Electrocardiography in myocardial infarction | |
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Purpose | detecting ischemia or acute coronary injury in emergency department |
Electrocardiography in suspected myocardial infarction has the main purpose of detecting ischemia or acute coronary injury in emergency department populations coming for symptoms of myocardial infarction (MI). Also, it can distinguish clinically different types of myocardial infarction.
The standard 12 lead electrocardiogram (ECG) has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture. [1] It is therefore desirable to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. [2] The standard 12 lead ECG also does not directly examine the right ventricle, and is relatively poor at examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG. [1] The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care. [3]
The 12 lead ECG is used to classify MI patients into one of three groups: [4]
The 2018 European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Health Federation Universal Definition of Myocardial Infarction for the ECG diagnosis of the ST segment elevation type of acute myocardial infarction require new ST elevation at J point of at least 1mm (0.1 mV) in two contiguous leads with the cut-points: ≥1 mm in all leads other than leads V2-V3. For leads V2-V3: ≥2 mm in men ≥40 years, ≥2.5 mm in men <40 years, or ≥1.5 mm in women regardless of age. This assumes usual calibration of 1mV/10mm. [5] These elevations must be present in anatomically contiguous leads. [4] (I, aVL, V5, V6 correspond to the lateral wall; V3-V4 correspond to the anterior wall ; V1-V2 correspond to the septal wall; II, III, aVF correspond to the inferior wall.) This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients. [6] Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. [7] The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm. [7] [8] [9]
There are heavily researched clinical decision tools such as the TIMI Scores which help prognose and diagnose STEMI based on clinical data. For example, TIMI scores are frequently used to take advantage of EKG findings to prognose patients with MI symptoms. [10] Based on symptoms and electrocardiographic findings, practitioners can differentiate between unstable angina, NSTEMI and STEMI, normally in the emergency room setting. [11] Other calculators such as the GRACE [12] and HEART [13] scores, assess other major cardiac events using electrocardiogram findings, both predicting mortality rates for 6 months and 6 weeks, respectively.[ citation needed ]
Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation. [14] In practice this is rarely seen, because it only exists for 2–30 minutes after the onset of infarction. [15] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia. [16]
In the first few hours the ST segments usually begin to rise. [17] Pathological Q waves may appear within hours or may take greater than 24 hr. [17] The T wave will generally become inverted in the first 24 hours, as the ST elevation begins to resolve. [17]
Long term changes of ECG include persistent Q waves (in 90% of cases) and persistent inverted T waves. [17] Persistent ST elevation is rare except in the presence of a ventricular aneurysm. [17]
Electrocardiography is the process of producing an electrocardiogram, a recording of the heart's electrical activity through repeated cardiac cycles. It is an electrogram of the heart which is a graph of voltage versus time of the electrical activity of the heart using electrodes placed on the skin. These electrodes detect the small electrical changes that are a consequence of cardiac muscle depolarization followed by repolarization during each cardiac cycle (heartbeat). Changes in the normal ECG pattern occur in numerous cardiac abnormalities, including:
In electrocardiography, the T wave represents the repolarization of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period or vulnerable period. The T wave contains more information than the QT interval. The T wave can be described by its symmetry, skewness, slope of ascending and descending limbs, amplitude and subintervals like the Tpeak–Tend interval.
Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.
Variant angina, also known as Prinzmetal angina,vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina. Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.
Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome.
Left bundle branch block (LBBB) is a conduction abnormality in the heart that can be seen on an electrocardiogram (ECG). In this condition, activation of the left ventricle of the heart is delayed, which causes the left ventricle to contract later than the right ventricle.
Acute pericarditis is a type of pericarditis usually lasting less than 6 weeks. It is the most common condition affecting the pericardium.
P2Y12 is a chemoreceptor for adenosine diphosphate (ADP) that belongs to the Gi class of a group of G protein-coupled (GPCR) purinergic receptors. This P2Y receptor family has several receptor subtypes with different pharmacological selectivity, which overlaps in some cases, for various adenosine and uridine nucleotides. The P2Y12 receptor is involved in platelet aggregation and is thus a biological target for the treatment of thromboembolisms and other clotting disorders. Two transcript variants encoding the same isoform have been identified for this gene.
Door-to-balloon is a time measurement in emergency cardiac care (ECC), specifically in the treatment of ST segment elevation myocardial infarction. The interval starts with the patient's arrival in the emergency department, and ends when a catheter guidewire crosses the culprit lesion in the cardiac cath lab. Because of the adage that "time is muscle", meaning that delays in treating a myocardial infarction increase the likelihood and amount of cardiac muscle damage due to localised hypoxia, ACC/AHA guidelines recommend a door-to-balloon interval of no more than 90 minutes. As of 2006 in the United States, fewer than half of STEMI patients received reperfusion with primary percutaneous coronary intervention (PCI) within the guideline-recommended timeframe. It has become a core quality measure for the Joint Commission on Accreditation of Healthcare Organizations (TJC).
The Thrombolysis In Myocardial Infarction (TIMI) Study Group, is an academic research organization (ARO) affiliated with Brigham and Women's Hospital and Harvard Medical School with a focus in the field of cardiovascular disease. The group has its headquarters in Boston, Massachusetts.
Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in people with unstable angina. Originally thought of as two separate types, A and B, it is now considered an evolving wave form, initially of biphasic T wave inversions and later becoming symmetrical, often deep, T wave inversions in the anterior precordial leads.
A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw. Often such pain occurs in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn. Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat, feeling tired, and decreased level of consciousness. About 30% of people have atypical symptoms. Women more often present without chest pain and instead have neck pain, arm pain or feel tired. Among those over 75 years old, about 5% have had an MI with little or no history of symptoms. An MI may cause heart failure, an irregular heartbeat, cardiogenic shock or cardiac arrest.
ST elevation refers to a finding on an electrocardiogram wherein the trace in the ST segment is abnormally high above the baseline.
ST depression refers to a finding on an electrocardiogram, wherein the trace in the ST segment is abnormally low below the baseline.
Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a heart attack. Reperfusion therapy includes drugs and surgery. The drugs are thrombolytics and fibrinolytics used in a process called thrombolysis. Surgeries performed may be minimally-invasive endovascular procedures such as a percutaneous coronary intervention (PCI), which involves coronary angioplasty. The angioplasty uses the insertion of a balloon and/or stents to open up the artery. Other surgeries performed are the more invasive bypass surgeries that graft arteries around blockages.
Francis Miller Fesmire was an American emergency physician and a nationally recognized expert in myocardial infarction. He authored numerous academic articles and assisted in the development of clinical guidelines on the standard of care in treating patients with suspected myocardial infarction by the American College of Emergency Physicians and the American Heart Association/American College of Cardiology. He performed numerous research investigations in chest pain patients, reporting the usefulness of continuous 12-lead ECG monitoring, two-hour delta cardiac marker testing, and nuclear cardiac stress testing in the emergency department. The culmination of his studies was The Erlanger Chest Pain Evaluation Protocol published in the Annals of Emergency Medicine in 2002. In 2011 he published a novel Nashville Skyline that received a 5 star review by ForeWord Reviews. His most recent research involved the risk stratification of chest pain patients in the emergency department.
A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers. A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.
Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the affected area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that inhibit clot formation; for a subset of patients invasive measures are also employed. Basic principles of management are the same for all types of acute coronary syndrome. However, some important aspects of treatment depend on the presence or absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction (NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is more often reserved for them. Long-term therapy is necessary for prevention of recurrent events and complications.
Sgarbossa's criteria are a set of electrocardiographic findings generally used to identify myocardial infarction in the presence of a left bundle branch block (LBBB) or a ventricular paced rhythm.
de Winter syndrome is an electrocardiogram (ECG) pattern which often represents sudden near blockage of the left anterior descending artery (LAD). Symptoms include chest pain, shortness of breath, and sweating.