EMS 44 was in the middle of a busy 12 hour shift. Most of the calls required ALS care and Frankie, an experienced paramedic, was behind on paperwork. Her partner Jacob, an EMT, was hoping to grab lunch when their tones went off to respond to an office building for a male patient with chest pain. After a short response, the building’s security directs the crew to the 5th floor where they find a 48-year-old male seated in a conference room. The crew immediately recognizes his skin is pale and diaphoretic. The patient reports he began having chest tightness this morning as he prepared for several meetings. Thinking it was anxiety, he took an Ativan pill and kept working. It has now been three hours and the pain has worsened and is radiating into his neck. While Jacob administers oxygen via nasal cannula and administers 324mg of chewable aspirin, Frankie places the patient on the cardiac monitor and obtains a 12-lead ECG.
Prehospital providers frequently monitor and manage patients complaining of chest pain. While not all patients with chest pain are experiencing acute coronary syndrome (ACS), it is important to maintain a high index of suspicion when ACS is in your differential diagnoses, particularly when patients have common complaints (Table 1). Acute coronary syndrome is the generic diagnoses encompassing patient presentations ranging from unstable angina (UA) to non-ST-segment elevation myocardial infarction, and ST-segment myocardial infarction (STEMI). Whenever ACS is suspected, it’s important to rapidly obtain a 12-lead electrocardiogram (ECG). A 12-lead is the single most important diagnostic test for ACS patients, and its findings drive a patient’s goal-directed therapy.1 It has been shown that paramedics can diagnose STEMI with an accuracy of over 90%.2 Prehospital 12-lead ECGs are proven to speed STEMI diagnosis and shorten the time from symptom onset to reperfusion, either from fibrinolytics or primary percutaneous coronary intervention (PCI) with balloon angioplasty in the cardiac catheterization lab.3 Paramedic activation of catheterization lab teams for patients experiencing STEMI can shorten door to balloon (d2b) times and increase a patient’s chance of experiencing catheterization within the recommended 90 minutes.2 Yet over 25% of patients who do not yet present with STEMI will still have ECG changes that can provide clinicians with clues to the patient’s disease process and drive their therapy.4 This month’s CE column builds upon the basics of 12-lead ECG interpretation and explores how to use a 12-lead ECG to accurately identify and understand the significance of the ECG changes occurring throughout acute coronary syndrome.
Table 1: Common ACS Patient Complaints1
Pain (pressures, squeezing, burning, with radiation)
Nausea (vagal stimulation)
Decreased exercise tolerance
Acute Coronary Syndrome
Patients with ACS experience a variety of cardiac related symptoms (Table 2) leading to a diagnosis of either angina or myocardial infarction. Atherosclerosis is the primary cause of ACS when a previously non-severe lesion—narrowing of a coronary artery—ruptures the vessel’s tunica intima leading to clot formation.1 Embolisms can also cause ACS; however, it is much less common. Each year 1.2 million people are admitted to U.S. hospitals with ACS, and as many as 47% are later discharged with a diagnosis of STEMI.5 Many of these patients are treated by prehospital providers. The prehospital assessment and management of these patients does make a difference, as even a diagnosis of ACS without a STEMI increases the risk of death. The six month mortality for non-STEMI is 13%, while unstable angina has a mortality of 8%.1
Table 2: Physical Findings Associated with ACS1
Hypotension (indicates cardiogenic shock)
Pulmonary edema (LV failure)
Cool, clammy skin
S3 and S4 heart tones
When evaluating a patient with chest pain it’s essential to rule in or out AMI. The 12-lead ECG is an essential tool, but studies have demonstrated that when cardiologists look at a 12-lead ECG without considering a patient’s clinical presentation they disagree on the diagnosis over 50% of the time.6 When considering an ECG, also consider looking for symptoms that strongly increase the likelihood of AMI—chest pain radiating to the left arm, to the right shoulder or to both arms; chest pain with diaphoresis; a third heart tone; or hypotension.6
Myocardial infarctions are described as either a STEMI or a non-STEMI. STEMI is diagnosed by the presence of ST-segment elevation on a 12-lead ECG. When ST-segment elevation is absent, non-ST segment elevation myocardial infarctions are diagnosed by the elevation of the cardiac enzyme troponin I in the presence of cardiac symptoms. Cardiology has shifted away from the previously used myocardial infarction descriptions of transmural and non-transmural as well as Q-wave and non Q-wave MI.1
The rapid acquisition of a 12-lead ECG is essential. Once STEMI is diagnosed, the American Heart Association (AHA) and American College of Cardiology Foundation have set a standard: the time from first medical contact to primary PCI should not exceed 90 minutes; when primary PCI is not available, first medical contact to fibrinolytics should not exceed 120 minutes.5 When a prehospital provider diagnoses STEMI or other significant changes on a 12-lead ECG they can help decrease myocardial tissue damage through therapeutic interventions and by providing timely access to definitive care for early reperfusion. There are three major causes of delays in STEMI patients’ access to definitive therapy for ACS, two of which occur in the prehospital phase of patient care: 1) patient recognition following symptom onset; 2) patient transport to the proper facility; and 3) delay from ED arrival until therapy—fibrinolytics or PCI—delivery.3
The History of the 12-lead ECG
We can trace this history of electrocardiograms back to 1887 when British physiologist Augustus Waller first recorded a human ECG with a capillary electrometer. Just two years later, in 1889, ventricular fibrillation was described in the British Journal of Medicine by John McWilliam. By 1891 physicists learned that by placing a terminal on a patient’s hands it’s possible to monitor and measure electrical deflections with each heart beat; these later were described as the P, QRS, and T complexes still used today. Willem Einthoven was the first to introduce the term the “electrocardiogram” in 1893, and really became the father of the ECG over the next two decades as he refined and improved techniques for ECG acquisition and accuracy. His famous Einthoven triangle was first presented in 1912 to the Chelsea Clinical Society in London and he standardized leads I, II and III; he went on to win the Nobel prize in 1924.
Leads aVR, aVL and aVF, and the chest leads, were all identified through the 1930s and early-1940s. All of these now-defined leads were first put together in 1942 by Emanuel Goldberger, creating the 12-lead ECG used today. It wasn’t until 1976 that the right-sided ECG was first described by LR Erhardt and right sided infarctions were recognized, and finally in 1993 the posterior ECG was described using v8 and v9, when the 15-lead ECG was described by Robert Zalenski.7
Placing a 12-lead ECG
ECGs require rapid placement and acquisition whenever symptoms are present; the 12-lead may be the only diagnostic tool to help identify an etiology for episodic symptoms such as transient syncope or intermittent chest pain. However, if the leads of the 12-lead are not properly placed, the resulting image will not be accurate and can lead to misinterpretation by the reader. Proper positioning is shown in Figure 1.
When placing leads for a 12-lead, begin by placing the four limb leads on the limbs; this means the leg leads go below the hips and the arm leads distal to the shoulder. To maintain proper orientation, all four leads are placed either proximally or distally. For example, if the leg legs are placed near the ankles, the arm leads must be placed near the wrists; leg leads placed near the thighs require arm leads placed on the deltoid muscle. Avoid placing electrodes directly over bone or over very hairy areas, as these will serve to impede the electrical reading. Hair should be shaved when necessary.
Chest leads are placed in their respective intercostal regions. It may be necessary to shave the chest to ensure firm electrode placement. Do not place electrodes over the breast tissue. V1 is placed in the fourth intercostal space just to the right of the sternum; V2 just to the left of the sternum in the fourth intercostal space as well. Next, place V4 in the fifth intercostal space on the midclavicular line; if a patient has excess breast tissue it may be lifted by using the back of a gloved hand so that V4 may be properly placed. Following V4 placement, place V3 at the midpoint of the line between V2 and V4. V6 is placed along the fifth intercostal space at the mid-axillary line. Note that this should be in line with the armpit and the intercostal space may curve slightly caudally. Finally, place V5 at the midpoint of the V4–V6 line.
Proper placement is extremely important as the each lead then looks at a specific region of the heart’s muscles. Figure 2 shows the 12-lead ECG’s leads and the muscle region, as well as the associated coronary artery. The coronary arteries and the heart’s regions are also shown in Figure 3.
With proper placement, the 12-lead offers a precise diagnostic snapshot of that moment’s electrical activity within the heart. ACS is an evolving process and when patients have ongoing symptoms, or a sudden condition change, it is prudent to repeat the 12-lead ECG. A recent study found an initial prehospital 12-lead ECG missed over 15% of STEMIs. Researchers found by repeating the 12-lead ECG, nearly 94% of STEMIs were captured by the second 12-lead and 100% (in this 325 patient study) were identified by the third 12-lead.8 It’s important to note all 12-leads were acquired within a maximum of 25 minutes of patient contact. This suggests it’s reasonable to repeat a 12-lead every 10 minutes during patient care, or whenever there is a significant change in patient condition (e.g., an increase in pain, sudden diaphoresis, nausea, blood pressure change). Do not rule out STEMI after a single prehospital 12-lead. Instead, perform repeat 12-leads throughout your entire course of prehospital care. Make repeating a 12-lead ECG easier by leaving the electrodes on the patient until you arrive at the emergency department.
A 12-lead ECG is not used to interpret a patient’s baseline rhythm, such as sinus rhythm, atrial fibrillation, sinus tachycardia or an accelerated junctional rhythm. This interpretation is best performed by obtaining a 3-lead tracing for 6–10 seconds. A 3-lead ECG is superior for rhythm interpretation because it allows three simultaneous views of the heart to better identify the regularity of the P-wave, QRS complex and T-wave, and by obtaining a 6 or 10 second strip you can more accurately determine the actual heart rate than you can on a 12-lead ECG. Since a 12-lead ECG changes leads every 3 seconds across the print out, marching out the pattern on the P, QRS and T waves is nearly impossible. The 12-lead ECG is used to look for evidence of abnormalities within the heart’s electrical system and evidence of myocardial tissue ischemia, injury and infarction. Normal 12-lead ECGs do not rule out a patient’s complaint from being cardiac in nature. However, significant ECG changes can rule in ACS. Further, there are many imitators which can cause ECG changes that look similar to STEMI (Table 3).
Table 3: Alternative Causes of ST-Segment Changes1
What Are You Looking For?
When reviewing a 12-lead ECG, look for evidence of myocardial ischemia, injury and infarction. Each repeated 12-lead throughout patient care can be valuable, as it can indicate if the patient’s ischemia or injury is improving or becoming worse based on the observed ST-segment changes between their 12-lead ECGs. Only a single 12-lead with significant changes is needed to diagnose ACS. The AHA recommends triaging your patient based on ECG interpretation as one of: ST elevation MI, high-risk unstable angina/non-ST elevation MI (ST depression or dynamic T-wave inversions), or low/intermediate risk ACS (non-diagnostic ECG only).3 This article focuses on the first two interpretations.
Myocardial ischemia occurs when there is inadequate blood flow to completely meet the oxygen demands of the myocardial cells distal to a lesion (narrowing of the blood vessel). While the blood flow inadequately meets the tissue’s needs, there still is some blood flow. Distal tissues thus become hypoxic resulting in pain, and over time they can fail to function normally. Improper cell function results in a variation in the heart’s electrical activity. When a 12-lead ECG is performed on a patient who has cardiac tissue experiencing myocardial ischemia, several changes may be seen, including:
Transient ST-segment elevation.
Transient ECG changes during the presentation of symptoms, which resolve when symptoms disappear, are strong predictors of underlying CAD and have great prognostic value.1 Recently, Jigar H. Patel, MD, and several research partners published their review of the presenting 12-lead ECG findings of over 175,000 patients who experienced non-STEMI in the American Journal of Cardiology. ST-segment depression was the most common initial abnormality (22.9% of patients), followed by T-wave inversion (14%) and then transient ST-segment elevation (2.9%). Surprisingly, they found 60% of NSTEMI patients had no ST-segment changes on their initial 12-lead. They then looked at the resulting disease pathology for these patient groups and found patients with ST-segment depression were most likely to have disease in the left main or proximal left anterior descending coronary artery, and most frequently went on to need coronary artery bypass surgery. However, patients with intermittent ST-segment elevation were most likely to need urgent cardiac catheterization.9
While there must be ST-segment elevation >1mm in at least two contiguous leads on a 12-lead ECG to diagnose STEMI, this type of rule does not exist to diagnose myocardial ischemia. When a 12-lead ECG has a narrow QRS complex (<0.12sec), any ST-segment depression is likely caused by myocardial ischemia; rhythms with widened QRS complexes may present with apparent ST-segment depression in the absence of myocardial ischemia. Further, the presence of ST-segment depression or T-wave inversion only needs to appear in a single lead to be suspicious for myocardial ischemia. There is one exception to this though. Uncontrolled rapid atrial fibrillation—over 120 beats per minute—has a propensity to cause transient ST-segment depression of >1mm. This transient depression does not consistently correspond to underlying coronary artery disease and is known as a strain pattern. When ST depression is observed in atrial fibrillation >120 beats per minute, focus on rate control before diagnosing myocardial ischemia.10
Once at the hospital, patients with cardiac related symptoms will have serial troponin I enzymes monitored. A diagnosis of non-STEMI is typically made with elevated quantitative troponin levels and a history consistent of ACS. Qualitative troponin levels (e.g., tests that say positive or negative) do not meet lab required accuracy standard to count as one of these tests.1 However, should your program use a qualitative troponin I test, its positive result can be used to rule in patients who warrant direct transport to a hospital with interventional cardiology capabilities.
An excellent example of transient ST-segment elevation was presented this summer in Prehospital Emergency Care by David Ross, MD, et al. His team presented a case of a 53-year-old male who presented to EMS with syncope and intermittent shortness of breath on ambulation. His resting supine 12-lead ECG was normal. When they attempted to obtain orthostatic vital signs, they noted apparent ECG changes on their monitor. A standing 12-lead ECG was performed when the patient developed dizziness, and ST-segment elevation was found in the inferior leads (II, III, aVF) with reciprocal depression in v1–v4. During preparation for transport the patient developed ventricular fibrillation and was shocked one time with ROSC and the return of consciousness. None of his successive 12-lead ECGs revealed ST-segment elevation, yet he received a stent in his circumflex coronary artery.11 Had these paramedics not performed repetitive 12-lead ECGs, valuable diagnostic information about this patient may have been missed.
12-lead ECG Changes Suggesting Myocardial Injury
Acute ischemic changes most frequently occur when a plaque lesion disrupts the tunica intima leading to clot formation. In the absence of a plaque rupture, sudden increased myocardial oxygen demands can also lead to ischemia when the lesion prevents adequate distal blood flow during periods of stress.1 When the disruption of blood flow in a coronary artery is not rapidly reversed the myocardial injury develops and presents as ST-segment elevation >1mm in at least two contiguous leads on the 12-lead ECG. Contiguous leads are leads that look at the same region of myocardial tissue and were described in Figure 2. Contiguous leads are not necessarily continuous or touching. For example, leads I and II are not contiguous leads, nor are leads I and aVR, yet they are next to one another. Understanding the contiguous leads is essential to interpreting a 12-lead ECG.
Rapidly interpreting a 12-lead ECG for the presence of STEMI can be difficult if you are not looking at 12-leads every day. Nearly 95% of prehospital STEMI presentations are either inferior or septal/anterior infarctions; 5% of STEMI presentations are lateral or posterior.12 Further, septal/anterior STEMIs are only recognized by paramedics in 78% of cases, leading to the potential for delayed cardiac cath lab activations as well as improper destination decisions.12 What does this mean?
First, prehospital providers can focus training on the most commonly seem STEMIs, those in the inferior and septal/anterior regions, and capture most STEMIs that providers will see; however, other STEMI injury patterns cannot be ignored. Second, it’s important to try to understand why we miss nearly a quarter of the STEMI presentations in the septal anterior leads. Currently no studies have presented evidence to suggest why prehospital providers struggle with the diagnosis of septal-anterior myocardial infarctions.
Another theory can be the assumption of needing to identify reciprocal changes. Reciprocal changes are not needed to diagnose STEMI. The presence of reciprocal changes rules out STEMI imitators; however, they are not always present during STEMI. In actuality, the presence any ST-segment depression on an ECG that is diagnostic for STEMI is associated with an increased frequency of hemodynamic instability.13
Prehospital 12-lead ECGs are incredibly important, as roughly 3% of patients will have STEMI identified on a prehospital 12-lead yet have the ST-segment elevation resolve with pharmacologic intervention by hospital arrival, and nearly 20% of patients can present with myocardial ischemia on a prehospital 12-lead that resolves by hospital arrival.14
Right Sided 12-lead ECG
When a patient’s 12-lead ECG presents with ST-segment elevation in leads II, III and/or aVF, they are diagnosed with an inferior wall STEMI. The inferior wall is perfused by the circumflex artery in 20% of patients and by the right coronary artery in 70%, while as many as 10% of patients experience some inferior wall perfusion by both arteries. While definitive identification of the location of a coronary artery occlusion can only be made in the catheterization lab, there is value in looking for evidence of right coronary artery involvement. You can try to rule in an occlusion of the right coronary artery by performing a right sided 12-lead ECG. A proximal right coronary artery occlusion is concerning because it results in infarction of the right ventricle, which leads to a loss of preload.
To identify a right coronary artery occlusion and a right ventricle infarction, take the electrode for lead v4 and place it in the fifth intercostal space, mid-clavicular line on the right side of the patient’s chest. Repeat the recording of the 12-lead ECG and label v4 as v4R. If v4R has >1mm of ST-segment elevation it is diagnostic for right ventricular infarction and an occlusion of the right coronary artery. Only one lead needs to be moved to the right side of the chest and be elevated to confirm a right ventricle infarction. If you choose, you may also all leads v3 through v6 to the right side by placing them each in their respective position on right side of the chest rather than the left. V1 and v2 would remain in their traditional locations. While >1mm ST-segment elevation in any lead v3R through v6R is diagnostic for right ventricle MI, only one lead is needed to make the diagnosis.
The absence of elevation in a right sided lead does not rule out right coronary involvement, it only rules out right ventricle involvement. This is an important distinction. When the right ventricle is not involved, the risk for a loss of preload is greatly decreased.
When the right ventricle is involved, prehospital care needs to focus on the maintenance of an adequate blood pressure and the administration of IV fluids while avoiding nitrates. However, if the right ventricle is not involved when a patient is experiencing an inferior wall STEMI, nitrates may be safely administered as long as the patient has an adequate blood pressure and hasn’t taken sildenafil-type drugs.
Left Main Disease
Traditionally it is taught that lead aVR is not used in the diagnosis of STEMI in a 12-lead ECG. While technically this is correct as aVR is not contiguous with any of the other leads, it actually does provide valuable diagnostic information. ST-segment elevation in aVR, particularly when >2mm, is indicative of left main coronary artery disease and is a strong predictor for increased morbidity and mortality, and the need for emergent coronary artery bypass grafting.15 It is not common to identify ST elevation in aVR because these patients rapidly deteriorate into cardiogenic shock and cardiac arrest. Patients with left main disease present severely ill and frequently have ST-segment depression in leads v1–v6 with the most pronounced depression in v4–v6. While the presence of aVR ST-segment elevation does not meet true “STEMI” criteria, its presence with associated ST-segment depression is strongly suspicious for left main disease and warrants catheterization lab notification.16
A left main occlusion signifies little to no blood flow to the left anterior descending and circumflex coronary arteries. Such a condition leads to patients rapidly developing profound hypotension, severe chest pain and left ventricle dysfunction. Patients with left main occlusions are very unlikely to have mild signs and symptoms. Should you suspect aVR elevation in a patient with minimal symptoms, look for another cause for the elevation other than left main disease.
Frankie obtains the 12-lead ECG and it shows 3mm of ST-segment depression in leads v5, v6 and lead I. She suspects her patient has ischemia in the lateral wall of the left ventricle. After moving the patient to the ambulance, she establishes IV access and confirms that the patient is not taking any erectile dysfunction medications such as sildenafil (Viagra). She notes the patient’s blood pressure remains about 140mmHg systolic and administers 0.4mg of nitroglycerine SL. After the second sublingual nitroglycerine, her patient reports relief of his pain, stating it is now a “2 out of 10.” Frankie repeats the 12-lead ECG and finds the ST-segment depression has resolved. Upon arrival in the emergency department she shows both 12-lead ECGs to the ED physician; the ED 12-lead ECG is normal. Because of Frankie’s initial 12-lead ECG, the patient is taken for a cardiac catheterization and receives a stent in his circumflex artery.
Coven D, et al. Acute Coronary Syndrome, Medscape, emedicine.medscape.com/article/1910735-overview.
Squire B, et al. Effect of prehospital cardiac catheterization lab activation on door-to-balloon time, mortality, and false-positive activation. Prehospital Emergency Care, 2014; 18: 1–8.
O’Connor R, et al. Part 10: acute coronary syndrome: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 2010; 122: s787–s817.
Thang ND, et al. ECG signs of acute myocardial ischemia in the prehospital setting of a suspected acute coronary syndrome and its association with outcomes. American Journal of Emergency Medicine, 2014; 32: 601–605.
Giugliano R, Brunwald E. The year in acute coronary syndrome. Journal of the American College of Cardiology, 2014; 63(3): 201–214.
Panju A, et al. Is this patient having a myocardial infarction? JAMA, 1998; v280(14): 1256–1263.
Jenkins D. A (not so) brief history of electrocardiography, ECG Library, www.ecglibrary.com/ecghist.html.
Verbeek PR, et al. Serial prehospital 12-lead electrocardiograms increase identification of ST-segment elevation myocardial infarction. Prehospital Emergency Care, 2012; 16: 109–114.
Patel J, et al. Influence of presenting electrocardiographic findings on the treatment and outcomes of patients with non-ST-segment elevation myocardial infarction. American Journal of Cardiology, 2014; 113: 256–261.
Pradhan R, et al. Predictive accuracy of ST depression during rapid atrial fibrillation on the presence of obstructive coronary artery disease. American Journal of Emergency Medicine, 2012; 30: 1042–1047.
Ross DW, et al. Acute coronary ischemia identified by EMS providers in a standing middle-aged male with atypical symptoms. Prehospital Emergency Care, 2014; 18: 450–455.
Celik D, et al. Characteristics of prehospital ST-segment elevation myocardial infarctions. Prehospital Emergency Care, 2013; 17(3): 299–303.
Chen T, et al. Prognostic significance of reciprocal ST-segment depression in patients with acute STEMI undergoing immediate invasive intervention. American Journal of Emergency Medicine, 2012; 30: 1865–1871.
Boothroyd L, et al. Information on myocardial ischemia and arrhythmias added by prehospital electrocardiograms. Prehospital Emergency Care, 2013; 17(2): 187–192.
Shinde RS, et al. ECG showing features of total left main coronary artery occlusion. Heart, 2006 May; 92(5): 670.
Nikus K, Eskola M. Electrocardiogram patterns in acute left main coronary artery occlusion. Journal of Electrocardiology, 2008; 41(6): 626–629.