Cardio Flashcards
(304 cards)
Define atherosclerosis
Inflammatory process characterised by Accumulation of lipids, macrophages, and smooth muscle cells in the intima of large and medium sized arteries, encased within a fibrous cap.
Outline the progression of atherosclerosis.
- High levels of cholesterol damages endothelium.
- LDLs pass in and out of the arterial wall in excess and accumulate in it, and there is undergoes oxidation and multiplies, leading to inflammation
- The inflammation releases chemoattractants, which attracts Macrophages try to break down, LDLs, turning into foam cells, which produce a LIPID CORE/FATTY STREAK
- This inflammatory reaction leads to tissue repair, so the smooth muscle proliferates forming a fibrous cap that encloses the lipid core.
Taken form netter illustrated pathology
Fully formed atherosclerotic plaques, can rupture -why is this?
What would a rupture plaque lead to?
The caps can rupture, this is down to the enzymatic activity breaking down the plaque more than it is being laid down. ==> this imbalance can be triggered by pneumonias/infection.
===>The microvessels in the plaque will Haemorrhage, which will lead to thrombus (clot formation and a subsequent blockage of the vessels
taken from Prof Simon Cross lecture
What are some risk factors for atherosclerosis?
What is the most significant risk factor for atherosclerosis?
age, gender, genetics, smoking, high blood pressure, high cholesterol, diabetes, and obesity.
Hypercholesterolemia is most significant RF for atherosclerosis
development
Atherosclerosis - when the endothelium is damaged, what happens that leads to inflammation?
the accumulation of LDL-cholesterol in the artery wall, which leads to the activation of inflammatory cells
Atherosclerosis - Once the endothelium wall is inflamed, what will begin to accumulate? What does this lead to?
As the endothelial cells become damaged, they begin to accumulate fats, such as cholesterol, triglycerides, and phospholipids. These fats oxidize and cause the formation of fatty plaques in the artery wall.
How does Aspirin help reduce cardiovascular disease? What type of drug is it?
It is a NSAID, can be over the counter, in cardiology, can act As an antiplatelet
It IRREVERNSIBILY blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.
taken from IHD Symposium - Acute coronary syndromes - Prof Robert Storey
What type of Drugs are
a) Clopidogrel and
b) GPIIba antagonists? What is their effect on the CV system?
a) P2Y12 receptor blockers - Drugs like Clopidogrel block the P2Y12 receptor to Reduce platelet activation
b) These block glycoprotein IIb/IIIa receptors on their platelet’s plasma membrane and inhibiting fibrinogen binding - also reduce platelet activation.
*BOTH ANTIPLATELET
taken from IHD Symposium - Acute coronary syndromes - Prof Robert Storey
What is the main cause of unstable angina, NSTEMI, and STEMI?
What are some other causes of these?
Unstable Angina and NSTEMI - Partial occlusion of coronary arteries
STEMI - complete or almost complete blockage of the coronary arteries
Most common cause -
Rupture of a fibrous cap of coronary artery plaque
Other causes:
- Coronary Spasm leading to less blood supply to myocardium
- Coronary Embolism
- Chest trauma
- Recreational drug use like Cocaine
What is the pathophysiology behind the main cause of ACS?
Rupture of a fibrous cap of coronary artery plaque
Leads to the Release of the lipid-rich atherogenic core,
Leads to causes adhesion, activation, and aggregation of platelets.
This initiates the coagulation cascade, causing a superimposed thrombus forming, leading to myocardial ischaemia/infarction
What are some key symptoms of MIs?
Acute chest pain >15 minutes
Pain that radiates to both arms, or just right arm, arms or jaw
Pain can also radiate down epigastrium (upper central part of abdoemen, or back
Diaphoresis - Sweating
Vomiting
Exertional chest pain
Breathlessness - Can be the only symptom
Syncope - Fainting
Distress, feeling of impending down
Patients with MIs can present with no pain!!
What is a Silent MI? What % of patients present with it, and it what populations is it most common?
MI without chest pain
30% of case of MI present without chest pain.
This is particularly important in:
* Women
* Those with diabetes
* The elderly
What investigations would you order for ACS/Suspected MI?
What would you look for on examination
ECG, as soon as possible
Blood Troponin Levels
FBC, Blood glucose,
Count Platelets -(due to Thrombocytopaenia, (low blood platelets) potentially occurring
Chest x-ray to look at other causes of central chest pain
Do a cardiac examination for
Pulse
BP
JVP
Murmurs
What are the ranges of troponin that are normal, and that could be indicative of an MI?
Troponin values <14ng/l normal = no MI, 14-30 ng/l = possible MI, >30ng/l = definite MI
ACS ECGs - what would you seen on an ECG with someone with unstable angina?
What is the gold standard test for diagnosing unstable angina, if Troponin test is -ve
An absence of ST elevation
typically no ECG changes
ST depression (indicates a worse prognosis), transient ST elevation, and T-wave changes may be seen
May also be Normal!!!
can be similar to NSTEMI
Gold standard test used to diagnose this condition - Angiography
What are other causes of Raised troponin other than MIs?
Causes include:
Renal failure
Myocarditis
PE
Pericarditis
Heart failure
Arrhythmia
What ECG changes would you see in a STEMI, immediately??
Peaked T wave (very tall T wave)
Raised ST-segment - this can return to normal within a few hours
Signs of a New LBBB —> M shaped waves in V6 - LBBB - become and change shape (wiLLiaM)
For any patient with new onset chest pain and LBBB on ECG you need to compare to an old ECG to see if the LBBB is new. If none is available, consider STEMI until proven otherwise.
taken from osmosis
What ECG changes would you see in a STEMI,
a) within 24 hours
b) within days
a) Inverted T waves – this may or may not persist
ST segment returns to normal.
Raised ST segments may persist if a left ventricular aneurysm develops
b) Pathological Q waves form – these may resolve in 10% of cases
Q wave is pathological if it is >25% of the height of the R wave, and/or it is greater than 1small square in width, and/or greater than 2 square squares in height
Q waves are also a sign of a previous MI – the changes in Q waves are generally permanent
picture credit - unknown
What is the first line acute management of ACS?
MONA
Morphine - For pain relief
Oxygen - ONLY IF SATS ARE LESS THAN 94% -
don’t need to give it if not!
Nitrates (GTN SPRAY) - typically fondaparinux in Sheffield - A GTN, Glyceryl Trinitrate
Aspirin 300mg chewed to increase absorption
Urgent ECG, IV access, Take history
What are nitrates, like GTN? Why are they given in ACS, and when would you not give them?
Nitrates like GTNs decrease amount of oxygen being used by heart.
==> Helps to reduce the workload on heart, prevents further damage to heart muscle.
Also help to open up the blood vessels, increasing blood flow to the heart
BUT don’t give with systolic BP <90, or with a HR <50, or left ventricular heart failure
As they lower blood pressure -
Once diagnosis of STEMI is confirmed, what is the definitive management?
Refer to cardiology urgently
First line, definitive
Percutaneous Coronary Intervention - only suitable if done within 2 HOURS OF ONSET
If PCI/angioplasty is not Available/over 2 hours - give Fibrinolysis with IV Tenecteplase
-
Aspirin, AND a PY12 inhibitor, eg
clopidogrel/ticagrelor
Give Heparin (anticoagulant)
Give Glycoprotien IIb inhibitor
Do not give anticoagulant therapy if the patient is likely to be eligible for primary PCI.
BUT – DONT GIVE FIBRINOLYSIS/THROMBOLYSIS TO THOSE WITHOUT ST ELEVATION
What do you do with your patient with suspected ACS/NSTEMI, who is unstable?
What is not considered in NSTEMI?
You need to get urgent input from seniors to arrange immediate invasive coronary angiography (with the intent to perform revascularisation) for any patient who has suspected NSTEMI and is clinically unstable
- it looks at the vessels of the heart with a dye
Do not wait for the results of troponin testing.
Thrombolysis is NOT INDICATED for NSTEMI
What is thrombolysis? When would you use it in ACS?
The second line treatment for STEMI
Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous.
From zerotofinals
How can you assess whether an NSTEMI patient would qualify for a PCI?
A Key part of management!!!
GRACE SCORE
This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
Taken from zerotofinals