Differential diagnosis
- Cardiovascular: stable angina, another form of ACS (unstable angina or NSTEMI), acute pericarditis, myocarditis, aortic stenosis, aortic dissection, pulmonary embolism.
- Respiratory: pneumonia, pneumothorax.
- Gastrointestinal: oesophageal spasm, gastro-oesophageal reflux disease, acute gastritis, cholecystitis, acute pancreatitis.
What is the diagnostic test for myocardial infarction?
You may also undergo:
- Chest X-ray. An X-ray image of your chest allows your doctor to check the size of your heart and its blood vessels and to look for fluid in your lungs.
- Echocardiogram. ...
- Coronary catheterization (angiogram). ...
- Exercise stress test. ...
- Cardiac computerized tomography (CT) or magnetic resonance imaging (MRI). ...
Which cardiac marker rises first in 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. Explore more on it. Subsequently, one may also ask, which enzymes are elevated in myocardial infarction?
Which enzymes are elevated in myocardial infarction?
- Myoglobin is found in cardiac and skeletal muscle.
- It is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as2 hours after an acute myocardial infarction.
- Myoglobin has high sensitivity but poor specificity. It may be useful for the early detection of myocardial infarction.
Is myocardial infarction life threatening?
The interrupted blood flow can damage or destroy part of the heart muscle. A heart attack, also called a myocardial infarction, can be fatal, but treatment has improved dramatically over the years. It's crucial to call 911 or emergency medical help if you think you might be having a heart attack.
What are the 4 types of myocardial infarction?
ST segment elevation myocardial infarction (STEMI) non-ST segment elevation myocardial infarction (NSTEMI) coronary spasm, or unstable angina.
What is the best nursing diagnosis for myocardial infarction?
End of dialog window. Nursing Diagnosis: Risk for Excess Fluid Volume due to diminished renal perfusion secondary to myocardial infarction. Desired Outcomes: The patient will be able to achieve body fluid equilibrium as displayed by blood pressure within normal range.
What are 3 common complications of a myocardial infarction?
Complications of MI include arrhythmic, mechanical, and inflammatory (early pericarditis and post-MI syndrome) sequelae, as well as left ventricular mural thrombus (LVMT) (see the following image).
What are examples of nursing diagnosis?
According to NANDA, some of the most common nursing diagnoses include pain, risk of infection, constipation, and body temperature imbalance.
What is Nanda approved nursing diagnosis?
A nursing diagnosis is defined by NANDA International (2013) as a clinical judgment concerning a human response to health conditions/life processes, or vulnerability for that response, by an individual, family, group, or community.
What are the main causes of myocardial infarction?
Most myocardial infarctions are due to underlying coronary artery disease, the leading cause of death in the United States. With coronary artery occlusion, the myocardium is deprived of oxygen. Prolonged deprivation of oxygen supply to the myocardium can lead to myocardial cell death and necrosis.
What tests are done for myocardial infarction?
TestsElectrocardiogram (ECG or EKG). This first test done to diagnose a heart attack records electrical signals as they travel through the heart. ... Blood tests. ... Chest X-ray. ... Echocardiogram. ... Coronary catheterization (angiogram). ... Cardiac CT or MRI .
What are the signs symptoms and complications of MI?
SymptomsChest pain that may feel like pressure, tightness, pain, squeezing or aching.Pain or discomfort that spreads to the shoulder, arm, back, neck, jaw, teeth or sometimes the upper belly.Cold sweat.Fatigue.Heartburn or indigestion.Lightheadedness or sudden dizziness.Nausea.Shortness of breath.
Is decreased cardiac output a nursing diagnosis?
Decreased Cardiac Output is a nursing diagnosis that refers to the cardiac output level below 4 liters per minute. The heart pumps blood to supply nutrients including oxygen to meet the body's metabolic demands.
Which is the priority management of a patient with MI?
Although the immediate priority in managing acute myocardial infarction is thrombolysis and reperfusion of the myocardium, a variety of other drug therapies such as heparin, β-adrenoceptor blockers, magnesium and insulin might also be considered in the early hours.
What is the diagnostic test for myocardial infarction?
Electrocardiogram (ECG or EKG). This first test done to diagnose a heart attack records electrical signals as they travel through the heart. Sticky patches (electrodes) are attached to the chest and sometimes the arms and legs. Signals are recorded as waves displayed on a monitor or printed on paper.
Which of the following are nursing interventions for chest pain?
Nursing ManagementManage chest pain.Bed rest.Provide oxygen.Administer aspirin and nitroglycerin.Place patient with head of the bed elevated at 45 degrees.Make patient comfortable.Hook up to monitor.Check vitals.More items...•
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.
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.
What is the red area on a ventricular endocardial activation map?
This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. Earliest activation is recorded in red; late activation shows as blue to magenta. Fragmented low-amplitude diastolic local electrocardiograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
What is the mottled appearance of the left ventricle?
Healing myocardial infarction, lateral left ventricle. In this heart, there is a variegated or mottled appearance to the lateral left ventricle (left). This infarct began 19 days prior to death.
What is the long axis view of the left ventricle?
Parasternal long-axis view of the left ventricle demonstrates a large inferobasal aneurysm. Note the wide neck and base of the aneurysm.
Why are younger patients overrepresented in MI cases?
Younger patients are overly represented in cases of missed MI. Most likely this is because of the inherent bias that MI is a disease of middle-aged and older individuals. Each patient with chest symptoms should be approached as an individual who could have the disease.
Is there necrosis in myocardium?
There is a large area of necrosis with hypereosinophilia of myocytes, with a rim of viable myocardium at the very bottom. At the border, there is chronic inflammation with early granulation tissue, with ingrowth of endothelial cells. Healing myocardial infarct.
What is the diagnosis of myocardial infarction?
At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings. A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department.
How long does it take for a myocardial infarct to be identified?
On gross examination, the infarct is not identifiable within the first 12 hours.
How many components are needed for a myocardial infarction?
The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-hour period.
What leads are used for right ventricular infarction?
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. The 12 lead ECG is used to classify patients into one of three groups: those with a so-called non-diagnostic or normal ECG.
What is the color of the 12 lead electrocardiogram?
12-lead electrocardiogram showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal changes (blue) in the inferior leads, indicative of an anterior wall myocardial infarction.
What are the changes in the cytoplasm of an infarcted cell?
Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so-called wavy fibers. Subsequently, the myocyte cytoplasm becomes more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the cell nucleus . The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, who phagocytose ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous ( collagenous) scar (which are typical steps in wound healing ). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells.
Why is an infarcted area revealed as an unstained pale zone?
Because dehydrogenases are depleted in the area of ischemic necrosis ( i.e., they leak out through the damaged cell membranes), an infarcted area is revealed as an unstained pale zone. Instead of a triphenyltetrazolium chloride dye, a LDH (lactate dehydrogenase) dye can also be used to visualize an area of necrosis.
What are the non-modifiable risk factors for myocardial infarction?
Some non-modifiable risk factors for myocardial infarction include advanced age, male gender (males tend to have myocardial infarction earlier in life), genetics (there is an increased risk of MI if a first-degree relative has a history of cardiovascular events before the age of 50). [6][8] The role of genetic loci that increase the risk for MI is under active investigation. [9][10]
What is the cause of myocardial infarction?
Myocardial infarction (MI), colloquially known as "heart attack," is caused by decreased or complete cessation of blood flow to a portion of the myocardium. Myocardial infarction may be"silent," and go undetected, or it could be a catastrophic event leading to hemodynamic deterioration and sudden death. Most myocardial infarctions are due to underlying coronary artery disease, the leading cause of death in the United States. With coronary artery occlusion, the myocardium is deprived of oxygen. Prolonged deprivation of oxygen supply to the myocardium can lead to myocardial cell death and necrosis. Patients can present with chest discomfort or pressure that can radiate to the neck, jaw, shoulder, or arm. In addition to the history and physical exam, myocardial ischemia may be associated with ECG changes and elevated biochemical markers such as cardiac troponins. This activity describes the pathophysiology, evaluation, and management of myocardial infarction and highlights the role of the interprofessional team in improving care for affected patients.
What is the best way to reduce myocardial oxygen consumption?
Beta-blockers:This group of drugs reduces myocardial oxygen consumption by lowering heart rate, blood pressure, and myocardial contractility. They block beta receptors in the body, including the heart, and reduce the effects of circulating catecholamines. Beta-blockers should not be used in suspected coronary vasospasm.
What imaging techniques are used to assess myocardial perfusion?
Different imaging techniques are used to assess myocardial perfusion, myocardial vi ability, myocardial thickness, thickening and motion, and the effect of myocyte loss on the kinetics of para-magnetic or radio-opaque contrast agents indicating myocardial fibrosis or scars.[14] Some imaging modalities that can be used are echocardiography, radionuclide imaging, and cardiac magnetic resonance imaging (cardiac MRI). Regional wall motion abnormalities induced by ischemia can be detected by echocardiography almost immediately after the onset of ischemia when greater than 20% transmural myocardial thickness is affected. Cardiac MRI provides an accurate assessment of myocardial structure and function. [14]
What are the risk factors for MI?
Other risk factors include a moderately high level of plasma homocysteine, which is an independent risk factor of MI. Elevated plasma homocysteine is potentially modifiable and can be treated with folic acid, vitamin B6, and vitamin B12. [7]
How old is the average person with MI?
The ARIC study also found that the average age at first MI is 65.6 years for males and 72.0 years for females. In the past decades, several studies have shown a declining incidence of MI in the United States. [12]
What is the cause of a heart attack?
Myocardial infarction (MI), colloquially known as “heart attack,” is caused by decreased or complete cessation of blood flow to a portion of the myocardium. Myocardial infarction may be “silent” and go undetected, or it could be a catastrophic event leading to hemodynamic deterioration and sudden death.[1] Most myocardial infarctions are due to underlying coronary artery disease, the leading cause of death in the United States. With coronary artery occlusion, the myocardium is deprived of oxygen. Prolonged deprivation of oxygen supply to the myocardium can lead to myocardial cell death and necrosis.[2] Patients can present with chest discomfort or pressure that can radiate to the neck, jaw, shoulder, or arm. In addition to the history and physical exam, myocardial ischemia may be associated with ECG changes and elevated biochemical markers such as cardiac troponins. [3][4]
What are the symptoms of acute myocardial infarction?
Symptoms of acute myocardial infarction and ischemia. Angina pectoris is the hallmark of myocardial ischemia. It is described as a retrosternal chest discomfort (pressure, heaviness, squeezing, burning or choking sensation). It is commonly accompanied by radiation of pain to the left shoulder and/or arm.
What is the name of the plaque that forms during an acute myocardial infarction?
Figure 1. Acute myocardial infarction is usually initiated by rupture or erosion of a vulnerable (unstable) atherosclerotic coronary plaque.
What is type 3 in cardiac biomarker?
Type 3: Myocardial infarction resulting in death when biomarker values are unavailable – Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in rare cases cardiac biomarkers were not collected.
How long does myocardial infarction pain last?
The pain lasts longer than 20 minutes in myocardial infarction. Shorter durations are usually episodes of unstable angina. As compared with stable angina pectoris, the symptoms during acute coronary syndromes are more pronounced, present at rest, and do not respond to nitroglycerin.
How many troponin samples are needed for myocardial infarction?
A diagnosis of myocardial infarction requires at least two troponin samples. One of these must be elevated (above the upper reference limit) and there should be a change between the two samples, such that troponin levels either rise or fall between the samples. This pattern (with falling or rising troponin) is required to differentiate acutely elevated troponin levels (i.e acute myocardial infarction) from chronically elevated troponin levels (e.g chronic kidney disease, which leads to reduced renal elimination of troponins from blood).
Is myocardial necrosis a firm evidence of myocardial necrosis?
Elevated levels of cardiac troponins is firm evidence of myocardial necrosis (i.e infarction). This is explained by the fact that there is no (or very little) turnover of myocardial cells and therefore myocardial troponins should not be detected in the blood.
Overview
Histopathology
Histopathological examination of the heart may reveal infarction at autopsy. Gross examination may reveal signs of myocardial infarction.
• A one-week-old myocardial infarction of the posterior left ventricle, with focal rupture, in fresh state (left) and after formalin fixation (right). The infarcted area is pale whereas the rupture is hemorrhagic (dark red).
Diagnostic criteria
According to the WHO criteria as revised in 2000, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.
Previous WHO criteria formulated in 1979 put less emphasis on cardiac biomarkers; according to these, a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of th…
Physical examination
The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can become irregular.
If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of t…
Electrocardiogram
The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. A serial ECG may be used to follow rapid changes in time. The standard 12 lead ECG 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…
Cardiac markers
Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Now, the markers most widely used in detection of MI are MB subtype of the enzyme creatine kinase and cardiac troponins T and I as they are more specific for myocardial injury. The cardiac troponins T and I which are released within 4–6 hours of an attac…
Angiography
In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (typically the radial or femoral artery ) and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter and a sequence of x-rays (fluoroscopy) is performed. Obstructed or narrowed …
See also