Yale 20: Acute Coronary Syndromes

Transcript

• 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.