Acute Coronary Syndromes

Question 1

What is Acute Coronary Syndrome?

Answer 1

Consists of Unstable angina, STEMI and NSTEMI

Question 2

What is a STEMI?

Answer 2

ST Elevation Myocardial Infarction

Question 3

What is a NON STEMI?

Answer 3

Non ST Elevation Myocardial Infarction

Question 4

What is the Pathophysiology of ACS?

Answer 4

Rupture of atherosclerotic plaque in coronary arteries leads to platelet aggregation. Platelet aggregation results in the release of vasoconstricting chemicals causing the blood vessel to narrow even further

Question 5

ACS S&S?

Answer 5

Angina/severe pain
Pain persists > 15 mins
Radiating chest pain arms, back, neck,upper abdo 
Nausea 
Vomiting 
indigestion 
Dyspnea 
Diaphoresis 
Syncope 
impending doom 
Chest pain not improved by GTN after 15 mins

Question 6

What three things does a 12 lead ECG help with?

Answer 6

• Targeted pre hospital treatment
• Transport to correct hospital (PPCI capable)
• Provide info to receiving unit to prep

12-Lead ECG recommended as soon as possible in chest pain presentations. (A normal ECG does not exclude ACS)

Question 7

ACS A&M

Answer 7

ABCDE
-12 Lead (If stemi or suspected with haemo instability then TCT
-TC Transfer with monitoring
-Admin Aspirin
-Admin GTN for pain, rpt if pain persists
Admin Clopidogrel (STEMI)
-Record Obs
-SOCRATES (cardiac pain?)
-Repeat GTN if indicated
-Consider DD

Question 8

What is an infarction?

Answer 8

Tissue death from lack of blood flow

Question 9

What are atherosclerotic plaques?

Answer 9

Composed of a hard fibrous cap with an inner interior of proteins, cholesterol,calcium,fat & wbc’s.
They form on the tunica intima of arteries.

Question 10

How are atherosclerotic plaques formed?

Answer 10

An irritant such as tobacco, irritates the tunica intima the slippery inner lining of endothelial cells within the artery.
The cells are damaged
Damaged site leads to build up of atherosclerotic plaque.
This process takes years

Question 11

How do atherosclerotic plaques cause MI’s?

Answer 11

Mechanical force of blood flow rips off fibrous cap exposing soft interior.
The composites of the soft interior are thrombogenic
Platelets interact with soft interior, build up and release coagulation chemicals.
Artery is now fully occluded
This process takes a few minutes

Question 12

What three coronary arteries are most commonly implicated in MI’s?

Answer 12

Left Anterior Descending (40-50%)
Right Coronary Artery (30-40%)
Left Circumflex Artery (15-20%)

Question 13

What ventricle does MI’s most commonly affect?

Answer 13

Left Ventricle

Question 14

What are the zones supplied by the LAD, RCA & LCA called?

Answer 14

Zone of Perfusion

Question 15

During an MI at what time frame does damage start to become irreversible?

Answer 15

20-40 minutes

At this point there is now a zone of necrosis.

Question 16

What is the first area of myocardium to be affect in an MI?

Answer 16

The inner third (it is furthest from artery and subject to higher pressures from heart cavity’s)

Question 17

If the blockage resolved and damage is limited to inner third what is this called?

Answer 17

Subendocardial Infarct
(partial infarct of wall)

Question 18

How is a subendocardial infarct represented on an ECG?

Answer 18

ST Segment depression

NSTEMI

Question 19

At what time frame does zone of necrosis cover entire heart wall?

Answer 19

3-6 hours

Question 20

What is it called when zone of necrosis covers entire heart wall?

Answer 20

Transmural Infarct

total infarct of wall

Question 21

How is a transmural infract represented on an ECG?

Answer 21

ST segment elevation

STEMI

Question 22

What % of MI’s are followed by another MI?

Answer 22

10%

Question 23

What are the complications of MI?

Answer 23

IMMEDIATE
Secondary MI
Arrhythmias
Cardiogenic Shock

TO FOLLOW
Pericarditis
Myocardial Rupture
Heart Failure