Acute MI Flashcards
When are thrombocytes drugs used and what do they treat?
NOT for MI (anymore)
Only for some types of strokes
How are MI’s usually treated
Mechanical disruption of clot via balloon and stent in catch lab
Name the AV valves on each side of the heart.
Left - Mitral
Right - Tricuspid
What is the function of:
- actin
- myosin
- troponin
- tropomyosin
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
How does muscle contraction occur with respect to the microfilament structures involved?
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
Which troponin subtype binds calcium?
Troponin c
Which troponin subtypes are released in cardiac cell death (e.g. MI)?
Which is usually measured?
Troponin T and I
T is usually measured
How can you distinguish cardiac from skeletal troponin?
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
Why do people having an MI get chest pain?
Why do people being treated to SVT get chest pain?
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.
Name the components of ACS.
Acute coronary syndrome consists of:
STEMI
NSTEMI
Unstable angina
Why is ACS a syndrome?
Because it is a group of conditions (signs and symptoms)caused by decreased blood flow to the coronary arteries.
What is the difference between stable and unstable angina?
Stopping the exertion/exercise in stable angina will stop the angina pain.
When does angina occur with respect to blood flow through the coronary arteries?
What plaque size results in this?
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.
Describe angina/MI pain.
What duration of pain would constitute MI over angina?
Central anterior chest
Crushing
Left arm
Neck
Angina <30 mins
MI >30 mins
By what two methods is oxygen demand compromised in coronary retry occlusion?
Hypoxia
Decreased cardiac output
Why does cardiac output decrease in coronary artery occlusion?
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.
How does hypoxia occur in coronary artery occlusion and how does it cause breathlessness and confusion?
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
Where does oedema occur in each heart side heart failure?
- right
- left
RHF = ankle oedema
LHF = pulmonary oedema
How does a coronary thrombus form?
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.
What 3 pharmacological mechanisms can interrupt the thrombus formation process?
How do they work (with examples)?
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)
What treatment is now preferred over fibrinolytics?
Why?
Mechanical reperfusion with balloon and stent in cath lab.
Faster reperfusion
Less stroke/bleed risk as site specific, not generalised fibrinolysis.
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?
STE and associated history
Straight to cath lab, no troponin
1/3 of patients
What is the indication for an NSTEMI?
What is the treatment?
Troponin required for diagnosis
Small capillary blockages by emboli as opposed to epicardial coronary artery blockage or non-occlusive thrombi
Requires anti-platelet treatment
How long does troponin tests take to run?
When should the bloods for these be taken?
4-6 hours
Should be taken on admission and again 3-6 hours later
What would blood tests and ECG show in:
1) STEMI
2) NSTEMI
3) Unstable angina
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
List some categories of drugs which improve heart oxygen supply and demand (anti-anginals) with their mechanism of action.
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
What is leg cramping/pain caused by walking short distances called?
Intermittent claudication
Occlusion of vessels from atherosclerotic plaques
Differentiate between stable angina, unstable angina, NSTEMI and STEMI in terms of pathology.
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
What material can be an emboli?
It is the transportation of ABNORMAL materials in the bloodstream impacting a vessel upstream
Thrombus fragments
Fat
Air
Many more
