Missing the Diagnosis of Acute MI: Challenging Presentations, Electrocardiographic Pearls, and Outcome-Effective Management Strategies
Author: William J. Brady, Jr., MD, Assistant Professor of Emergency Medicine and Internal Medicine; Medical Director, Chest Pain Center, Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA.
Peer Reviewers: Corey M. Slovis, MD, FACP, FACEP, Professor and Chairman, Department of Emergency Medicine, Vanderbilt University School of Medicine, Nashville, TN.
Frank Ruiz, MD, Assistant Professor of Surgery, University of California-San Francisco; Department of Emergency Services, San Francisco General Hospital, San Francisco, CA.
Missing the diagnosis of myocardial infarction (MI) is one of most anxiety-producing clinical scenarios in the practice of emergency medicine. We know where the diagnostic "weak" links are: the younger patient with chest pain, the elderly individual with atypical manifestations, the patient with left bundle branch block (LBBB), the individual with altered mental status, the diabetic, and many other high-risk subgroups. Yet despite all of the critical pathways, the heightened awareness, the safeguards, and the sophisticated diagnostic modalities that have been pressed into service to prevent such a mishap, it still happens. ED physicians miss the diagnosis of acute MI, and we have a continuing litany of lawsuits that testify as to just how devastating this error can be.
To prevent misdiagnosis or underrecognition of acute MI, patients presenting to the ED with acute chest discomfort of potential ischemic origin are usually evaluated with three principal clinical or laboratory modalities: a detailed history of the acute event; a 12-lead electrocardiogram (ECG); and measurement of cardiac enzymes and other serum markers of myocardial injury. Using a combination of these tools, the diagnosis of acute myocardial infarction (AMI) can usually be suspected and confirmed clinically, and when the ECG is diagnostic, the presence of AMI can be established rapidly upon presentation to the ED. For example, the 50-year-old male diabetic patient who presents to the ED complaining of substernal chest pressure, diaphoresis, and nausea with an ECG demonstrating ST-segment/T-wave abnormality usually does not present much of a diagnostic challenge; in this case, AMI or acute coronary ischemia is the most likely etiology of the patient’s chief complaint. Individuals with this "classical constellation" of symptoms are usually not among the approximately 4% of patients with AMI who are inappropriately discharged from the ED.1,2
On the other hand, "atypical presentations" are noted in approximately 10-30% of the general AMI population.3-9 Many factors challenge the emergency physician (EP) when evaluating such patients, in whom confirmation of the diagnosis of AMI can be very difficult. These factors include patient age, alternate chief complaints, atypical discomfort, certain comorbid states, indeterminate ECG patterns, and the presence of a normal or nondiagnostic ECG. Patient age complicates the clinical picture in two ways. First, the EP may feel that the patient is "too young" to be at risk for AMI. While most cases of AMI occur in patients over the age of 40, a significant minority of patients with AMI are encountered in the "younger than 40" age group, especially smokers and those with a history of cocaine abuse. Second, in the elderly patient, many factors, including autonomic neuropathy, CNS status, comorbid diseases, and pre-existing mental status abnormalities, contribute to a higher frequency of atypical presentations. In this population, AMI may present with "anginal equivalent" chief complaints such as shortness of breath, "silent" MI, or neurologic complaints such as confusion.
Because a strong suspicion for, or confirmation of, AMI has important implications on mortality-reducing interventions such as angioplasty and thrombolysis, the ED physician must recognize unusual or subtle presentations in order to maximize clinical outcomes. This article outlines potential pitfalls in the diagnosis of AMI, presents unusual or subtle ECG findings that strongly suggest MI, and characterizes atypical presentations in specific patient subgroups that will direct the clinician toward the appropriate diagnosis.
The Editor
Historical Features, Atypical Presentations, and Potential Clinical Pitfalls
Atypical Presentations. Not infrequently, patients with AMI complain of little more than dyspnea or weakness. In some cases, chest discomfort may be noted as minor, and in others, the patient will complain of no chest pain whatsoever. Alternative chief complaints, which represent anginal equivalent syndromes or responses to pain, typically include dyspnea, diaphoresis, nausea, and emesis. The most frequently encountered anginal equivalent chief complaint is dyspnea, which is more common in the elderly and is reported in approximately 15% of all patients with AMI.1-3 Isolated emesis or diaphoresis is a very unusual presentation of AMI. On the other hand, the elderly patient may present with acute weakness, syncope, altered mental status, or cerebral infarction. Although weakness and syncope rarely occur as the sole manifestation of AMI in individuals younger than 70 years of age, these symptoms increase in frequency in the older population. Among neurological symptoms, confusion is reported in about 20% of patients with MI who are 85 years of age or older.4,5 MI is rarely associated with acute stroke in younger patients, whereas in the elderly patient, approximately 10% of cases are characterized by the coexisting coronary and cerebral ischemic syndromes.8,9
Chest Symptoms. When chest discomfort is noted as a major complaint, it may be characterized by so-called "atypical" features. Atypical presentations of ischemia-induced chest pain include cases in which the sensation is located in the epigastrium or back. Individuals in whom the pain is reported to have a sharp or burning quality (atypical quality) or found to have reproducible nature on palpation (atypical examination) frequently present diagnostic challenges. When chest discomfort is described as "burning" or "indigestion-like," features that may suggest a gastrointestinal source for the discomfort, the diagnosis of AMI must be suspected because these complaints are reported in approximately 50% of adult cases with confirmed ischemic coronary syndromes. Moreover, patients noted "sharp," "knife-like," or pleuritic pain in about one-fourth of acute ischemic syndromes. The physical examination may also demonstrate reproducible chest wall pain in a significant minority of AMI patients, potentially mimicking a musculoskeletal diagnosis.1-4
Comorbid Conditions. Certain disease states may obscure the physician’s ability to make the diagnosis of AMI. For example, patients with a history of diabetes mellitus (DM) who have undergone cardiac transplantation or who use immunosuppressive medications frequently present with atypical manifestations of AMI. In other cases, patients with dementia or other functional impairments that affect communication may be unable to describe in sufficient detail all the sensations that typically are associated with an acute coronary ischemic event. Some patients may have altered pain perception as a result of past cardiothoracic surgery, stroke, degenerative neurologic conditions, or spinal cord injury. Of special concern is the cocaine user who presents with chest discomfort but does not admit to illicit substance abuse. This is a high-risk population. Consequently, younger patients who are suspected of using cocaine and present with an "atypical" chest complaint should be evaluated for possible AMI.
The Electrocardiogram. A double-edged sword, the ECG can be a powerful clinical tool for assisting in the evaluation, treatment, and disposition of patients who present with atypical symptoms. However, it must be appreciated that the ECG is plagued by significant shortcomings and indeterminate conduction profiles, which include: 1) confounding or obfuscating patterns such as LBBB, ventricular-paced rhythms (VPR), and left ventricular hypertrophy (LVH); 2) evolving patterns of cardiac injury; 3) interpreting the significance of a "normal" ECG or those with "nonspecific ST-segment-T-wave changes" (NSSTTW); 4) the non-Q wave myocardial infarction (NQWMI); and 5) acute, isolated posterior myocardial infarction (PMI).
From a practical clinical perspective, confounding patterns such as LBBB, VPR, and LVH frequently obscure the typical ECG findings of AMI. In this regard, LBBB and VPR are encountered on the ECGs of patients with AMI in 2-6% and in 0.1-5.0% of cases, respectively.20 In addition, LVH is a frequent ECG finding but is noted in only 7-8% of AMI patients and up to 45% of patients with unstable angina.20-23 Overall, the ECG does not provide conclusive evidence of AMI in up to 50% of cases presenting in the ED. In these cases, the ECG may be entirely normal, nonspecifically abnormal, or clearly abnormal but without pathologic ST-segment elevation indicative of transmural infarct.
The initial ECG is interpreted as normal or with NSSTTW in up to 10% of documented AMI cases in the ED.9-11 The ECG that provides clear evidence of acute ischemia but does not demonstrate an obvious infarct is encountered in up to 50% of patients found to have myocardial infarction. This last group of patients will either evolve electrocardiographically into a transmural AMI with ST-segment elevation (approximately 10%) or continue to demonstrate ST-segment depression with T-wave abnormality. Elevated cardiac enzymes will confirm the diagnosis of NQWMI in the remaining 40%.20-22
Medically Unattended and Silent Myocardial Infarction. Unrecognized AMI occurs with an annual incidence of approximately 2 cases per 1000 persons at risk.9 The unrecognized event includes the medically unattended AMI (i.e., the patient did not seek medical attention due to either denial or misperception of the cause), individuals with silent infarction, and the patient with MI who was inappropriately discharged from the ED. Large population studies have demonstrated that 25% of all MIs are not medically attended, with an increased prevalence among diabetic and elderly patients.10-12 These studies have used long-term surveillance of the ECG as the principal diagnostic tool. Of these unattended infarcts, approximately half were "silent," and the patient did not recall any symptoms that could be attributed to a myocardial ischemic event. The remaining half experienced either typical symptoms that they ignored or atypical complaints that they felt were due to an alternative nonthreatening illness. Patients with AMI who are inappropriately discharged from the ED represent 2-4% of all cases of MI.1,2 This group is composed of patients with both typical and atypical presentations.
Medical and Legal Considerations
It should be emphasized that a minority of patients with AMI are inappropriately sent home from the ED.1,2 Interestingly, the vast majority of these cases involve young patients with unsuspected AMI and elderly patients with atypical presentations. Despite the low percentage of inappropriate diagnoses, missed MI is the third leading cause of malpractice claims, accounting for 20% of all dollars spent for legal damage awards. Forty percent of all claims have resulted in payments to the plaintiff, with an average award of $220,000. Among all specialties, emergency medicine physicians are the third most likely to be sued for failing to diagnose AMI, and they are the leading physician group in terms of amount of indemnity, with an average award of $280,000 per case.13
Table 1 presents information that is derived from the 1996 Physician Insurers Association of American (PIAA) survey of "missed myocardial infarction" malpractice claims.13 These findings are characteristic of physician-patient encounters in which cash awards were made to individuals in whom MI was missed. They do not necessarily represent features of the medically unrecognized AMI. The clinical presentation of the missed AMI in the PIAA survey includes all age groups, although 50% of these cases were less than 50 years of age. Seventy percent of patients in the PIAA study lacked a previous history of ischemic heart disease. Chest discomfort was the chief or secondary complaint in most cases, which the majority of patients described as typical; anginal equivalent complaints were encountered in a minority of cases.
The ECG was misinterpreted and/or incorrectly used in 25%; incorrect use is defined as excessive reliance on a single "negative" study or the characterization of NSSTTW findings as normal. Other diagnostic tests were misused in 6% of cases and were characterized by an over-reliance on a single negative serum marker. In order of occurrence, incorrect initial diagnoses included gastrointestinal, musculoskeletal, and noncardiac chest pain syndromes. Factors determined during litigation that may have led to a misdiagnosis included: failure to order study (ECG); the diagnosis of AMI was not considered; there was an inappropriate discharge from the ED; interpretation of tests was incorrect; and there was an over-reliance on negative studies (i.e., "negative" ECG or single serum marker).
Studies in the the medical literature point to many of the same risk factors that predispose to missing AMI. From the medical malpractice perspective, high-risk patients include women, individuals younger than 50 years of age, and patients with no past history of ischemic heart disease. Missed MI is also more common in patients who present with an anginal equivalent complaint or atypical discomfort, when there is excessive reliance on the ECG or single serum markers, and when studies are interpreted incorrectly.1,2,10-12 When one considers both medically unattended and inappropriately discharged patients with subsequently documented AMI, young patients without a past history of heart disease as well as women and older men represent high-risk populations for misdiagnosis. One large ED study of missed AMI found that ECG misinterpretation accounted for 25% of undiagnosed cases; a similar percentage were incorrectly felt to have stable presentations of ischemic heart disease rather than acute infarct.1 The clinical outcome associated with a missed AMI is considerably worse in the immediate post-infarct period. However, with appropriate medical attention, the prognosis of a missed MI is similar to the recognized AMI.
Clinical Correlates Associated with Atypical Presentations
A number of personality traits, behavioral patterns, psychiatric issues, coexisting conditions, and underlying risk factors account for atypical presentations of AMI and underscore the difficulties associated with making the diagnosis of MI. (See Table 2.) For example, many individuals with either "silent" ischemia or clinically unrecognized MI demonstrate higher pain thresholds. In addition, specific personality traits or behavior patterns may make it difficult for the EP to assess the risk of AMI based on the patient’s clinical history. In this regard, the diagnosis may be especially difficult in individuals who score highly in neuropsychiatric testing in areas of "masculinity," "calmness," "independence," and "low anxiety." These patients also demonstrate relatively low rates of presenting to physicians for other, noncardiac medical problems. Such health-care access patterns and personality issues appear to correlate with higher pain thresholds. In addition, the stoic patient, the patient who exhibits denial, and the patient with psychiatric diseaseparticularly those with major depression or psychosismake evaluation more difficult.
It has been postulated that peripheral and CNS dysfunction can cause "silent" ischemia, increase the risk for clinically unrecognized infarction, and produce atypical presentations of AMI. In particular, diabetic neuropathy has been suggested as one common risk factor. Sensory, motor, and autonomic neuropathies are seen more often among diabetic patients with AMI. Although this explanation sounds plausible, it has not held up to clinical scrutiny. For example, diabetic patients with and without demonstrable neuropathy appear to have a similar incidence of atypical manifestation and missed or unrecognized AMI.8,14
Recent studies have suggested that CNS abnormalities may play a greater role in such presentations.14,15 "Silent" ischemia, characterized by dynamic ST-segment abnormality and absence of symptoms, has been observed in patients with diverse backgrounds, including diabetics, the elderly, and the normal "host." Of special clinical concern is the observation that these patients will manifest symptoms of ischemia on some occasions, while at other times, "silent" ischemia will be encountered. Explanations for such altered presentations include past CNS injury due to stroke, multiple sclerosis, amyotrophic lateral sclerosis, spinal cord traumatic injury, and the effects of comorbid states and concurrent medical therapies.
Miscommunication and faulty interpretation of historical features represent additional pitfalls in evaluation. For example, the patient may perceive the pain as gastrointestinal or musculoskeletal in nature, in which case he or she may refer to the symptoms as "indigestion" or "a pulled muscle," respectively. The physician may be led down the wrong diagnostic pathway if specific questions are not asked or if the patient’s "diagnosis" is accepted without medical exploration. In addition, a patient may describe the pain as "sharp" to imply sudden onset of discomfort, whereas to the physician, this description it may imply a musculoskeletal etiology. Finally, the elderly patient may present with altered mental status, which represents a major diagnostic challenge.
Profiles and Patterns Associated with Atypical Presentations
The EP will encounter atypical features of AMI in approximately 10-30% of patients with MI.3-9 Factors contributing to this clinical presentation include patient age, alternate chief complaints, atypical discomfort, and the presence of comorbid conditions.
Unusual Chief Complaints. Anginal equivalent complaints, which occur in the setting of "painless" AMI, classically include dyspnea, diaphoresis, nausea, and emesis. (See Table 3.) Other anginal equivalent symptoms that must be considered include cough, palpitations, and anxiety. The most frequently encountered anginal equivalent chief complaint is dyspnea, which is found in 10-17% of patients with AMI and is often caused by pulmonary edema.3-5 Isolated emesis and diaphoresis are quite rare, with a prevalence of 1-3%.3-5 The geriatric patient may also present atypically, with acute weakness observed in 3-8% and syncope in 3-5% of patients.6,7
Unexplained sinus tachycardia, bronchospasm resulting from cardiogenic asthma, and new-onset lower-extremity edema have all been reported as anginal equivalent presentations for AMI. Anginal equivalent syndromes are more common in the setting of acute mental status abnormalities and cerebrovascular attacks (CVAs). Overall, fewer than 1% of patients who present to the ED with altered mentation will be found to have AMI.15a Less-pronounced mental status abnormalities, including confusion and lethargy, have been reported in about 5% of elderly patients with documented AMI. MI is associated with acute stroke in approximately 5-9% of patients over 60 years of age.7
Atypical Pain Syndromes. Discomfort associated with AMI may be "atypical" from a number of different perspectives. For example, pain may be noted in an atypical location and the patient may complain of epigastric, neck, arm, or back discomfort. The discomfort may be perceived as a sharp sensation or as having a burning quality. Finally, the discomfort may be reproducible on palpation, which can suggest a musculoskeletal rather than ischemic etiology.
The discomfort may be located in a non-chest anatomic region. In many cases, the discomfort is only experienced in the epigastrium, anterior neck or jaw, or in the left upper extremity. Although symptoms referred to these locations do not represent the classic presentation of an acute coronary ischemic event, their presence usually does not challenge the physician’s diagnostic ability, since these pain distributions are suggestive of a coronary ischemic source. Rarely, the discomfort may be located in the back, posterior neck, and right arm. Other unusual presentations include cephalgia as well as hip and lower back pain.
The description of chest discomfort can range from the classic "crushing, heaviness, pressure-like" to the atypical "sharp, knife-like." If one considers all patients presenting to the ED with complaints such as "crushing" or "pressure-like," chest pain, about one-half will have an acute coronary ischemic syndrome; about 50% of these cases will be associated with AMI and the remainder with unstable angina.16 Of those whose discomfort cannot be explained by acute coronary ischemia, the remainder are found to have gastrointestinal, pulmonary, and musculoskeletal diagnoses. In an adult population presenting with chest pain, chest discomfort described as "burning" or "indigestion-like" was reported in 23% of patients who were found to have AMI and in 21% of those with unstable angina.16 Patients note "sharp," "knife-like," or pleuritic pain in 19-23% of cases caused by an acute coronary ischemic syndrome.17 Finally, the physical examination may complicate the diagnosis, especially when reproducible chest wall pain is present, which is seen in up to 15% of confirmed cases.18
The Young Patient. While most cases of AMI occur in patients over 40 years of age, a significant minority (2-6%) are encountered in younger patients.19 The vast majority present with typical features of AMI and exhibit similar rates of diagnostic and nondiagnostic ECGs. The diagnosis may be especially difficult in a young patient who presents either with atypical discomfort or an anginal equivalent complaint and demonstrates a nondiagnostic ECG. A positive family history for heart disease, cocaine abuse, and tobacco use are almost universally present in the risk-factor profile for younger patients with AMI. Because AMI can occur in the young patient, the ED physician must not rule out this possibility without a thorough evaluation. Many chest pain policies and clinical protocols, including those of the American College of Emergency Physicians, recommend the use of the 12-lead ECG in younger patients who present with chest pain.
The Elderly Patient. Advanced age almost always has an impact on the ED physician’s ability to evaluate the patient and assess the potential for AMI. In fact, several studies have demonstrated that evaluation of acute chest pain, confirmation of the correct diagnosis, and initiation of appropriate therapies is compromised in geriatric patients.6,7 Coexisting disease states and medication use contribute to make the elderly patient with AMI a diagnostic challenge. The increased incidence of atypical presentations among the elderly translates into clinically unrecognized AMI. For example, in one large autopsy series of elderly patients, the correct diagnosis of AMI was made in less than half the patients prior to death; the "elder" elderly (age > 85 years) constituted a large portion of this group of patients with the postmortem diagnosis of MI.
The presentation of AMI in the elderly is frequently nonclassical; atypical presentations are encountered with increasing frequency in older populations.6,7 The spectrum of presentation changes significantly with increasing age. In patients less than 85 years of age, chest pain is less frequent, while anginal equivalent complaints are noted more often; nevertheless, chest pain still is found in the majority of cases.6,7 Stroke, weakness, and altered mentation become more common with increasing age and frequently are not accompanied by typical chest discomfort. The incidence of "painless" AMI increases dramatically with age and is seen in 60-70% of elderly patients over 85. These patients typically present with an anginal equivalent complaint or CNS syndrome such as a change in mental status. If one considers all elderly patients with altered mental status in an ED population, however, the diagnosis of AMI is found in only 1% of these cases.15a As might be expected, the elderly frequently present with complications of AMI rather than the symptoms of the acute ischemic event. For example, elderly patients who present with the sudden onset of unexplained congestive heart failure should be evaluated for AMI. Similarly, the elderly patient who presents with bradycardia, atrioventricular block, or ventricular arrhythmia should be ruled out for MI while appropriate therapies and other evaluations are performed.6,7
The Diabetic Patient. Patients with diabetes mellitus (DM) experience AMI at an earlier age, are more likely to have atypical manifestations, and have the diagnosis of MI missed more often than those without DM. Medically unrecognized AMI is felt to occur in approximately 40% of patients with DM compared to the 25% rate for the non-DM population.8 Autopsy studies have demonstrated that myocardial damage without an antemortem diagnosis of MI, which indicates a medically unattended, previous infarct, is three times more frequent in the diabetic than the nondiabetic patient. As with the elderly AMI patient, numerous factors contribute to atypical manifestations of acute ischemic heart disease in the DM patient, including polyneuropathy, an altered perception of cardiac pain, and extensive comorbidity. The diabetic patient’s abnormal perception of MI may lead to atypical or less impressive symptoms of AMI. Atypical symptoms such as dyspnea, confusion, fatigue, and emesis may be the presenting complaints in up to 40% of diabetics with AMI.8
Although the ECG is an essential modality for evaluating patients with chest pain, a number of unusual, misleading, or confounding ECG patterns may reduce the value of the 12-lead ECG. These include: confounding ECG patterns (LBBB, ventricular paced rhythms, and left ventricular hypertrophy); normal and nonspecific readings (i.e., the nondiagnostic ECG); evolving patterns; the non-Q wave MI; and other issues, such as acute posterior wall MI. Each of these will be considered separately.
Diagnosing AMI in the Presence of LBBB. The electrocardiographic diagnosis of ischemic heart disease is made more difficult in the setting of LBBB. While this pattern may confound the early electrocardiographic evaluation of a potentially ischemic patient, the ECG is not entirely without value. (See ECG interpretation supplementFigures 1A, 1B, and 3.) Some authorities claim that the electrocardiographic diagnosis of AMI is impossible in the presence of LBBB, while others believe that the diagnosis is often possible, if not straightforward and "disarmingly easy."20,21 Generally speaking, right bundle branch block (RBBB) does not present the same diagnostic dilemma as LBBB, inasmuch as the electrocardiographic diagnosis of AMI in the patient with co-existing RBBB usually is not problematic.22
In LBBB, the ventricular depolarization pattern is abnormal, with activation of the ventricles occurring from the right to the left, a direction opposite from the norm. Since the left ventricle cannot be depolarized from the left bundle branch, the impulse must proceed down the right bundle and across the interventricular septum, eventually reaching the left ventricle. The activation of the right ventricle occurs first, followed closely by the interventricular septum. Electrical depolarization of the left ventricle then occurs. After leaving the right bundle branch, the impulse travels through the myocardium rather than the specialized conduction fibers, which results in a prolonged duration of ventricular depolarization and the characteristically widened QRS complex (> 0.12 seconds).
In the patient with LBBB, the 12-lead ECG records the abnormal ventricular activation as it moves from right to left, producing a broad, mainly negative QS or rS complex in lead V1. In lead V6, late intrinsicoid deflection is noted, resulting in a positive, monophasic R wave; similar structures are frequently found in leads I and aVl. Poor R-wave progression or QS complexes are noted in the right-to-mid precordial leads, rarely extending beyond leads V4 or V5. QS complexes may also be encountered in leads III and aVf. The anticipated or expected ST-segment-T-wave configurations are discordant (i.e., they are directed opposite from the terminal portion of the QRS complex). This relationship is called QRS complex-ST-segment/T-wave axes discordanceor, the rule of appropriate discordance.
In this situation, leads with either QS or rS complexes may have markedly elevated ST segments, mimicking AMI. Leads with large monophasic R waves demonstrate ST-segment depression. The T wave, especially in the right- to mid-precordial leads, has a convex upward shape or a tall, vaulting appearance, similar to the hyperacute T wave of early MI. The T waves in leads with the monophasic R waves are frequently inverted. Loss of this normal discordant relationship in patients with LBBB may imply an acute process, such as AMI. (See ECG interpretation supplementFigures 1A and 1B.) An inspection of the ECG in patients with LBBB must be performed, looking for a loss of this QRS complex-ST segment/T-wave axes discordance.
A group of authors has developed a clinical prediction rule to assist in the ECG diagnosis of AMI in the setting of LBBB. They have identified three criteria suggestive of acute infarction.23 (See Table 4.) The ECG criteria suggesting a diagnosis of AMI, ranked with a scoring system based on the probability of such a diagnosis, include: ST segment elevation greater than 1 mm, which is concordant with the QRS complex (score of 5); ST-segment depression greater than 1 mm in leads V1, V2, or V3 (score of 3); and ST segment elevation greater than 5 mm which is discordant with the QRS complex (score of 2). A total score of 3 or more suggests that the patient is likely experiencing an AMI based on the ECG criteria. With a score less than 3, the electrocardiographic diagnosis is less assured, requiring additional evaluation. This clinical prediction instrument supports the contention that a detailed knowledge of the associated, or anticipated, ST segment-T wave changes resulting from the abnormal ventricular conduction of the LBBB is a must. Such an understanding of the ECG in LBBB allows the clinician to recognize unanticipated morphologies that may be suspicious for AMI. (See ECG interpretation supplementFigure 2.)
Ventricular-Paced Rhythm (VPR). A ventricular-paced rhythm may mask acute ischemic changes associated with MI much as the presence of LBBB can. (See ECG interpretation supplementFigures 3A, 3B, 3C, and Figure 4.) The patient with a VPR is encountered in a minority of cases involving AMI, ranging from 0.1% to 5%. As the population ages, however, physicians can be expected to encounter such electrocardiographic patterns more often. Furthermore, the early electrocardiographic diagnosis of AMI in patients with ventricular pacemakers is important in that this population is relatively older and is more likely to have pre-existing heart disease; these patients with cardiovascular comorbidity may benefit from a more aggressive therapeutic approach in the setting of AMI.
In right VPR, the ventricular depolarization pattern is abnormal with activation of the ventricles occurring from the right to the left, resembling an LBBB pattern in most cases. The activation of the right ventricle occurs first, followed closely by the interventricular septum. Electrical depolarization of the left ventricle then occurs. The impulse travels through the myocardium rather than the specialized conduction fibers, resulting in a prolonged duration of ventricular depolarization and a markedly widened QRS complex. A pacer spike (i.e., a narrow negative or positive deflection) is seen in most electrocardiographic leads immediately preceding the QRS complex.
In the patient with VPR, the 12-lead ECG records the abnormal ventricular activation as it moves from right to left, producing a broad, mainly negative QS or rS complex in leads V1 to V6 with either poor R-wave progression or QS complexes. A large monophasic R wave is encountered in leads I and aVL and, on occasion, in leads V5 and V6. QS complexes may also be encountered in leads II, III, and aVF. The anticipated or expected ST-segment/T-wave configurations are discordant, directed opposite from the terminal portion of the QRS complex. This relationship is called QRS complex-T wave axes discordance or the rule of appropriate discordance and is similar to the electrocardiographic principles applied in the setting of LBBB. Accordingly, leads with QS complexes may have marked ST-segment elevation, mimicking AMI. Leads with a large monophasic R wave demonstrate ST-segment depression. The T wave, especially in the right to mid-precordial and inferior leads, has a convex upward shape or a tall, vaulting appearance, similar to the hyperacute T wave of early MI. The T waves in leads with the monophasic R wave are frequently inverted. An inspection of the ECG in patients with VPR must be performed, looking for a loss of this QRS complex-T wave axes discordance. Loss of this normal discordance in patients with VPR may imply an acute process, such as AMI. (See ECG interpretation supplementFigures 3A, 3B, and 3C.)
In 1996, Sgarbossa et al published a report detailing the electrocardiographic changes encountered in patients with VPR experiencing AMI.24 Three ECG criteria were found to be useful in the early diagnosis of AMI including: discordant ST segment elevation ³ 5 mm; concordant ST segment elevation ³ 1 mm; and ST segment depression ³ 1 mm in leads V1, V2, or V3. (See ECG interpretation supplementFigure 4.) Interestingly, no criteria involving QRS complex or T-wave morphologies were found to be useful. This article addresses the diagnosis of AMI in the setting of VPR early in the patient’s presentation. Much of the existing cardiology literature exploring this issue does not distinguish between past MI and AMI. Unfortunately, the electrocardiographic tools recommended are cumbersome, difficult to use at the bedside, and not reliable. Finally, the sensitivity and specificity of these past criteria are not impressive. See ECG interpretation supplement, Figures 3A, 3B, 3C, and 4 for examples of the 12-lead ECG in a patient with VPR and AMI with these electrocardiographic criteria.
The most useful criterion found in this analysis is discordant ST segment elevation of 5 mm or more, which violates the rule of appropriate discordance with an inappropriate degree of discordant elevation.24 (See ECG interpretation supplementFigure 4D.) Repolarization changes of ventricular-paced rhythms should produce ST segment elevation of less magnitude in the "normal" state. (See ECG interpretation supplementFigure 4A.) ECG criterion #2 (see ECG interpretation supplementFigure 4B) and #3 (see ECG interpretation supplementFigure 4C) outlined above are examples of infractions of the rule of appropriate discordance, concordant ST segment elevation, and ST segment depression (limited to leads V1, V2, or V3), respectively. The physician must realize, however, that these ST segment changes are only suggestive of AMI and that management decisions must be made with these caveats in mind.
Left Ventricular Hypertrophy (LVH). The final electrocardiographic pattern encountered in chest pain patients that may confound the evaluation is LVH, a term that refers to a total increase in left ventricular mass and does not distinguish between concentric hypertrophy and dilation. A number of electrocardiographic criteria and findings have been devised to assist the physician in making the diagnosis of LVH. In general, these systems lack sensitivity, yet demonstrate significant specificity ranging from 93% to 96%.28 Unfortunately, the various scoring systems are cumbersome and difficult to use unless employed on a regular basis.
Two basic guidelines for electrocardiographic diagnosis that the ED physician should use are: greater than 11 mm positive deflection (R wave) in lead aVL; and the sum of the S wave in leads V1 or V2 and the R wave in leads V5 or V6 equalling 35 mm or more in a patient over age 35. Ultimate confirmation of LVH is made via echocardiography.
Significant ST segment-T wave abnormalities are the new "norm" in patients with LVH on the ECG and may mask early findings consistent with acute coronary ischemia. This "masking effect," however, occurs to a lesser extent than encountered in the LBBB and VPR situations. Conversely, the new waveform morphologies, particularly the ST segment changes noted in the right anterior and inferior distributions, are the most frequently encountered form of non-infarctional ST segment elevation seen in chest pain; these ST segment-T wave abnormalities may lead the uninformed physician in the wrong diagnostic direction (i.e., toward initiating therapies directed at AMI when this situation does not in fact exist).25
LVH is associated with poor R-wave progression and loss of the septal R wave in the right to mid-precordial leads, most commonly producing a QS pattern in leads V1, V2, and V3. (See ECG interpretation supplementFigure 5.) As predicted by the rule of appropriate discordance, ST segment elevation is encountered in this distribution along with prominent, "hyperacute" T waves. The ST segment elevation seen in this distribution may be greater than 5 mm in height. These ST-segment/T-wave abnormalities resemble the electrocardiographic findings associated with anteroseptal AMI and, at times, are difficult to distinguish from AMI in the chest pain patient. The "strain" pattern, characterized by asymmetric biphasic or inverted T waves in leads with prominent R waves in patients with LVH, is frequently misinterpreted as acute ischemia. Such findings are usually encountered in leads I, aVL, V5, and V6. It is important to realize that significant variability may be encountered in the "strain" pattern. The T wave may be minimally inverted, or the inversion may be greater than 5 mm in depth. These T wave abnormalities may also be encountered in patients lacking prominent voltage (i.e., large S and R waves).22
The diagnosis of AMI in patients with LVH may be difficult.22 In general, the QS complexes are usually located in leads V1 and V2, rarely extending beyond lead V3. The ST segment elevation encountered in this distribution is difficult to distinguish from that associated with AMI. The initial, up-sloping portion of the ST segment-T wave complex is frequently concave in LVH compared to the either flattened or convex pattern observed in the AMI patient. This morphologic observation should only be used as a guideline. As with most guidelines, it is not infallible; patients with ST segment elevation due to AMI may demonstrate transient concavity of this portion of the waveform.
Normal and Nondiagnostic ECG. One landmark study of adult chest pain patients managed in the ED found that approximately 20% of patients had an absolutely normal 12-lead ECG.16 In this study, the description "absolutely normal" was defined as the absence of NSSTTW, atrioventricular block, intraventricular conduction delay, repolarization changes, and other sinus rhythm, including both sinus bradycardia and tachycardia. As might be expected, the final diagnoses in this group of chest pain patients with a normal 12-lead ECG in the ED included numerous gastrointestinal, musculoskeletal, and pulmonary syndromes. A small percentage had a diagnosis of unstable angina (4%) and AMI (1%). Similar findings have been reported in another study that demonstrated that patients with a normal ECG and classic symptoms of angina are still at risk of having acute coronary ischemic syndrome, with 3% of such patients having a final hospital diagnosis of AMI.26 In addition, it has been shown that over-reliance on a normal ECG in a patient with anginal chest pain who is currently pain-free should also be avoided.
Patients who initially have a normal ECG but go on to develop AMI during hospitalization are usually sensation-free or minimally uncomfortable upon presentation. Furthermore, these patients frequently lack a past history of ischemic heart disease. These findings reinforce the teaching point that the history is the most important tool used in the evaluation of chest pain patients and that excessive reliance on a normal ECG in a patient with a classic description of anginal chest pain can lead to a missed diagnosis of AMI. Conversely, a normal ECG in a patient with a low clinical likelihood (i.e., an atypical presentation) of ischemic heart disease provides strong evidence against the possibility of acute coronary ischemic syndrome.
The patient with a normal ECG must be managed based on an analysis of the clinical history, risk factors, and the ECG. A patient with a reasonable clinical likelihood of experiencing an acute coronary ischemic event despite a normal ECG should be admitted to the hospital for additional therapy, aggressive monitoring, and further diagnostic evaluation. The EP must realize that the chest-pain patient with an initial ECG not suggestive of transmural infarct should undergo serial electrocardiographic examinations at a frequency appropriate for the clinical situation. This type of patient scenario (i.e., acute anginal chest discomfort with a nondiagnostic ECG) obviously warrants aggressive medical therapy aimed at halting the ischemic cascade. The use of such a serial approach identifies the patient with the nondiagnostic ECG who evolves into the diagnostic category with pathologic ST segment changes. With continued discomfort or other undesired clinical findings, repeat ECGs must be performed. When practiced at a chest pain center environment, the use of serial ECGs assisted in establishing the diagnosis of AMI in approximately 10% of patients ultimately found to have MI.3 Such a practice, while recognized as a standard approach, may be omitted unintentionally in the often hectic ED environment after the EP has made arrangements for in-hospital disposition with the consulting physician. Another strategy that may be useful in detecting the evolving ischemic syndrome with electrocardiography is the use of ST segment trend monitoring that may alert the health care provider to dynamic ST segment abnormality earlier in the patient’s course. Such an approach has been found to be helpful in cases involving the initial, nondiagnostic ECG as well as in instances characterized by electrocardiographic confounding patterns, such as LBBB, VPR, and LVH.
Non-specific ST/T-Wave Changes. The ECG may be described as "nondiagnostic" if NSSTTW are noted. These nonspecific changes are defined as less than 1 mm ST segment depression or ST segment elevation with or without abnormal morphology and blunted, flattened, or biphasic T waves without obvious inversion or hyperacuity. Other electrocardiographic features that may produce nondiagnostic changes include sinus tachycardia and bradycardia or artifactual phenomena such as a wandering or irregular baseline. One study noted that adult chest-pain patients with nonspecific or other nondiagnostic electrocardiographic features had a relatively low risk of AMI, ranging from 3% to 4%, but a significant risk of unstable angina, which occurred in approximately one-fifth of all such cases.16 Other investigators have found that approximately 6% of patients with AMI demonstrate a "nonspecifically abnormal" ECG on presentation.
Once again, it must be emphasized that the ECG is fallible, and the ED physician must rely on the clinical history. The nondiagnostic ECG is exactly what the name implies: nondiagnostic. Over-reliance on the nondiagnostic ECG is an approach that is fraught with both error and danger. Granted, few patients with such an electrocardiographic interpretation suffer AMI, but a significant minority experience an unstable coronary syndrome that, if not appropriately managed, may progress to an acute infarct or other ischemic sequelae.
Alternatively, in a somewhat different application of the term, the nondiagnostic ECG is initially encountered in 50-75% of patients ultimately found to have experienced an MI. With this use of the descriptor "nondiagnostic," the clinician is referring to the lack of pathologic ST segment elevation noted on the ECG. Significant ST segment depression and/or T wave changes may be seen in these situations; these findings are suggestive of an active coronary ischemic event.
Previously Abnormal ECG. Some patients are known to have an electrocardiographic abnormality due to past coronary heart disease or LVH. For example, in a group of adult chest pain patients with electrocardiographic abnormalities known to be oldischemic abnormality (T wave inversions or ST segment depression), evidence of old infarction (pathologic Q waves), or LVH with strain without interval changethe final hospital diagnoses included AMI in 7% and unstable angina in 48%.16
The Evolving ECG. The evolving ECG represents another electrocardiographic challenge for the ED physician. The ECG is noted to be "diagnostic" of AMI in only 25-50% of cases based upon the initial encounter in the ED; this figure, however, increases to 66% with the use of the chest pain center with its dedicated staff, potential increased scrutiny, and enhanced monitoring capabilities.3 In this instance, "diagnostic" refers to pathologic ST segment elevation, indicative of acute, transmural MI. Several factors contribute to this relatively low rate of initial diagnostic findings, including incomplete, progressive pathophysiology as well as the non-Q wave (subendocardial) MI. The EP must realize that the chest pain patient with an initial ECG not suggestive of transmural infarct should undergo serial electrocardiographic examinations at a frequency appropriate for the clinical situation.
The Non-Q Wave Myocardial Infarction. The patient with a non-Q wave MI (NQWMI), also referred to as the subendocardial MI, represents approximately 25-40% of all cases of AMI.3,27 The infarct is nontransmural, as indicated in the acute phase by the absence of pathologic ST segment elevation and ultimately by the lack of significant Q waves. The diagnosis is made in the patient with chest pain (or equivalent complaint) who demonstrates biochemical evidence of MI with abnormal cardiac enzymes or other serum markers.
Typically, ST segment depression and/or T wave inversions are noted on the ECG. In a number of patients experiencing NQWMI, the initial and subsequent ECGs demonstrate only NSSTTW. The ECG is less often indicative of acute injury (i.e., diagnostic in this group of patients on presentation when compared to the Q wave AMI group). Conversely, the NQWMI patient population more often demonstrates significant electrocardiographic abnormalities on presentation compared to the transmural group.27
The NQWMI results from an incomplete arterial occlusion with myocyte death. The actual infarct is generally described as "small," and it has a good short-term prognosis and is associated with a low risk of death, pump failure, and malignant arrhythmia. The intermediate and long-term prognoses, however, are less favorable; these patients are at increased risk of recurrent chest pain with infarct. The incomplete arterial occlusion that produced the initial infarct leaves viable myocardium at risk in an area of compromised perfusion. Such patients should undergo additional cardiac evaluation after the initial infarct period to identify the subgroup requiring further therapies. With respect to acute therapy, patients with NQWMI have not been shown to benefit from the use of thrombolytic agents. The value of primary angioplasty has not been answered conclusively. These patients potentially benefit from the use of nitrates, aspirin, heparin, beta-adrenergic-blocking agents, and other such therapies; the use of urgent cardiac catheterization obviously is made by the cardiologist who should be involved early the patient’s course. The elderly population tends to experience the NQWMI more often than other patient groups; unfortunately, it is this same population that also presents with other atypical or diagnostic confounding manifestations of AMI.
Posterior Wall AMI. Posterior AMI (PMI) refers to infarction of the dorsal area of the heart and, in most cases, pathophysiologically involves either the left circumflex or the right coronary artery with its posterior descending branch. As predicted from the coronary anatomy, posterior AMI most often occurs along with acute inferior or lateral myocardial infarction. True, isolated posterior AMI does occur but is rare.
Because the endocardial surface of the posterior wall faces the precordial leads, the electrocardiographic changes resulting from AMI will be reversed. An R wave with increased voltage in the right precordial leads (V1 to V3) is the major electrocardiographic feature associated with PMI. An R/S wave ratio greater than 1.0 in leads V1 or V2 is another suggestive finding.28 Table 6, Figure 6, and Figure 7 (see ECG interpretation supplement) illustrate the electrocardiographic findings consistent with PMI and give examples of a PMI noted on the ECG. ST segment depression with a prominent, upright T wave in a similar distribution are highly correlated with PMI. If one considers the "reverse nature" of these electrocardiographic abnormalities when applied to the posterior wall, the findings have more ominous implications. The tall R wave is actually a significant Q wave while the ST segment-T wave abnormalities represent ST segment elevation with inverted T wave. When interpreting the ECG in an appropriate patient, the finding of ST segment depression in the right precordial leads should suggest either anterior wall ischemia or acute posterior wall MI.
The EP may employ additional-lead ECGs in select cases, looking for involvement of the posterior wall in patients with co-existing inferior or lateral acute infarct. Alternatively, in a chest-pain patient with a high clinical suspicion for AMI who has ST segment depression noted only in the right precordial leads, the additional-lead ECG may reveal PMI. The use of additional-lead ECGs in all adult chest-pain patients encountered in the ED has not yielded therapeutic or diagnostic benefit.29 Unsuspected PMI was not noted in this population; moreover, therapeutic and disposition decisions were not altered. When considering a higher risk population, additional lead ECGs did have an impact on the rate of diagnosis of PMI.30 Greater than 1 mm ST segment elevation in the posterior leads, V8 and V9, confirms the presence of PMI and is felt to be superior to the findings noted in leads V1 through V3.30 (See ECG interpretation supplementFigure 7.) The posterior leads are placed on the left back. (See ECG interpretation supplementFigure 8.)
Outcome-effective evaluation of patients at risk for AMI requires an awareness that clinical presentations and ECG findings may be atypical and nonclassical. For example, the young patient with cardiac risk factors and a chest pain syndrome with unexplained accompanying symptoms such as emesis or diaphoresis should undergo electrocardiographic evaluation. In contrast, the elderly patient with AMI is more likely to present with atypical manifestations such as dyspnea or a stroke syndrome. Accordingly, the ED physician should actively exclude AMI in all older patients presenting with unexplained cardiac, respiratory, and neurologic syndromes. Similar logic applies to the patient with DM.
Detailed knowledge of anticipated ST segment-T wave changes resulting from the abnormal ventricular conduction disturbances such as LBBB and VPR is mandatory. A more thorough understanding of atypical ECG manifestation of AMI will permit the clinician to recognize the unusual morphologies of AMI and initiate proper management aimed at reperfusion, thereby optimizing therapy of patients with evolving MI. Specifically, abnormalities of the ST segment-T wave complexes that are not consistent with the altered ventricular conduction should alert the physician to the possibility of acute ischemic ECG changes.21,22,31,32 The performance of serial ECGs may demonstrate the dynamic electrocardiographic changes usually encountered in those patients with acute ischemia.33
Finally, the ED physician must have a working knowledge of LVH and its spectrum of associated ST segment-T wave abnormalities. This information will help clinicians distinguish between acute ischemic changes and anticipated electrocardiographic abnormalities of LVH. Other strategies, similar to those suggested for both the LBBB and VPR situations, include serial ECGs, ST segment trend monitoring, and comparison with past studies.
References
1. McCarthy BD, Beshansky JR, D’Agostino RB, et al. Missed diagnosis of acute myocardial infarction in the emergency department: Results from a multicenter study. Ann Emerg Med 1993;22:579-582.
2. Lee TH, Rouan GW, Weisberg MC, et al. Clinical characteristics and natural history of patients with acute myocardial infarction sent home from the emergency department. Am J Cardiol 1987;60:219-224.
3. Brady WJ. Personal communication (unpublished data), University of Virginia Health Sciences Center, Charlottesville, VA; 1997.
4. Lusiani L, Perrone A, Pesavento R, et al. Prevalence, clinical features, and acute course of atypical myocardial infarction. Angiology 1994;45:49-55.
5. Uretski B, Farquhar D, Berenzin A. Symptomatic myocardial infarction without chest pain: Prevalence and clinical course. Am J Cardiol 1977;40:498-503.
6. Aronow WS. Prevalence of presenting symptoms of recognized acute myocardial infarction and of unrecognized healed myocardial infarction in elderly patients. Am J Cardiol 1987;60:1182-1187.
7. Bayer AJ, Chadha JS, Farag RR, et al. Changing presentation of myocardial infarction with increasing old age. J Am Geriatr Soc 1986;34:263-266.
8. Jacoby RM, Nesto RW. Acute myocardial infarction in the diabetic patient: Pathophysiology, clinical course, and prognosis. J Am Coll Cardiol 1992;20:736-744.
9. Bertolet BD, Hill JA. Unrecognized myocardial infarction. Cardiovasc Clin 1989;20:173-182.
10. Margolis JR, Kannel WB, Feinleib M, et al. Clinical features of unrecognized myocardial infarctionsilent and symptomatic. Eighteen-year follow-up: The Framingham study. Am J Cardiol 1973;32:1-7.
11. Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction. An update on the Framingham study. N Engl J Med 1984;311:1144-1147.
12. Yano K, MacLean CJ. The incidence and prognosis of unrecognized myocardial infarction in the Honolulu, Hawaii, Heart Program. Arch Intern Med 1989;149:1528-1532.
13. Anonymous (Physician Insurers Association of America). Acute myocardial infarction study. Rockville, MD: Physician Insurers Association of America; May 1996.
14. Theron HDT, Steyn AF, Raan HED, et al. Autonomic neuropathy and atypical myocardial infarction in a diabetic clinic population. S Afr Med J 1987;72:253-254.
15. Rosen SD, Paulesu E, Nihiyannopoulos P, et al. Silent ischemia as a central problem: Regional brain activation compared in silent and painful myocardial ischemia. Ann Intern Med 1996;124:939-949.
15a. Brady WJ, Fines R, Huff JS, et al. Altered mental status in the emergency department: Etiology, outcome, and evaluation. Acad Emerg Med 1997;4:abstract pending.
16. Lee T, Cook F, Weisberg M, et al. Acute chest pain in the emergency room: Identification and examination of low-risk patients. Arch Intern Med 1985;145:65-69.
17. Tierney WM, Fitzgerald J, McHenry R. Physician estimates of the probability of myocardial infarction in emergency room patients with chest pain. Med Decis Making 1986;6:12-17.
18. McElroy JB. Angina pectoris with coexisting skeletal chest pain. Am Heart J 1963;66:96-99.
19. Jalowiec DA, Hill JA. Myocardial infarction in the young and in women. Cardiovasc Clin 1989;20:197-206.
20. Marriott HJL. Myocardial infarction. In: Marriott HJL, ed. Practical Electrocardiography. 8th ed., Baltimore: Williams & Wilkins; 1988:419-450.
21. Brady WJ, Aufderheide TP. Left bundle branch block pattern complicating the electrocardiographic evaluation of acute myocardial infarction. Acad Emerg Med 1997;4:56-62.
22. Aufderheide TP, Brady WJ. Electrocardiography in the patient with myocardial ischemia or infarction. In: Gibler WB, Aufderheide TP, eds. Emergency Cardiac Care. St. Louis: Mosby-Year Book; 1994.
23. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle branch block. N Engl J Med 1996;334:481-487.
24. Sgarbossa EB, Piniski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. Am J Cardiol 1996;77:423-424.
25. Otto LA, Aufderheide TP. Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis of acute myocardial infarction. Ann Emerg Med 1994;23:17-24.
26. Rouan GW, Lee TH, Cook EF, et al. Clinical characteristics of patients with acute myocardial infarction and nonspecific electrocardiograms. Clin Res 1987;35:360A.
27. Fesmire FM, Percy RF, Wears RL, et al. Initial ECG in Q wave and non-Q wave myocardial infarction. Ann Emerg Med 1985;18:741-746.
28. Goldberger AL. Myocardial Infarction: Electrocardiographic Differential Diagnosis. 4th ed. St. Louis: Mosby; 1991.
29. Brady WJ, Chang N, Hwang V, et al. The 15-lead electrocardiogram in emergency department chest pain patients: Comparison to the 12-lead electrocardiogram. Acad Emerg Med 1997;4:abstract pending.
30. Zalenski RJ, Cook D, Rydman R. Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: The 15-lead ECG. Ann Emerg Med 1993;22:786-791.
31. Hands ME, Cook EF, Stone PH, et al. Electrocardiographic diagnosis of myocardial infarction in the presence of complete left bundle branch block. Am Heart J 1988;116:23-31.
32. Kuhn M. ECG diagnosis of acute myocardial infarction in patients with bundle branch block. Ann Emerg Med 1988;17:633-639.
33. Fesmire FM. ECG diagnosis of acute myocardial infarction in the presence of left bundle branch block in patients undergoing continuous ECG monitoring. Ann Emerg Med 1995;26:69-82.
Physician CME Questions
73. Isolated emesis or diaphoresis is:
A. a common presentation for AMI in the younger patients.
B. a more common presentation for AMI than chest pain.
C. is a very unusual presentation for AMI.
74. The following comorbid conditions may obscure a physician’s ability to diagnose AMI:
A. History of diabetes mellitus
B. Patients who have undergone cardiac transplantation
C. Patients with dementia
D. Patients on immunosuppressive medications
75. The initial ECG is interpreted as being normal or as having non-specific ST/T wave changes in:
A. less than 1% of patients with documented MI.
B. up to 10% of patients with documented MI.
C. about one-third of patients with documented MI.
D. the majority of patients with documented MI.
76. The ED physician can expect to encounter so-called "atypical" features of AMI in approximately:
A. 5% of patients with MI
B. 10-30% of patients with MI
C. 40-50% of patients with MI
77. The incidence of "painless" AMI is seen in about what percentage of elderly patients over the age of 85?
A. 10-20%
B. 20-30%
C. 30-40%
D. 40-50%
78. In patients with a ventricular-paced rhythm (VPR), the most useful criterion for suggesting the presence of AMI is:
A. upward sloping, then concave ST-T segment in leads V1, V2, and V3.
B. concordant ST elevation of 1 mm in leads II, III, and AVF.
C. discordant ST segment elevation of 5 mm or more
D. none of the above
79. ECG criteria suggesting the presence of an AMI in a patient with LBBB include:
A. ST segment elevation greater than 1 mm, which is concordant with the QRS complex.
B. ST-T segment depression greater than 1 mm in leads V1, V2, or V3.
C. ST segment elevation greater than 5 mm which is discordant with the QRS complex
D. all of the above
80. The nondiagnostic ECG is initially encountered in:
A. about 10% of patients who ultimately have MI confirmed.
B. about 10-25% of patients who ultimately have MI confirmed.
C. about 25-50% of patients who ultimately have MI confirmed.
D. about 50-75% of patients who ultimately have MI confirmed.
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