1. ACS / CAD Flashcards
What is the pathology behind coronary artery disease?
- There is an increased amount of cholesterol in the blood
- This cholesterol binds to damaged sections of the arterial wall
- White blood cells flood to the area to try and remove the cholesterol, kicking off an inflammatory process known as atherosclerosis
- Over time, this increases in size to a plaque, which eventually bulges into the vessel and obstructs blood flow
What are the non-modifiable risk factors for coronary artery disease?
- increasing age
- male sex
- family history of CAD
- Caucasian ethnicity
What causes stable angina?
Partial occlusion in a coronary artery that allows adequate blood flow to the rest of the heart at rest, but upon exercise or emotion, it does not, so results in ischaemia to part of the heart downstream from the clot
How is the pain in angina described?
Tight / Heavy strangling feeling in the chest, which does not radiate
What is unstable angina
It is the next progression from stable angina. It is a constant heaviness / tightness in the individuals chest, even when at rest
How else can angina be characterised other than stable and unstable?
Typical and atypical
What is the difference between typical angina and atypical angina? What if there is only 1 criteria met?
Typical angina has these 3 characteristics;
- Constricting discomfort in the front of the chest
- Brought on by physical exertion
- Relieved by rest or GTN within about 5 minutes.
If only 2 of these criteria are met, then it is described as atypical angina. If only 1 of the criteria is met, it is said to be non-cardiac chest pain.
What is an NSTEMI?
Non-ST elevation myocardial infarction.
It is the progression from unstable angina.
It is one of the ACS.
It is when the plaque embolises, blocking a smaller artery downstream, causing infarction distally and then ischaemia proximally
It is said to cause a subendocardial infarction
What is a STEMI?
ST elevation myocardial infarction.
It is more severe than a NSTEMI
It is when the plaque builds up and fully excludes the artery, causing widespread infarction distally, which slowly progresses proximally unless the occlusion resolves.
It is said to cause a transmural infarction
What are the 3 conditions that are included as an Acute Coronary Syndrome (ACS)?
- unstable angina
- NSTEMI
- STEMI
From most likely to least likely, in which coronary arteries do plaques commonly occur?
- Left anterior descending
- Right coronary artery
- Left circumflex artery
Are NSTEMIs or STEMIs more common?
NSTEMIs are twice as common as STEMIs
What is the hospital mortality rate of STEMIs and NSTEMIs?
What about after 6 months and beyond?
STEMI - 7% hospital mortality
NSTEMI - 3.5% hospital mortality
However after 6 months, they both have the same mortality rate, and then by 4 years, those who had an NSTEMI are 2x more likely to die
What are the 3 layers of the heart?
Endocardium - layer closest to the heart
Myocardium - muscle layer in the middle
Epicardium - this is otherwise known as the viceral layer of serous pericardium
Distal to this is the pericardial cavity, parietal layer of serous pericardium and then the fibrous later of pericardium
Where does the endocardium receive its blood supply from?
It receives oxygen directly from the blood in the ventricles and atria
In which layers of the heart are the coronary arteries found?
The major coronary arteries are found in the epicardium, with the smaller branches penetrating through into the myocardium
What effect does tachycardia have on blood flow to the cardiac muscles?
As it requires more effort, it is increasing the myocardial oxygen demand. In addition, it decreases coronary blood flow, as the duration of diastole is shortened.
Name the key branches of the right coronary artery
- right marginal artery
- posterior descending artery
Name the key branches of the left coronary artery
- left circumflex artery
- left anterior descending artery
- left marginal artery
What are the symptoms that someone with an ACS presents with?
- Central chest pain described as a crushing pain or tightness
- Radiating pain to the neck, arms (mainly left) and jaw
- Diaphoresis (sweating) due to sympathetic activation
- Nausea and vomiting due to parasympathetic response
If the pain goes away when the person rests, then this is usually stable angina.
What 3 investigations are typically performed on someone with chest pain, and what does each of them look at/for?
- ECG
- Check for / rule out STEMI or NTEMI - Blood Test
- FBC
- EUC
- Glucose
- Lipids
- Cardiac Markers - X-Ray
- To rule out other differentials, but don’t wait for this to start treatment
When should the first ECG be done on someone with chest pain?
Either in the ambulance or within 10 minutes of arrival at hospital
When should the ECG be repeated on those with chest pain?
At 3 hours, 6 hours, and then 24 hours after the initial chest pain was reported.
More importantly, it should also be repeated if they report current chest pain.
Why are ECGs not definitive?
20% of individuals with an ACS have a completely normal ECG
What ECG changes do you see in unstable angina?
You do not see any changes normally, but you can sometimes see a T-wave inversion
On an ECG, apart from the obvious, what should you look for in someone with a STEMI?
A left bundle branch block (LBBB)
How do you identify a left bundle branch block on an ECG?
Use the mnemonic ‘WILLIAM’
L reminds you its a ‘L’eft bundle branch block, and the ‘W’ (1st letter) and ‘M’ (6th letter) remind you to look at the 1st and 6th chest lead.
In the 1st lead you would see a widened QRS complex with a W shape (pointing down), and in the 6th lead you see a widened QRS with an M shape (pointing up).
What are the main cardiac markers that can be seen after an MI?
- troponins T and I
- Creatine-Kinase MB (CK-MB)
- Myoglobulin
Which cardiac marker is the gold standard to test for an MI?
Troponin T and Troponin I
At what point do troponin levels rise? When do they reach their peak? For how long can they be elevated in the blood for?
Rise after 2-4 hours of the MI
Reach their peak after 12-24 hours of the MI
Stay at elevated levels in the blood for up to a week
What cardiac markers increase in unstable angina?
None
Do cardiac markers increase more in STEMI or NSTEMI?
They increase slightly in NSTEMI, and more in a STEMI
What is the pharmacological management of those with a current STEMI?
3 categories
- Anti-ischaemic agents
- Anti-platlet agents
- Anticoagulation agents
Theres also the MOAN acronym
Name some anti-ischaemic agents used to treat ACS.
- Beta blockers
- Nitrates
- Calcium channel blockers
Name some anti-platlet agents used to treat ACS.
- aspirin
- clopidogrel
- ticagrelor
Name some anti-coagulation agents used to treat ACS.
Indirect Inhibitors
- Unfractionated heparin
- Low molecular weight heparin
- Factor Xa inhibitors
Direct inhibitors
- Dabigatran
- Apixaban
- Bivalirudin
After pharmacological management, what additional management occurs for those with a STEMI?
They get an emergency reperfusion, usually a primary percutaneous coronary intervention (PCI).
What management occurs for those with a NSTEMI?
For those with an NSTEMI, they get catagorised into high and low risk.
Those in high risk are commenced on antiplatelets, anticoagulant therapy and beta blockers. You can also consider glycoprotein IIb/ IIa inhibitor and revascularization.
Low risk patients however just require continuous monitoring of cardiac markers and ECG to see if any changes will occur. If there are changes that occur, then it’s possible that they can move into the high risk management category. If there are no changes that occur in the low risk patients, then a follow up cardiologist referral is suggested.
What long-term management is the same for all ACS patients?
- Lifestyle modifications - includes quitting smoking, reducing alcohol intake, losing weight, increasing activity
- Pharmacology therapy - this can be remembered using the mnemonic ABAS.
- Ace inhibitors / Angiotensin II receptor antagonist - This reduces blood pressure and reduces workload of the heart. ACE inhibitors should be given to everyone, and those intolerant of it should be given angiotensin II receptor blockers.
- Beta blockers - this lowers blood pressure and heart rate. It should be given to all those with left ventricular impairment (LVEF <40%)
- Aspirin and clopidogrel/ticargrelor - to help prevent clots forming. Aspirin is for life and dual antiplatelet therapy is for 12 months
- Statins - Given to everyone in order to reduce cholesterol levels, aiming for LDL < 1.8mmol/l
If a patient is on ACE inhibitors and bete blockers, and their left ventricular ejection fraction is still <35%, then they are also commenced on aldosterone antagonists.
