Acute Coronary Syndrome 1 & 2

Front 1

Pathophysiological difference between stable and unstable angina?

Back 1

Stable angina is due to exertion and
increased demand in presence of stenosis; gets better with rest

Unstable angina is due to ruptured
clot and occlussion; decreased
supply; doesn't improve with rest

Front 2

Pathophysiological difference between unstable angina and NSTEMI?

Back 2

unstable angina = ischemia with no cell death

NSTEMI = ischemia with cell death of ONLY the endocardium

Front 3

Pathophysiological difference between NSTEMI and STEMI?

Back 3

Difference between NSTEMI and STEMI
is incomplete occlusion with death in the
endocardium vs complete occlusion with death in ALL layers (endo, myo, epi)

Front 4

Describe the characteristics of a stable plaque

Back 4

Thick fibrous cap with a smaller lipid rich core

Front 5

Describe the characteristics of an unstable plaque? Where is it most likely to rupture?

Back 5

Thin fibrous cap with lots of lipid

shoulder of the plaque = lots of inflammatory
cells in the area where abnormal and normal
endothelium meet —> Increased sheer stress at the shoulder makes it the most
prone to the rupture

Front 6

What is the most common source of an occlusive embolism in an MI?

Back 6

It’s more common to have a small occlusion rupture and create a big clot and cause an MI than it is to have a big occlusion rupture and cause an MI

"Dont think of an MI as slowly stenosing a vessel"

Front 7

How long can the myocardium last without O2 supply?

How does it do this?

What happens once this system is depleted?

Back 7

10-20 minutes via glycogenolysis

Once this is depleted low ATP causes the membrane to break down and release enzymes, (eg troponin) and the wall becomes stiff

Front 8

Low ATP leading to a stiff wall initially causes the wall to be _____, which progresses to the wall being ______. Finally the wall will become _______ because the infarcted area will bulge outward.

Back 8

hypokinetic > akinetic > dyskinetic

Low ATP leading to a stiff wall initially causes the wall to be hypokinetic, which progresses to the wall being akinetic. Finally the wall will become dyskinteic because the infarcted area will bulge outward.

Front 9

Clinical presentation of AMI?

Back 9

Chest discomfort

Sudden death/arrhythmia

SOB

Nausea/vomiting

diaphoresis

weakness/syncope

mild fever

anxiety/feeling of impending doom

Front 10

What is the first sign of complete occlusion (STEMI) on 12-lead EKG?

Back 10

Peaked "hyperacute" T-waves followed by ST elevation

Front 11

What change on EKG indicates necrosis and follows ST elevation?

When does this occur?

Back 11

Q-waves and decreased R-wave amplitude; occurs within hours

Front 12

What change occurs in the T-wave 1-2 days after occlusion? Is this permanent?

Back 12

T-wave inversion; can return back to normal

Front 13

Ultimate changes seen on EKG of an "old" MI (weeks later)

Back 13

ST and T are normal

Q waves remain

Front 14

Describe the evolution of the NSTEMI from initial presentation to weeks later

Back 14

Presents with ST depression or T-wave inversion with a complete return to normal weeks later (no Qs)

Front 15

How do you distinguish unstable angina from NSTEMI clinically?

Back 15

troponins

Front 16

1. What organs release troponins?

2. How long after MI do troponins elevate?

3. How long do they remain elevated?

4. What does the level of elevation represent?

Back 16

1. Only the heart

2. 2-3 hours

3. Remain elevated for 10-14 days

4. Level of elevation quantifies damage and risk for sudden death (and other outcomes)

Front 17

What is a drawback of troponins staying elevated? How do you work around this?

Back 17

If a pt with a recent MI presents a second time with chest pain etc, troponins can't be used diagnostically.

Use CKMB

Front 18

When does CKMB elevate? When does it return to normal?

Back 18

Elevates within 24 hours and returns to normal within 48-72 hours.

Front 19

Definition of Acute MI?

Back 19

1. Typical rise and fall of biochemical markers of necrosis (troponin or CKMB) with at least one of the following:

a. ischemic symptoms

b. development of pathologic Q-waves

c. ischemic EKG changes (ST depression; Twave inversion)

d. coronary intervention

OR

2. Pathological findings of acute MI

Front 20

What are the anti-ischemic therapies for ACS?

(Figure 7.10)

Back 20

1. Beta-blocker

2. Nitrates

3. +/- Calcium channel blocker

Front 21

How do each of the following contribute to anti-ischemia?

1. Beta-blocker

2. Nitrates

3. Calcium channel blocker

Back 21

1. Beta-blocker = decrease in oxygen demand, sympathetic tone, dysrrhythmias, infarct extension, and cardiac rupture.

2. Nitrates = venodilation and pain relief

3. Calcium channel blocker = decrease heart rate and contractility thru vasodilation

Front 22

"When should you use CCBs?"

Back 22

"When someone comes in with ACS and they are tachycardic and htn can’t take a beta blocker cause of bronchospasm etc"

or for recurrent ischemia after beta blockers and nitrates have been fully used

Front 23

What are the "general measures" for ACS?

(Figure 7.10)

Back 23

1. Pain control with morphine

2. Supplemental O2 as needed

3. Nitrates are also considered pain control

Front 24

How do each of the following contribute to ACS?

1. Morphine

2. Supplemental O2

Back 24

1. morphine = reduce pain and anxiety which reduce myocardial O2 needs

2. O2 = treats hypoxemia

Front 25

1. What are the two categories of antithrombic therapy for ACS?

2. What is the basis for their use?

(Figure 7.10)

Back 25

1. Antiplatelet agents and Anticoagulants

2. Prevents further propagation of the partially occlusive intracoronary thrombus while facilitating its dissolution by endogenous mechanisms

Front 26

What are the recommended antiplatelet drugs for ACS?

Back 26

ASA and clopidogrel are recommended in combination

Front 27

When is a GP IIb/IIIa antagonist recommended?

Back 27

abciximab is recommended for the highest risk pts and usually only if they are about to get PCI

Front 28

What are the recommended anticoagulant drugs for ACS? How many should you use in one pt?

Back 28

Use one:

Low Molec weight heparin

Unfractionated heparin

Front 29

What are the adjunctive therapies for ACS?

Back 29

1. ACEI/ARB

2. Statins

Front 30

Rationale for the use of an ACEI or ARB?

Back 30

limit ventricular remodeling

reduce incidence of heart failure, recurrent ischemia, and mortality.

Front 31

Rationale for the use of statins?

Back 31

reduce mortality rates

improve endothelial dysfunction, inhibit platelet aggregation, impair thrombus formation

Front 32

Two major treatment options for STEMI?

Back 32

Thrombolytics

Percutaneous Coronary Intervention (PCI)

Front 33

Physiologic basis for the use of thrombolytics?

Back 33

80% of occlusions are due to thrombus.

Accelerate the lysis of occlusive thrombus in STEMI and recanalization of the artery

Front 34

Benefits of thrombolytic therapy?

Back 34

reduce mortality

Improve LV function

Reduce incidence of CHF

Reduce arrhythmias

Front 35

Indications for fibrinolytic therapy?

Back 35

STEMI and Emergent PCI NOT available within 90 minutes

Front 36

Indications for PCI?

Back 36

STEMI and if the balloon can be inflated in the artery within 90 minutes

Front 37

How do you determine if a pt with unstable angina or NSTEMI should get PCI?

Back 37

TIMI score

Front 38

What are the 7 categories of the TIMI score and how many do you need to use PCI?

Back 38

>/= 3 of the following:

1. >65 y/o

2. 3 or more CAD risk factors

3. known coronary stenosis of >/= 50% by prior angiography

4. ST segment deviations on presenting EKG

5. At least two anginal episodes in prior 24 hrs

6. Use of ASA in prior 7 days (implies ASA resistance)

7. Elevated troponin or CKMB

Front 39

Complications of acute MI? (6)

Back 39

1.Recurrent ischemia

2. Post MI angina

3. reinfarction/infarct extension

4. Pericarditis

5. Post MI Syndrome (Dresseler's syndrome)

6. Thromboembolism

Front 40

Treatment for acute pericarditis post MI

Back 40

ASA

Front 41

What is dresseler's syndrome?

Back 41

pericarditis that occurs weeks after pt leaves the hospital; might be d/t to spilling of myocardial enzymes into the circulation; body develops immune response to those enzymes and then
reacts to them on the myocardium

Front 42

Mechanism of post MI thromboembolism?

Back 42

blood pools in the area of impaired LV contraction

Front 43

Electrical complications of MI (7)

Back 43

1. V-fib

2. V-tach

3. Accelerated Idioventricular Rhythm

4. A-fib

5. Sinus Tach

6. Sinus Brady

7. AV nodal or Bundle branch block

Front 44

Mechanical complications of Acute MI (8)

Back 44

1. LV pump failure

2. Cardiogenic shock

3. RV infarct

4. Infarct expansion

5. Myocardial rupture

6. VSD (especially in septal MIs)

7. Papillary muscle rupture

8. LV free wall rupture

Front 45

The most important predictor of post-MI outcome is

Back 45

the extent of LV dysfunction

Front 46

Standard discharge therapy for a post MI pt

Back 46

1. ASA

2. B-blocker

3. Statins

4. ACE inhibitors if LV dysfunction

5. Aldosterone antagonist if signs of heart failure

6. Treat risk factors (smoking, DM, obesity etc)

Front 47

When is an implated defibrillator indicated as part of post MI care?

Back 47

Pts with an EF < 0.30

(went with the book definition; edit as you see fit)