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Acute Coronary Syndrome (Heart Attack) - Unstable Angina vs NSTEMI vs STEMI | With ECGs
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acute coronary syndrome is a spectrum of conditions resulting from the formation of a thrombus in the coronary arteries following rupture of an atherosclerotic plaque they include unstable angina non-st elevation myocardial infarction and st elevation myocardial infarction the heart is supplied with blood via the coronary arteries which are connected to the aorta near the aortic valve when the heart is in diastole the backflow of blood to the aortic valve leads to the coronary arteries being perfused there are two main coronary arteries the left and the right the left coronary artery divides into the left anterior descending artery which supplies the left ventricle and interventricular septum as well as some of the right ventricle then there is the left marginal artery that supplies the left ventricle and the circumflex artery that supplies the left atrium and part of the left ventricle the right coronary artery supplies the right atrium including the sa and av nodes and the right ventricle over time these arteries can become atherosclerotic which is the formation of fatty plaques on the walls atherosclerotic plaques have a fibrous cap that contains cell debris lipids and inflammatory cells that all together make up a thrombogenic substance in some cases these plaques develop over years and extend far enough into the lumen of the vessel to narrow it which can lead to ischemia if the demand increases such as during exercise this is what happens in stable angina a slow change over time however in acute coronary syndrome these plaques rupture then the thrombogenic material is exposed to blood leading to formation of a clot which causes a very sudden reduction in blood flow to the cardiac cells and therefore ischemia depending on the severity of the reduction of flow we can see the different spectrums of acute coronary syndrome in unstable angina the myocytes are ischemic but are not yet necrosed and no cell death has occurred in non-st elevation myocardial infarction and st elevation myocardial infarction there is death of some of the myocytes the non-st and st portion of the name refers to the elevation of the st segment in the ecg the reason this occurs is because in stemi there is typically a complete occlusion of the coronary artery and therefore transmural necrosis meaning the death of the cardiac myocytes extends across the entire thickness of the wall whereas in n-stemi this only extends through a portion of the wall typically risk factors are divided into modifiable and non-modifiable modifiable ones include smoking hypertension diabetes and hyperlipidemia obesity and drug use including cocaine non-modifiable ones include age male sex family history and ethnicity clinically each one can present similarly symptoms include chest pain or discomfort often described as heavy or dull with radiation to the jaw arm or shoulder that comes on at rest upper back pain and epigastric pain or indigestion-like symptoms are also possible symptoms of acute coronary syndrome these were previously termed atypical symptoms patients can also complain of lightheadedness nausea or vomiting sudden heavy sweating known as diaphoresis palpitations and dyspnea or shortness of breath however bear in mind that people may present without chest pain this happens more commonly in women than in males and therefore the presentation may be more subtle and is more commonly missed this is also true for older patients and patients with diabetes an ecg is a key part of the diagnosis as the name suggests for diagnosis of stemi there must be elevations in the st segment specifically in two contiguous leads of at least one millimeter in height except in leads v2 and v3 where it must be 1.5 millimeters in women or two millimeters in men a new left bundle branch block is also included in criteria for stemi each lead corresponds to different parts of the hat and can suggest the location of the event leads v1 to v4 are known as the anterior or septal leads and roughly represent the left anterior descending artery leads 1 avl v5 and v6 are known as lateral leads which represent the left circumflex artery and part of the left anterior descending artery leads 2 3 and avf are the inferior leads showing part of the right coronary artery or the left circumflex leads of v7 v8 and v9 are required to see the posterior aspect of the heart there are typically reciprocal st depressions in opposite leads to the occlusion which may be the only findings in posterior stemi pathological key waves may also develop in large infarctions in non-st elevation acute coronary syndrome which includes both n-stemi and unstable angina the hallmark is st depressions and t-wave inversions in contrast to stemi these changes do not necessarily represent the affected vessels q-waves are typically not present and this also coincides with the fact that n stemies are smaller in factions than stemis generally t wave inversions alongside st segment changes indicate ongoing ischemia however isolated t-wave inversions are post-ischemic meaning they occur after the ischemic episode also remember that the st segment is especially challenging in paste or known left bundle branch blocks which is where criteria such as the scabosa criteria are used in rare cases the ecgs can be normal the primary lab investigation is use of cardiac troponin eye assays a protein released from the cardiac myocytes upon cell death exact values vary by lab but generally values above the 99th percentile are considered abnormal levels generally rise from 2 hours after the onset of chest pain and peak at around 12 to 48 hours they can remain elevated for between 4 and 15 days coronary angiography is the definitive investigation and provides visualization of the affected coronaries especially prior to primary percutaneous coronary intervention a chest x-ray is not directly involved in the workup but it can reveal pomona edema or cardiomegaly but may also reveal other causes of chest pain echocardiography isn't done routinely acutely but can be done to evaluate secondary complications such as disruption to valves or a tamponade general management involves analgesia which is often morphine oxygen therapy as required to maintain saturations above 94 provided there is not another appropriate range such as in chronic obstructive pulmonary disease the use of nitrates most commonly glycerol trinitrate sublingually or via intravenous infusion aspirin is also used in most cases this is remembered with the pneumonic mona antiometics such as metaclopramide may also be added patients with stemi undergo reperfusion therapy as early as possible if the onset of chest pain was within 12 hours high risk non-st elevation acute coronary syndrome patients should also be considered primary percutaneous coronary intervention which involves inserting a balloon and stent into the clogged coronary artery to reintroduce blood flow is preferred if it can be performed within 90 minutes of medical contact while fibrinolytic therapy is preferred if this is not feasible this involves the use of tissue plasminogen activators like altiplays to tenecta plays or retiplase further medical therapy for confirmed stemi and non-st elevation acute coronary syndrome includes additional anti-platelets like the p2 y12 inhibitors ticagrelor or clopidogrel and anticoagulation such as unfractionated heparin intravenously or low molecular weight heparin subcutaneously secondary prevention medications include statins as not only do they help prevent dyslipidemia but they also provide plaque stabilization an ace inhibitor or angiotensin receptor blocker are also included and beta blockers are used if there is evidence of left ventricular systolic dysfunction
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