Acute myocardial infarction

Question 1

In terms of the physiological course of MI, why do people get chest pain?

Answer 1

• The metabolism is interrupted

- ADP is not being recharged to ATP so adenosine accumulates, causing angina

Question 2

What is the clinical significance of glycerol trinitrate (GTN)

Answer 2

• Used as relief for angina
• It relaxes blood vessels in your body causing them to widen and this reduces the strain on your heart, making it easier to pump blood around your body

Question 3

How can we relieve angina?

Answer 3

• Rest

- GTN

Question 4

What are the triggers of angina?

Answer 4

• cold
• exercise
• meals
• psychological stress

Question 5

Describe the site&radiation of myocardial ischaemia

Answer 5

• Diffuse
• Anterior chest
• Left arm
• Neck

Question 6

What is the significance of the duration of angina?

Answer 6

<30 mins= angina

<30 mins= MI

Question 7

As your heart becomes more damaged what does this mean for the relationship between CO and left ventricular end diastolic pressure (Frank Starling mechanism)

Answer 7

• Decreases

- relationship shown by line on graph becomes much flatter

Question 8

Outline the difference between a stable and unstable plaque

Answer 8

Stable plaque: contains fibrous cap; doesnt change in frequency and doesnt worsen over time
Unstable plaque: fibrous plaque eroded, becomes very thrombotic; can occur with or without physical exertion and rest; medicine may not relieve symptoms

Question 9

When macrophages are activated in the process of atherosclerosis what results?

Answer 9

induce intimal smooth muscle cell death and degrade matrix in the fibrous cap

Question 10

What are the 2 types of reperfusion?

Answer 10

• Mechanical

- Pharmacological

Question 11

What are cardiac biomarkers;

Answer 11

-markers to evaluate heart function
-Troponin tests measure the levels of troponin t and i.
These proteins are released when the heart muscle has been damaged

Question 12

Which drugs improve supply demand imbalance of the heart

Answer 12

• Anti-anginals including….
• beta-adrenoceptor blockers
• L-type calcium channel blockers
• Nitrates
• ATP-sensitive potassium channel openers
• If (funny current) channel blockers

Question 13

What are the non-modifiable cardiovascular risk factors

Answer 13

• family history
• age
• sex

Question 14

What are the modifiable cardiovascular risk factors

Answer 14

• Smoking
• high cholesterol
• high BP
• diabetes
• obesity/diet/exercise
• XS alcohol

Question 15

When is troponin NOT used to indicate a MI?

Answer 15

-When an ST elevation is present

Question 16

Describe ST elevation MI and its treatment

Answer 16

-Caused by a sudden complete blockage of a coronary artery
Treatment:
1.) Percutaneous coronary intervention
2.) Clot busting mechanism
3.) Coronary artery bypass graft

Question 17

Describe non-ST elevation MI and its treatment

Answer 17

-Has troponin release,so used to diagnose MI
-symptoms are chest and neck pain
-severely narrowed artery but the artery is not usually completely blocked
Treatment= often to do with minimizing blood clotting…
1.) anti platelets
2.)anti coagulants
3.) nitrates
4.) statins
5.)Beta blockers
6.) ACE inhibitors
7.) angiotensin receptor blockers (ARB’s)
8.) Angioplasty
9.) Percutaneous coronary intervention

Question 18

What different types of oedema does heart failure of the right and left heart result in

Answer 18

right heart failure= ankle oedema

left heart failure=pulmonary oedema

Question 19

How are the macrophages activated during atherosclerosis?

Answer 19

The cholesterol brawl of the plaque is a result of frustrated phagocytosis ( the macrophages thinking that the cholesterol is a foreign body and trying to digest it
-In this process the macrophages are activated and secrete enzymes that break down proteins resulting in disruption of the atherosclerotic plaque

Question 20

What is the soft interior core of the atherosclerotic plaque made up of?

Answer 20

• Fat
• cholesterol
• proteins
• calcium
• WBCs

Question 21

What is a subendocardial infarct?

Answer 21

• If patient damage is limited to the inner 1/3rd
• Partial infarct of the wall
• An ECG done at this point would show no ST elevation (NSTEMI)

Question 22

What is a transmural infarct?

Answer 22

• After about 3-6 hours the zone of necrosis extends through the entire wall thickness
• would show up as an STEMI following an ECG
• Infarct involving the whole wall thickness

Question 23

What are the symptoms of MI?

Answer 23

• chest pain/pressure (may be referred to left arm/jaw)
• diaphoresis
• nausea
• fatigue
• dyspnea

Question 24

Which 3 key proteins can be released following irreversible damage to heart cells and what can they be used for?

Answer 24

• results from membrane damage
• proteins can escape and enter the bloodstream
  1. ) Troponin I
  2. ) Troponin T
  3. ) CK-MB (creatine kinase M-B)
• Troponin I&T levels can be elevated in the blood 2-4 hours after MI; they usually peak after 48hours and stay elevated for 7-10days
• CK-MB starts to arise 2-4 hours after infarction; peaks around 24 hours and stays elevated for 48hours. As it returns the normal quickly it helps to diagnose REINFARCTION

Question 25

What complications may arise from MI?

Answer 25

• arrythmia (high risk immediately after MI)
• cardiogeneic shock= heart can’t pump enough blood
• Pericarditis= inflammed tissues, invaded by neutrophils
• scarring of the heart, resulting in growth/mishape of the heart as the scarred areas do not help to pump blood so other areas have to compensate