The Ecg In Acute Myocardial Infarction And Unstable Angina Pdf

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Rapid risk stratification by emergency department ED physicians to evaluate patients with chest pain for predicting the short-term occurrence of major adverse cardiac event MACE is crucial. The aim of this study was to investigate the predictive value of platelet-lymphocyte ratio PLR levels and compare with the modified heart score m-HS and stress testing to predict the severity of high-risk patients with unstable angina pectoris UAP in the ED. This study is prospective which included patients with UAP and control healthy subjects.

Diagnosis of Acute Coronary Syndrome

A more recent article on acute coronary syndrome is available. Diagnosis requires an electrocardiogram and a careful review for signs and symptoms of cardiac ischemia. In acute coronary syndrome, common electrocardiographic abnormalities include T-wave tenting or inversion, ST-segment elevation or depression including J-point elevation in multiple leads , and pathologic Q waves. Risk stratification allows appropriate referral of patients to a chest pain center or emergency department, where cardiac enzyme levels can be assessed.

Most high-risk patients should be hospitalized. Intermediate-risk patients should undergo a structured evaluation, often in a chest pain unit. Many low-risk patients can be discharged with appropriate follow-up.

Troponin T or I generally is the most sensitive determinant of acute coronary syndrome, although the MB isoenzyme of creatine kinase also is used. Early markers of acute ischemia include myoglobin and creatine kinase—MB subforms or isoforms , when available.

In the future, advanced diagnostic modalities, such as myocardial perfusion imaging, may have a role in reducing unnecessary hospitalizations. The likelihood of acute coronary syndrome low, intermediate, high should be determined in all patients who present with chest pain.

A lead ECG should be obtained within 10 minutes of presentation in patients with ongoing chest pain. When used by trained physicians, the Acute Cardiac Ischemia Time-Insensitive Predictive Instrument a computerized, decision-making program built into the electrocardiogram machine results in a significant reduction in hospital admissions of patients who do not have acute coronary syndrome.

Differentiating acute coronary syndrome from noncardiac chest pain is the primary diagnostic challenge. The initial assessment requires a focused history including risk factor analysis , a physical examination, an electrocardiogram ECG and, frequently, serum cardiac marker determinations Table 1. New transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema or rales. T-wave flattening or inversion of T waves in leads with dominant R waves.

Adapted from Braunwald E, et al. Unstable angina: diagnosis and management. Rockville, Md. Symptoms of acute coronary syndrome include chest pain, referred pain, nausea, vomiting, dyspnea, diaphoresis, and light-headedness. Some patients may present without chest pain; in one review, 2 sudden dyspnea was the sole presenting feature in 4 to 14 percent of patients with acute myocardial infarction.

Pain may be referred to either arm, the jaw, the neck, the back, or even the abdomen. Pain radiating to the shoulder, left arm, or both arms somewhat increases the likelihood of acute coronary syndrome likelihood ratio [LR]: 1. Typical angina is described as pain that is substernal, occurs on exertion, and is relieved with rest. Patients with all three of these features have a greater likelihood of having acute coronary syndrome than patients with none, one, or even two of these features.

Only about 2 percent of patients with cocaine-associated chest pain have acute coronary syndrome. Atypical symptoms do not necessarily rule out acute coronary syndrome. One study 5 found the syndrome in 22 percent of patients who presented to emergency departments with sharp or stabbing pain. However, a combination of atypical symptoms improves identification of low-risk patients. The same study 5 demonstrated that patients presenting with sharp or stabbing pain, pleuritic pain, and positional chest pain had only a 3 percent likelihood of having acute coronary syndrome.

The physical examination in patients with acute coronary syndrome frequently is normal. Ominous physical findings include a new mitral regurgitation murmur, hypotension, pulmonary rales, a new third heart sound S 3 gallop , and new jugular venous distention. Chest-wall tenderness reduces the likelihood of acute coronary syndrome -LR: 0. The likelihood of silent ischemia traditionally has been thought to be greater in patients with diabetes.

However, in a prospective observational study 6 of patients with symptoms suggestive of coronary artery disease on presentation to the emergency department of a cardiac referral center, symptoms did not differ significantly in patients with and without diabetes. The increased frequency of ischemic changes noted on screening ECGs in patients with diabetes simply may reflect their greater baseline risk of coronary artery disease.

Any patient with a history suggestive of acute coronary syndrome should be evaluated in a facility that has ECG and cardiac monitoring equipment. The likelihood of acute infarction is 1. Accuracy is enhanced when the ECG is obtained in a patient with ongoing chest pain.

The characteristics of common ECG abnormalities in specific anatomic locations are presented in Table 2. ST-segment elevation in leads V 1 , V 2 , and V 3 plus any of the features below:. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med ;, The predictive value of the ECG varies markedly, depending on the baseline risk pretest probability for coronary artery disease in a given patient.

The number and magnitude of ECG abnormalities also affect sensitivity and specificity. The magnitude of an ECG abnormality affects diagnostic accuracy. One group of investigators 13 found that the diagnosis of NSTEMI is greater than three times more likely in patients with chest pain whose ECG showed ST-segment depression in three or more leads or ST-segment depressions that were greater than or equal to 0.

Subendocardial ischemia classically results in ST-segment depression and T-wave inversion. Transmural myocardial ischemia results in ST-segment elevation with the vector shifted toward the involved epicardial layer, and without treatment typically results in STEMI.

Serial cardiac marker determinations confirm myocardial injury or infarction in more than 90 percent of patients with J-point elevation in the limb leads.

Significant Q waves greater than 0. Abnormal Q waves usually develop within the first day, and T-wave inversion and normalization of ST segments occur within hours to days. Serum cardiac marker determinations play a vital role in the diagnosis of acute myocardial infarction. Serum markers such as aspartate transaminase, lactate dehydrogenase, and lactate dehydrogenase subforms no longer are used because they lack cardiac specificity and their delayed elevation precludes early diagnosis.

Information from references 16 through Creatine kinase CK is an enzyme that is found in striated muscle and tissues of the brain, kidney, lung, and gastrointestinal tract. This widely available marker has low sensitivity and specificity for cardiac damage. Furthermore, CK levels may be elevated in a number of noncardiac conditions, including trauma, seizures, renal insufficiency, hyperthermia, and hyperthyroidism. The serum CK level rises within three to eight hours after myocardial injury, peaks by 12 to 24 hours, and returns to baseline within three to four days.

Although CK commonly was measured serially along with CK-MB at the time of hospital admission and six to 12 hours after admission, this marker largely has been replaced by cardiac troponins and CK-MB. CK-MB is much more cardiac specific than CK alone, and is useful for the early diagnosis of acute myocardial infarction. Like the CK level, the peak CK-MB level does not predict infarct size; however, it can be used to detect early reinfarction. CK-MB may be further characterized into subforms or isoforms.

The CK-MB subform assay takes about 25 minutes to perform. However, the CK-MB subform assay is not yet widely available. Troponins T, I, C are found in striated and cardiac muscle. Unlike troponin I levels, troponin T levels may be elevated in patients with renal disease, polymyositis, or dermatomyositis.

The cardiac troponins typically are measured at emergency department admission and repeated in six to 12 hours. The cardiac troponins may remain elevated up to two weeks after symptom onset, which makes them useful as late markers of recent acute myocardial infarction. An elevated troponin T or I level is helpful in identifying patients at increased risk for death or the development of acute myocardial infarction.

The troponins also can help identify low-risk patients who may be sent home with close follow-up. Bedside troponin assays are being developed. Myoglobin is a low-molecular-weight protein that is present in both cardiac and skeletal muscle. It can be detected in the serum as early as two hours after myocardial necrosis begins. Myoglobin has low cardiac specificity but high sensitivity, which makes it most useful for ruling out myocardial infarction if the level is normal in the first four to eight hours after the onset of symptoms.

Time changes in the myoglobin value also can be extremely helpful. Combining a doubling of the baseline myoglobin level at two hours after symptom onset with an abnormal myoglobin test at six hours after symptom onset increases the sensitivity to 95 percent at six hours. Myoglobin should be used in conjunction with other serum markers, because its level peaks and falls rapidly in patients with ischemia. No assessment protocol or constellation of tests is totally accurate in diagnosing acute coronary syndrome.

From 1 to 4 percent of patients ultimately proven to have acute coronary syndrome are sent home from the emergency department. A suggested approach to the evaluation of patients with chest pain or symptoms consistent with acute coronary syndrome is provided in Figure 1. When a patient presents with chest pain or symptoms suggestive of acute coronary syndrome, vital signs should be obtained, the patient should be monitored, and a focused but careful history should be obtained.

A lead ECG should be obtained within 10 minutes of presentation. Suggested approach to the evaluation of patients with chest pain or symptoms suggestive of ACS. Risk stratification then should be performed using the criteria in Table 1. Use of this instrument in an emergency department resulted in no change in appropriate admission of patients who had acute coronary syndrome. The benefit of its use was a significant reduction in hospital admissions of patients who did not have acute coronary syndrome.

Patients who are at high risk for acute coronary syndrome should be admitted to a coronary care unit. Patients at intermediate risk may be monitored in a telemetry bed in an inpatient setting or a chest pain unit.

A chest pain unit is a specialized unit within an emergency department or a medical center; the unit is dedicated to careful monitoring and aggressive implementation of diagnostic protocols clinical guidelines for the evaluation of acute coronary syndrome. Most low-risk patients may undergo early exercise testing or can be discharged with careful outpatient follow-up.

Although protocols for chest pain units may vary somewhat, one protocol 28 that has been shown to be safe and cost-effective in an intermediate-risk population consists of the following:.

Admission to the cardiac care unit or a telemetry bed on the cardiology service for patients with elevated cardiac enzyme levels, recurrent chest pain consistent with unstable angina, or significant ventricular arrhythmias;. An exercise treadmill test for patients without abnormal findings on the initial tests, or a nuclear stress test or echocardiographic stress test;.

Use of this type of systematic approach has the potential to improve the ability of physicians to care for patients with possible acute coronary syndrome, as well as reduce the likelihood of medical error. Already a member or subscriber? Log in. Address correspondence to Suraj A.

The ECG in Acute Myocardial Infarction and Unstable Angina

This open-access and indexed, peer-reviewed journal publishes review articles ideal for the busy physician. While there is a codified definition of STEMI, challenges in diagnosis remain due to variability in electrocardiogram ECG presentation, conditions with similar presentations, variability in the electrical manifestation of ST-segment elevation on ECG, and systems issues with access to rapid diagnosis that can make this diagnosis challenging. This article aims to review these challenges. Disclosure: The authors have no conflicts of interest to declare. Received: 03 February Accepted: 10 May Citation: US Cardiology Review ;10 2 —4.

Skip to main content Skip to table of contents. Advertisement Hide. This service is more advanced with JavaScript available. Front Matter Pages i-ix. Pages Determining the size of the area at risk, the severity of ischemia, and identifying the site of occlusion in the culprit coronary artery.

A more recent article on acute coronary syndrome is available. Diagnosis requires an electrocardiogram and a careful review for signs and symptoms of cardiac ischemia. In acute coronary syndrome, common electrocardiographic abnormalities include T-wave tenting or inversion, ST-segment elevation or depression including J-point elevation in multiple leads , and pathologic Q waves. Risk stratification allows appropriate referral of patients to a chest pain center or emergency department, where cardiac enzyme levels can be assessed. Most high-risk patients should be hospitalized.

AMI and (b) hyperacute T waves. Because immediate PCI may be indicated for some cases of unstable angina and non—ST-. Elevation AMI (UA/NSTEMI), we.

Acute Coronary Syndromes

Coronary artery disease CAD risk factors include family history of CAD, diabetes, hypertension, hyperlipidemia, and tobacco use. Beyond that time, most patients have a clinical course similar to those with chronic stable angina. To view other topics, please log in or purchase a subscription. The Washington Manual of Medical Therapeutics helps you diagnose and treat hundreds of medical conditions.

Unstable Angina

ECG Interpretation

Unstable angina results from acute obstruction of a coronary artery without myocardial infarction. Symptoms include chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis is by ECG and the presence or absence of serologic markers. Treatment is with antiplatelet drugs, anticoagulants, nitrates, statins, and beta-blockers. Coronary angiography with percutaneous intervention or coronary artery bypass surgery is often necessary. See also Overview of Acute Coronary Syndromes.

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A Novel Index for Prompt Prediction of Severity in Patients with Unstable Angina Pectoris

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  1. Marize 01.06.2021 at 08:39

    The electrocardiogram (ECG) remains the most accessible and inexpensive diagnostic tool to evaluate the patient presenting with symptoms suggestive of The ECG in Acute Myocardial Infarction and Unstable Angina Download book PDF.

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    The ECG in acute myocardial infarction and unstable angina Diagnosis and risk Get a printable copy (PDF file) of the complete article (K), or click on a.

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