The symptoms of acute myocardial infarction
Heart Attack
Death of heart muscle caused by a loss of blood supply.
Which morphologic findings are characteristic of myocardial ischemia (mi)?
The earliest morphologic characteristic of MI occurs between 12 and 24 hours after the onset of chest pain. Hypereosinophilia of the cytoplasm as assessed by hematoxylin-eosin staining is characteristic of myocardial ischemia (see the first image below).
What are the diagnostic criteria for an mi?
An MI is diagnosed when two of the following criteria are met: Symptoms of ischemia New ST-segment changes or a left bundle branch block (LBBB) Presence of pathological Q waves on the ECG Imaging study showing new regional wall motion abnormality Presence of an intracoronary thrombus at autopsy or angiography
What is the pathology of acute myocardial infarction (MI)?
Pathology of Acute Myocardial Infarction. Author: Allen Patrick Burke, MD; Chief Editor: Allen Patrick Burke, MD more... Acute myocardial infarction (MI) indicates irreversible myocardial injury resulting in necrosis of a significant portion of myocardium (generally >1 cm).
What are the microscopic findings of an infarct?
Microscopic Findings. The border areas show prominent neutrophil infiltration by 48 hours. At 3-5 days, the central portion of the infarct shows loss of myocyte nuclei and striations; in smaller infarcts, neutrophils invade the infarct and fragment, resulting in more severe karyorrhexis (nuclear dust).
What are the pathophysiology of myocardial infarction?
In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function.
What are four indicators of an MI?
Symptoms of acute myocardial infarction include chest pain or discomfort with or without dyspnea, nausea, and diaphoresis. Women and patients with diabetes are more likely to present with atypical symptoms, and 20% of acute MI are silent. Diagnosis is by ECG and cardiac markers.
What factors are considered when diagnosing an acute MI?
An MI is diagnosed when two of the following criteria are met:Symptoms of ischemia.New ST-segment changes or a left bundle branch block (LBBB)Presence of pathological Q waves on the ECG.Imaging study showing new regional wall motion abnormality.Presence of an intracoronary thrombus at autopsy or angiography.
What is the pathophysiology of stemi?
Pathophysiology. STEMI is caused by acute, total occlusion of an epicardial coronary artery, most often due to atherosclerotic plaque rupture/erosion and subsequent thrombus formation.
What is the best indicator of a myocardial infarction?
The most sensitive early marker for myocardial infarction is myoglobin. Troponin levels should be measured at presentation and again 10-12 hours after the onset of symptoms.
What are the morphologic findings in myocardial infarction?
The gross morphologic appearance of a myocardial infarction can vary....Myocardial Infarction (MI)Time from OnsetGross Morphologic Finding24 - 72 HoursPallor with some hyperemia3 - 7 DaysHyperemic border with central yellowing10 - 21 DaysMaximally yellow and soft with vascular margins7 weeksWhite fibrosis1 more row
What is the pathophysiology of coronary artery disease?
The hallmark of the pathophysiology of CAD is the development of atherosclerotic plaque. Plaque is a build-up of fatty material that narrows the vessel lumen and impedes the blood flow.
What is the pathophysiology of ST elevation?
ST segment elevation occurs because when the ventricle is at rest and therefore repolarized, the depolarized ischemic region generates electrical currents that are traveling away from the recording electrode; therefore, the baseline voltage prior to the QRS complex is depressed (red line before R wave).
What is the pathophysiology of myocardial infarction?
Pathophysiology of myocardial infarction consists of the events that lead to the damage and/or death of heart muscles. Read on to know all about this pathophysiology... Pathophysiology of myocardial infarction consists of the events that lead to the damage and/or death of heart muscles. Read on to know all about this pathophysiology….
What is the most common etiological factor in myocardial infarction?
As mentioned earlier, the most common etiological factor is the presence of an atherosclerotic plaque in the region of the coronary arteries.
What is plaque in arteries?
Plaque in arteries is a condition wherein there is the presence of a blockade in the form of a plug made of cholesterol, lipids, and platelets among other cells. The actual development of a plaque, that is large enough to cause atherosclerosis symptoms, takes years to form.
What is MI in medical terms?
Key Points. Acute myocardial infarction (MI) is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms of acute myocardial infarction include chest pain or discomfort with or without dyspnea, nausea, and diaphoresis. Women and patients with diabetes are more likely to present with atypical symptoms, ...
What are the markers of myocardial cell injury?
Cardiac markers (serum markers of myocardial cell injury) are cardiac enzymes (eg, creatine kinase-MB isoenzyme [CK-MB]) and cell contents (eg, troponin I, troponin T, myoglobin) that are released into the bloodstream after myocardial cell necrosis. The markers appear at different times after injury, and levels decrease at different rates. Sensitivity and specificity for myocardial cell injury vary significantly among these markers, but the troponins (cTn) are the most sensitive and specific and are now the markers of choice. Recently, several new, highly sensitive assays of cardiac troponin (hs-cTn) that are also very precise have become available. These assays can reliably measure cTn levels (T or I) as low as 0.003 to 0.006 ng/mL (3 to 6 pg/mL); some research assays go as low as 0.001 ng/mL (1 pg/mL).
Is NSTEMI the same as STEMI?
Symptoms of NSTEMI and STEMI are the same. Days to weeks before the event, about two thirds of patients experience prodromal symptoms, including unstable or crescendo angina, shortness of breath, and fatigue.
What does MI mean in cardiac?
However, cardiac markers are not elevated. [1][2][3] An MI results in irreversible damage to the heart muscle due to a lack of oxygen. An MI may lead to impairment in diastolic and systolic function and make the patient prone to arrhythmias. In addition, an MI can lead to a number of serious complications.
What is the most common cause of myocardial infarction?
Among patients suffering from acute myocardial infarction, 70% of fatal events are due to occlusion from atherosclerotic plaques. As atherosclerosis is the predominant cause of acute myocardial infarction, risk-factors for atherosclerotic disease are often mitigated in the prevention of disease.
How many people die from acute myocardial infarction?
The prevalence of the disease approaches three million people worldwide, with more than one million deaths in the United States annually.
How many people die from myocardial infarctions annually?
Acute myocardial infarctions are one of the leading causes of death in the developed world, with prevalence approaching three million people worldwide, with more than one million deaths in the United States annually. This activity reviews the presentation, evaluation, and management of patients with acute myocardial infarctions and highlights ...
What happens to the monocytes in an atherosclerotic rupture?
This leads to decreased oxygen delivery through the coronary artery resulting in decreased oxygenation of the myocardium.
What is MI in a heart?
Etiology. Acute myocardial infarction (MI) results from lack of oxygen supply to the working myocardium. Regional infarcts are due to lack of blood flow that occurs when an epicardial artery is blocked by atheroma or thrombus, or other obstructions.
What is the infiltrate at the border of an acute myocardial infarct?
Acute myocardial infarct. After 24 hours, there is a neutrophilic infiltrate at the border of the infarct. Viable myocardium is at the left, and neutrophils with apoptosis (karyorrhexis) are seen infiltrating the necrotic muscle. This patient experienced abdominal pain 35 hours prior to death.
How long does it take for a neutrophil to invade a karyote?
At 3-5 days, the central portion of the infarct shows loss of myocyte nuclei and striations; in smaller infarcts, neutrophils invade the infarct and fragment, resulting in more severe karyorrhexis (nuclear dust). By 5-7 days, macrophages and fibroblasts begin to appear in the border areas.
What is the earliest change in myocardial infarct?
Acute myocardial infarct. The earliest change is hypereosinophilia (above) with an intense pink cytoplasm. There is no inflammation at border between the necrotic myocardium and the viable myocardium (left and below), indicating that the necrosis is about 12-24 hours in age. View Media Gallery.
What is an acute myocardial infarction?
Acute myocardial infarction (MI) indicates irreversible myocardial injury resulting in necrosis of a significant portion of myocardium (generally >1 cm). The term "acute" denotes infarction less than 3-5 days old, when the inflammatory infiltrate is primarily neutrophilic. Acute MI may be either of the nonreperfusion type, in which case the obstruction to blood flow is permanent, or of the reperfusion type, in which the obstruction or lack of blood flow is long enough in duration (generally hours) but is reversed or restored after myocardial cell death occurs.
What is the purpose of immunohistochemistry?
Immunohistochemistry. Immunohistochemistry is of limited use in the diagnosis of acute myocardial infarction (MI). Immunolocalization of complement or fibrin may be helpful in identifying areas of myocyte necrosis, where there is leakage of extracellular proteins into the myocytes.
What is the earliest change that can be grossly discerned in the evolution of acute myocardial in
The earliest change that can be grossly discerned in the evolution of acute myocardial infarction (MI) is pallor of the myocardium, which is visible 12 hours or later after the onset of irreversible ischemia.
What is the case study of John?
Cardiovascular Case Study#N#John is a 76-year-old man with a long history of stable angina and hypertension. He is prescribed nitroglycerin tablets as needed for chest pain and lisinopril for his hypertension. John has noticed that his chest pain is occurring with increasing frequency and less activity is required to initiate the symptoms; however, the pain subsides quickly with rest and one or two nitroglycerin tablets.#N#John is awakened from sleep with chest pain and shortness of breath. The pain is much more severe than his usual anginal pain and radiates to the jaw and the left arm. He experienced some nausea and became diaphoretic and pale. Upon admission to the local emergency department, he was noted to have significant ST-segment elevation on a 12-lead electrocardiogram (ECG).#N#Discussion Questions:#N#1. What diagnosis is consistent with John’s history and physical exam?#N#2. Please differentiate between a STEMI and Non-STEMI.#N#3. What are the pathophysiological findings specifying an MI?#N#4.What are the differences between angina, silent ischemia, and myocardial ischemia?#N#5.Provide a description of the three factors associated with Sudden Cardiac Death.#N#6.What are the possible complications post-MI might the NP be aware of when caring for John?#N#John is a 76-year-old man with a long history of stable angina and hypertension. He is prescribed nitroglycerin tablets as needed for chest pain and lisinopril for his hypertension. John has noticed that his chest pain is occurring with increasing frequency and less activity is required to initiate the symptoms; however, the pain subsides quickly with rest and one or two nitroglycerin tablets.#N#John is awakened from sleep with chest pain and shortness of breath. The pain is much more severe than his usual anginal pain and radiates to the jaw and the left arm. He experienced some nausea and became diaphoretic and pale. Upon admission to the local emergency department, he was noted to have significant ST-segment elevation on a 12-lead electrocardiogram (ECG).#N#Discussion Questions:#N#1. What diagnosis is consistent with John’s history and physical exam?#N#2. Please differentiate between a STEMI and Non-STEMI.#N#3. What are the pathophysiological findings specifying an MI?#N#4.What are the differences between angina, silent ischemia, and myocardial ischemia?#N#5.Provide a description of the three factors associated with Sudden Cardiac Death.#N#6.What are the possible complications post-MI might the NP be aware of when caring for John?
What is the difference between angina and silent ischemia?
CASE STUDY 3. Angina is defined as the chest pain occurring due to ischemia of the cardiac muscles. Silent ischemia is also the inadequate supply of oxygen to the heart muscles but does not cause.