Chest pain complaint might be one of the most common calls that EMS providers face. It’s also one of the vaguest. Thanks to education about “heart attacks,” the public has learned to recognize chest pain early and to call often. Often, EMS providers can clear patients of any cardiac risk by taking a good history and doing a thorough physical assessment. Not all chest pain patients require a 12-lead ECG; of those that do, our ECG assessment is often a quick look for “ST elevation” and a review of the computer interpretation of the leads, and it always includes a nagging in the back of our minds to “treat the patient, not the monitor.”
The 12-lead ECG is a staple of modern EMS care and has been implemented in the field with a broad spectrum of training, from those who learned it as new paramedics to those who were trained after years of working without it. Most of us know that ST elevation is bad; remember that there’s something to fear in ST depression, and admit that inverted T waves are just plain confusing. Somewhere, dusty and long pushed to the back of our memories, is something about significant Q waves and something called “R-prime.” So we take a look at the ST-segment, argue about what is—and isn’t—elevation, decide on a course of action and slide our ECG printout in with the rest of our paperwork. After all, even emergency physicians agree that the ECG is helpful in supporting a good clinical assessment, not replacing it.1
The reality is that ST elevation is a poor indicator for diagnosing acute myocardial infarction (AMI) (see Figure 1).1 In one emergency department (ED) study, the cause of the ST elevation was AMI in only 15–31% of cases. The rest of resulted from other causes, including left ventricular hypertrophy (LVH), benign early repolarization (BER), pericarditis, left bundle branch blocks (LBBB) and ventricular paced rhythms (VPR), to name a few.2 Each has a classic presentation that’s subtly different from ST elevation caused by an AMI.
Granted, pulling out a pair of calipers to measure T waves in the back of a bumpy ambulance will inevitably lead to headaches and minor trauma. But a quick, 10-second look (and some practice) at what would otherwise be dismissively called “a 12-lead with ST elevation” can teach us much more about our patients, in the morphologies of the ST segment and elsewhere in the ECG.
Before we discuss electrocardiographic morphologies, we should define what’s normal. Of course, between patient movement, ambulance movement and population variance, “normal” is perhaps the rarest form of ECG.
The normal ECG starts with a PR segment, measured from the beginning of the P wave, and ends at the QRS. The QRS ends at the J, or “junction” point, which marks the beginning of the ST segment. This follows a straight line to the T wave, a slightly pronounced, usually asymmetrical wave caused by ventricular repolarization.3 The TP segment connects the last beat to the next and defines the “isoelectric line” by which all elevation and depression is measured. In the normal ECG, the PR segment, the ST segment and the TP segment start and finish at the same elevation. Remember that ST elevation is measured at the J point. If the J point is below the TP segment, you’re looking at depression.3 A depressed J point with an ST segment that curves up above the isoelectric line and then back down is still depression.
In the classic ST-elevation MI, or isoelectric line, the segment is usually “non-concave,” which means it bows up rather than back down toward the isoelectric line. In a well-developed MI, the segment is often indistinguishable from the T wave, and together they form an ominous sign that has earned the very appropriate title “the tombstone.” This non-concave morphology appears almost exclusively in cases of acute infarction.2 This appearance in two or more contiguous leads, which are leads that view the same side of the heart, is considered diagnostic. Reciprocal depression in leads on the opposite side—such as the lateral leads I and aVL, if the elevation is in leads II, III and aVF—is even more definitive of AMI.3
In subtle but important ways, however, ST elevation often doesn’t follow the above pattern; most cases of ST elevation aren’t caused by an AMI.1 Although ST elevation may have any number of different etiologies, we’ll look at some of the more common ones.
Left Ventricular Hypertrophy (LVH)
LVH is responsible for up to 30% of ST elevation.2 It’s defined as an increase in mass to the left ventricle, often in response to chronic hypertension. As the heart beats continuously against a higher diastolic afterload, cardiac tissue surrounding the left ventricle grows, stealing space, and thus volume, from its ventricle. The long-term prognosis for these patients is poor because the condition eventually leads to decreased diastolic and systolic function.4 These patients often develop close relationships with their cardiologists and emergency departments as cardiac function drops, and their risk of AMI and other cardiac disease climbs. As the left ventricle loses its ability to move blood, the pump backs up into the left atria and then into the lungs; many of our CHF patients will demonstrate the signature QRS pattern of LVH (see Figure 2). Exaggerated QRS complexes dominate the precordial leads, resembling the tracing of a large earthquake.
The most common criteria for LVH diagnoses were established in 1949. Take the largest negative deflection from the isoelectric line of VI and V2 (“S” wave), whichever is larger, and count the small boxes. Then take the largest positive deflection of V5 or V6 (“R” wave), whichever is larger, and add it to the total from VI or V2. If the result is greater than 35, your suspicion for LVH should be high. The equation can be simplified to the following: S(V1 or V2) + R(V5 or V6)>35.
Left lateral leads 1, aVL, V5 and V6 often have large positive R waves and ST depression with inverted T waves. The ST segment in these leads is usually non-concave. (Fear not … “the tombstone” applies to elevation only,) The segment starts from a depressed J point and curves down gradually into the T wave, which abruptly returns to the isoelectric line.5 In septal leads V1 and V2, the long, negative S wave is usually accompanied with ST elevation caused by altered repolarization patterns of the cardiac tissue.6 This elevation is usually concave, as opposed to the non-concave appearance of AMI. But use caution in these leads; early AMI can sometimes manifest as an elevated concave ST segment.2
Unfortunately, identifying LVH doesn’t mean you’re out of the woods of cardiac suspicion. Chronic hypertension and LVH are two major risk factors for cardiac disease. ST elevation due to LVH may be hiding a STEMI underneath its concave ST segment. The same may be said for a left bundle branch block.
In the normal conduction of the heart, the electrical impulse initiated in the right atrium travels through the internodal pathways to the AV node, down through the bundle of His and eventually down to the right and left bundles. In this way, the cardiac muscle contracts sequentially and efficiently. A BBB (see Figure 3), however, slows or stops the conduction through one of the bundles. The block is often caused by death of the specialized conduction cells that transmit the electrical impulse, leaving the affected myocardium primed to contract, but without a signal. This could be caused by cardiac surgery, endocarditis, LVH or AMI, to name some of the more common pathologies.7
When the normal bundle pathway is disrupted, the electric impulse arrives to the affected ventricle from the unaffected one through the slower-contracting myocardial cells, resulting in a QRS greater than 0.12 seconds (three small boxes), and often, the classic “rabbit ear” R or S wave. In LBBB, the depolarizing signal to contract arrives from the right ventricular myocardium (see Figure 4). The vector that repolarization follows results in a negative S wave in V1, and often a unique pattern of ST elevation.
T waves, in the normal ECG, are positive in leads I, II and V3 through V6. In a LBBB, however, this isn’t true. Because of the changes in the vector or repolarization, T waves in a BBB should move in the opposite direction of the last deflection of the QRS. This is called “discordance.” To put this simply, if your QRS leaves you with a mountain, the T wave should be a valley, and vice versa. If you have identified LBBB using the above criteria, expect the negative QRS in V1 and V2 to have moderate ST elevation and large discordant T waves. The positive R waves of V5 and V6 will have ST depression with discordant negative T waves.
QRS complexes and T waves that are either both positive or both negative display concordance. Concordant positive T waves after a positive QRS are indicative of ischemia, and along with ST elevation is one highly specific sign of AMI in the presence of LBBB. Elevation of more than 5 mm in ST segments following a negative QRS is another sign.8 Depression in reciprocal leads in the latter case would prove even more definitive. This is important because LBBB places patients at extremely high risk for cardiovascular complication.2
The pericardial sac is attached to the diaphragm, sternum and costal cartilage. It’s designed to not only minimize friction for the constantly active heart, but also to create a barrier for infection that might be transferred from other surrounding organs. Like all structures, however, the sac is an imperfect solution. Pericarditis, or inflammation of this sac, is one of the leading causes of effusion to the pericardial space (see Figure 5).9 Although 83% of cases are idiopathic, sometimes end stage renal disease, lupus or cardiac surgery with subsequent infection is to blame. Uremia, trauma, human immunodeficiency virus and AMI are other causes. As many as 11–50% of rheumatoid arthritis patients are diagnosed with pericarditis post-mortem.9
A good clinical assessment and patient history will often reveal a febrile patient complaining of a “sharp” or “stabbing” chest pain that may change with movement or inspiration. And, it may radiate in a classically “cardiac” way—to the left arm and neck. Supine positioning may increase pain, while leaning forward alleviates the pain. Associated symptoms include dyspnea or tachypnea, and dysphagia. If TB is to blame, such symptoms as fever, night sweats and weight loss are common. Cardiac auscultation may reveal a friction rub, although this is transient in nature and appears only about half the time.9
On initial inspection, the classic ECG of early pericarditis is alarming. Elevation across numerous leads may trigger a primal paramedic response that brings out the nitro and aspirin, but take a closer look: The ST elevation, which may be in every lead but aVR and V1, will usually be concave like ST elevation in LVH, as if it could hold water. A notched J point, which gives the ST segment the appearance of a fish hook lying on its back, is often present in this concave elevation. If you look to the PR segment, there will be depression in the leads with ST elevation. This depression is so suggestive of early onset pericarditis that it’s considered “almost diagnostic.” If you have trouble recognizing the depression, look for reciprocal PR elevation in lead aVR, which clinicians have an easier time recognizing.10
As the disease progresses, T-wave inversion may be present. (Remember that the T waves are normally upright in II, III and V3 through V6.) If the disease progresses unchecked, pericardial effusion followed by tamponade may ensue. This may cause electrical alternans—a condition in which the ECG voltage of each beat may be different from the last as the heart shifts inside its oversized sac. Low ECG voltage caused by transmission through higher fluid volume may also be present, but this is hard to recognize without a baseline ECG for comparison.2 This might be a good time to take a look for Beck’s triad of jugular venous distension, hypotension and muffled heart tones. Coupled with a good assessment of your patient, your suspicion for myopericarditis in this ECG should be high.
BER resembles pericarditis because of a diffuse, concave ST elevation in numerous leads. The difference is that the PR interval isn’t depressed, and there are pronounced, concordant T waves. The catch, however, is that you may never see this condition on an ECG. As the name implies, these patients, who are usually less than 40 years old and predominantly African-American, have no increased risk to their long-term health. In fact, one study found they generally have lower cholesterol, lower blood pressures, lower BMI and were less likely to report illnesses in general.11 They’re probably less likely to have cardiac-type complaints, thus you’re less likely to introduce them to your 12-lead cables. If you happen to see an ECG with ST elevation that looks like it was simply lifted from the baseline across many leads, look for tall, symmetrical and concordant T waves in the precordial leads.2 These findings are classic indicators of BER.
To be thorough, we should include patients with ventricular pacemakers. Most of us are well versed in the wide, dramatic rhythms following the spike of a ventricular pacemaker, and all bets are off when it comes to diagnosing morphologies. Like LBBB, repolarization pathways are different in the cardiac tissue of these patients, and ST morphologies are varied and unpredictable. Carry a high index of suspicion in these patients, and trust your assessment over the monitor.
Now comes the inevitable question of what to do with all this information. Paramedics don’t have the luxury of an old ECG to compare their tracing with, and the eye of the experienced cardiologist in the cath lab is substituted with the eye of the field clinician, viewing a 3" wide strip by the light of a flashlight, or if they’re lucky, in the back of a moving ambulance. We’ve identified the most common causes of ST elevation, but if we follow the old motto “treat the patient, not the monitor,” our treatment may be affected very little. After all, the paramedic with a high index of suspicion for ACS or AMI will recognize that AMI is one of the common causes for LVH, LBBB, pericarditis and paced rhythms. ST elevation that doesn’t resemble the classic ST morphology of AMI may only be covering up a lesser elevation that does.
Like the concordant T waves in LBBB, there are other ways to find cardiac injury in a patient with the above conditions, such as ST depression or significant Q waves. But none of these findings alone will ever replace the thorough clinical assessment of an educated paramedic. JEMS
1. Brady WJ & Morris F. Electrocardiographic ST-segment elevation in adults with chest pain. J Accid Emerg Med. 1999;16(6):433–439.
2. Brady WJ. ST segment and T wave abnormalities not caused by acute coronary syndromes. Emerg Med Clin N Am. 2006;24(1):91–111.
3. Garcia TB. 12-Lead ECG; The Art of Interpretation. 2001; Jones & Bartlett Learning: Sudbury, Mass., pp. 309, 312, 409–410, 2001.
4. Riaz K & Ahmed A. (April 20, 2010) Hypertensive heart disease. In Medscape Reference. Retrieved January 2011, from http://emedicine.medscape.com/article/162449-overview.
5. Rykert HE & Hepburn J. Electrocardiographic abnormalities characteristic of certain cases of arterial hypertension. Am Heart J. 1935;10(7):942–954.
6. Huwez FU, Pringle SD & Macfarlane FW. Variable patterns of ST-T abnormalities in patients with left ventricular hypertrophy and normal coronary arteries. Br Heart J. 1992;67(4):304–307.
7. Kakavand B. (April 14, 2010) Bundle branch block: Left. In Medscape Reference. Retrieved January 2011, from http://emedicine.medscape.com/article/895064-overview.
8. 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(8):481–487.
9. Spangler S, Aronoff GR, Fly CA, et al. (April 20, 2010) Acute Pericarditis. In Medscape Reference. http://emedicine.medscape.com/article/156951-overview.
10. Spodick DH. Differential diagnosis of the electrocardiogram in early repolarization and acute pericarditis. N Engl J Med. 1976;295:523–526.
11. Klatsky AL, Oehm R, Cooper RA, et al. The early repolarization variant electrocardiogram: Correlates and consequences. Am J Med. 2003;115(3):171–177.
- Aghel A & Krasuski RA. A 37-year-old man with chest pain, ECG changes, and elevated cardiac enzymes. Cleve Clin J Med. 2009;73(3)199–205.
- Hameed W, Razi MS, Khan MA, et al. Electrocardiographic diagnosis of left ventricular hypertrophy: Comparison with echocardiography. Pak J Physiol. 2005;1(1–2).
- Marinella MA. Electrocardiographic manifestations and differential diagnosis of acute pericarditis. Am Fam Physician. 1998;57(4):699–704.
- Merce J, Sagrista SJ, Permanyer MG, et al. Pericardial effusion in the elderly: A different disease? Rev Esp Cardiol. 2000;53(11):1432–1436.
- Estok L & Wallach F. Cardiac tamponade in a patient with AIDS: A review of pericardial disease in patients with HIV infection. Mt Sinai J Med. 1998;65(1):33–39.
This article originally appeared in July 2011 JEMS as “Elevation Imposters: When the classic approach to ECG interpretation isn’t enough.”