17 and 18. Acute Coronary Syndrome and chronic coronary artery diseaes Flashcards

1
Q

UA, NSTEMI, STEMI are result of:

A

acute atheromatous plaque rupture with variable degree of coronary lumen obstruction

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2
Q

Tx recommendation for ACS

A

Best rest, analgesics, Oxygen, Statins, Beta blockers and nitrates

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3
Q

With ACS, you IG will form a thrombus as a result of

A

Plaque rupture which causes: Platelet activation/adhesion/aggregation Activation of Coag factors

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4
Q

What tx would you want to give someone right away with Thrombus formation during ACS?

A

Antiplatelets: aspririn/Clopidigrel/Prasurgrel/Ticagrelor OR Antithrombics: heparin/LMWH/Direct thrombin inhbitors

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5
Q

Once we know patient has ACS… what is our goal?

A

Reperfusion: #1 immediate PCI and use Thrombolytics (in UA and NSTEMI, still have some flow, so give drugs and hold off on PCI>> reevaluate in few weeks) Do cardiac Catheterization: PCI or CABG

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6
Q

What ECG and lab findings do we expect to see in STEMI?

A

ST elevation (but not always) and elevated CK and CK-MB pt will have chest pain, diaphoresis, and perhaps hitsory of DM, HTN, smoking

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7
Q

Recommend reperfusion of infarct related to STEMI?

A

IV throbmolytic therapy Emergency coronary interevention

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8
Q

How would you get acute left to right intracardiac shunt?

A

IV septum rupture

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9
Q

What would you expect to see in pt with NSTEMI on ECG and in labs

A

will have elevated enZ but will NOT have elevated ST; will be DEPRESSED!

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10
Q

Partial thrombotic occlusion of the vessel lumen results in

A

NSTEMI

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11
Q

Role of thrombolytic agents in NSTEMI

A

NONE… we don’t use them

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12
Q

General on IHD

A

leading cause of death worldwide –>after 40; risk of devo CAD is 49% men and 32% women

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13
Q

MOst common cause of IHD

A

obstruction of coronary arteries by atheromatous plaque also congenital issues, vasculitis or radiation

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14
Q

How are ACS and IHD similar?

A

Both are caused by restrictive blood flow to myocardium d/t flow restrictions in coronary arteries Supply/demand mismatch

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15
Q

Chronic stable angina on ECG and labs?

A

only ST depression during episode.. goes away and CK and MB-CK are normal

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16
Q

How will a pt with IHD present at clinic?

A

chronic chest discomfort (stable angina), have heart fail, cardiac arrythmias or have sudden death. (very similar to acute MI but more chronic in nature)

17
Q

What can we give to someone with Angina pectoris?

A

Nitroglycerin or rest

18
Q

Diagnosis of CAD: Early finding on ECG Late findings on ECG

A

Early we see ST elevation; shows that we’ve had injury Later we will see development of Q waves

19
Q

In a timeline of MI: Immidately before MI starts: Within hours after MI: Weeks later:

A

T wave inversion ST elevation Significant Q wave only

20
Q

Leads to look at for LATERAL wall damage

A

V5, V6

I, aVL

21
Q

Inferior wall leads

A

II, III, aVF

22
Q

Anterior wall leads

A

V2-V4

23
Q

Damage to LAD is likely to show up on which leads

A

V1-V6

I

aVL

(anterior leads)

24
Q

Damage to RCA likely to show up on which leads?

A

Inferior ones:

II, III, aVF

25
Q

Damage to CIRC likely to show up on which leads

A

I, aVL, V5-V6

(Lateral leads)

26
Q

What type of data do we collect during stress testing?

A

look for ECG changes (twave inversions, ST depression or elevation)

Do imaging for wall mostion abnormalities or defect

27
Q

Whats an option for stress testing in those that can’t exercise?

A

Dobutamine; will increase HR and contractility

Adenosine: cause arterial dilation for normal arteries, abnormal ones will not dilate

28
Q

What is the Gold Standard for Diagnosis of obstructed coronary blood flow?

A

Angiography

lesions of >70% are considered significant

29
Q

What medical tx can we give to pts with decreased cornary blood flow?

A

Antiplats: apsirin or ADP-R inhibitors

Beta blocks

Ca+ blockers

ACEI

Nitrates

STatins

30
Q

Aspirin therapy in pts with exsisting CAD will reduce future events by:

A

25%

31
Q

Whats all the cool shit that Beta blockers do?

A

Decrease O2 demand via decrease HR, BP, and contractility

Decrease V fib risk

Decrease automaticity; increased electrophysiologic threshold

Bradycardia wil prolong diastole thus improves diastolic perfusion

REDUCTION IN REMODELING and improves LV hemodynamics to reduce infarct

reduce risk of mortality after MI by 23%

32
Q

Metoprolol and Carvelilol are examples of what kind of drugs?

A

Beta blockers

selective for beta 1

33
Q

Overall effect of Ca+ Channel Blockers

A

reduce myocardial O2 demand and increase O2 supply

Helpful in pts with Prinzmetal

No mortality benefit, just symptom relief

34
Q

When are ACE I really beneficial

A

For pt with low LV ejection fraction after MI… can help up to 26%

(still helpful after MI by reducing mortality by 22%)

35
Q

Action of Nitrates

A

relax vascular smooth muscle

Mostly in the VENOUS system which reduces PRELOAD==> thus reduces myocardial wall tension and oxygen requirements

36
Q

Would we do revascularization for crhonic CAD?

A

we can do it electivly for symtomatic lesions:

PCI such as balloon or stent or a surgical bypass

** do this AFTER we’ve tried medical therapy and antianginal therapy as well as lifestyle changes

37
Q

What situations would CABG be preferred over PCI?

A

Left main

Triple vessel

Double vessel with proximal LAD and LVEF <50%

Diabetics

38
Q

Sequela of Chronic CAD

A

Cardiomyopathy (heart fail)

LV aneurysms

Ventricular Arrhthmias/Sudden Death

39
Q

Cardiac Arrest risk is higher post MI especially if:

A

Left ventricular ejection fraction is depressed

*put in implantable cardiac defribilatory if you have LVEF