Acute myocardial infarction Flashcards
In terms of the physiological course of MI, why do people get chest pain?
- The metabolism is interrupted
- ADP is not being recharged to ATP so adenosine accumulates, causing angina
What is the clinical significance of glycerol trinitrate (GTN)
- 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
How can we relieve angina?
- Rest
- GTN
What are the triggers of angina?
- cold
- exercise
- meals
- psychological stress
Describe the site&radiation of myocardial ischaemia
- Diffuse
- Anterior chest
- Left arm
- Neck
What is the significance of the duration of angina?
<30 mins= angina
<30 mins= MI
As your heart becomes more damaged what does this mean for the relationship between CO and left ventricular end diastolic pressure (Frank Starling mechanism)
- Decreases
- relationship shown by line on graph becomes much flatter
Outline the difference between a stable and unstable plaque
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
When macrophages are activated in the process of atherosclerosis what results?
induce intimal smooth muscle cell death and degrade matrix in the fibrous cap
What are the 2 types of reperfusion?
- Mechanical
- Pharmacological
What are cardiac biomarkers;
-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
Which drugs improve supply demand imbalance of the heart
- Anti-anginals including….
- beta-adrenoceptor blockers
- L-type calcium channel blockers
- Nitrates
- ATP-sensitive potassium channel openers
- If (funny current) channel blockers
What are the non-modifiable cardiovascular risk factors
- family history
- age
- sex
What are the modifiable cardiovascular risk factors
- Smoking
- high cholesterol
- high BP
- diabetes
- obesity/diet/exercise
- XS alcohol
When is troponin NOT used to indicate a MI?
-When an ST elevation is present
Describe ST elevation MI and its treatment
-Caused by a sudden complete blockage of a coronary artery Treatment: 1.) Percutaneous coronary intervention 2.) Clot busting mechanism 3.) Coronary artery bypass graft
Describe non-ST elevation MI and its treatment
-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
What different types of oedema does heart failure of the right and left heart result in
right heart failure= ankle oedema
left heart failure=pulmonary oedema
How are the macrophages activated during atherosclerosis?
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
What is the soft interior core of the atherosclerotic plaque made up of?
- Fat
- cholesterol
- proteins
- calcium
- WBCs
What is a subendocardial infarct?
- 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)
What is a transmural infarct?
- 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
What are the symptoms of MI?
- chest pain/pressure (may be referred to left arm/jaw)
- diaphoresis
- nausea
- fatigue
- dyspnea
Which 3 key proteins can be released following irreversible damage to heart cells and what can they be used for?
- 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
What complications may arise from MI?
- 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
