What is acute myocardial infarction?
It is part of a spectrum of conditions that result from myocardial ischemia known as an acute coronary syndrome. Get more details on acute coronary syndrome here. Acute MI includes both non-ST segment elevation myocardial infarction in short NSTEMI and ST-segment elevation myocardial infarction - STEMI. Reduced O2 supply to the heart.
Which medications are used in the treatment of acute myocardial infarction (MI)?
The dose of aspirin for acute MI is 160-325 mg, chewed or swallowed as soon as possible after symptom onset. This dose should be continued for several days, after which a maintenance dose of 75-325 mg daily should be taken indefinitely. [ 14] Heparin.
What is the mortality and morbidity of acute myocardial infarction (MI)?
MI results in death for 300,000 to 400,000 people (see also Cardiac Arrest ). Acute myocardial infarction (MI), along with unstable angina, is considered an acute coronary syndrome. Acute MI includes both non ST segment elevation myocardial infarction (NSTEMI) and ST segment elevation myocardial infarction (STEMI).
What are the different types of myocardial infarction?
Based on the causative mechanism, myocardial infarction can be classified into five types: Type 1: This is the commonest type. It occurs due to a primary coronary event such as atherosclerotic plaque rupture, fissuring, coronary dissection or erosion. It is also referred to as a spontaneous myocardial infarction.
What is the standard treatment for an acute myocardial infarction?
The standard regimen is an initial bolus of 5000 units, followed by an infusion of 1000 units per hour adjusted after 6 hours for APTT. ACE inhibitors reduce the mortality of myocardial infarction and this benefit is seen within the first 30 days.
What are the treatment options for myocardial infarction?
The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of 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 correct order of Mona?
MONA is a mnemonic that stands for: Morphine, Oxygen, Nitrates, and Aspirin. These are the four primary interventions that are performed when treating a patient with Heart Attack/Myocardial Infarction (MI).
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).
How is AMI diagnosed?
Diagnosis is easy and based on simple principals of good history, physical examination, early and complete 12 lead electrocardiogram and use of echocardiography which should be available in the emergency triage area. Subsequently biomarkers are also available for documentation and risk stratification.
What is a type 5 myocardial infarction?
Coronary artery bypass grafting (CABG)–related MI is termed type 5 MI. Coronary procedure–related MI ≤48 hours after the index procedure is arbitrarily defined by an elevation of cTn values >5 times for type 4a MI and >10 times for type 5 MI of the 99th percentile URL in patients with normal baseline values.
What is a Type 3 myocardial infarction?
The type 3 myocardial infarction was defined according to the Universal definition of myocardial infarction, that is, cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new left bundle branch block, but death occurring before blood samples could be obtained, before ...
Which myocardial infarction type is most severe?
An ST-elevation myocardial infarction (STEMI) is a type of heart attack that is more serious and has a greater risk of serious complications and death.
Do you give aspirin or nitroglycerin first?
This study hypothesizes that the order of administering these drugs is important, and giving aspirin several minutes before nitroglycerin can lead to a better patient outcome and theoretically can help in re-vascularization.
What are the 3 cardiac enzymes?
Cardiac enzymes ― also known as cardiac biomarkers ― include myoglobin, troponin and creatine kinase.
What is Mona in myocardial infarction?
The mnemonic, MONA, which stands for morphine, oxygen, nitroglycerin, and aspirin, is used to recall the initial management of patients with chest pain (ie, suspected acute coronary syndrome).
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.
What are the biomarkers used for acute myocardial infarction?
Cardiac biomarkers are useful in the diagnosis of acute myocardial infarction, specifically non-ST-elevation MI. Troponin is the most specific lab test and has two isoforms, I and T. Troponins peak at 12 hours and persist for seven days. Creatinine kinase MB is also specific to the myocardium. It peaks at ten hours; however, it normalizes within two to three days. LDH peaks over 72 hours and normalizes over ten to 14 hours. In clinical practice, LDH is not used to diagnose acute MI. Finally, MB has very low specificity for the myocardium and is not used clinically; it quickly rises and normalizes. High-sensitivity troponin has recently been approved for use in the United States after having been heavily studied and utilized in Europe. Although it is more sensitive than conventional troponin, it is also less specific. Thus, potential challenges include numerous false-positive interpretations. [3]
How long does it take for myocardial infarction to change?
The histology of myocardial infarction changes over the time-course of the disease. At time 0, there are no microscopic histologic changes. Under light microscopy, within 0.5 to 4 hours, waviness of fibers at the periphery of the tissue is seen. Glycogen is depleted. At 4 to 12 hours, the myocardium undergoes coagulation necrosis and edema. At 12 to 24 hours, the gross specimen becomes dark and mottled. There are contraction band necrosis and neutrophil predominance on histopathology. At 1 to 3 days, there is a loss of nuclei, and at 3 to 7 days, macrophages appear to remove apoptosis cells. At 7 to10 days, granulation tissue appears. At 10 days and onward, there is collagen one deposition. After 2 months, the myocardium is scarred.
What causes decreased blood flow in myocardial infarction?
Decreased coronary blood flow is multifactorial. Atherosclerotic plaques classically rupture and lead to thrombosis, contributing to acutely decreased blood flow in the coronary. Other etiologies of decreased oxygenation/myocardial ischemia include coronary artery embolism, which accounts for 2.9% of patients, cocaine-induced ischemia, coronary dissection, and coronary vasospasm. [4][5]
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 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.
What happens to the thrombus during an atherosclerotic rupture?
Atherosclerotic rupture leads to an inflammatory cascade of monocytes and macrophages, thrombus formation, and platelet aggregation. This leads to decreased oxygen delivery through the coronary artery resulting in decreased oxygenation of the myocardium. The inability to produce ATP in the mitochondria leads to the ischemic cascade, and therefore apoptosis (cell death) of the endocardium or myocardial infarction.
What is an AMI episode?
An AMI episode is defined by the admission of an eligible Medicare fee-for-service beneficiary to a hospital paid under the Inpatient Prospective Payment System (IPPS) that eventually results in a discharge paid under MS-DRG 280 (Acute myocardial infarction, discharged alive with MCC), MS-DRG 281 (Acute myocardial infarction, discharged alive with CC), MS-DRG 282 (Acute myocardial infarction, discharged alive without CC/MCC). In addition to AMI MS-DRGs, an MS-DRG for percutaneous catheter insertion (PCI) which includes an AMI ICD-10-CM diagnosis code in any diagnosis (i.e. 1-25) position on the IPPS claim will initiate an AMI Model episode. The following PCI MS-DRGs are eligible to initiate an AMI episode, as long as the criterion for AMI diagnosis code as specified previously is met: MS-DRG 246 (Percutaneous cardiovascular procedures with drug-eluting stent with MCC or 4+
What is episode of care?
The episode of care begins with an admission to a participant hospital of a beneficiary who is ultimately discharged under an AMI MS-DRG 280-282, or who is discharged under PCI MS-DRGs 246-251 with AMI ICD-10-CM diagnosis code in any diagnosis (i.e. 1-25) position on the IPPS claim and ends 90 days post-discharge in order to cover an extended period of recovery for beneficiaries. The episode includes all related items and services paid under Medicare Part A and Part B for all Medicare fee-for-service beneficiaries, with the exception of certain exclusions. The following categories of items and services are included in the episodes: physicians' services; inpatient hospital services (including hospital readmissions); inpatient psychiatric facility (IPF) services; long-term care hospital (LTCH) services; inpatient rehabilitation facility (IRF) services; skilled nursing facility (SNF) services; home health agency (HHA) services; hospital outpatient services; outpatient therapy services; clinical laboratory services; durable medical equipment (DME); Part B drugs; hospice; and some per beneficiary per month (PBPM) care management payments under models tested under Section 1115A of the Social Security Act. Unrelated services are excluded from the episode. Unrelated services are for acute clinical conditions not arising from existing episode-related chronic clinical conditions or complications of the AMI treatment; and chronic conditions that are generally not affected by treatment during hospitalization for the AMI or care during the 90-day post-discharge period. The complete list of exclusions can be found on our website at: https://innovation.cms.gov/initiatives/epm, accompanied by the list of excluded MS-DRGs for readmissions during the episode and ICD-10-CM diagnosis codes for Part B services.
How to classify an infarct as STEMI?
Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the ECG. Volume of myocardium destroyed can be roughly estimated by the extent and duration of CK elevation or by peak levels of more commonly measured cardiac troponins.
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 is the treatment for STEMI?
For patients with STEMI: Immediate percutaneous coronary intervention or fibrinolytics
What is RV dysfunction?
RV dysfunction should be considered in any patient who has inferoposterior infarction and elevated jugular venous pressure with hypo tension or shock.
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).
What is ST-T in a nontransmural infarct?
Nontransmural (including subendocardial) infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities. Subendocardial infarcts usually involve the inner one third of myocardium, where wall tension is highest and myocardial blood flow is most vulnerable to circulatory changes. These infarcts may follow prolonged hypotension.
When to do angiography for NSTEMI?
Patients with uncomplicated NSTEMI whose symptoms have resolved typically undergo angiography within the first 24 to 48 hours of hospitalization to detect lesions that may require treatment.