Acute MI

Question 1

When are thrombocytes drugs used and what do they treat?

Answer 1

NOT for MI (anymore)

Only for some types of strokes

Question 2

How are MI’s usually treated

Answer 2

Mechanical disruption of clot via balloon and stent in catch lab

Question 3

Name the AV valves on each side of the heart.

Answer 3

Left - Mitral

Right - Tricuspid

Question 4

What is the function of:

• actin
• myosin
• troponin
• tropomyosin

Answer 4

Myosin are the heads (thick)
Actin are the thin filaments
Troponin is a complex of proteins that sit on tropomyosin
Tropomyosin blocks the binding site on the actin to which the myosin heads bind

Question 5

How does muscle contraction occur with respect to the microfilament structures involved?

Answer 5

Calcium binds to troponin
This causes conformational change for tropomyosin to move and unblock the myosin binding sites on the actin
Actin and myosin then bind

Question 6

Which troponin subtype binds calcium?

Answer 6

Troponin c

Question 7

Which troponin subtypes are released in cardiac cell death (e.g. MI)?

Which is usually measured?

Answer 7

Troponin T and I

T is usually measured

Question 8

How can you distinguish cardiac from skeletal troponin?

Answer 8

There are cardiac specific troponin T and I isoforms compared to those of skeletal muscle

Multiple cardiac T isoforms
One cardiac I isoform
No cardiac C isoforms

Question 9

Why do people having an MI get chest pain?

Why do people being treated to SVT get chest pain?

Answer 9

Because nerve endings are triggered by ATP breakdown products.

Adenosine is a breakdown ATP product, therefore angina will be caused by any treatment with this same mechanism. SVT is treated with adenosine.

Question 10

Name the components of ACS.

Answer 10

Acute coronary syndrome consists of:

STEMI
NSTEMI
Unstable angina

Question 11

Why is ACS a syndrome?

Answer 11

Because it is a group of conditions (signs and symptoms)caused by decreased blood flow to the coronary arteries.

Question 12

What is the difference between stable and unstable angina?

Answer 12

Stopping the exertion/exercise in stable angina will stop the angina pain.

Question 13

When does angina occur with respect to blood flow through the coronary arteries?

What plaque size results in this?

Answer 13

Angina occurs when ‘coronary flow reserve’ is affected, this being the maximal increase in blood flow through the coronary arteries above the normal resting volume.

A plaque size of greater than 50% affects coronary flow reserve, therefore ON EXERTION with a plaque size of GREATER THAN 50% angina will occur.

Question 14

Describe angina/MI pain.

What duration of pain would constitute MI over angina?

Answer 14

Central anterior chest
Crushing
Left arm
Neck

Angina <30 mins
MI >30 mins

Question 15

By what two methods is oxygen demand compromised in coronary retry occlusion?

Answer 15

Hypoxia

Decreased cardiac output

Question 16

Why does cardiac output decrease in coronary artery occlusion?

Answer 16

Function of the area the artery supplies shits down to preserve energy usage, therefore contraction stops.

The pump is less efficient and unable to compensate for preload due to not being able to increase CO as much. Starling reflex can NOT compensate.

Question 17

How does hypoxia occur in coronary artery occlusion and how does it cause breathlessness and confusion?

Answer 17

Heart pump less efficient
Can not overcome preload easily
LV pressure increases
Therefore LA pressure increases (as the pressure backs up)
Therefore pulmonary venous pressure increases (as the pressure backs up)
Hydrostatic pressure increases
Fluid transudates into the interstitium
Pulmonary oedema occurs
Air space between alveoli and capillaries increases
Gas exchange is inhibited
This causes hypoxia and breathlessness, with the brain receiving less oxygen resulting is dizziness

Question 18

Where does oedema occur in each heart side heart failure?

• right
• left

Answer 18

RHF = ankle oedema

LHF = pulmonary oedema

Question 19

How does a coronary thrombus form?

Answer 19

Blood flow sheers the endothelial lining of the plaque exposing the collagen/cholesterol underneath.

Platelets then adhere to this, in a process called deposition or aggregation.

The clotting cascade is initiated as a result.

A fibrin mesh forms to which RBC’s attach.

Question 20

What 3 pharmacological mechanisms can interrupt the thrombus formation process?

How do they work (with examples)?

Answer 20

Statins = lowers cholesterol

Aspirin = anti-platelet = stops platelets aggregate and depose on the exposed collagen/cholesterol surface

Clot busting drugs = fibrinolytics (not used anymore) = break down fibrin mesh =streptokinase/urokinase/tissue plasminogen activators (alteplase)

Question 21

What treatment is now preferred over fibrinolytics?

Why?

Answer 21

Mechanical reperfusion with balloon and stent in cath lab.

Faster reperfusion
Less stroke/bleed risk as site specific, not generalised fibrinolysis.

Question 22

What is the indication for an STEMI?

What is the treatment?

How many patients have a STEMI out of those in total having MI’s?

Answer 22

STE and associated history

Straight to cath lab, no troponin

1/3 of patients

Question 23

What is the indication for an NSTEMI?

What is the treatment?

Answer 23

Troponin required for diagnosis

Small capillary blockages by emboli as opposed to epicardial coronary artery blockage or non-occlusive thrombi

Requires anti-platelet treatment

Question 24

How long does troponin tests take to run?

When should the bloods for these be taken?

Answer 24

4-6 hours

Should be taken on admission and again 3-6 hours later

Question 25

What would blood tests and ECG show in:

1) STEMI
2) NSTEMI
3) Unstable angina

Answer 25

All have chest pain and other aspects of suggesting Hx…

1) STE and troponin on bloods
2) Normal ECG but troponin on bloods
3) Normal ECH and NO troponin on bloods

Question 26

List some categories of drugs which improve heart oxygen supply and demand (anti-anginals) with their mechanism of action.

Answer 26

Beta blockers - negative inotropic and chronotropic effects, increases coronary perfusion time in diastole

If channel blockers (Ivabridine) - slows HR

Nitrites - smooth muscle relaxation (vessel dilation)

L-type (DHP) calcium channel blockers

Question 27

What is leg cramping/pain caused by walking short distances called?

Answer 27

Intermittent claudication

Occlusion of vessels from atherosclerotic plaques

Question 28

Differentiate between stable angina, unstable angina, NSTEMI and STEMI in terms of pathology.

Answer 28

Stable angina = atherosclerotic plaque, increased oxygen demand, vessel unable to dilate to meet demand, angina stops when exertion stops

Unstable angina = plaque ruptures, thrombus forms, partial occlusion but no infarct to the myocardium. Occurs at rest and progresses rapidly, no relief when exertion stopped (as no exertion)

NSTEMI = plaque rupture, thrombus formation partial occlusion with subendocardial myocardial infarct

STEMI = plaque rupture, thrombus formation, full occlusion, transmural myocardial infarct

Question 29

What material can be an emboli?

Answer 29

It is the transportation of ABNORMAL materials in the bloodstream impacting a vessel upstream

Thrombus fragments
Fat
Air
Many more