0:00 acute coronary syndrome is a spectrum of
0:03 conditions resulting from the formation
0:05 of a thrombus in the coronary arteries
0:08 following rupture of an atherosclerotic
0:10 plaque
0:12 they include unstable angina
0:14 non-st elevation myocardial infarction
0:17 and st elevation myocardial infarction
0:21 the heart is supplied with blood via the
0:24 coronary arteries which are connected to
0:26 the aorta near the aortic valve
0:29 when the heart is in diastole the
0:31 backflow of blood to the aortic valve
0:34 leads to the coronary arteries being
0:36 perfused
0:37 there are two main coronary arteries the
0:40 left and the right
0:42 the left coronary artery divides into
0:44 the left anterior descending artery
0:47 which supplies the left ventricle and
0:49 interventricular septum as well as some
0:52 of the right ventricle
0:53 then there is the left marginal artery
0:56 that supplies the left ventricle and the
0:58 circumflex artery that supplies the left
1:01 atrium and part of the left ventricle
1:04 the right coronary artery supplies the
1:06 right atrium including the sa and av
1:09 nodes and the right ventricle
1:12 over time these arteries can become
1:15 atherosclerotic
1:16 which is the formation of fatty plaques
1:19 on the walls
1:20 atherosclerotic plaques have a fibrous
1:23 cap that contains cell debris lipids and
1:26 inflammatory cells that all together
1:29 make up a thrombogenic substance
1:32 in some cases these plaques develop over
1:35 years and extend far enough into the
1:37 lumen of the vessel to narrow it which
1:40 can lead to ischemia if the demand
1:42 increases such as during exercise
1:46 this is what happens in stable angina a
1:48 slow change over time
1:51 however in acute coronary syndrome these
1:54 plaques rupture then the thrombogenic
1:56 material is exposed to blood leading to
1:59 formation of a clot which causes a very
2:02 sudden reduction in blood flow to the
2:04 cardiac cells and therefore ischemia
2:08 depending on the severity of the
2:09 reduction of flow we can see the
2:12 different spectrums of acute coronary
2:14 syndrome
2:15 in unstable angina the myocytes are
2:18 ischemic but are not yet necrosed and no
2:21 cell death has occurred
2:23 in non-st elevation myocardial
2:25 infarction and st elevation myocardial
2:28 infarction there is death of some of the
2:30 myocytes
2:32 the non-st and st portion of the name
2:35 refers to the elevation of the st
2:37 segment in the ecg the reason this
2:40 occurs is because in stemi there is
2:43 typically a complete occlusion of the
2:45 coronary artery and therefore transmural
2:48 necrosis meaning the death of the
2:50 cardiac myocytes extends across the
2:53 entire thickness of the wall whereas in
2:56 n-stemi this only extends through a
2:58 portion of the wall typically
3:01 risk factors are divided into modifiable
3:03 and non-modifiable
3:06 modifiable ones include smoking
3:08 hypertension diabetes and hyperlipidemia
3:12 obesity and drug use including cocaine
3:16 non-modifiable ones include age male sex
3:20 family history and ethnicity
3:23 clinically each one can present
3:25 similarly
3:26 symptoms include chest pain or
3:28 discomfort often described as heavy or
3:31 dull with radiation to the jaw arm or
3:34 shoulder that comes on at rest
3:37 upper back pain and epigastric pain or
3:40 indigestion-like symptoms are also
3:42 possible symptoms of acute coronary
3:44 syndrome these were previously termed
3:47 atypical symptoms
3:49 patients can also complain of
3:51 lightheadedness nausea or vomiting
3:54 sudden heavy sweating known as
3:55 diaphoresis palpitations and dyspnea or
3:59 shortness of breath however bear in mind
4:02 that people may present without chest
4:04 pain this happens more commonly in women
4:07 than in males and therefore the
4:09 presentation may be more subtle and is
4:11 more commonly missed this is also true
4:14 for older patients and patients with
4:16 diabetes
4:17 an ecg is a key part of the diagnosis
4:21 as the name suggests for diagnosis of
4:24 stemi there must be elevations in the st
4:27 segment specifically in two contiguous
4:30 leads of at least one millimeter in
4:32 height
4:33 except in leads v2 and v3 where it must
4:36 be 1.5 millimeters in women or two
4:39 millimeters in men a new left bundle
4:42 branch block is also included in
4:44 criteria for stemi
4:46 each lead corresponds to different parts
4:49 of the hat and can suggest the location
4:51 of the event
4:53 leads v1 to v4 are known as the anterior
4:56 or septal leads and roughly represent
4:59 the left anterior descending artery
5:02 leads 1 avl v5 and v6 are known as
5:06 lateral leads which represent the left
5:09 circumflex artery and part of the left
5:11 anterior descending artery leads 2 3 and
5:15 avf are the inferior leads
5:18 showing part of the right coronary
5:20 artery or the left circumflex
5:23 leads of v7 v8 and v9 are required to
5:27 see the posterior aspect of the heart
5:30 there are typically reciprocal st
5:32 depressions in opposite leads to the
5:34 occlusion which may be the only findings
5:37 in posterior stemi pathological key
5:40 waves may also develop in large
5:42 infarctions
5:43 in non-st elevation acute coronary
5:46 syndrome which includes both n-stemi and
5:50 unstable angina the hallmark is st
5:53 depressions and t-wave inversions
5:56 in contrast to stemi these changes do
5:59 not necessarily represent the affected
6:01 vessels
6:03 q-waves are typically not present and
6:05 this also coincides with the fact that n
6:08 stemies are smaller in factions than
6:10 stemis generally
6:12 t wave inversions alongside st segment
6:15 changes indicate ongoing ischemia
6:18 however isolated t-wave inversions are
6:21 post-ischemic meaning they occur after
6:24 the ischemic episode
6:26 also remember that the st segment is
6:28 especially challenging in paste or known
6:31 left bundle branch blocks which is where
6:34 criteria such as the scabosa criteria
6:36 are used
6:37 in rare cases the ecgs can be normal
6:41 the primary lab investigation is use of
6:44 cardiac troponin eye assays a protein
6:47 released from the cardiac myocytes upon
6:50 cell death
6:51 exact values vary by lab but generally
6:54 values above the 99th percentile are
6:57 considered abnormal
6:59 levels generally rise from 2 hours after
7:02 the onset of chest pain and peak at
7:04 around 12 to 48 hours they can remain
7:07 elevated for between 4 and 15 days
7:11 coronary angiography is the definitive
7:13 investigation and provides visualization
7:16 of the affected coronaries especially
7:18 prior to primary percutaneous coronary
7:21 intervention a chest x-ray is not
7:24 directly involved in the workup but it
7:26 can reveal pomona edema or cardiomegaly
7:29 but may also reveal other causes of
7:31 chest pain
7:32 echocardiography isn't done routinely
7:35 acutely but can be done to evaluate
7:37 secondary complications such as
7:39 disruption to valves or a tamponade
7:43 general management involves analgesia
7:45 which is often morphine oxygen therapy
7:48 as required to maintain saturations
7:51 above 94
7:52 provided there is not another
7:54 appropriate range such as in chronic
7:56 obstructive pulmonary disease the use of
7:59 nitrates most commonly glycerol
8:01 trinitrate sublingually or via
8:04 intravenous infusion
8:05 aspirin is also used in most cases this
8:08 is remembered with the pneumonic mona
8:11 antiometics such as metaclopramide may
8:14 also be added
8:15 patients with stemi undergo reperfusion
8:18 therapy as early as possible if the
8:20 onset of chest pain was within 12 hours
8:23 high risk non-st elevation acute
8:25 coronary syndrome patients should also
8:27 be considered
8:29 primary percutaneous coronary
8:31 intervention which involves inserting a
8:33 balloon and stent into the clogged
8:35 coronary artery to reintroduce blood
8:37 flow is preferred if it can be performed
8:40 within 90 minutes of medical contact
8:43 while fibrinolytic therapy is preferred
8:46 if this is not feasible
8:48 this involves the use of tissue
8:50 plasminogen activators like altiplays to
8:53 tenecta plays or retiplase
8:55 further medical therapy for confirmed
8:57 stemi and non-st elevation acute
9:00 coronary syndrome includes additional
9:02 anti-platelets like the p2 y12
9:05 inhibitors ticagrelor or clopidogrel and
9:09 anticoagulation such as unfractionated
9:11 heparin intravenously or low molecular
9:14 weight heparin subcutaneously
9:17 secondary prevention medications include
9:19 statins as not only do they help prevent
9:22 dyslipidemia but they also provide
9:24 plaque stabilization
9:26 an ace inhibitor or angiotensin receptor
9:29 blocker are also included and beta
9:32 blockers are used if there is evidence
9:34 of left ventricular systolic dysfunction
Chrome Extension