI can be identified by obtaining serial ECGs. The ST-segment elevation associated with BER will not evolve over the minutes to hours a patient is with EMS, and it will remain unchanged despite treatment. In addition, there will be no reciprocal changes in BER. The presence of reciprocal changes indicates STEMI.

Treatment

There is no treatment for BER. Prehospital treatment should center on the clinical signs and symptoms presented by the patient. The patient in this case should receive oxygen via the appropriate device and flow rate to maintain a saturation of at least 94%. Intravenous access should be obtained, the patient placed on the cardiac monitor and serial 12-lead ECGs performed en route to the emergency department. Arguably this patient could be transported via basic life support, but her complaint of chest pain is a valid argument for ALS transport.

Is there danger in treating BER as a STEMI? Will the administration of nitroglycerin, aspirin and morphine be detrimental in these patients? There is, of course, a risk with administering any medication. Giving nitroglycerin, for example, can lead to hypotension. In addition, there are costs involved in initiating a STEMI activation and preparing a cath lab for what turns out to be BER. That said, the risks of not treating a legitimate STEMI are greater than the risks of treating BER as a STEMI. Use sound clinical judgment, and if there is any uncertainty or concern as to the etiology of the ECG findings, contact a medical control physician.

Case #2: Acute Pericarditis

A 54-year-old male presents conscious, alert and oriented, sitting upright in a chair, complaining of chest pain. He says the pain started about 24 hours ago and has been getting worse since. He describes it as sharp, radiating to his neck, reproducible with movement, and 7 on a scale of 0–10. He denies any difficulty breathing, nausea or vomiting, dizziness, weakness, syncope, and abdominal or back pain. His lung sounds are clear and equal bilaterally, though you note he winces when taking a deep breath. He says deep inspiration makes the pain worse. The patient has no past medical history, takes no medications and has no known drug allergies. He mentions he saw his personal physician last week for a viral upper respiratory infection, and that his father and uncle both died of heart attacks in their 50s.

When you ask him to lay supine on the stretcher for an abdominal exam, he refuses and says lying flat “makes the pain worse—I couldn’t sleep last night.” Vital signs are: HR, 92/min.; BP, 132/82 mmHg; RR, 16/min. with good tidal volume; SpO2, 97% on room air; temperature, 101.9°F (38.8°C) tympanic. You perform a 12-lead ECG, shown in Figure 4. What is your interpretation of this ECG? How would you treat this patient?

Pericarditis is an inflammation of the pericardium, the double-layered fibrous sac that envelops the heart. Causes of pericarditis include infection, metabolic diseases, systemic diseases, cancer and injury to the pericardium. Pericarditis can also be idiopathic. Specific etiologies are listed in Table 2.

Pericarditis can occur acutely or chronically, and can result in pericardial effusion and resultant cardiac tamponade. Acute pericarditis is recorded in about 0.1% of hospitalized patients and 5% of patients treated in emergency departments for nonischemic chest pain.7

The 12-lead ECG is a fairly reliable diagnostic tool that can help supplement your clinical suspicion of pericarditis. The ECG changes characteristic of pericarditis occur in four stages:8–10

Stage 1:

ST elevation in multiple leads (typically concave up);

PR depression in limb leads (I, II, III, aVL, aVF) and precordial leads (V2–V6) (Figure 5);

ST-segment depression in leads aVR and V1;

“Knuckle sign” in aVR: The PR segment in aVR is rounded and elevated above the baseline, like a knuckle.

Stage 2: ST segments return to isoelectric line, T-waves flatten in multiple leads;

Stage 3: Flattened T-waves become inverted in multiple leads;

Stage 4: ECG returns to normal.

Widespread ST-segment changes in most or all limb and precordial leads occur when the infection of the pericardium involves and irritates the epicardium (the topmost layer of the heart). These changes can help differentiate acute pericarditis from benign early repolarization. PR depression in pericarditis is thought to be due to atrial wall injury, and its presence in pericarditis can help differentiate the T-wave inversion characteristic of benign early repolarization from acute pericarditis.11

Arguably the most significant and readily identifiable changes occur in the first stage, during the first few hours to days of the illness. These changes can easily be distinguished from a STEMI.

The most common symptom associated with acute pericarditis is chest pain (present in more than 95% of patients) that may worsen with inspiration, coughing or movement.12 Pain is often described as retrosternal or precordial and may radiate to the back, shoulder (in particular the trapezius ridge), neck or jaw, much like the pain associated with acute myocardial infarction. Typically a patient will describe pain that is more severe when lying supine and relieved (but not necessarily absent) when sitting up and/or leaning forward.13 The clinical exam hallmark of pericarditis is the pleural friction rub, caused by the creation of friction between the inflamed parietal and visceral pericardium. A pleural friction rub can be very difficult to auscultate in a noisy prehospital environment. You can increase your likelihood of hearing it by placing the diaphragm of your stethoscope at the lower left sternal border while having the patient lean forward.

Other clinical exam findings associated with pericarditis include fever, tachypnea and dyspnea, dysphagia and tachycardia. Tachycardia can occur secondary to the pain associated with pericarditis, as well as in response to the hemodynamic insult that can occur with pericardial effusion and tamponade.

Differentiating Between STEMI and Pericarditis

At first look this patient has signs and symptoms highly suggestive of ACS and STEMI. He is in his 50s, experiencing an episode of chest pain that radiates to his neck, has a family history of death from AMI and has ST-segment elevation. In this particular case, a close look at the HPI and clinical exam findings helps considerably in differentiating this patient’s pericarditis from ACS and STEMI.

This patient had a history of recent viral illness, increasing the risk for pericarditis. The positional nature of his pain (worse when lying supine) is not characteristic of ACS, nor is relief of pain while leaning forward. Both of these clinical findings should suggest a non-ACS etiology of the chest pain. Auscultation of a pleural friction rub would further increase the suspicion of pericarditis. Arguably, assessment of heart sounds is not a skill that is frequently practiced by paramedics in the field due to a lack of perceived utility and the real difficulty of hearing heart sounds in our noisy environment. However, a pleural friction rub is pretty distinct from normal heart sound. A clinician with very limited experience auscultating normal heart sounds may well be able to detect a friction rub. This patient also had a fever, which is not a sign typically associated with AMI, though it can occur in the postinfarction period.14

In his series “Emergency ECG Video of the Week,” Amal Mattu, MD, suggests looking for factors strongly associated with AMI. When evaluating a 12-lead ECG to determine pericarditis versus STEMI, you should ask yourself three questions:15

Is there reciprocal ST-segment depression in any leads excluding aVR and V1? If there is, the patient is having a STEMI. If not, then ask yourself…

Is the ST-segment morphology convex or horizontal? If it is, the patient is having a STEMI. If not, then ask yourself…

Is the ST-segment elevation greater in lead III than in lead II? If it is, it’s a STEMI.

A close examination of the patient’s 12-lead (Figure 4) reveals no ST-segment depression outside of aVR and V1, concave-up ST-segment morphology, and ST-segment elevation in lead III that is less than the elevation in lead II.

In addition, there are other subtle inconsistencies with STEMI. Consider the widespread ST-segment elevation that includes leads II, III, aVF and V2–V6. In STEMI, ST-segment elevation is localized to the areas of myocardium supplied by the occluded coronary artery. If this were a STEMI, the 12-lead ECG pattern would indicate occlusion of both the left and right coronary arteries. In other words, this patient would be having a massive AMI. The patient’s clinical condition does not support this, as he is quite stable. Aside from a slightly elevated heart rate, his vital signs are normal, and his skin is pink, warm and dry. This is contrary to what would be expected in a patient having a significant AMI.

In addition, the ST segments are concave, and there is PR depression in multiple leads, both suggestive of pericarditis and not consistent with STEMI.

Treatment

The treatment of acute pericarditis uncomplicated by pericardial effusion and/or tamponade is supportive only. Place the patient on supplemental oxygen via a device and flow rate sufficient to maintain a saturation of at least 94%. Obtain intravenous access and place the patient on the cardiac monitor. Perform serial 12-lead ECGs to continually evaluate for any changes in the ST segments consistent with STEMI. If you elect to not treat for STEMI because you think the patient has pericarditis (or any other STEMI imitator), obtain serial ECGs. Pericarditis does not result in reciprocal changes, nor should you see evolving or increasing ST-segment elevation. If serial ECGs develop reciprocal changes or worsening ST-segment elevation, transport the patient to a STEMI center and activate a STEMI alert, as this is inconsistent with pericarditis and more suggestive of STEMI.

Patients with pericarditis can experience significant pain, and consideration of pain control is warranted. Nonsteroidal anti-inflammatory drugs are an option frequently utilized in the emergency department, with ibuprofen commonly preferred for its limited side effects. Ibuprofen in fact has a desired side effect: increased coronary blood flow.16 In the absence of ibuprofen, you can consider the use of other analgesics such as morphine or fentanyl, but weigh their potential risks (decreased level of consciousness, respiratory depression, hypotension) against the perceived benefits.

Case #3: Brugada Syndrome

A 24-year-old male presents conscious and alert, lying supine on the ground after a syncopal episode. The patient is a Chinese national and arrived in your city yesterday. Through an interpreter he says he has felt fine but is a “bit tired” from his long air travel. He describes an acute onset of dizziness while walking. He was assisted to the floor by his brother, who reports the patient lost consciousness for 30–60 seconds. No seizure activity was noted. The patient denies any chest pain or discomfort, difficulty breathing, nausea or vomiting, and abdominal or head pain. He is currently being treated with antibiotics for a cellulitis on his left leg but has no other significant medical history, medications or allergies. He informs you that his father died of a heart attack at 40. Vital signs are: HR, 92/min.; BP, 136/72 mmHg; RR, 14/min. with good tidal volume; SpO2, 98% on room air; temperature, 102.0°F (38.8°C) tympanic. You perform a 12-lead ECG, shown in Figure 6. What is your interpretation of this ECG? How would you treat this patient?

Brugada syndrome is an autosomal dominant genetic disorder characterized by abnormal ECG findings and an increased risk of sudden cardiac death. The genetic disorder results in defective myocardial sodium channels that shorten the action potential (a type of sodium channelopathy) and increase the risk of cardiac arrhythmia, including venticular tachycardia, with or without a pulse, and ventricular fibrillation.

The ECG characteristics of Brugada pattern and syndrome are not always present but can be exacerbated by a number of factors, including fever, hypothermia, drugs (alpha agonists, beta blockers, calcium channel blockers, cocaine, alcohol, tricyclic antidepressants), electrolyte abnormalities (hyper- and hypokalemia, hypercalcemia), myocardial ischemia, and electrical cardiac interventions such as pacing and cardioversion. During a period of stress brought about by one of these factors, the patient experiences myocardial irritability, the characteristic ECG pattern emerges, and the risk of cardiac dysrhythmia increases.

The prevalence of ECG changes typical of Brugada pattern are particularly high in males of Asian descent.17 The first onset of symptoms (VT, VF, syncope, sudden death) and therefore diagnosis is around 40 years old, though Brugada syndrome can be diagnosed at any age.

 A patient with ST elevation in V1 and V2 is said to have a Brugada pattern. To be diagnosed with Brugada syndrome, a patient must have the typical ECG features as well as one of the following clinical criteria:

History of VF/VT;

Family history of sudden cardiac death;

Family history of coved-type ECG pattern;

Agonal respirations during sleep;

Inducibility of VT/VF during electrophysiology study.

The ST-segment elevations characteristic of Brugada syndrome are not always present on ECG, but are frequently “unmasked” by one of the multiple factors previously listed. Specific ECG changes are:

Typically found in V1–V2;

RBBB or incomplete RBBB pattern;

ST-segment elevation;

Coved type (Figure 7);

Saddle type (Figure 8).

Moving the V1 and V2 leads up one intercostal space may increase the sensitivity of the ST-segment changes, making identification of the ECG pattern of Brugada syndrome easier.18 The coved ST-segment pattern is the most concerning, as it seems to be more associated with adverse outcomes than the saddle pattern.

There are no clinical exam findings associated with Brugada pattern or syndrome. Patients who experience cardiac dysrhythmia secondary to Brugada syndrome may experience syncope during a tachydysrhythmic event or cardiac arrest during episodes of VF/VT.

There are multiple factors that can result in the unmasking of the ECG patterns characteristic of Brugada syndrome. The clinical exam and HPI findings associated with such factors may be present.

Differentiating Between Brugada Syndrome and STEMI

In this particular case, a syncopal episode in a healthy male of Asian descent should immediately increase your suspicion of Brugada syndrome. The presence of any of the exacerbating factors listed above, along with syncope and ST-segment elevation in V1 and V2, should also increase your suspicion. In addition, the patient has a fever as a result of his cellulitis, a readily identifiable exacerbating factor.

In the presence of witnessed ventricular dysrhythmia, the differentiation between STEMI and the ST-segment elevation in V1 and V2 characteristic of Brugada syndrome is made much more difficult. Prehospital providers should treat for STEMI rather than risk missing the diagnosis in any patient with Brugada syndrome and witnessed ventricular dysrhythmia.

Treatment

There is no treatment for Brugada syndrome. The patient in this case should receive oxygen via the appropriate device and flow rate to maintain a saturation of at least 94%. Obtain intravenous access, place the patient on the cardiac monitor and perform serial 12-lead ECGs en route to the emergency department.

If a patient presents with Brugada syndrome and concomitant cardiac dysrhythmia, treat the dysrhythmia per your local protocols with medication or the appropriate electrical intervention. Amiodarone is the most effective antidysrhythmic for the treatment and prevention of ventricular dysrhythmias associated with Brugada syndrome.19 In-hospital treatment is focused on the implantation of a cardioverter-defibrillator device, and patients will usually be referred for genetic testing.

Case #4: Left Bundle Branch Block

A 42-year-old female presents conscious, alert and oriented, sitting on a couch in her living room and complaining of gastrointestinal distress. She says she awoke this morning “feeling sick to my stomach” and over the past four hours has experienced worsening nausea, abdominal cramping and weakness. She feels like she might have to move her bowels but has not experienced any diarrhea. When you ask if she’s having any chest pain or discomfort, she says, “I feel like I’m having my normal reflux discomfort, though a little bit worse today.” She describes the discomfort as a burning sensation that runs up from her epigastrium into her throat, nonreproducible, and a 3 on a scale of 0–10. She has not vomited and also denies any shortness of breath, syncope, dizziness, or neck or shoulder or back pain.

The patient describes a past medical history significant for cardiovascular disease, hyperlipidemia, hypertension and one myocardial infarction five years prior, with a stent placement. Your clinical exam reveals mild discomfort with palpation to all four abdominal quadrants. Vital signs are: HR, 72/min.; BP, 118/52 mmHg; RR, 16/min. with good tidal volume; SpO2, 97% on room air; temperature, 98.7°F (37.0°C) tympanic. You perform a 12-lead ECG, shown in Figure 9. What is your interpretation of this ECG? How would you treat this patient?

Left bundle branch block (LBBB) is an ECG pattern that results when the normal path of electrical impulses through the His-Purkinje system is altered. This results in aberrant electrical flow through the ventricular myocardium and a widening of the QRS (greater than 0.12 secs.) on the ECG. LBBB can occur secondary to chronic and progressive disease of the heart’s electrical conduction system, or acutely from AMI. It can even be identified in young, healthy persons with structurally normal hearts, though this is uncommon. The prevalence of LBBB increases with age, reaching 5.7% by age 80.20 Approximately 2% of all patients who present with suspected ACS will have LBBB.21 These patients are more likely to be older, female and have a history of cardiovascular disease, hypertension and congestive heart failure than non-BBB patients with ACS.22

A task force composed of representatives from the American Heart Association, American College of Cardiology and Heart Rhythm Society has defined the electrocardiographic features of LBBB. Their definition includes the following:23            

QRS duration greater than or equal to 120 ms in adults;

Broad notched or slurred R-wave in leads I, aVL, V5 and V6;

Absent Q-waves in leads I, V5 and V6;

ST and T-waves opposite in direction to the QRS complex (discordance);

Depressed ST segments and/or negative T-waves in leads with negative QRS (discordance) are generally abnormal and may be a sign of underlying ischemia.

A normal LBBB will follow the rule of appropriate discordance. Discordance is said to be present when the QRS and ST segments are on opposite sides of the baseline (Figure 10). Discordance should occur in all 12 leads. If the deflection of the QRS complex is primarily upward, the ST segment and T-wave will deflect downward, below the baseline. So in LBBB, when the QRS is primarily above the baseline and the ST segment is below, discordance is present, and that is normal and good. Conversely, every time the deflection of the QRS complex is primarily downward, the ST segment will be in the opposite direction and above the baseline. So in LBBB, when the QRS is primarily below the baseline and the ST segment is above, discordance is present, and that is normal and good. To summarize, in a normal LBBB the main deflections of the QRS and ST segments go in opposite directions from the baseline. In some cases the ST segment may be at the isoelectric line, and that is OK.

What is not OK is when the ST segment and T-wave are both clearly in the same direction as the main deflection of the QRS complex. This situation, termed concordance, is indicative of myocardial ischemia. Concordance with ST-segment elevation present in any lead is considered a STEMI.

There are no clinical exam findings directly related to LBBB. However, a patient may exhibit findings consistent with cardiovascular disease.

Differentiating Between LBBB and STEMI

It’s a common misconception that you cannot identify a STEMI in a patient with a LBBB or who is being paced (patients being paced will have a wide QRS that appears as a LBBB). This is not true, and in fact sometimes you can identify myocardial ischemia, in the form of a STEMI, in the presence of a LBBB using Sgarbossa’s criteria. In 1996, cardiologist Elena Sgarbossa and colleagues published an analysis from the GUSTO-1 trial suggesting criteria potentially useful for diagnosis of AMI in the setting of LBBB.24 Sgarbossa proposed three criteria, identified as criteria A, B and C (Figure 11):

Concordant ST elevation of 1 mm or more in any lead with a positive QRS complex (the deflection of the QRS is primarily upward, and there is ST elevation greater than or equal to 1 mm);

Concordant ST depression of 1 mm or more in V1–V3 (in V1–V3 the deflection of the QRS is primarily downward, and there is ST depression greater than or equal to 1 mm);

Excessively discordant ST elevation (5 mm or more) in any lead with a negative QRS complex.

A 12-lead ECG needs only one lead exhibiting Sgarbossa criteria A or B to be called a STEMI. Patients who meet Sgarbossa A or B criteria are said to have a STEMI, and a cardiac catheterization lab should be activated. Positive A and B criteria are accurate more than 90% of the time. If these criteria are not met, it is unlikely the patient is having an AMI.

Sgarbossa’s C criterion has been found to be not as predictive as A and B, so many clinicians ignore it. That this criterion, based on a simple number (5 mm of ST elevation), is not accurate makes intuitive sense: Any large, negative QRS would be expected to have a proportionally large ST segment, as a large depolarization (QRS) would be expected to result in an equally large repolarization (T-wave). Nonetheless, EMS providers should consider the presence of Sgarbossa C criteria as a positive indicator for STEMI.

In the absence of any of Sgarbossa A, B or C criteria, you can assume your patient is not having a myocardial infarction in the presence of a LBBB or paced rhythm (Diagram 1).

The patient in the case presented with numerous symptoms that could be consistent with ACS: nausea, weakness, abdominal discomfort and chest discomfort she describes as her normal reflux pain. When you consider she is female and can be expected to exhibit atypical symptoms of ACS, this should at least get you thinking about ACS. Then there is her 12-lead ECG (Figure 9) to consider; it clearly shows a LBBB with ST-segment elevation. However, her 12-lead ECG was not positive for any of the Sgarbossa criteria, so hers can be considered a “normal” LBBB without a STEMI equivalent.

Treatment

There is no treatment for LBBB in the hemodynamically stable patient. In patients who are hemodynamically unstable, treatment centers on the underlying problem, not the LBBB. The patient in the case presented with a LBBB that was not positive for any of the Sgarbossa criteria. In addition, her clinical findings and HPI were more consistent with GI distress than ACS. Therefore, she should not be treated for STEMI but managed as a patient with GI distress.

Conclusion

STEMI imitators can be readily identified with a good understanding of the history of present illness, a thorough clinical exam and an understanding of the ECG patterns typical for the imitators. If a patient presents with a suspected STEMI imitator, there is any change in their symptoms, or there are persistent clinical symptoms suggesting AMI in the presence of a suspected STEMI imitator, perform serial ECGs. In one study, 11% of patients with an eventual STEMI had an initial ECG that was nondiagnostic for STEMI, and 72% of patients with eventual STEMI developed a diagnostic ECG within 90 minutes.26 When in doubt, consistently reevaluate and perform serial ECGs!

References

Tikkanen JT, Anttonen O, Junttila MJ. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med, 2009; 361(26): 2,529.

Sinner MF, Reinhard W, Muller M, et al. Association of early repolarization pattern on ECG with risk of cardiac and all-cause mortality: a population-based prospective cohort study (MONICA/KORA). PLoS Med, 2010 Jul 27; 7(7): e1000314.

Haissaguerre M, Derval N, Sacher F. Sudden cardiac arrest associated with early repolarization. N Engl J Med, 2008; 358(19): 2,016.

Rosso R, Kogan E, Belhassen B. J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance. J Am Coll Cardiol, 2008; 52(15): 1,231.

Derval N, Simpson CS, Birnie DH, et al. Prevalence and characteristics of early repolarization in the CASPER registry: cardiac arrest survivors with preserved ejection fraction registry. J Am Coll Cardiol, 2011 Aug; 58(7): 722–8.

Burns E. Benign early repolarization. Life in the Fast Lane, https://lifeinthefastlane.com/ecg-library/benign-early-repolarisation/.

Spodick DH. Acute cardiac tamponade. N Engl J Med, 2003; 349(7): 684.

Niermann JT. Chapter 59: “The Cardiomyopathies, Myocarditis, and Pericardial Disease: Introduction.” In: Tintinalli JE, et al., Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed. New York: McGraw-Hill, 2011.

Jouriles NJ. Chapter 82. “Pericardial and Myocardial Disease.” In: Marx J, Hockberger R, Walls R, Rosen’s Emergency Medicine, 8th ed. Mosby, 2013.

Nickson, C. Pericarditis. Life in the Fast Lane, https://lifeinthefastlane.com/ecg-library/basics/pericarditis/.

Rathore S, Dodds PA. Diagnosing chest pain: characteristic ECG changes in acute pericarditis. Heart, 2007 Sep; 93(9): 1,063.

Imazio M, Demichelis B, et al. Day-hospital treatment of acute pericarditis: a management program for outpatient therapy. J Am Coll Cardiol, 2004; 43(6): 1,042.

Rahman A, Liu D. Pericarditis—clinical features and management. Aust Fam Physician, 2011 Oct; 40(10): 791–6.

Kacprzak M, Kidawa M, Zielinska M. Fever in myocardial infarction: is it still common, is it still predictive? Cardiol J, 2012; 19(4): 369–73.

Mattu A. ECG findings in pericarditis vs. STEMI. Emergency ECG Video of the Week, https://ekgumem.tumblr.com/post/30868011279/ecg-findings-in-pericarditis-vs-stemi-episode.

Wang K, Asinger RW, Marriott HJ. ST-segment elevation in conditions other that acute myocardial infarction. N Engl J Med, 2003 Nov 27; 349(22): 2,128–35.

Alings M, Wilde A. “Brugada” syndrome: clinical data and suggested pathophysiological mechanism. Circulation, 1999; 99(5): 666.

Sangwatanaroj S, Prechawat S, Sunsaneewitayakul B, et al. New electrocardiographic leads and the procainamide test for the detection of the Brugada sign in sudden unexplained death syndrome survivors and their relatives. Eur Heart J, 2001; 22(24): 2,290.

Wylie JV, Garlitski AC. Brugada syndrome. UpToDate, www.uptodate.com/contents/brugada-syndrome.

Eriksson P, Hansson PO, Eriksson H, et al. Bundle-branch block in a general male population: the study of men born 1913. Circulation, 1998; 98(22): 2,494.

Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol, 2012; 60: 96–105.

Bansilal S, Aneja A, Mathew V, et al. Long-term cardiovascular outcomes in patients with angina pectoris presenting with bundle branch block. Am J Cardiol, 2011 Jun 1; 107(11): 1,565–70.

Surawicz B, Childers R, Deal BJ, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part III: intraventricular conduction disturbances: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol, 2009 mar 17; 53(11): 976–81.

Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med, 1996; 334: 481–7.

Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med, 2012; 60(6): 766–76.

Riley RF et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram. Amer Heart J, 2013; 165(1): 50–6.

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is performance improvement coordinator for VitaLink/AirLink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. E-mail kcollopy@colgatealumni.org.

Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California, San Francisco. E-mail sean.kivlehan@gmail.com.

Scott R. Snyder, BS, NREMT-P, is a faculty member at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. E-mail scottrsnyder@me.com.