CE Article: Common STEMI Imitators: Part 2

As we discussed last month, 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. A STEMI imitator (Table 1) can place a patient at 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. The November article covered benign early repolarization (BER), acute pericarditis, Brugada syndrome and left bundle branch block (LBBB). This month’s article continues a case-based approach to explore some additional STEMI imitators.

Case #1: Ventricular Paced Rhythm

An obese 60-year-old male presents conscious, alert and oriented to person, place, time and event, sitting on a couch, complaining of chest discomfort. He describes an acute onset of discomfort about an hour ago after eating dinner. The discomfort is described as retrosternal, nonreproducible, burning, nonradiating, and a 6 on a scale of 0–10. It is slightly relieved with belching. He says he’s been experiencing the discomfort “about every day or two” for the past three weeks, and tonight the pain is worse. He also describes frequent episodes of dysphagia and regurgitation that started about three weeks ago.

The patient denies any difficulty breathing, nausea, vomiting, weakness, dizziness, syncope, and abdominal or back pain. His past medical history includes two AMIs, with a ventricular pacemaker implant three years ago; hypertension; type 2 diabetes; a sliding hiatal hernia diagnosed three months ago; and a 46-pack-a-year smoking history. His medications include aspirin, Plavix, diltiazem and glimepiride, and he has no known drug allergies.

Your clinical exam reveals nothing remarkable. He has no JVD or peripheral edema, and his lungs are clear and equal bilaterally. There is no trauma to his chest, and no pain with palpation of his chest wall or sternum. His pacemaker implant site appears normal. His blood glucose is 112 mg/dL; other vitals are HR, 72/min.; BP, 128/72 mmHg; RR, 12/min. with good tidal volume; SpO₂, 97% on room air; temperature, 98.1ºF (36.7ºC) tympanic. Per your protocol you perform a 12-lead ECG, shown in Figure 1. What is your interpretation of this ECG? Do you think the patient is having a STEMI?

There are many clinical situations and circumstances in which a pacemaker implant is considered, but two factors drive the decision of permanent cardiac pacing more than others: the presence of a symptomatic bradydysrhythmia and the location of the conduction dysfunction. The two most common indications for pacemaker implantation are sinus node dysfunction and atrioventricular (AV) block.¹ Examples of sinus node dysfunction include symptomatic sinus bradycardia, chronic heart rates below 40 bpm. while awake in minimally symptomatic patients, sinus node dysfunction in patients with unexplained syncope, and sinus node disease.² Symptomatic chronotropic incompetence is broadly defined as the inability of the heart to increase its rate with increased activity or demand. It is common in persons with cardiovascular disease.³ Examples of AV block that may require the use of a permanent cardiac pacemaker include first-degree AV block (in cases where a very long PR interval effectively creates AV disassociation and hemodynamic instability), Mobitz I or Mobitz II second-degree AV block, and third-degree AV block.²

In atrial pacing, the pacemaker wire is placed in the right atrium. The ECG will show a pacemaker spike followed by a P-wave, the morphology of which depends on the exact placement of the pacemaker wire. P-waves can be normal, small, inverted or biphasic. The P-wave is followed by a PR interval and QRS that is normal for that patient.

In ventricular pacing, the pacemaker spike is followed by a wide QRS. As the patient in our scenario had a ventricular pacemaker, its specific ECG characteristics will be discussed below.

With dual-chamber atrioventricular sequential pacing, pacing wires are placed in the atrium and the ventricle. The ECG pattern depends on two possible starting points. In the first case, if the patient’s sinus node rate (heart rate) is greater than the programmed rate of the pacer, an electrical impulse will originate from the AV node and no pacer spike will appear before the P-wave. Depending on the condition of the AV node, there may or may not be a pacer spike before the QRS: If the AV node is functioning properly and allows the atrial impulse through, a native QRS will appear. If the AV node is dysfunctional and does not allow the atrial impulse through, a pacer spike will appear and a wide QRS will be present. In the second case, if the patient’s inherent sinus node rate is lower than the programmed rate of the pacer, then the pacer will fire, resulting in a pacer spike before the P-wave. If the AV node allows the impulse through, a normal QRS will appear. If the AV node is dysfunctional and does not allow the impulse through, the ventricular pacer will fire, and a pacer spike will appear before the paced QRS complex.

In biventricular pacing, pacing wires are placed in the right atrium, right ventricle and coronary sinus, which stimulates the left ventricle. The ECG characteristics of biventricular pacing are complex and beyond the scope of this article, and they may present with features characteristic of atrial pacing, ventricular pacing or both.

ECG Findings

The pacemaker lead of a ventricular pacemaker is typically placed in the apex of the right ventricle. As such, the ECG pattern associated with a right ventricular paced rhythm typically has a left bundle branch block (LBBB) appearance, since the right ventricle is depolarized before the left ventricle. The pacemaker lead may sometimes be placed higher up in the right ventricle, resulting in an LBBB pattern with a variable axis. Typical ECG morphology for a right ventricular paced rhythm mirrors that of LBBB and includes:

• Pacemaker spike preceding the QRS;

• 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).

Atrial activity, as evidenced by the presence of a P-wave, may or may not be present. Factors that influence whether a P-wave is present include the patient’s underlying rhythm, the atrial rate and the occurrence of retrograde ventriculoatrial conduction of the pacemaker impulse through the atrioventricular node.⁴

Worth noting is that newer-generation pacemakers can have very small, almost imperceptible pacemaker spikes compared to older pacemakers, which had relatively large, easily discernible spikes. The amplitude of any pacemaker spike depends on the patient’s position, lead’s position and type of lead being viewed. A pacemaker spike may be difficult to see in some or even all leads. Anyone who interprets ECGs should develop the habit of deliberately looking for these smaller pacer spikes, which can easily be overlooked.

Other than seeing or palpating the implanted pacemaker during a clinical exam, there are no clinical exam findings that are specific or even suggestive for an implanted pacemaker. A paced rhythm is an ECG entity without any clinical manifestations.      

Differentiating Between Paced Rhythm and STEMI

A ventricular paced rhythm will typically have an LBBB ECG morphology. As is the case with LBBB, it’s a common misconception that you cannot identify a STEMI in a patient with a ventricular paced rhythm. This is not true, and in fact sometimes you can identify myocardial ischemia, in the form of a STEMI, in the presence of a ventricular paced rhythm using the same Sgarbossa criteria used with LBBB discussed in Part 1. Recall that there are three Sgarbossa criteria, identified as A, B and C:

A—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);  

B—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);

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

Thirty-two patients in the GUSTO-1 trial (the results from which Sgarbossa and colleagues determined their criteria) presented with a ventricular paced rhythm, accounting for 0.1% of enrolled patients. Sgarbossa criteria C proved to be the only ECG criteria with a high specificity and statistical significance for the diagnosis of acute myocardial infarction.⁵ Sgarbossa criteria A and B are considered to have “acceptable” specificity.⁶

Patients with a ventricular paced rhythm who meet Sgarbossa C criteria should be considered to have a STEMI, and a cardiac catheterization lab should be activated. Patients with who meet Sgarbossa criteria A or B present a diagnostic challenge, and a medical control physician should be contacted. Ideally the ECG would be transmitted to the medical control physician, who could then assist with a determination regarding transport to a STEMI center and activation of a cardiac catheterization lab.

The patient in our opening case presented with ST-segment elevation in leads II, III, aVF and V2–V4, but he does not meet Sgarbossa criteria A, B or C, so should be considered to not be having a STEMI.

It is worth reinforcing the concept of serial ECGs in any patient with suspected acute coronary syndrome. Serial ECGs, performed every 10–15 minutes at most, should be performed an all patients with suspected ACS. The role of serial ECGs in identifying myocardial ischemia and infarction was reinforced by the Myocardial Infarction Triage and Intervention (MITI) project.⁷ The MITI trial had a number of findings directly applicable to EMS:

• ECG abnormalities secondary to AMI could be identified on a prehospital ECG within 90 minutes of symptom onset;

• Serial ECGs were more effective at identifying patients with myocardial ischemia or infarction;

• ST-segment changes between serial ECGs improved overall sensitivity from 36% to 46%;

• When all ECG abnormalities were considered (ST segment, T-waves, Q-waves, LBBB), the diagnostic sensitivity of the ECG increased from 80% to 87%.

In summary, perform serial ECGs! Your likelihood of identifying an evolving STEMI is greater if you do. In addition, serial ECGs can help with the identification of STEMI imitators, which will not show ST-segment evolution over time and multiple ECGs.

Treatment

There is no treatment needed for a normally paced cardiac rhythm. Prehospital treatment should center on the clinical signs and symptoms presented by the patient. The patient in this case has clinical exam and history findings strongly suggestive of gastroesophageal reflux disease (GERD); his description of his pain is more characteristic of GERD than acute coronary syndrome, and his history of smoking, diabetes and obesity are all risk factors for GERD. In addition, we have determined that the ST-segment elevation on his 12-lead ECG is normal for his ventricular pacemaker, and he does not meet criteria for STEMI activation.

That said, the patient does have a history of AMI as well as risk factors, so ALS transport would be prudent. The patient in this case should receive oxygen if necessary via the appropriate device and flow rate to maintain an oxygen saturation of at least 94%. Intravenous access should be obtained, and the patient placed on a 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 his complaint of chest pain is a valid argument for ALS transport.

Case #2: Subarachnoid Hemorrhage

A 38-year-old male presents unconscious, supine on his bed with snoring respirations. He withdraws from painful stimuli and mutters incomprehensible sounds. His wife says he suffered an acute onset of a “really bad headache—he said it was the worst he’d ever had” about an hour ago during sexual intercourse, and the patient has become increasingly disoriented since and lost consciousness about five minutes ago, after which she called EMS. She says he complained of nausea and vomited twice, and also seemed to be intolerant of bright light, avoiding the brightly lit areas of his house and retreating to his bedroom, where he closed the window blinds. The patient has a history of hypertension treated with hydrochlorothiazide, and has no known drug allergies. In addition, his wife reports he’s an 18-pack-a-year smoker and a recovering alcoholic sober for a month.

Your physical exam reveals no trauma to his head, neck, chest, abdomen or pelvis. His pupils are equal and reactive to light bilaterally, and he withdraws to painful stimuli, showing purposeful and equal movement to all of his extremities. His blood glucose is 133 mg/dL. Vital signs are: HR, 60/min.; BP, 168/110 mmHg; RR, 12/min. with shallow tidal volume; SpO₂, 86% on room air; temperature, 98.8ºF (37.1ºC) tympanic. Per your protocol you perform a 12-lead ECG, shown in Figure 2. What is your interpretation of this ECG? Do you think the patient is having a STEMI?

The most common cause of subarachnoid hemorrhage (SAH) is the rupture of a cerebral arterial aneurysm. The ruptured cerebral artery then pumps high-pressure blood into the cerebrospinal fluid and the space between the surface of the brain and the subarachnoid membrane. SAH secondary to a ruptured arterial aneurysm tends to bleed rapidly, resulting in a fast increase in intracranial pressure (ICP). Other causes of SAH include bleeding diathesis (unusual susceptibility to bleeding), vascular malformations, drug use, illicit drug use and trauma. These etiologies tend to bleed more slowly, and clinical manifestations may take days to weeks to appear.

Cardiac complications are not uncommon in the time period immediately following subarachnoid hemorrhage or ischemic stroke. In the dynamic prehospital environment, it can be difficult to determine if the cardiac findings are caused by the intracranial event, the cause of the intracranial event or completely unrelated.⁸ Intracranial hemorrhage (SAH or intracerebral hemorrhage) with increased ICP and other central nervous system events such as traumatic brain injury and ischemic stroke resulting in cerebral edema can produce ECG abnormalities that can mimic myocardial ischemia.⁹

ECG Findings

The ECG findings associated with increased ICP include:^8–10

• Nonspecific ST changes;

• Ischemic ST changes (depression and elevation);

• Diffuse T-wave inversion and enlargement, especially in precordial leads;

• Prolonged QT interval;

• Brady- and tachydysrhythmias.

Intracranial bleeds can produce ischemic-looking ECGs. However, most patients will have an altered level of consciousness. In addition, intracranial events produce a prolonged QT and deep T-waves. Ischemic ST-segment elevation and flipped T-waves are usually not associated with QT prolongation, a finding that can help identify ECG changes associated with increased ICP and SAH.

The exact reasons for the ECG changes that can accompany increased ICP are not well understood. One hypothesis is that increased ICP may result in a catecholamine surge, stressing the myocardium and resulting in ischemic changes. Vagus nerve stimulation may also play a role. In addition, elevated ICP and intracranial events may result in increased left ventricular pressure and subsequent subendocardial hemorrhage. As such, ICP and CNS events may actually induce myocardial damage, which produces the ECG abnormalities.⁸

The patient with ECG changes secondary to SAH and increased ICP will present with the characteristic clinical exam findings expected from the various etiologies of increased ICP. There are no clinical exam findings directly related to the ECG manifestations of increased ICP.

Differentiating Between SAH and STEMI

Differentiating between SAH and AMI can be difficult early in the progression of SAH. Both etiologies can present with dizziness, nausea and vomiting, and altered mental status early in their progression.

Arguably it becomes easier to differentiate AMI from SAH as SAH progresses, and AMI will not present with the neurologic findings (unequal pupils), bradycardia and hypertension characteristic of SAH and increased ICP. In the case above, the patient presented with a history and clinical exam findings that strongly suggested acute SAH and increased ICP as the etiology of his decreased level of consciousness. He had a history of acute onset of severe headache, nausea and vomiting, and photophobia. He was also exhibiting signs of increased ICP: bradycardia and hypertension. In addition, he had risk factors for SAH: cigarette smoking, hypertension and heavy alcohol consumption.

Treatment

In the absence of AMI, there is no treatment for the ECG manifestations of SAH and increased ICP. Treatment of the patient in this case should focus on his increased ICP. ALS care is warranted. The patient in this case should receive oxygen if necessary via the appropriate device and flow rate to maintain an oxygen saturation of at least 94%, intravenous access should be obtained and, if he exhibits signs of severe herniation (fixed and dilated pupil, severe hypertension and bradycardia, posturing, seizures), a fluid challenge could be administered in an attempt to increase preload and ultimately blood pressure to better maintain cerebral perfusion in the face of increased ICP. Place the patient on the cardiac monitor and obtain serial 12-lead ECGs en route to the emergency department (for medical emergencies) or trauma center (for trauma emergencies), as there is a risk of cardiac complications secondary to increased ICP.

Case #3: Left Ventricular Hypertrophy

A 73-year-old female presents conscious, alert and oriented to person, place, time and event, sitting on a chair in her backyard, complaining of dizziness and weakness. She says she was working in her garden for the past two hours without rest, food or water. You note that it is 90ºF with high humidity. She describes a gradual onset of weakness over the past two hours, then experienced dizziness when she got up from her hands and knees to go into her home to escape the heat that was, as she describes it, “really getting to me.” She denies syncope, chest pain or discomfort, difficulty breathing, abdominal or back pain, and headache. She has a history of hypertension and diabetes for which she takes metoprolol, diltiazem and glyburide. She has been compliant with her medications and has no known drug allergies.

Your clinical exam reveals dry mucous membranes, lung sounds that are clear and equal bilaterally, and no jugular venous distention or peripheral edema. You observe no pronator drift, facial droop or slurred speech. All other finds are normal. Her blood glucose is 102 mg/dL. Other vitals: HR, 70/min.; BP, 98/52 mmHg; RR, 12/min. with good tidal volume; SpO₂, 96% on room air; temperature, 98.6ºF (37ºC) tympanic. Per your protocol you perform a 12-lead ECG, shown in Figure 3. What is your interpretation of this ECG? Do you think the patient is having a STEMI?

Left ventricular hypertrophy (LVH) is a condition in which there is an increase in the size of the myocardial fibers in the left ventricle of the heart. Any condition that impedes the forward movement of blood from the left ventricle will create a back pressure, requiring the heart to work harder to move blood forward into the aorta. As a result of the ventricular muscle working harder, it becomes larger.

LVH is not an acute condition; it can take weeks to months to years to develop. Etiologies of LVH include hypertension (the most common cause), aortic stenosis (second most common), aortic regurgitation, mitral regurgitation, coarctation of the aorta and hypertrophic cardiomyopathy. Patients with LVH from any of these etiologies are at increased risk for cardiovascular complications including congestive heart failure and cardiac dysrhythmias.¹¹ It is also a blood pressure-independent risk factor for sudden death, acute myocardial infarction and other cardiovascular morbidity and mortality.¹²

ECG Findings

The ECG can be useful but is not the best tool for diagnosing LVH; electrocardiography is the best and preferred method. ECG is a relatively insensitive method of detecting LVH, and patients with clinically significant LVH may have relatively normal ECGs.¹³ This is not to say LVH is rare. In fact, one study concluded that LVH was the most common cause of ST-segment elevation in patients with chest pain presenting to the emergency department.¹⁴

There is no single best ECG criteria for hypertrophy of any of the cardiac chambers (atria and ventricles). Several different sets of criteria have been proposed, with varying sensitivities and specificities. The characteristics of LVH include:^11,12,15

• Increased QRS voltage;

• Scott criteria;

• Limb leads:

R in I plus S in 3 more than 25 mm;

R in aVL more than 11 mm or greater than 18 mm if left axis is present;

R in aVF more than 20 mm;

S in aVR more than 14 mm;

• Precordial leads:

S in V1 or V2 plus R in V5 or V6 more than 35 mm;

R in V5 or V6 more than 26 mm;

R plus S in any V lead more than 45 mm;

• Increased QRS duration;

• Left axis deviation;

• ST-segment and T-wave abnormalities in the left-sided leads, especially V1–V3 (ST-segment elevation, downsloping ST-segment depression and T-wave inversion);

• Left atrial abnormality/enlargement.

Another widely used criteria is the Sokolow-Lyon criteria, which states that LVH is present if the sum of the amplitude of the S-wave in lead V1 plus the amplitude of the R-wave in V5 or V6 (whichever is the tallest) is 35 mm or more, and/or the R wave in aVL is greater than or equal to 11 mm.

The patient with ECG changes secondary to LVH will present with the characteristic clinical exam findings expected from the various etiologies of LVH, which include hypertension, aortic stenosis, aortic regurgitation, mitral regurgitation, coarctation of the aorta and hypertrophic cardiomyopathy. There are no clinical exam finds directly related to the ECG manifestations of LVH.

Differentiating Between LVH and STEMI

Differentiating between LVH and STEMI can be difficult. A true STEMI will have reciprocal ECG changes, while ST-segment elevation secondary to LVH will not.

As detailed in the ECG criteria above, LVH usually presents with ST-segment elevation in the anterior leads. Therefore, ST segment elevation in the inferior, lateral, right-sided or posterior leads should be considered a STEMI. The true difficulty lies in differentiating an anterior MI from LVH. A group out of University of California-Davis has put together an algorithm to better predict which ST-segment elevation in LVH is a true STEMI.¹⁶ This algorithm has not yet been validated, and the authors acknowledge it “may augment interpretation” but is by no means definitive. The authors found that measuring the relative amount of ST-segment elevation was more sensitive and specific for STEMI than measuring the absolute ST-segment elevation. To determine the relative ST-segment elevation, it is normalized against the difference of the preceding R- and S-waves to give a percentage (%STE; Figure 4). In this calculation, %STE = (height of T-P segment to J-point)/(height of R-wave minus depth of S-wave).

The authors found that legitimate STEMIs had a greater percent STE versus false STEMIs in LVH. If the percent STE was less than 25%, a STEMI could be ruled out. If the percent STE was greater than 25%, the sensitivity and specificity for legitimate STEMI were 77% and 91%, respectively.

The steps involved in using the algorithm are as follows:

1. Are the ST elevations in leads V1–V3? If yes, go to step 2. If they’re in other leads, it’s a STEMI.

2. Is the %STE greater than 25%? If no, it’s not a STEMI. If yes, go to step 3.

3. Are there more than three leads with ST elevation? If yes, it’s a STEMI. If no, go to step 4.

4. Are the T-wave inversions present in V1–V3? If yes, it’s a STEMI. If no, it’s not a STEMI.

Using these criteria, the patient in our case does not meet the criteria for STEMI. Her ST-segment elevation can be considered normal with her LVH. In addition, while she does have weakness and dizziness, and as an elderly diabetic female we would expect her to present with atypical chest pain with AMI, her history and clinical exam strongly suggest that she may be dehydrated from long hours working in a warm environment.

Treatment

In the absence of true STEMI, there is no treatment for the ECG manifestations of LVH. Treatment of the patient in this case should focus on her weakness and dizziness, and these complaints warrant ALS-level care. Administer oxygen if necessary via the appropriate device and flow rate to maintain an oxygen saturation of at least 94%, obtain intravenous access, and a fluid challenge could be administered in an attempt to increase her blood pressure. Place the patient on a cardiac monitor and obtain serial 12-lead ECGs en route to the emergency department, just to be certain the ST-segment elevation is not evolving or that reciprocal changes don’t emerge, both of which would indicate an evolving STEMI.

Conclusion

Hopefully, this month’s CE article reinforced the message from last month: STEMI imitators can be readily identified with a good understanding of the HPI, a thorough clinical exam and an understanding of the ECG patterns typical for the imitators. If a patient presents with a suspected STEMI imitator, if there is any change in their symptoms or there are persistent clinical symptoms suggestive of AMI in the presence of a suspected STEMI imitator, perform serial ECGs. If you find yourself wanting to identify a 12-lead ECG pattern as a STEMI imitator, continue to reevaluate and perform serial ECGs! When in doubt, always err on the side of caution: Call it a STEMI and treat it as such.

References

1. Birnie D, Williams K, et al. Reasons for escalating pacemaker implants. Am J Cardiol, 2006; 98(1): 93.

2. Hayes DL. Indications for permanent cardiac pacing. UpToDate.com, www.uptodate.com/contents/indications-for-permanent-cardiac-pacing.

3. Brubaker PH, Kitzman DW. Chronotropic incompetence: causes, consequences, and management. Circulation, 2011; 123: 1,010–20.

4. Prutkin JM. ECG tutorial: Pacemakers. UpToDate.com, www.uptodate.com/contents/ecg-tutorial-pacemakers.

5. Sgarbossa EB, Pinski SL, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. Am J Cardiol, 1996; 77(5): 423.

6. Goldberger AL. Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm. UpToDate.com, www.uptodate.com/contents/electrocardiographic-diagnosis-of-myocardial-infarction-in-the-presence-of-bundle-branch-block-or-a-paced-rhythm.

7. Kudenchuk PJ, Maynard C, et al. Utility of the prehospital electrocardiogram in diagnosing acute coronary syndromes: the Myocardial Infarction Triage and Intervention (MITI) Project. J Am Coll Cardiol, 1998; 32(1): 17.

8. Chalela JA, Jacobs TL. Cardiac complications of stroke. UpToDate.com, www.uptodate.com/contents/cardiac-complications-of-stroke.

9. Burns E. Raised intracranial pressure. Life in the Fast Lane, https://lifeinthefastlane.com/ecg-library/raised-intracranial-pressure/.  

10. Singer RJ, Ogilvy CS, Rordorf G. Clinical manifestations and diagnosis of aneurysmal subarachnoid hemorrhage. UpToDate.com, www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-aneurysmal-subarachnoid-hemorrhage.

11. Goldberger AL. Electrocardiographic diagnosis of left ventricular hypertrophy. UpToDate.com, www.uptodate.com/contents/electrocardiographic-diagnosis-of-left-ventricular-hypertrophy.

12. Podrid PJ. Left ventricular hypertrophy and arrhythmia. UpToDate.com, www.uptodate.com/contents/left-ventricular-hypertrophy-and-arrhythmia.'

13. Burns E. Left ventricular hypertrophy. Life in the Fast Lane, https://lifeinthefastlane.com/ecg-library/basics/left-ventricular-hypertrophy/.

14. Brady WJ, Perron AD, et al. Cause of ST segment abnormality in ED chest pain patients. Am J Emerg Med, 2001 Jan; 19(1): 25–8.

15. Prutkin JM. ECG tutorial: Chamber enlargement and hypertrophy. UpToDate.com, www.uptodate.com/contents/ecg-tutorial-chamber-enlargement-and-hypertrophy.

16. Armstrong EJ, Kulkami AR, et al. Electrocardiographic criteria for ST-elevation myocardial infarction in patients with left ventricular hypertrophy. Am J Cardiol, 2012 Oct 1; 110(7): 977–83.

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.

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.

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.