Acute Coronary Syndrome (Exam 1)

Question 1

Acute Coronary Syndrome

Answer 1

Umbrella term for complication where blood supply to the heart muscle is suddenly blocked

Heart Tissue is dying

Medical emergency

Question 2

Prinzmetal Variant Angina

Answer 2

When the coronary artery vasospasms

Decrease blood flow to the cardiac tissue

Increase risk of myocardial ischemia

Question 3

Unstable Angina

Answer 3

Rupture of plaque that leads to thrombus formation in the vessel

Question 4

ACS 3 conditions

Answer 4

Unstable angina (blood supply)

Non-ST-Segment elevation MI (some blood supply)

ST-segment elevation MI (No blood flow)

Question 5

Unstable angina

Answer 5

New or changing chest pain caused by ischemia

Question 6

NSTEMI

Answer 6

non-ST segment elevation myocardial infarction

Question 7

STEMI

Answer 7

ST segment elevation myocardial infarction

Life threatening

Question 8

Prinzmetal Angina: Cause

Answer 8

Coronary artery spasm due to damage of the coronary artery

Underlying cause = Endothelial dysfunction (damage)

Question 9

Prinzmetal Angina: CAD and Timing

Answer 9

(CAD) may or may not be present

Timing:
-Rest
-Minimal exertion
-Night

Question 10

Prinzmetal Angina: ECG changes

Answer 10

Elevated ST segment

Monitor them closely

Question 11

Prinzmetal Angina: Treatment

Answer 11

Nitrate (vasodilate)

Question 12

Unstable Plaque —>ACS

Answer 12

1. Size of lipid core
   -If plaque has large lipid core it will be more unstable
2. Inflammation
   -CRP levels
   -Ongoing
3. Smooth muscle cells
   -Proliferation into intima (middle lining of blood vessel)

Question 13

Unstable Angina

Answer 13

Chest pain occurring fo the first time

Chest pain that more severe than usual with chronic angina (new regions or worse)

Emergency situation (call 911)

Question 14

Unstable Angina: Pathophysiology

Answer 14

Ruptured plaque + Thrombus forms

Size of clot and size of blockage determines the amount of blood flow that is loss

Question 15

Unstable Angina: Why is there no infarction?

Answer 15

Occlusion is partial

Thrombus dissolves

Question 16

Unstable Angina: ECG changes

Answer 16

Normal

Might see ischemic changes, typically transient (Changes go back to normal)

Question 17

Unstable Angina: Elevated cardiac enzymes

Answer 17

None

Question 18

Theory of Plaque Rupture

Answer 18

INCREASED SNS ACTIVITY

Contributing factors
(Stress) (Exercise) (Circadian Rhythms)

Increase in BP, HR, and Force of contraction
=
Increase force of coronary artery blood flow
=
Increase force exerted against injured endothelium
=
PLAQUE RUPTURE
=
Platelets adhere to plaque
=
Releases substance that attract more platelets and contribute to vasospasm
=
THROMBUS FORMATION

Question 19

ACS versus stable angina

Answer 19

Severity and duration

Relief with nitrates

Additional pain descriptors

Accompanying symptoms

(FEELING OF IMPENDING DOOM)

Question 20

Women atypically symptoms

Answer 20

Heartburn

GI

Cold sweat and unusual tiredness

Sudden dizziness

Question 21

S/S of MI

Answer 21

Diaphoresis

Dyspnea

Extreme anxiety

Levine’s sign (hand to chest) (First to chest)

Pallor

Retrosternal crushing chest pain that radiates

Weak pulses

Question 22

What is an acute MI

Answer 22

Ruptured plaque + Thrombus that disrupts blood flow is disruption and is prolonged or total

Prolonged ischemia and irreversible necrosis

Question 23

MI: ECG changes

Answer 23

Will be ECG changes

Question 24

MI: Cardiac Enzymes that are elevated

Answer 24

Increase in troponin levels (they will trend up with the infarction)

Question 25

MIs are classified by ECG finding

Answer 25

STEMI NSTEMI

Question 26

Ischemia vs infarction

Answer 26

Ischemia is when O2 supply does not meet the demands Infarction = tissue death

Question 27

ATP and Myocardial

Answer 27

Adenosine Triphosphate (energy source of cellular function) Myocardial cells cannot store and need a constant supply of O2 to make ATP When O2 goes down ATP supply goes down Heart loses ability to contract because there is no energy source

Question 28

With MI Irreversible injury occurs within

Answer 28

30 min - 4 hr

Question 29

MI: Tissue necrosis begins by

Answer 29

4 hours

Question 30

MI: Necrotic tissue is cleared away by

Answer 30

1-2 weeks but the myocardium tissue is weak and likely to rupture

Question 31

MI: Tough fibrous scar tissue replaces necrotic tissue by

Answer 31

6 weeks Electrical impulses struggle to move through scar tissues

Question 32

Three zone of injury

Answer 32

Ischemia Injury Infarciton

Question 33

Zone Damage: Infarction

Answer 33

= Necrosis MI cells are dead The cells can not be recovered but can stop in from increasing

Question 34

Zone Damage: Injury

Answer 34

Some tissue recovery possible Can still perfuse it and restore it to become viable Not dead yet

Question 35

Zone Damage: Ischemia

Answer 35

Full recovery possible

Question 36

How do we keep a patient from extending the size of the infarction

Answer 36

Increase oxygen Decrease the demand on the heart

Question 37

With an acute MI the amount damage of heart tissue depends on three factors

Answer 37

1. Location or level of occlusion in the coronary artery (large or small vessel) 2. Length of time that the coronary artery has been occluded 3. Hearts availability to collateral circulation

Question 38

STEMI versus NSTEMI: ST segment

Answer 38

STEMI = Elevated NSTEMI = Depression or normal

Question 39

STEMI versus NSTEMI: QRS

Answer 39

STEMI = Usually pathologic (wide), develops over ours NSTEMI = Normal

Question 40

STEMI versus NSTEMI: T wave

Answer 40

STEMI = Peaked, then inverted NSTEMI = Inverted

Question 41

STEMI versus NSTEMI: Troponin I

Answer 41

Elevated in both

Question 42

STEMI versus NSTEMI: Size of infarct

Answer 42

STEMI = Larger NSTEMI = Smaller

Question 43

STEMI versus NSTEMI: Outcomes

Answer 43

STEMI = Poor NSTEMI = Better

Question 44

Left Anterior Descending Artery

Answer 44

The LAD artery supplies the left ventricle Most common artery involved in MI WIDOWMAKER