Coronary Artery Disease | Clinical Medicine

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0:06what's up Ninja nerds in this video

0:08today we're talking about coronary

0:10artery disease this is going to be a

0:11part of our clinical science section if

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0:15understand this topic with some great

0:17notes some great illustrations go down

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0:42swagoo there all right we're going to

0:44start talking about CAD so CD diseases

0:47of the coronary artery is what it is

0:50we're not going to go through we should

0:51have already covered this in our basic

0:53kind of foundational science Concepts

0:55about the coronary vascular Anatomy what

0:57I really want us to do to really kind of

0:58get straight to the point here

1:00is here we have a section of the heart

1:02so I took and I cut the heart and I can

1:05see here parts of the ventricle so

1:07here's going to be my right ventricle

1:09and here's my left ventricle this will

1:11be the posterior portion and then over

1:15here coming out of the Whiteboard like

1:16it's going to punch you in the face this

1:17is the anterior portion

1:19what happens is you have vessels that

1:22are going to be supplying this big

1:23chunky muscle of the actual heart what

1:25are those those are the coronary vessels

1:27and the most basic concept there is four

1:29that I really need you guys to remember

1:30one here in the posterior portion guess

1:33what it's not that hard it's called the

1:35posterior descending artery we're going

1:37to abbreviate that as the

1:39PDA it doesn't take a rocket scientist

1:42to figure out that this supplies the

1:44posterior portion of the heart it'll

1:46Supply a little bit of the right

1:46ventricle a little bit of the left

1:48ventricle as well

1:49the other one which is going to be on

1:51this right part here is called the right

1:54coronary artery this one supplies the

1:57right ventricle and parts of the

1:59inferior portion of the left ventricle

2:01this right here is the Big Daddy this is

2:04the Mack Daddy of all the coronary

2:05vessels this is the one that you don't

2:06want to get occluded this is called the

2:08lad or the left anterior descending

2:11artery this one supplies the septum IT

2:14Supplies the anterior wall of the left

2:16ventricle and it even gives off some of

2:17the lateral wall of the left ventricle

2:19so really really important artery

2:21and the last one here that we have we're

2:23going to zoom in on in just a second

2:25here this one is called the left

2:26circumflex artery which we're going to

2:28abbreviate lcx and that supplies the

2:30lateral wall of the left ventricle so

2:33when we talk about coronary artery

2:34disease it's a disease of these vessels

2:36so we have to zoom in on a chunk of this

2:38vessel in the associated myocardium

2:39that's what we're going to do here so

2:41we're zooming in on this puppy so this

2:43is a zoom in view

2:45of that that portion there

2:47so here we're going to have a portion of

2:48the left circumflex artery and here's a

2:50piece of myocardium

2:52what happens in patients who have

2:53coronary artery disease is the most

2:56common cause of that disease is

2:58atherosclerosis that is by far the most

3:00common cause so then we have to ask

3:02ourselves the question what is

3:04atherosclerosis and what causes

3:06atherosclerosis atherosclerosis is these

3:08fatty plaques that develop within the

3:10wall of the actual blood vessel and

3:12include the actual blood flow what leads

3:15to this I want you to remember the

3:16mnemonic sad CHF

3:19so sad CHF will give you the following

3:22things to remember one is smoking

3:25second is Advanced age

3:27now when I specifically talk about this

3:29one I'm talking about greater than 45

3:31for males and greater than 55 for

3:32females don't forget that

3:34D got the diabetes the C is for

3:38cholesterol so this one's kind of a

3:39funky one right so cholesterol is high

3:43now when I talk about cholesterol being

3:46high which ones am I specifically

3:47talking about that's the real problem

3:49here there's two of them it's high LDL

3:52and then a weird one that kind of

3:53doesn't completely go along with this is

3:55low HDL so don't forget that as well so

3:56a dyslipidemia the next one is

3:58hypertension and finally a family

4:01history of coronary artery disease

4:04so these particular risk factors will

4:07then do what it'll stimulate this vessel

4:10to become diseased it'll cause plaques

4:12to form within the actual coronary

4:14vessel now when that happens look what

4:16we get we can get two particular

4:17scenarios here you see this vessel here

4:19now look you got this big old

4:21atherosclerotic plaque

4:23the big difference here

4:25is that this is called stable current

4:27coronary artery disease because what

4:28happens is the plaque is kind of covered

4:30by this fibrous tissue

4:32and the interesting thing about this

4:34plaque is that it's very stable but what

4:36you will notice is that look at the

4:38lumen in comparison here the Lumen is

4:41significantly smaller so because of this

4:43what's going to happen to the actual

4:45blood flow in this particular area here

4:47there's going to be a reduction in the

4:50oxygen supply

4:52if I have a reduction in oxygen supply

4:54because of having this big old stenosis

4:57aluminal stenosis of the coronary vessel

4:59that's going to lead to less oxygen

5:01being delivered to The myocardium

5:03now that may lead to ischemia but

5:05generally these patients don't have a

5:06lot of ischemic symptoms the chest pain

5:08is the primary classic finding

5:10what really leads to this is something

5:12else this myocardium

5:15decides to say all right you're giving

5:17me a very little oxygen

5:19but what if for some reason I decide to

5:21consume more oxygen huh that's

5:24interesting so what would be a reason

5:26why the patient would decide to have an

5:28increase in the oxygen consumption maybe

5:31they're demanding more let's use that

5:33term so there's an increase in the O2

5:36demand now the reason for the reduced O2

5:38Supply is this plaque

5:42this plaque is causing the reduced

5:44oxygen supply what would be causing the

5:46increase in oxygen demand

5:48there's two particular reasons that I

5:51want you to think about one is the

5:53patient's heart rate decides to go

5:55through the stinking roof they decide to

5:57tack away maybe in the 170s 180s

6:00whatever it may be that's causing the

6:02heart rate to go up if the heart rate

6:04goes up the heart has to beat faster it

6:05has to work harder and consume more

6:07oxygen if the demand goes up and the

6:10supply is low you create a mismatch and

6:12a recipe for ischemia so that's one

6:15particular reason so if we have these

6:17two particular things here this is a

6:19recipe for what ischemia and what is

6:22ischemia ischemia can be simply defined

6:25as a reduction in perfusion to the

6:29tissue and it's inadequate to meet the

6:31tissues demands so that's the big

6:33stimulus here now what's another reason

6:35why the O2 demand can go up another one

6:37is high blood pressure if the patient

6:39has hypertension they decide to shoot

6:41their blood pressure up so now they're

6:43afterload's crazy high if their

6:45afterload is crazy crazy high now the

6:48heart is going to have to beat so much

6:49harder to generate enough stroke volume

6:51to push blood out of the heart

6:54that's the big concept here and so this

6:56is why this is so interesting because in

6:58patients who have stable coronary artery

7:00disease when they're at rest

7:01they don't really have any angina

7:04what really starts to happen is when

7:07they start to exert themselves and

7:09increase their oxygen demand then they

7:11develop angina and so one of the classic

7:14findings of CAD is that in these

7:16patients they have ischemia but

7:18generally this ischemia what's the way

7:20that they'll present they'll present

7:21with angina so let's actually do this in

7:24red here because this is the classic

7:26finding of patients who have stable CAD

7:29but this angina is very very specific

7:34in the sense that the angina will only

7:37actually do what increase or occur

7:40whenever the patient is exerting an

7:42increase in their demand and so this is

7:44angina that is

7:47worse

7:50with exertion

7:53because if you exert yourself you decide

7:55to go running you decide to walk or you

7:57whatever it may be you increase your

7:59heart rate increase your blood pressure

8:00you increase the demand

8:01then if you decide to decrease the

8:04demand you stop exerting yourself what

8:06would happen the demand would go down

8:07and the ischemia should actually go away

8:11so this would get better

8:13with rest

8:16this is generally the classic finding of

8:18patients who have stable CAD they have a

8:21stable plaque reducing Supply if you

8:22increase their demand this will cause

8:25worsening ischemia all right

8:28neck next concept here this is the scary

8:30one this is the one that most people are

8:33frightened of in CAD

8:34they have a disease coronary artery

8:36right we're just using this left

8:37circumflex as an example

8:39they have a plaque

8:40maybe the plaque is somewhat stable but

8:43it's not completely stable at certain

8:46parts

8:46and what happens is this plaque

8:49decides to rupture

8:51so you get what's called a plaque

8:53rupture a plaque

8:55rupture and why is that bad well if you

8:58rupture that plaque you expose that

9:00inner cheesy material which is highly

9:03thrombogenic

9:05when it's extremely thrombogenic what

9:07happens here

9:08when you have this massive plaque

9:10rupture platelets love to come and stick

9:13to this

9:15and then you develop this thrombus oh my

9:19gosh that's terrifying so you have a

9:20plaque rupture and this creates a

9:22thrombus that forms on the actual plaque

9:26when you have a thrombus that forms on

9:28top of the plaque now what happens to

9:30your O2 Supply here it's massively

9:33decreased and so what happens in these

9:35particular patient populations is their

9:37O2 Supply

9:39is incredibly low

9:42and if you have an incredibly low O2

9:44Supply you're going to stop perfusing

9:47The myocardium and The myocardium here

9:49is going to start becoming as chemic

9:52and that's the scary part of acute

9:54coronary syndrome but we have to be able

9:56to differentiate these because they're a

9:58Teensy bit different in nomenclature and

10:00understanding the actual disease process

10:03so let's say here I take three

10:04particular types of acute coronary

10:06syndromes

10:07in one scenario I rupture the plaque

10:10when I rupture the plaque it does kind

10:13of really kind of bust open a lot of

10:16this thrombus starts to form

10:18and then same thing here for nstemi I

10:21rupture the plaque

10:23a lot of thrombus begins to form

10:26so we call this what

10:28for these two this is a sub

10:33total

10:35occlusion

10:37now when I have a subtotal occlusion

10:40because I form this this rhombus on the

10:42plaque

10:43then I'm reducing the blood supply C

10:45very very significantly right

10:48so definitely for both of these I'm

10:50going to have a reduction in O2 Supply

10:52very very low O2 Supply

10:55but the big primary difference here

10:59is what happens to The myocardium

11:02now you're not giving enough oxygen to

11:04the tissue

11:05in this particular scenario if I have

11:07the patient having ischemia of their sub

11:11endocardial layer so I have what's

11:12called sub-endocardial ischemia that is

11:15more specific for unstable angina

11:17so this is going to be again a sub

11:21endocardial

11:25ischemia

11:27and here is the big big difference

11:30I reduce the supply

11:32my sub-endocardial layer begins to start

11:34screaming

11:36but here's the other thing I don't kill

11:38any tissue none of the tissue dies and

11:40so there's a particular molecule that

11:42leaks from these tissues whenever

11:44there's tissue death you guys know what

11:45that's called troponins I know you guys

11:47are all screaming at home right so

11:49troponins so what would I say

11:52troponins what would I say about the

11:55troponins would they be positive or

11:56negative they should be negative right

11:59so that should be one particular thing

12:01they shouldn't really have a troponin

12:02bump and on top of that what we'll learn

12:04a little bit later is is they shouldn't

12:06have any ST segment like elevation they

12:09may have because of this ischemia they

12:12may have what's called some ST segment

12:15depressions or

12:17some T wave inversions

12:21and that's the other thing that we'll

12:22actually remember for these two but

12:24we'll go over that when we get into the

12:25diagnostic section

12:27now you're probably like okay these are

12:28kind of the same though Zach you said a

12:29subtotal occlusion for both of these so

12:31what's the difference between unstable

12:32engine and stemi well really with an in

12:35stemi

12:36I actually have my Supply so low

12:39that I actually began to infarct so it's

12:42no longer sub-endocardial ischemia this

12:44is called a sub

12:47endocardial

12:49infarct and that is the big difference

12:51here I actually am causing death

12:55of the tissue

12:57if there is death of the tissue what

12:59will leak out as a result

13:02troponins

13:04and so if the troponins are leaking out

13:05they should be positive if we were to

13:08test them so we will have a positive

13:12troponin leak and the last thing is is

13:15this is a small infarct it doesn't cause

13:17St elevation but it does cause SC

13:20depression

13:21or

13:23T wave inversion

13:26and that is how we really kind of

13:27differentiate between these two when it

13:29comes down to the pathophysiology

13:32the last one here

13:34is going to be for the stemi and for the

13:36stemi this one is primarily

13:39a total occlusion

13:42a complete total occlusion of that

13:44entire coronary vessel so this vessel is

13:47completely jacked up

13:48it is filled to the brim with clot

13:51if I completely clot off this entire

13:54Lumen do I have any blood supply no

13:58and so the difference between these is

14:00that these have very little Supply

14:02this one's completely choked off there

14:05is zero O2 Supply

14:08and if I get no oxygen supply to The

14:10myocardium what begins to happen it gets

14:13ticked off and the entire

14:15myocardium begins to become damaged

14:19and because the entire tissue is damaged

14:21we call this transmural this is a

14:25transmural

14:26infarct the entire wall gets jacked up

14:30that's no bueno what would happen to the

14:33troponins

14:35through the roof

14:36these usually will bump pretty high

14:39and then the last thing is this will

14:42definitely present with ST segment

14:44elevation that's where we get the name

14:46so we'll see particularly ST segment

14:48elevation we'll get into the details of

14:51that a little bit later but they should

14:52have a positive troponin

14:55because of the transmittal infarct St

14:58elevation because of the transmeral

14:59infarct and that is how we

15:01pathophysiologically describe semi

15:03the last thing the last thing that I

15:05want you guys to understand here is

15:07for stable CAD they present with Angela

15:09worse with exertion better with rest

15:11because it's particularly exertional

15:13dependent

15:15for acute coronary syndromes their type

15:17of angina is a little bit different

15:20for these guys for the acute coronary

15:23syndromes acute coronary syndrome

15:25findings

15:27these guys present particularly with

15:30angina same thing same thing but

15:34this can occur

15:36at rest

15:38and it is more intense so there's an

15:40increased intensity of that pain it is

15:43much much more intense and there is an

15:45increase in

15:47frequency of the pain so when you're

15:49trying to compare the two

15:51between an acute coronary syndrome

15:53angina and a stable angina this is

15:56really the big difference if it occurs

15:58at rest it's intense and it's occurring

16:01more more frequently that's more

16:03concerning for an acute coronary

16:04syndrome if it's an engine that occurs

16:06with exertion and improves with the rest

16:08of what we call Nitro which we'll talk

16:09about the treatment section that's

16:11stable angina

16:13the other thing that I want to talk

16:14about really quickly is this classic

16:15finding of angina if you will so when

16:18patients present with angina it is a

16:20substernal type of chest pain it's a

16:21squeezing choking type of pain and

16:24generally this can you want to watch out

16:26for radiate to the left neck left face

16:29left arm all right other Associated

16:32symptoms that can be atypical findings

16:34or anginal equivalents is epigastric

16:37abdominal pain and some nausea and

16:39diaphoresis so watch out for that all

16:42right let's now take this understanding

16:44that we have the pathophysiology and

16:46move into what happens if a patient does

16:49infarct they damage their myocardium

16:51what are some issues or complications

16:53that can arise all right my friends so

16:55now the patient has come in they have

16:57developed an nstemi or a stemi so they

16:59have infarcted some of their tissue when

17:02a patient has infarcted some of their

17:04tissue you're going to start seeing

17:06potential issues and complications arise

17:08what are those issues what are those

17:10complications that we have to be weary

17:12of because it can have a high mortality

17:14rate

17:15so one of the big things is when you

17:17start to infarct the tissue it can

17:18increase the risk of arrhythmias

17:19arrhythmias usually developed within the

17:22first 24 hours after a patient has had

17:24some type of nstemi or stemi so this is

17:26the one that you want to watch out for

17:28very early in that course

17:30what can happen is

17:32one of the things that you can actually

17:33see here is you know whenever patients

17:35develop what's called a RCA occlusion

17:37right so they have develop what's called

17:38a right coronary artery occlusion do you

17:41guys remember which parts of the heart

17:43that's applied it's pretty sure for

17:45right the right ventricle and inferior

17:47aspect of the left ventricle but another

17:50thing is it gives like this little

17:51branch that supplies the AV node and

17:54sometimes in patients who get these RCA

17:56occlusions you can actually destroy this

17:59structure here so here's you have your

18:01AV node and you go into your bundle

18:02branches I can actually destroy this

18:06structure here and if I have an RCA

18:08occlusion that leads to an AV node

18:14destruction

18:16now what's going to be the problem with

18:18that this is supposed to be able to

18:19allow for electrical activity to go from

18:21the Atria into the ventricles now you

18:23lose that you're going to start

18:24developing AV blocks and so this patient

18:27could develop a AV block that could

18:29precipitate a profound

18:32bradycardia

18:33and so this is something that you want

18:35to watch out for watch out for like

18:36second degree heart blocks third degree

18:38heart blocks this is something that can

18:39be potentially evident so the patients

18:41develop an RCA occlusion this RCA

18:43occlusion could potentially cause AV no

18:45destruction which could then lose the

18:48electrical connection between the Atria

18:49and the ventricles precipitating the AV

18:51block and now the actual infra uh

18:55nodal components or like the purkinje

18:58system now have to take over the actual

18:59rate of the heart and that will lead to

19:01a profound beta bradycardia all right so

19:03that's one thing to watch out for so if

19:05you have a patient who has then had an

19:06nstemi or stemi check potentially if

19:08they have bradycardia you really want to

19:10watch out for that as a potential

19:11complication

19:13the other thing that can happen and you

19:15usually see this with any kind of like

19:17lad or left Circ kind of occlusions this

19:21is usually going to affect the left side

19:23of the heart so whenever these patients

19:25actually develop an infarct they start

19:27to damage this left ventricular tissue

19:29and whenever you damage this left

19:31ventricular tissue you infarct it now

19:34you create a re-entrant circuit so LED

19:37left circumflex occlusions can increase

19:38what's called re-entrant

19:42circuits

19:44the problem with that is is that if you

19:47create re-entrant circuits within the

19:49ventricle this can create a ventricular

19:52Rhythm and that is absolutely terrifying

19:55because you know what these patients can

19:57potentially develop

19:58if they develop this reentrant circuit

20:00and starts flying off these kind of

20:02electrical activities the patient can

20:04potentially go into what's called

20:05ventricular tachycardia

20:07that could potentially go to ventricular

20:10fibrillation and then from there sudden

20:13cardiac death so you really want to

20:15watch out for

20:16these potential complications and

20:19patients who develop an end stemi or

20:21stemi and again just to remind you when

20:23is this the most profound usually you

20:26want to watch out and the first

20:2924 hours after an end stemi or a stemi

20:32for particular types of arrhythmias

20:34all right so these are the two big ones

20:36that I want you to remember here the

20:37next really really scary one that you

20:40can't miss and again this is usually

20:42most common in the first 24 hours as

20:45well

20:46is acute heart failure this is one of

20:49the big causes of acute heart failure so

20:51with arrhythmias particularly V tag

20:53v-fib or profound AV blocks like

20:56bradycardia you want to think about

20:57myocardial ischemia from acute heart

21:00failure you want to think about

21:01myocardial ischemia as well think about

21:03it it's pretty straightforward let's see

21:05here we have the left ventricle and then

21:07I decide to develop a let's say a

21:09massive lad occlusion you can get this

21:13from your your left Circle but I'd say

21:15the left of the lad would probably be

21:16the most disastrous one to have because

21:19it supplies the septum the Apex and even

21:22a part

21:24of the lateral wall you imagine knocking

21:27this thing out oh my gosh that'd be

21:29terrifying so if you infarct this entire

21:31tissue what are you going to do you're

21:33going to drop the contractility now now

21:36you've caused damage to multiple

21:37myocardial tissues you drop the left

21:39ventricular contractility you're going

21:41to drop the left ventricular ejection

21:43fraction

21:44if you drop the left ventricular

21:46ejection fraction now you're not getting

21:48blood out of the heart so the problem

21:50with this is is that if I damage this

21:52tissue I'm not going to be able to get

21:54blood out of the left ventricle and out

21:57into the aorta this process

22:00is going to be inhibited so there's

22:03going to be a drop in what's that called

22:05the volume that gets pumped out of the

22:06heart within one minute microtic output

22:09so my cardiac output will drop

22:11then I won't perfuse tissues if the

22:14cardiac output drops enough what's that

22:15formula blood pressure is equal to

22:17cardiac output times the systemic

22:18vascular resistance if my cardiac output

22:21goes down enough it can potentially drop

22:22my blood pressure so the patient may

22:24develop hypotension

22:28but the most worrisome complication here

22:30is if that hypotension leads to reduced

22:32perfusion to the tissue it can put a

22:34patient into what's called cardiogenic

22:36shock so this is when they're not

22:38perfusing the tissues and you want to

22:40watch out for like potentially

22:42multi-system organ failure other organs

22:45are going to start failing such as the

22:46kidneys right and that's a really really

22:49big thing to watch out for so again

22:50because you lose you have this led

22:52occlusion you knock out a big portion of

22:55the left ventricular contractility you

22:58reduce the left ventricular ejection

22:59fraction and what happens is that drops

23:02the cardiac output that can lead to

23:03hypotension and can stimulate a patient

23:06going into cardiogenic shock so you

23:08really want to watch out for this a

23:09reduction in contractility a reduction

23:11in left ventricular ejection fraction

23:12then precipitating this low cardiac

23:15output and cardiogenic shock here's the

23:18other scary thing

23:19if the blood can't go forward so you

23:21have a problem getting blood going

23:22forward

23:23where will it go then

23:25what happens is the blood will start

23:28backing up into the left atrium and when

23:31it backs up into the left atrium it'll

23:33go back into your pulmonary circulation

23:36when it goes back into the pulmonary

23:37circulation where do you think it's

23:38going to go it's going to go right into

23:40the lungs my friend

23:41and then what's going to happen is

23:42you're going to start filling the lungs

23:44with fluid because the hydrostatic

23:45pressure and the pulmonary veins are

23:47going to start increasing and fluid is

23:49going to leak out and these patients

23:51will develop a profound

23:53pulmonary edema

23:55so you want to watch out for these

23:56patients developing pulmonary

23:59edema

24:01and this can lead to

24:03hypoxia

24:05so if you have a patient

24:07who has just had an instamy or stemi

24:10they now are developing features of

24:12pulmonary edema such as dyspnea or watch

24:15out for that as well they can also

24:16develop not just profound hypoxia but

24:18they may develop dyspnea so watch out

24:21for dyspnea as well

24:24or hypoxia so if you have a patient who

24:26has an nstemi or stemi

24:29massive LED occlusion they knock out the

24:31actual contractility they lose their

24:33left ventricular ejection fraction they

24:35don't pump blood out so develop

24:36hypotension and perform perfusion to the

24:38tissues and pulmonary edema this is

24:42something that you want to think about

24:43as acute heart failure and a patient

24:44who's had an MI all right that's this

24:46one very very scary one you really want

24:49to get on top of that one the next one

24:50is pericarditis this one is actually one

24:53of the nice ones like if you wanted to

24:54get any complication this is probably

24:55the ones you want to get because this is

24:58the one where it's not going to have a

25:00super high mortality rate it's not fun I

25:02don't want to deny that but it's not

25:04going to be the scary one so if you

25:05develop an infarct generally anywhere

25:06near the pericardium

25:09you're going to have infarction of

25:10tissue right neutrophils macrophages

25:13will all come into this area and try to

25:15clean it up and lay down some

25:16granulation tissue but there's going to

25:18be a lot of inflammation in this area

25:19it's not out of this world to think that

25:23the inflammation will extend to the

25:26nearby pericardium

25:29and if it extends to the nearby

25:31pericardium this can cause inflammation

25:33of the pericardium which will lead to

25:34pericarditis now when patients present

25:37with pericarditis they present with

25:39what's called a pleuritic that's one of

25:41the big differences here so sometimes

25:42what gets scary and hard to suss out

25:44with these patients is they had

25:47an MI they came in because they

25:49presented with chest pain now they're

25:50presenting with chest pain again you

25:52have to be able to differentiate the two

25:54is it squeezing is it choking is it feel

25:56like there's someone sitting on your

25:57chest kind of pain radiates to the left

25:59jaw neck arm

26:00or is it this type of pain where it's a

26:03kind of more of a pain that hurts

26:04whenever you're taking breaths does it

26:07actually change whenever you kind of

26:08lean forward a little bit and offload

26:10the pressure on the pericardium so

26:12there's a positional component of it

26:14that's more suggestive of pericarditis

26:17another thing is that you want to listen

26:19because if the pericardium gets really

26:21really inflamed

26:22the layers start kind of actually

26:24rubbing up against one another and it

26:26creates a weird rub on auscultation we

26:28call it a friction rub

26:30we call it a friction rub

26:32and so generally

26:33in patients who have low grade fevers

26:36a pleuritic chest pain a positional type

26:39of chest pain another one great for your

26:41boards is a chest pain that radiates to

26:43the trapezius that's classic in your

26:46vignette so don't forget that one as

26:47well but if her presents like this

26:50after having some type of cardiac event

26:52you definitely want to think about

26:54pericarditis now sometimes and I and I

26:56hate it we start thinking could there be

26:58another component to this like there's

27:00two different types of pericarditis this

27:03is called fibrinous pericarditis right

27:04so there's two types

27:06one is called

27:08fibernous and the other one is called

27:10dresslers

27:12how do I suss out the two

27:14amphibians pericarditis it's usually

27:17very soon

27:19generally one to three days after having

27:21the cardiac event so that's one thing so

27:22if you have a patient who's

27:23approximately one to three days

27:26post MI

27:28it's more likely februinous for your

27:30exams in True Life this isn't truly that

27:32important

27:33but if it's free exams dresslers is

27:36usually a little bit later so it's a

27:37kind of pleuritic chest pain with a

27:38friction rub that comes generally about

27:4014 days two weeks after an MI so

27:43approximately two weeks

27:46post

27:47am I and that's one of the things that

27:49they may try to trip you up on your exam

27:51in true life it's not that important but

27:53for your exams something to not forget

27:55about

27:56all right so we've got a rhythmias we

27:58got acute heart failure we got the

27:59pericarditis we come down to the ones

28:01that usually cause sudden hemodynamic

28:04collapse and these are terrifying as

28:06well

28:07these I'd say are less common in the new

28:09reperfusion era which we have PCI is the

28:12primary way that we reperfuse people

28:14but complications that can arise and a

28:18patient who gets an LED occlusion

28:20all right so an LED occlusion

28:22what happens is

28:24is one of the parts

28:26that can get really jacked up here is

28:28the interventricular septum

28:30so whenever there is a infarct

28:34of the interventricular septum you

28:36damage this tissue so now look this

28:38endocriticular septum is all jacked up

28:40it's all infarcted

28:42what can happen is sometimes when the

28:45tissue is super weak and a chronic it

28:47can actually be thin enough that you can

28:49rupture the septum and you can create

28:51what's called a ventricular septal

28:53defect and look at this now when I

28:56rupture this puppy I have a big hole in

29:00between the left ventricle and the right

29:01ventricle and generally blood is going

29:03to go from the high pressure system and

29:05to the low pressure system so it'll go

29:06from the left ventricle into the right

29:07ventricle what that will do is that will

29:09cause the patient to present with a

29:12murmur so usually they're present with a

29:14murmur

29:15some type of holocystolic murmur so if

29:18you hear a new murmur on the patient

29:19definitely one of these things that you

29:21want to think about

29:22and it'll precipitate heart failure

29:24generally it'll cause the patient to go

29:26into a right heart failure before they

29:28go into left heart failure so it's more

29:30common that they'll get right greater

29:32than left because think about it you're

29:33overloading the right ventricle blood is

29:36squirting from the left ventricle into

29:37the right ventricle and you're

29:39overloading the right ventricle so

29:40that's something to think about but in a

29:42patient who presents with hemodynamic

29:43collapse in a hole of systolic murmur

29:45think about a vsd

29:48the other one that's also really

29:50interesting as well that you really want

29:52to think about here is going to be a

29:54patient who presents with what's called

29:55a papillary muscle rupture

29:58so let's say that they have an occlusion

30:00here and this occlusion what it does is

30:03it knocks out

30:05the blood flow particularly this you can

30:08you can see with a bunch of different

30:09types you can see this usually with

30:10inferior ischemia so usually right

30:13ventricular or RCA occlusion so if a

30:16patient develops like an RCA occlusion

30:18what can happen

30:20is this can cause a papillary muscle

30:22ischemia

30:24so this will cause papillary

30:28muscle

30:30ischemia

30:32or infarct let's actually let's say

30:34infant so again you have an occlusion

30:36there you're infarcting the tissue

30:37that's in stemming and stemi you develop

30:39an infarct of the papillary muscle

30:41when you infarct that tissue now it's

30:44supposed to be holding onto the chordae

30:46tendine it can't hold on to the chord

30:48A10 anymore

30:49and so if you can't hold on to this

30:50chordatanine what is it going to do this

30:52sucker is going to break right off it

30:54was supposed to be anchoring it down now

30:56look at it's flapping in the Wind

30:59because of that you can't hold this

31:01valve down

31:02and what happens is this valve becomes

31:05super unstable and it can easily

31:07whenever the patient goes into like

31:09statistically whenever they have what's

31:11called ventricular systole this valve

31:13can blow right open

31:15and now you get something called

31:17regurgitation now a regurgitant jet

31:21instead of going this way

31:23can fly back into the left atrium

31:26and so you really want to watch out for

31:28that so when a patient develops on RCA

31:30occlusion they infarct their papillary

31:31muscle what happens is they can develop

31:33what's called

31:35acute

31:37mitral regurgitation

31:40and that will cause a murmur Believe It

31:42or Not similar to a vsd a hollow

31:46systolic

31:47murmur

31:50and we'll put the patient in two

31:52heart failure

31:54usually in this particular scenario left

31:57more than right obviously because it's

32:00going to be affecting the left side now

32:02so these are the things that you really

32:03want to watch out for pretty scary one

32:05again not as common in the reperfusion

32:07era

32:08this last one is probably the most

32:10terrifying this one I feel like most

32:12people usually just die because they go

32:13into PE arrests because they're left

32:15ventricle just explodes but what happens

32:17is you get a really big LED occlusion

32:22usually in combination with the left

32:23circumflex but what happens is you

32:26infarct this entire left ventricular

32:28free wall

32:30imagine this whole thing is dead

32:33super weak as it becomes weak

32:36boom

32:37this entire free wall ruptures oh my

32:40gosh this is so terrifying blood that's

32:42in your left ventricle will then squirt

32:44out

32:45right into your pericardium

32:48as the Blood starts filling into the

32:50pericardium what is this called

32:53hemopericardium

32:54imagine all that pressure from here left

32:56ventricle just squirting blood into that

32:58pericardium that is terrifying so what

33:00happens is you get an LED occlusion you

33:03get a free

33:05wall

33:06infarct

33:09this thing causes a free

33:12wall

33:14rupture

33:16and this will push a patient into what's

33:17called what is this when you have a lot

33:19of blood

33:20that's accumulating within the

33:21pericardium

33:22and it's squeezing on the heart not

33:25allowing for it to properly fill it's

33:26called cardiac tamponade so this is

33:28another one that you want to watch out

33:29for we'll talk about this in the

33:31pericardial disease section but you want

33:33to watch out for a patient developing

33:35that Bex Triad right so the jugular

33:37venous extension the hypotension and the

33:39muffled heart sounds that would be

33:40another really really big one

33:42and then again you can potentially see

33:44signs of like pulses paradoxes but again

33:46we'll go over all that in the

33:47pericardial disease section all right

33:49this is another potential complication

33:52the last one that I want you guys to

33:53watch out for here

33:54is again another type of LED occlusion

33:57so if you get an LED occlusion

34:02and then what happens is it infarcts

34:04this particular tissue here right so you

34:06could develop some depth of this tissue

34:08then what happens is something kind of

34:09weird it ruptures but it doesn't rupture

34:12the way that you would normally think so

34:14it doesn't completely rupture the free

34:17wall

34:18and what happens is you develop a

34:19rupture here but it's kind of contained

34:22there's like a fibrin kind of like clot

34:24that's kind of stabilizing the rupture

34:26so it doesn't allow blood to empty into

34:28the actual pericardial cavity so it's a

34:30contained rupture we don't call this an

34:33aneurysm per se even though it kind of

34:36looks like it it's a pseudoane or a

34:38contained rupture so we call this it

34:40creates a pseudo

34:43aneurysm

34:46the problem with this is that now blood

34:49can kind of just

34:51stay in this area this can create like a

34:53stasis of blood flow what happens when

34:56you create stasis of blood flow clots

34:58Virgos Triad right and so then this can

35:00lead to clots forming here and if you

35:03get a clot that forms right in here

35:06and then it decides to flick a part of

35:08that clot off what do you get thrombo

35:10and bottle complications that patient

35:11gets like a stroke or something right so

35:13you want to watch out for thrombo

35:17and belai

35:19these are the big big things that I want

35:21you guys to associate in patients who

35:22have had an end stemi or a stemi all

35:25right now that we've covered all the

35:27pathophys the issues and the

35:29complications of myocardial ischemia and

35:30coronary artery disease now we're going

35:32to do is we're going to learn how to

35:33diagnose these diseases a patient comes

35:35in they have anginal chest pain and the

35:37classic way that I taught you guys what

35:39do we do first thing EKG you can add on

35:42some cardiac biomarkers like troponin

35:43and ckmb but they're not always going to

35:46be the first test of choice ECG should

35:48be the first test once you've done that

35:50if you see this it's normal there's

35:52nothing really bad about this you can

35:54get a troponin if it's negative that

35:55again supports the concept that maybe

35:57this is a stress induced ischemy and we

36:00didn't stress them enough so maybe this

36:02is stable angina

36:03we'll talk about the workup of that in a

36:05little bit if you have a patient who

36:07doesn't have stress induced angina then

36:09you're thinking that they have an acute

36:11coronary syndrome that this doesn't

36:12require change in demand so that's going

36:14to be things like T wave inversions ST

36:16segment depressions and then you're

36:18thinking about things like an N stami or

36:20an unstable angina how do I determine

36:22that I want to know which one developed

36:23an infarct that's the importance of the

36:25pathophysiology if it's ischemia they'll

36:27have a negative troponin that's unstable

36:29Angela if the troponin is positive that

36:31means that they had an infarct that's an

36:33nstemi

36:34if I see this so that's a stemi right

36:37there right that's a big old Tombstone

36:39thing you know things are puckering up

36:41down there that's not good this is St

36:42elevation this should make you think

36:44about a stemi if you checked at your

36:46opponent and it's positive it would be

36:49way more suggestive of an SD segment

36:51elevation of mine there is this

36:53potential though that if you see St

36:55elevation and a patient known as cocaine

36:56tripped hand smoking younger respond to

36:58calcium channel blockers and their

37:00troponin is negative it's a little bit

37:02more suggestive of vasospastic angina

37:04all right that's how I would start this

37:06process chest pain EKG cardiac

37:09biomarkers determine if the patient has

37:11the worst case scenario which is a stemi

37:14if they have a stemming what do I do I

37:18want to know where the heck that stem is

37:20so then I'm going to try to localize the

37:22stemi and this is where EKGs are going

37:23to be a little bit more helpful in your

37:25exam

37:26so what they'll do is they'll say hey

37:27here's an EKG what do you think is the

37:29vessel that's occluded

37:30so the first one here is going to be an

37:32anterior and I told you that's V1 to V4

37:34I look for any St elevation in these

37:36leads and if you see that that would be

37:38suggested that the LED may be occluded

37:41if you're looking at the next one which

37:42is an inferior one you're looking at two

37:453 in avf and I see SD elevations maybe

37:47the right coronary artery is occluded

37:50with that being said if you think are

37:51right if you have an inferior Mi you

37:53should always do right-sided chest

37:54leaves just as a quick aside because it

37:56may show that the right ventricle is

37:58actually becoming infarcted and that's

37:59important to be able to identify

38:01but nonetheless lateral the left

38:03circumflex

38:04it's one and then AVL and then V5 and V6

38:08you're looking for St elevations there

38:10and that would suggest the left

38:11circumflex is occluded and then lastly

38:13if I see St depressions or T wave

38:15inversions in B1 to V3 I slap on the

38:17posterior chest leads in V7 to v9 and I

38:20see SD elevations that's suggestive of a

38:22PDA occlusion this is the way that they

38:24could try to test you on the exam as to

38:25where the actual stemi you think is

38:27occurring which vessel is diseased or

38:29occluded

38:30now with that being said ECGs are really

38:33really good combining it with an

38:35echocardiogram is even better

38:38because what you're doing is you're kind

38:39of making a correlation between the

38:42chest leads where you think the vessel

38:44is actually occluded and then

38:45correlating that with wall motion

38:47abnormalities where the areas of the

38:49ventricles aren't Contracting very well

38:50with the vascular territory so you can

38:53kind of see here I'm not going to go

38:54crazy because you won't be heavily

38:55tested on this but if you see V1 to V4

38:58St elevations and you look on the Echo

38:59and you see that the this territory the

39:01LED isn't Contracting well then you can

39:03say oh man I really think that this

39:05person is having a stemi and this kind

39:07of correlates

39:08and you can even correlate this with

39:10nstemi's as well but that's an important

39:13thing to do is to correlate hey anterior

39:15wall motion on rally hey maybe the LEDs

39:16knocked out RV is not Contracting very

39:19well they have an inferior wall motion

39:20abnormality maybe the RCA is knocked out

39:22left circumflex knocked out oh maybe

39:24that lateral wall isn't really

39:25Contracting very well or maybe the

39:26posterior walls are Contracting very

39:28well correlate your Echo with your ECG

39:31all right lastly in most patients on

39:34your clinical vignette you're going to

39:36get the ECG you're going to see that

39:37they have SD segment elevation maybe you

39:38get a troponin that's positive they're

39:40having crushing chest pain what's the

39:42test of choice but it's also the

39:44therapeutic like option in these

39:46patients it's usually going to get a

39:47coronary angiogram the benefit of this

39:50is that you're going to be for most

39:51patients when they get in the angiogram

39:52you're showing the occlusion but you're

39:55also going to treat the occlusion you're

39:57going to go in and put a stent in that

39:58area you're going to balloon it open and

40:00put in a stent but this is a really good

40:02test and probably the best test to find

40:04where the occlusion is so again you'll

40:06snake a catheter up there shoot contrast

40:08and look to see which of the vessels are

40:10not filling and where is the occlusion

40:11and again that's one of the best

40:13possible tests you could do

40:15all right so if a patient has a stemi go

40:18through that progression what's the ECG

40:20show where would a potentially localized

40:23correlated with your Echo and send them

40:25to the actual cath lab to find the

40:27occlusion and then treat the occlusion

40:29if they present with a normal ECG and a

40:31normal troponin then we're thinking

40:33about that stable angina patient but we

40:35still are scared because they have

40:36anginal chest pain we would want to send

40:39them for a stress test

40:40so we've ruled out ACS

40:42and we're going to say can the patient

40:44exercise if they can then you want to go

40:46ahead and do what's called stress

40:47exercise testing and so what we'll do is

40:50we'll kind of say okay there's a couple

40:51different options we could do here

40:53we can get a baseline ECG

40:55or we can do what's called a myocardial

40:56perfusion imaging where we give them

40:58like a radioactive tracer that shows

40:59areas of perfusion in their heart or we

41:02can do an echocardiogram and see if it's

41:03squeezing normally

41:05once we do that we're going to make them

41:06work out get them on a treadmill and

41:09have them Reach the kind of a target

41:10heart rate

41:12once we've done that and they start to

41:14experience maybe any symptoms or they

41:16get tachy arrhythmias or we actually

41:18repeat the ECG MPI or echocardiogram

41:20what are we looking for after we've

41:22really stressed the heart if I see on

41:24the ECG oh there are signs of ischemia

41:26that's stress-induced ischemia that

41:29would be helpful in telling me that this

41:30is a positive stress test if I didn't do

41:32the ECG test and I did the MPI then I'd

41:35be looking for areas of poor perfusion

41:37if I have to make them work out and I

41:39increase their demand now these errors

41:41are going to becoming suffering they're

41:43going to suffer now

41:44and the last thing if I do an

41:45echocardiogram and I see areas that

41:48aren't Contracting very well maybe they

41:50have an lad really big plaque there and

41:53I see that their anterior wall isn't

41:54Contracting very well after I had them

41:56exercise I could say oh there we go we

41:58have stress to induced wall motion

41:59abnormalities so these are all ways that

42:01if this happens and we see these changes

42:03that's a positive test

42:06now the reasons why you would do an NPR

42:09an echocardiogram because usually this

42:11is the first line is if their ECG has

42:13some weird things on them usually if

42:15they have like a left bundle it makes it

42:17really hard or if they have Q waves it

42:18makes a little bit difficult so you may

42:20do an echo or an MPI in those scenarios

42:22okay

42:23but we go to the other end of this

42:25algorithm which is the patient cannot

42:27exercise maybe they have terrible

42:28osteoarthritis they have some type of

42:30like rheumatological condition where

42:31they can't ambulate they just they can't

42:33do these things they can't exercise at

42:34all in those scenarios then you have to

42:36kind of precipitate the same increase in

42:38demand by giving them drugs two of the

42:41things that we would do is we would

42:43again get a baseline MPI or an

42:45echocardiogram and then we would give

42:47them a medication that would either

42:49really reduce the supply or increase

42:51their demand

42:53one is adenosine or dipridamole and what

42:55it does it decrease the supply it's

42:57actually really cool I'll show you how

42:58it does it in a second but I'm going to

43:00get the Baseline see what it looks like

43:01and then give them this drug and what it

43:03should do is if they have stress induced

43:05ischemia it should produce cold spots on

43:07their MPI

43:09I could also do the same concept give

43:11them an echo look for any like

43:13contractions of their ventricles give

43:15them dobutamine that should make their

43:17heart have to pump faster and pump

43:19harder which will increase the demand

43:21and it should show wall motion

43:23abnormalities and that would be a

43:24potential stress-induced ischemia

43:27now let's explain this adenosine or

43:28dipyridamole it's actually really cool

43:30it's called coronary steel syndrome here

43:32we give diaperinol or adenosine what it

43:33does is it does not vasodilate the

43:35disease vessel and it dilates the normal

43:37healthy vessels if you dilute a vessel

43:40you reduce the systemic vascular

43:41resistance and you drop the pressure in

43:43this area and it's easier for blood to

43:45flow in this direction

43:46but then what happens is you don't

43:48dilate this vessel the pressure doesn't

43:50drop in this area and now blood won't

43:52want to go this way it'll want to go to

43:53the lower pressure circuit and so this

43:56is literally going to steal blood away

43:57from the diseased area the supply is

43:59already reduced you're going to reduce

44:00it even more and that's going to

44:03precipitate ischemia and cause poor

44:05areas of perfusion

44:07so that's the concept of this pretty

44:09interesting

44:10either way you do any of these tests and

44:12it becomes positive usually the next

44:14thing is to say okay let's try to treat

44:16the patient we know that they have some

44:18type of stress this ischemia let's try

44:19to get them a little bit better

44:20but if we have any inkling that this

44:22patient may need to kind of go and get

44:23revascularized do something like a

44:25coronary angiogram look for the actual

44:27occlusion determine the severity of it

44:29or coronary CTA it's non-invasive and

44:31this will help you to determine to look

44:33at the actual vascular lesion so here's

44:34a coronary CTA and then here is a

44:36coronary angiogram to look for any kind

44:38of lesions that are present so you can

44:39see here's like this little stenotic

44:41area

44:42and you can see kind of stenotic areas

44:43here as well

44:44but that's the concept now after we've

44:47done this we've now determined the

44:49approach for stable Cad and the approach

44:51for stemi the approach for patients who

44:53have nstemi and unstable angina you

44:55really kind of just determine them

44:56already you determine if it's unstable

44:58angina or nstemi based upon the troponin

45:00and you're going to treat those guys

45:02relatively the same

45:03now that we've done this how do we go

45:05about treating the first patient which

45:07is the stable patient well the first

45:09thing is you don't want that plaque to

45:10rupture

45:11but more importantly if that plaque does

45:13rupture I don't want to thrombus to form

45:15on the plaque because it'll become

45:17subtotally or totally occluded and then

45:19I end up with an ACS scenario

45:21so how do I do that aspirin simple next

45:24thing is I really want to reduce their

45:25anginal chest pain so I want to reduce

45:27the oxygen demand so the ways that I can

45:29do this nitroglycerin because that

45:30reduces preload and dilates the coronary

45:32vessels and the second thing which is

45:34even more beneficial than that is beta

45:36blockers there is other drugs so there's

45:38not just nitroglycerin this is short

45:39acting but the drugs that you can give

45:41for long acting effect would be things

45:43like isosorbide dinitrate and there is

45:46the benefit of calcium channel blockers

45:48as well so it's usually beta blockers

45:50then PRN sublingual nitroglycerin

45:53long-acting isosorbidden nitrate which

45:56is another type of nitro and last line

45:58is usually calcium channel blockers and

46:00then after that there's another one

46:01called renolazine but we're not going to

46:03go there

46:04all right you've treated the patient

46:06with Aspirin you put them on a beta

46:07blocker they have sublingual Nitro

46:08you've treated them with isosorbent

46:09nitrate but now the patient has a

46:12positive stress test that is really

46:14really bad

46:15they have an angiogram which they got

46:16and it showed really really bad lesions

46:18like an lad that was like super stonotic

46:21or they have been symptomatic despite

46:24aspirin despite statins despite a beta

46:26blocker isosorbent to nitrate sublingual

46:28Nitro Etc and they're still having chest

46:31pain these patients have to be

46:32revascularized

46:34so when you want to revascularize these

46:35there's two options there's PCI or

46:37cabbage how do I determine

46:39if there's no left main lesion no left

46:42main coronary artery lesion they have

46:44less than three vessels that are plaqued

46:46up and they have a normal left

46:48ventricular EF it is preferable to do a

46:51PCI so a percutaneous coronary

46:53intervention

46:54now what we do is is we open up the

46:57artery we take a balloon we inflate the

46:59balloon and they're going to kind of try

47:01to open up and expand this area then

47:03what you're going to do is is you're

47:04going to pull back the balloon and leave

47:06in this stent which is going to

47:09hopefully keep this vessel nice and open

47:11that is the concept here but once we

47:13place this stent in we do not want the

47:16stent to clod off

47:18and we'll talk about what we'll do for

47:19that in a second

47:21what about the patient who gets the

47:22Cabbage it's the exact opposite they got

47:24a left main coronary artery lesion they

47:26got three or more vessels that are

47:27plaqued up and they're EF stinks

47:30probably better for these patients to

47:31get a cabbage a coronary artery bypass

47:33graph so they have a lesion like right

47:35here I'll take a graft and I'll move

47:38this over this way and sometimes we'll

47:40take like the internal mammary artery or

47:42we'll take the greater saphenous vein

47:44and we'll take those veins cut pieces of

47:47them and use them as the graphs to

47:49bypass these lesions you see how we're

47:51bypassing all of these lesions here

47:53that's the concept

47:55but to come back here we put the stent

47:57in when I put a stent in I don't want it

47:59to throw on bows and so I'll put them on

48:02Dual anti-platelets so in other words

48:04they'll be on aspirin plus something

48:06like Clopidogrel or decagitalor for at

48:08least one year then after that year you

48:12can downgrade to just one of those

48:13anti-platelets whether it's aspirin or

48:16it's Clopidogrel but I have to keep this

48:18on so that they don't stent uh thrombos

48:21this stent because that's terrible

48:23they can develop a reinfarction

48:25so that's the concept here here is the

48:27actual kind of like stent here and I

48:30want to prevent this I do not want them

48:32just like completely thrombos that stent

48:34all right

48:36the last thing is you can add them on

48:37statins as well statins help to prevent

48:39the actual plaque from continuing to

48:40hopefully get bigger and bigger and

48:42bigger we don't want that so again

48:43standard therapy aspirin beta blocker

48:46Nitro sublingual PRN isosorbet and

48:48nitrate for long-term control beta

48:50blockers if need be add on the Statin

48:52they're still symptomatic angiogram

48:54shells high risk lesions the stress test

48:56is really bad revascularize them PCI

48:59based upon this cabbage based upon this

49:01if they get the stent they need do

49:04anti-platelet therapy for a year

49:06all right unstable angina and nstemi

49:09it's similar

49:11you first want to prevent the thrombus

49:13from propagating so you give them

49:14aspirin plus Clopidogrel plus Heparin

49:18that's the big difference you see how

49:19the we load them with this before we

49:22even revascularize them so we load them

49:24with Aspirin plus Clopidogrel plus

49:26Heparin so it's called dual

49:27anti-platelet therapy plus heparin now

49:31if I want to revascularize the patient

49:33with unstable angina or an ends to me I

49:35need to have particular indications and

49:38there's usually three one as I do what's

49:41called a wrist stratification tool

49:43called the temi score there is other

49:45ones out there this is the one that

49:46sometimes is tested on this step too if

49:48the Timmy score is greater than three

49:50that in that kind of predicts a higher

49:53mortality rate for these patients and

49:55that means that they should probably go

49:56to the cath lab and get revascularized

49:58the next one is if they develop

50:01cardiogenic shock remember I told you

50:02the two big complications of Mis is vtac

50:06vfib because you can cause a ventricular

50:07arrhythmia or cardiogenic shock from a

50:10really nasty infarction

50:12if that happens where there's

50:14hemodynamic or electrical instability

50:16they need to go to the cath lab because

50:17the cause of their instability is the

50:20occlusion

50:21and the last one here is refractory

50:23angina they're symptomatic despite

50:25aspirin dual antibody therapy Heparin

50:28they're symptomatic despite beta

50:29blockers Nitro morphine statins all of

50:32those things they need to get

50:33revascularized and the decision of which

50:35revascularization technique is the same

50:38and then if you stent them you need dual

50:40anti-plated therapy for at least one

50:42year

50:43okay we come to stemi

50:46if a patient has a stemi it is the exact

50:48same process you load them up you give

50:50them 325 of aspirin you load them up

50:52with Clopidogrel or take Agra you load

50:54them up with Heparin and put them on a

50:55Heparin infusion and they go to the cath

50:57lab as soon as they possibly can and

51:00again most of the time you're going to

51:02be placing a stent and these rare

51:04scenarios you may be considering a

51:06cabbage but most of the time you're

51:08going to be going to the cath lab

51:10what if the patient is at a hospital

51:13that does not have a PCI capable

51:15facility

51:16then you give them the TPA and you

51:19transport them as quickly as you

51:21possibly can to a PCI cable facility to

51:24put a stent in no matter what even if

51:26they get TPA the guidelines say that

51:28they should still get PCI done

51:30that is the concept here

51:32all right the last thing that I want to

51:34add on here is after the patient has

51:36received revascularization you want to

51:39prevent ventricular remodeling because

51:41this has been shown to be beneficial if

51:43the patient is hypertensive or their

51:45blood pressure can tolerate it you want

51:47to get them on ACE inhibitors or arbs

51:49because it's been shown to reduce the

51:51ventricular Remodeling and that is the

51:54treatment for stemming and that my

51:56friends covers coronary artery disease I

51:58hope you guys liked it hope it made

51:59sense and I hope it helped as always

52:00until next time

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52:11foreign

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