Yale 20: Acute Coronary Syndromes

December 20, 2023

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00:03Hello everyone.
00:04My name is Sonia and I'm a P GY3
00:06Internal Medicine resident here at Yale.
00:08This is the Yale 20 video on acute
00:11coronary syndrome and chest pain.
00:12I developed this video with the
00:14help of Doctor Lawrence Young,
00:15who's a professor here in Cardiology.
00:18Here's a quick outline on
00:19what we're going to cover.
00:20First, we can talk about the
00:22anatomy and pathophysiology
00:23of acute coronary syndromes.
00:25Go through a 5 minute bedside assessment,
00:27touch on the diagnosis and work
00:29up as well as treatment.
00:30Learn how to write up the assessment and
00:32plan in your note and then summarize.
00:34Take home points.
00:38Let's briefly review our coronary anatomy.
00:40The left and right coronary
00:42arteries come off of the aorta.
00:44On the left side we have the
00:46left main coronary artery,
00:47which then branches into the left
00:49anterior descending or the LED and the
00:52left circumflex artery or the Cirque.
00:54The LED comes down the intraventricular
00:56septum and gives off multiple diagonal
00:58and septal perforating branches,
01:00which together supply the left atrium,
01:03left ventricle and the
01:05intraventricular septum.
01:06The circumflex wraps posterior laterally
01:08and gives off marginal branches
01:11which supply the apex of the heart.
01:13On the right side,
01:14we have the right coronary artery,
01:15which gives off many important branches
01:18including the SA nodal and the AB nodal
01:21branches which supply the conduction system.
01:23It also provides atrial,
01:25ventricular and marginal branches
01:26to supply the right side.
01:2890% of the time,
01:29the right coronary artery will end
01:31as the posterior descending artery,
01:33which is what determines dominance
01:3610% of the time.
01:37The posterior descending artery
01:38comes off of the left circumflex,
01:40which is a left dominant system.
01:42As you can see here,
01:43the arteries supply multiple different
01:45territories and can lead to a
01:47variety of clinical presentations
01:49of acute coronary syndrome.
01:51Now let's delve into some pathophysiology.
01:53Acute coronary syndrome is a
01:55spectrum of cardiac dysfunction.
01:57On the left,
01:58we have a healthy coronary artery.
02:00Over time,
02:01atherosclerotic plaques can build up,
02:03which creates supply demand mismatch and
02:05reduced oxygen delivery to cardiac myocytes.
02:08In patients,
02:09this manifests as chest pain or angina.
02:12Patients who have angina with
02:14exertion have stable angina,
02:16which is not on the spectrum
02:18of acute coronary syndromes.
02:19Patients who have chest pain or
02:22angina at rest have unstable angina.
02:24These patients are essentially having
02:26ischemia without infarction and thus
02:29they don't have elevated troponin or any St.
02:31elevations on their EKG.
02:32But this does need to be further
02:35monitored and evaluated as it can
02:37progress to either STEMI or end STEMI.
02:42Sometimes this plaque can rupture which
02:44leads to thrombosis where the area
02:46for blood flow is even more narrowed,
02:48worsening any existing
02:50supply demand mismatch.
02:51But as we can see here,
02:52the vessel is not totally occluded,
02:54therefore blood supply is limited furthest
02:57from the vessel or in the sub endocardium.
03:00These patients will have elevated troponins
03:02due to myocardial cell death and on
03:05their EKG they will not have typical St.
03:07elevations but may have other
03:09EKG changes such as St.
03:11depressions or T wave inversions which
03:13we will discuss later in the video.
03:17On the far right we have a totally
03:20occluded coronary artery which
03:21results in cell death the entire
03:23thickness of the myocardium and this
03:25is what produces characteristic St.
03:27elevations on EKG along with
03:29elevated troponin.
03:33Now let's take it to the bedside.
03:35One of the four nurses lets you know that a
03:37patient is having eight out of 10 chest pain.
03:39This is definitely something I would go
03:41evaluate in person. First things first,
03:43you want to make sure your patient is
03:45stable by grabbing a set of vitals.
03:46Then, while I talk to the patient and
03:48assess them and get their chest pain story,
03:50I would ask the nurse to grab an EKG
03:53and be prepared to drop troponins.
03:55Characteristic symptoms of acute
03:57coronary syndromes include chest
03:59pain that's central substernal,
04:01described as heaviness, crushing,
04:03gripping, or pressure.
04:05It's typically worse with exertion and gets
04:07better with rest or sublingual nitroglycerin.
04:11There is kind of new terminology in
04:12the way we're describing chest pain.
04:14Previously we used to use words
04:16like typical and atypical,
04:17but now the guidelines recommend
04:18describing chest pain as cardiac,
04:20possibly cardiac and non cardiac,
04:23and we can see here different descriptors
04:25and the probability of ischemia based
04:27on what symptoms patients are having.
04:29Other symptoms include diaphoresis,
04:32nausea, and often abdominal discomfort,
04:35which can mimic indigestion.
04:37These non characteristic symptoms
04:38of acute coronary syndromes are
04:40thought to occur more frequently
04:41in women and older patients,
04:43and so your degree of suspicion
04:45for acute coronary syndromes needs
04:47to be higher in these groups.
04:48On exam, you're looking for signs or
04:50symptoms of poor cardiac function,
04:52including jugular, venous distension,
04:54leg edema or crackles,
04:56or hypotension.
04:57You may also see hypertension
05:00given high sympathetic drive in the
05:02acute setting and then bradycardia
05:04may be suggestive of RV ischemia
05:06or right ventricular embarked.
05:10The differential for acute
05:11chest pain is pretty broad,
05:13and there's several other can't
05:15misdiagnosis that can masquerade
05:16as acute coronary syndrome,
05:18such as aortic aneurysm or dissection,
05:21pneumothorax, pulmonary embolisms,
05:24or any type of gastric or
05:26esophageal perforation.
05:27Some other key fiscal exam pearls are
05:29that if you have chest pain that's
05:32reproducible on exam or tender to palpation,
05:34should think of MSK etiologies such
05:37as costochondritis or rib fractures.
05:39If you have pain that's positional,
05:41such as pain that improves
05:43with leaning forward,
05:44that's thought to be related to
05:46pericarditis or pericardial inflammation.
05:48And if you have chest pain that's
05:50worsened with deep inspiration,
05:51it's characteristic of pleurisy.
05:55You've thought through your
05:56differential and assess your patient,
05:57and the nurse hands you the EKG.
05:59How do you make a diagnosis?
06:01STEMI is diagnosed based on STEMI criteria,
06:03which is St.
06:05elevations over 1mm and two contiguous
06:08leads except for leads V2 and V3,
06:11which differ by age and gender as seen below.
06:14The key is looking for changes in
06:16contiguous leads as well as St.
06:18depressions in electrically opposite leads
06:20in areas that correlate anatomically.
06:23As we can see here, 2-3 and ADF are inferior.
06:26Leads correlating with RCA
06:28territory V1 is interceptal,
06:31V2 to V4 are anterior leads correlating
06:34with left anterior descending territory,
06:36V5 to V6 are interolateral and
06:38one ADL are high lateral leads.
06:41These all correlate with
06:43left circumflex territory.
06:45In addition to St.
06:46elevations,
06:47you should also look for STEMI
06:49equivalents which can represent
06:50ongoing ischemia such as T wave
06:52abnormalities like hyper acute T waves.
06:54This can happen within minutes of
06:56ischemia and often precedes to St.
06:58changes.
06:58So here's an example where we see hyper
07:02acute T waves and most prominently
07:06V2V3V4 and they're often bulky,
07:09wide at the base and localized
07:10to the anatomic area of infarct.
07:12So this here would be the LED territory.
07:16You can also have biphasic
07:17or deeply inverted T waves,
07:19which are known as Wellens pattern.
07:20So here's an example of Wellens type
07:23A which are the biphasic T waves.
07:25We can see their most prominent
07:28here in B2 and B3.
07:31And here's an example of Wellens type B,
07:33which is deep symmetric inverted
07:35T waves as we can see here in
07:37the precordial leads,
07:38most notably in
07:41B2B3B4B5 and B6.
07:42And this is highly specific for critical
07:45LED stenosis as with Welland's type A.
07:48So to make a diagnosis of Welland's syndrome,
07:50you'll see deep inverted or biphasic T waves,
07:54most commonly in V2 to V3 can also be seen
07:57in V1 to V6 as seen in this EKG minimal St.
08:00elevations less than 1mm.
08:02There's no precordial Q waves,
08:04there's preserved R wave progression.
08:06There's a history of recent angina and
08:08the EKG that you get with the biphasic or
08:11inverted T waves is in a pain Free State
08:13because often when these patients have
08:15chest pain the T waves become upright,
08:17which is known as pseudo normalization.
08:19The management implication is because these
08:22patients typically have critical LED disease,
08:24they do need to be taken for
08:28urgent coronary angiography.
08:30St.
08:30depressions in V1 to V3 with the Pulmona R
08:33wave is also a semi equivalent because this
08:35represents A posterior myocardial infarction.
08:38We can go through an example here.
08:40So on this EKG we most notably see St.
08:43elevations in leads 2-3
08:46AVF as well as V5 and V6.
08:49So this localizes to the inferior
08:51and lateral territories.
08:52Whenever you have inferior St.
08:54elevations, you always have to check to
08:56see if the infarct has spread posteriorly,
08:58which you can see reflected
09:00reciprocally as St.
09:01depressions and V1 to V3.
09:04As we can see here, we do have St.
09:06depressions in these leads.
09:08If we were to turn these leads upside down,
09:09we'd see St.
09:11elevations.
09:11This is consistent overall with an
09:14inferior lateral posterior STEMI.
09:15And again,
09:16this is because anatomically,
09:17the right coronary artery
09:19usually ends and terminates as
09:21the posterior descending artery.
09:23If we wanted to confirm this diagnosis,
09:25we could place posterior leads
09:28which are V7 to V9 and see the St.
09:32elevations with these leads.
09:34Important to note is that to diagnose
09:35a posterior STEMI you only need St.
09:38elevations that are .5mm,
09:39and this is associated with worst
09:42outcomes as it represents a
09:44larger area of infarction.
09:46A new
09:47left bundle branch block
09:48is also a STEMI equivalent.
09:49In these situations we use Scarbosa
09:51criteria, which we will not go
09:53into too much detail about,
09:54but the principle is you're looking
09:56for inappropriate concordance with St.
09:58segments or excessive discordance,
10:01And then other patterns
10:02of ischemia that may be suggestive of
10:04end STEMI or unstable angina include St.
10:07depressions that localize to a
10:09specific area or T wave inversions.
10:12You could also see Q waves,
10:14which are evidence of a completed infarct,
10:15as these usually occur 12 hours
10:17after the initial ischemic insult.
10:20Now that we've learned how to
10:22diagnose acute coronary syndromes,
10:23we can focus on the management.
10:25I'd say one of the most important and
10:27time sensitive decisions that needs to be
10:29made in the management of acute coronary
10:32syndromes is regarding re vascularization.
10:34If you think you see St.
10:35elevations or any STEMI equivalents,
10:38I would call cardiology right away to
10:40confirm these findings and if true,
10:42activate the Cath lab Guidelines suggest
10:44that these patients should be emergently
10:47re vascularized within 90 minutes.
10:49Sometimes in situations where patients
10:51aren't close to Cath lab facilities,
10:53TPA may be used,
10:54but this is very infrequent in
10:57large academic centers like PO.
10:59If you don't see any St.
11:00elevations,
11:01but the patient has EKG changes
11:03or troponins consistent with
11:05end STEMI or unstable angina,
11:07they may meet criteria for immediate
11:09invasive angiography within two
11:11hours if they have any of the
11:13following hemodynamic instability,
11:14new left ventricular dysfunction
11:16or dropped ejection fraction,
11:19persistent chest pain at rest
11:21despite optimal medical management,
11:23up trending troponins or dynamic EKG changes,
11:26sustained ventricular arrhythmias,
11:28or evidence of late presenting MI like
11:31a new VSD or mitral regurgitation.
11:33If you don't see any of these findings,
11:35you have some time to get serial Ekgs
11:38and trend troponins and can further
11:40risk stratify with risk stratification
11:42tools like Grace and Timmy.
11:45These will help determine if a patient
11:47may benefit from early invasive
11:49angiography which is within 24 hours
11:51delayed invasive angiography which
11:53is in 48 to 72 hours or an ischemia
11:55guided approach which is based
11:57on further stress testing and or
12:00anatomic imaging which is usually
12:01reserved for lower risk patients.
12:03There are two key ways that
12:05patients can be revascularized.
12:07The first is via percutaneous
12:09coronary intervention,
12:10which is done in the Cath lab.
12:11In this,
12:12the operator gains access via the
12:14femoral or radial arteries and is
12:16able to snake a catheter up to the
12:18coronary arteries where they shoot
12:20dye to help identify any blockages.
12:22They can then open up the blood
12:24vessels via angioplasty and place
12:26a stent to keep the artery patent.
12:28Historically bare metal stents were placed,
12:31but nowadays you'll see drug eluting
12:33stents being placed due to the
12:35reduced rates of instant restenosis.
12:37If you have a patient that's
12:38had a stent placed,
12:39they need to be on dual antiplatelet
12:42therapy for at least one year after.
12:44The 2nd way that patients are
12:46revascularized is via coronary artery bypass
12:48surgery. In this, the
12:51surgeon takes vessels from elsewhere
12:53like the saphenous vein or the
12:55internal thoracic mammary artery
12:56and actually bypasses the blockage.
12:59There are three key indications that
13:00we need to know for which patients
13:03should be considered for cabbage.
13:04The 1st is left mean coronary artery disease,
13:07second is 2 vessel disease with
13:10left ventricular dysfunction and
13:11the third is 3 vessel disease,
13:13especially if the patient has diabetes.
13:16Now more and more we're also seeing
13:17the evolution of complex PCI which can
13:19be used when patients have complicated
13:22coronary anatomy like left mean disease,
13:24chronic total occlusions,
13:25calcific lesions or bifurcation
13:27lesions and can sometimes also be
13:29used as an alternative for surgery,
13:31especially if the patient isn't
13:33a good surgical candidate.
13:38Patients with acute coronary syndromes
13:40are also started on medical therapies.
13:42Regardless of whether they
13:44are revascularized initially,
13:45they should still be started on
13:47medications from various classes.
13:49The 1st is antiplatelet agents which
13:51prevent platelet activation are
13:53thereby anti thrombotic patients will
13:55usually be started on two agents,
13:57aspirin which is a Cox 1 inhibitor and
14:00then one other agent which is either
14:03Ticagralor Brilinta or Plavix Clopidogrel.
14:05Both of these work on P2Y12 and ADP which
14:09are involved in platelet aggregation.
14:11The difference between the two
14:13is that Ticagralor is the active
14:15drug and Plavix is a pro drug that
14:17needs to be metabolized and that
14:20metabolism depends on CYP 2C19.
14:22And so some patients are non
14:23responders to Plavix due to a
14:25loss of function in that gene.
14:26And so the effect of Plavix is less
14:29predictable in the population.
14:30But the benefit of using Plavix
14:32is that it's cheaper.
14:33So you can kind of just weigh the
14:35benefits and risks of each of those.
14:37And then the other note I'll make
14:38is that if you are suspicious
14:40about multi vessel disease,
14:41often patients will just be loaded
14:43with aspirin and they'll hold off
14:45on the 2nd antiplatelet agent.
14:46And that's because if they are going to
14:48go to surgery and they get that agent,
14:50they have to wait five days for
14:52that to wash out to reduce the
14:53risk of bleeding during surgery.
14:57The other major medication that
14:59we use is anticoagulation,
15:00which usually consists of
15:02a heparin drip or Lovenox.
15:03This is empirically continued for 48
15:05hours to prevent clot propagation.
15:08And then there's a couple of medications
15:10patients are started on long term to
15:12reduce their risk of adverse cardiac
15:14events and negative remodeling.
15:16The 1st is beta blockers.
15:18These work by reducing oxygen
15:19demand and also reducing the heart
15:21rate which thereby increases
15:23diastolic filling time which is
15:25when the coronaries are perfused.
15:27We also start Aces and Arbs which
15:30prevent negative remodeling over time and
15:32then moderate or high intensity statin.
15:35Then finally for symptoms we use anti
15:37anginals which mostly consist of nitrates.
15:40These reduce oxygen demand in our veno
15:43dilators and acute anginal attacks.
15:45We use sublingual and IV nitroglycerin
15:48because they avoid the GI system and
15:51nitrates are metabolized via first
15:52class metabolism and so an oral nitrate
15:55is not going to be as effective acutely.
15:59And then in terms of further work up
16:01and management on all these patients,
16:03we like to kind of further risk stratify
16:05them by checking a hemoglobin A1,
16:06CA lipid panel,
16:08getting an echocardiogram the subsequent
16:09day to evaluate if there's any
16:12regional wall motion abnormalities or
16:14changes to their ejection fraction.
16:16Then also focusing on
16:17modifiable lifestyle factors like encouraging
16:20smoking cessation and
16:21weight loss and exercise.
16:25Now we know how to diagnose and manage acute
16:27coronary syndromes and we can summarize
16:29it in an assessment and plan in the note.
16:32Things I like to focus on are the type
16:33of acute coronary syndrome, the location,
16:35any findings of the ischemic work up
16:37like if the patient underwent EKG,
16:39left heart Cath or any other type of
16:42ischemic evaluation and the treatment.
16:43So here's an example of how I
16:45would write up a patient,
16:46Miss S She's a 59 year old with a past
16:48medical history significant for hypertension,
16:50hyperlipidemia, tobacco use,
16:51who initially presented with eight
16:53out of 10 substernal chest pain
16:55at rest and her EKG showed St.
16:57elevations into three ABF.
16:59Ultimately,
17:00she was found to have a 90% occlusion of
17:02the RCA status post one drug eluting stent.
17:05So her presentation is consistent
17:06with an inferior STEMI.
17:08For this,
17:08we'll continue her dual antiplatelet
17:10therapy with aspirin and Brilinta.
17:12We'll start her on a high intensity statin,
17:14she'll get an echocardiogram
17:15and if that is normal then we'll
17:17start her on metoprolatartraate.
17:19We'll switch out her amlodipine to
17:21lisinopril which has cardio protective
17:23benefit and acute coronary syndromes
17:24and we'll also refer her to a smoking
17:27cessation program upon discharge.
17:29We can wrap up with some take home points.
17:31First is understanding the spectrum
17:32of acute coronary syndromes which
17:34includes unstable angina where patients
17:36present with chest pain at rest but
17:39don't necessarily have troponin or
17:40EKG changes because they're having
17:42ischemia Without evidence of infarction.
17:44Patients can have end STEMI
17:46characterized by sub endocardial
17:47ischemia which does not produce St.
17:49elevations on EKG but they can still
17:52have AC depressions or T wave inversions.
17:54They will have an elevated troponin
17:56and STEMI characterized by transviral
17:58infarction which produces the
18:00street elevations on EKG as well
18:02as elevated troponin.
18:04You can also localize the lesion based
18:05on the pattern and distribution of St.
18:07Changes 2-3 ADF are inferior
18:10leads correlating with the right
18:12coronary artery territory.
18:141A D LV5V6 are lateral leads which
18:17correlate with the circumflex territory
18:19and V1 to V4 are your anterior leads
18:22corresponding with LED territory.
18:24It's also very important to triage
18:26who goes to the Cath lab emergently
18:28versus urgently versus on a
18:30selective angiography basis.
18:31After further ischemic testing and
18:34monitoring and then recognizing the
18:36cornerstones and medical management
18:37of acute coronary syndromes which
18:39includes antiplatelet agents,
18:41anticoagulation,
18:41high intensity statin and things to
18:44prevent further adverse cardiovascular
18:46events like smoking cessations,
18:49beta blockers, aces,
18:50herbs and weight loss,
18:52here are some of the sources used
18:53in this video and some more information.
18:55The Life in the Fast Line website
18:57is really great for practicing
18:59identifying STEMI and STEMI equivalents.
19:01A lot of the Ek GS in this video
19:03are from this website.
19:04I also cited the most recent guidelines,
19:06the 2021 AHAACC guidelines and up
19:09to date which has some really great
19:11algorithms on managing and STEMI,
19:12STEMI and unstable angina.
19:14Thank you guys so much.
19:15This is the Yale 20 video.