Myocardial Infarction Flashcards
What is MI?
Basically when the heart muscles die from narrowed or blocked coronary arteries
What’s the cause of MI?
PACT
Platelet aggregation
Atherosclerosis
Coronary artery stenosis or spasm
Thrombosis
Modifiable and non modifiable risk factors?
Modi = HOT
NON = GIlF
MODIFIABLE
Hyperlipidemia, Hyperglycemia, HTN, Hypercholesteremia
Obesity
Tobacco use
NON
Gender - male more common
Increase in age
Lipoprotein
Family history or genetics
Why do diabetics go unnoticed?
Bc they have dead nerves due to diabetic neuropathy
S+S of MI?
PT PISS
FIRST! Chest pain
Pale peripheries and face
Tingling sensation in arm/hand
Pain @ shoulder, neck, L) arm, jaw
Indigestion like pain developing into intense chest pain
SOB
Sweating
Patho for MI?
MI happens when there is a sustained myocardial ischemia due to blockage of the coronary artery.
MOST common cause is a thrombus forming after the atherosclerotic plaque in the coronary artery ruptures.
Now this prolonged ischemia leads to irreversible hypoxia damage to the affected section of the heart (which is dependent on the vessels involved). And this will result in myocytes necrosis and will affect areas surrounding the zone of necrosis (infarct area)
What are the potential effects on the surrounding muscle cells?
There is
Myocardial stunning, hibernation and remodelling
Stunning = temporary loss of contractility lasting hours to days after reperfusion
Hibernation = prolonged loss of contractility when there is sustained ischemia
Remodelling = permanent loss of contractility with cellular hypertrophy.
What are the 2 types of MI?
STEMI (transmural)
Full thickness necrosis due to permanent blockage and ST segment is elevated
NSTEMI (subendocardial)
Partial thickness necrosis due to temporary blockage and NO ST elevation
What happens after from NSTEMI OR STEMI?
There’s a breakdown of the cell membrane leaking cardiac enzymes into the blood and results in contractile dysfunction and potential dysrrhytmia = heart failure
Diagnostic tests?
How does it relate to cardiovascular system?
ECG is one of the first investigations when a pt arrives with chest pain or suspected MI. It can diagnose ischemia and MI bc ischemia to the heart affects the cardiac conduction which can be seen as characteristic changes in the ECG.
The specific changes depend on where the infarction is located, size of area affected and the duration of the infarction.
The ECG measures electrical activity of the heart that is detectable through the skin. Usually measured as voltage over time. 10 electrodes are placed on the skin to measure 12 leads that record cardiac repolarisation and depolarisation throughout the cardiac cycle from differing directions. The leads are placed on both arms and legs with V1 to V6 leads that are placed at the anterior thoracic region.
The waveform is P Q R S T waves.
What are the ECG changes associated with MI?
Peaked T waves
Inverted T waves
ST elevation
ST depression
What is Peaked T waves?
Ischemia @ endocardium
What is inverted T waves?
Ischemia @ epicardium
What does ST elevation mean? BUT?
Transmural infarction
No O2 - heart muscles have died.
BUT! This could also mean elevated potassium levels so we need to check the troponin T levels
What is ST depression?
Subendocardial ischemia.
Low O2 - partial blockage
What would you expect from the blood tests?
I would expect cardiac enzymes, lipid and cholesterol levels to be high.
Enzymes confirm MI
Lipid and cholesterol confirms likelihood of atherosclerosis
We already talked about how due to the breakdown of myocardial cell membrane that proteins leak out of the myocytes and become detectable in the blood. Elevated cardiac enzymes are a significant marker for MI such as TROPONIN T
TROPONIN T CONFIRMS MI!!!!!
Number 1 indicator for MI. Contractile protein is only released from the myocytes when necrosis happened. So it’s highly sensitive and specific to cardiac muscle cell damage.
Troponin might not be detectable for up to 6 hours after onset of MI. So it’s usually measured on presentation and again after 10-12 hrs after onset.
Complications both Acute and Chronic
ACUTE
Cardiogenic shock - severely low BP
Dysrhythmias = heart glitches slipping into deadly rhythms. DE FIB BEFORE CPR!!!!!!!!!! - Mike had AF after de fib.
CHRONIC
HF+HF = Heart Failure => Heavy Fluids. S+S weight gain, JVD
Other pericarditis
Mitral valve prolapse
What are the steps? WHAT ARE THE 3 GOALS?
NOW
NEXT
AFTER
AVOID
NOW = MONA
NEXT = ANGIOPLASTY/THROMBOLYSIS
AFTER = PREVENTION/REST HEART
AVOID = NSAIDS
GOALS =
DECREASE HEART WORKLOAD
INCREASE O2 DELIVERY TO BODY TISSUES
REPERFUSE THE HEART WALL.
Elaborate on NOW
On admission pts gets placed on monitor, ECG taken, IV inserted, OBS taken and given medications. MONA
Morphine = Helps the heart relax to decrease workload = Relieves chest pain if not from sublingual or IV nitroglycerin
O2 = If SPO2 below 92% for perfusion
Nitroglycerin = Potent Vasodilator = Opens coronary arteries to provide O2 to heart muscle = decreases myocardial oxygen consumption and cardiac workload.
Aspirin = Slows platelet aggregation reducing the risk of further occlusion or RE occlusion of coronary arteries.
Elaborate on NEXT = Angioplasty
Re perfusion should be initiated ASAP.
Primary percutaneous intervention/angioplasty is performed in a timely fashion and is the go to choice in pts with acute ST elevation to STEMI MI. It’s to reperfuse the heart by inserting a catheter into the blocked or narrowed coronary artery to restore blood flow. To do this, we need to perform an angiogram. We inject a contrast agent into the blood stream to make the blood vessels visible on the X ray to assess damage.
Once located, angioplasty can be done.
The contrast however is very hard on the kidneys. It’s a thick dye highlighter to find blockage but for the kidneys it’s hard to wash this out of the blood. It’s like dumping cement into the washing machine of the body. So checking for increased levels of creatinine should be key.
Elaborate on NEXT = Thrombolysis
This is used when angioplasty isn’t available. Called CLOT BUSTER!
Enoxaparin is a low molecular weight heparin that prevents original arterial clot from expanding. It also allows the clot to breakdown, open blood vessels up and inhibits new clot formation. SC or IV
Tenecteplase is a fibrinolytic that binds to fibrin that holds blood clots together. It converts plasminogen to plasmin which dissolves the fibrin holding the clot together. Given IV and should be given ASAP after MI.
HUGE BLEED RISK! 8 hr window
No injections - no central lines - only pre existing IV
Elaborate on AFTER
We need to prevent and stabilise the clot.
So prior to D/C, aspirin can be prescribed. Aspirin PREVENT platelet AGGREGATION preventing blood clotting.
Anti coagulants like clopidogrel can be given with aspirin as it INHIBITS platelet ACTIVATION. Often also to prevent thrombosis after angioplasty.
And we also need the heart to rest.
So beta blockers = Metoprolol = reduces HR, CO and BP from inhibiting CATECHOLAMINES.
Nitroglycerin spray can be given to relax smooth muscles, decrease cardiac workload
Cholesterol lowering medications = Simvastatin - INHIBITS cholesterol synthesis. Should be taken at evening as the synthesis takes place as NOCTE. No grapefruit juice
Lastly LIFESTYLE CHANGE IS IMPORTANT = nicotine patches to stop smoking, change diet to low salt and fat. Plenty fruit and veggies. Monitor weight. DRESS
DIET = LOW sodium and fluids 2g/2L per day
Reduce = stress, alcohol, caffeine and animal fats
Exercise
Stop smoking
Stop sex
