Acute coronary Syndomre Flashcards
Define an ACS?
Any sudden cardiac event suspected to be related to occlusion of the coronary arteries
What are the risk factors for an ACS?
Older Age
Male
Smoker
FH
Low Exercise/Poor diet
Hypercholesterolaemia
Hypertension
Diabetes
What are the symptoms of an ACS?
SOB
Chest Pain:
(retrosternal, radiating to arms neck/jaw) Tight band/pressure/heaviness
Cold Sweat/Nausea
Fatigue
Sense of Impending Doom
Near Syncope/dizziness
Incomplete or unchanged relief with rest & GTN
Some may also show palpitations, anxiety or a sense of impending doom
What is an atypical ACS presentation?
In people with reduced pain sensation such as the elderly, diabetics and women ACS can present as:
SOB
Signs of heart failure (i.e. pulmonary oedema, raised JVP etc)
nausea/vomiting
But without the classic chest pain
What causes an ACS?
Usually a complicated atheroma growing a thrombus and/or embolising
Also Vasospasm & vasoconstriction
What do we do first to investigate an ACS?
An ECG asap, in the ambulance if possible.
ST elevation indicates acute heart damage telling us its a STEMI
What do we do for a STEMI?
MONAC + LMWH & B-blocker
PCI in the form of angioplasty +/- stenting (within 2 hours of event or 90mins of hostpital admission)
Failing that Thrombolysis (within 90 mins of event)
How does thrombolysis work and what agents are used?
Recombinant Tissue Plasminogen Activators (rtPA) such as alteplase or bacterial enzymes such as streptokinase
Alteplase converts plasminogen -> plasmin mainly in the presence of fibrin (so is a Fibrin Specific Agent)
Streptokinase activates plasmin systemically which can lyse other plasma proteins leading to a bleeding tendency (its a non-fibrin specific thrombolytic)
What cant streptokinase be used more than once?
Its bacterial so the patient will grow immune and may even have an allergic reaction to a 2nd dose.
If treatment is needed for a 2nd MI then it will be rtPA.
If theres no ST elevation how do we distinguish between NSTEMI & UAP?
Blood Tests for biomarkers of myocardial necrosis.
The main one is cardiac troponin (cTn), specifically type I & T (type C is present in blood anyway) if present it indicates an NSTEMI & if absent its UAP.
How do we treat NSTEMI/UAP?
Analgesia: Morphine
Vasodilators: IV Nitrates (e.g. GTN or isosorbide dinitrate) + CCBs (amlodipine)
Slow Heart Rate to lower O2 demand: RL CCBs (diltiazem) and/or Beta Blocker (Atenolol)
Anti-platelets: Aspirin + Clopidogrel/Ticagrelor
Anti-coagulant: LMWH (or Fondaparinux if used quickly)
Specialist: Glycoprotein IIa/IIIb receptor blockers (GP2a/3b blockers)
Once stabilised Do a CT coronary Angiogram and possibly follow with PCI or CABG
What is involved in secondary prevention of ACS?
Lifestyle:
- Smoking Cessation
- Healthy limits for alcohol consumption
- Daily Exercise & healthier diet (with weight loss if applicable)
Medication:
- Aspirin + Clopidogrel for 1 year (dual anti-platelet therapy) then aspirin alone indefinetely
- Warfarin
- Beta-blockers to reduce average O2 demand of heart (e.g. Metopolol/Atenolol)
- Statins to lower cholesterol & so reduce risk of atheroma
- ACEI/ARB to control Blood Pressure (e.g. Ramipril/Losarten respectively)
When would thrombolytics be contraindicated?
When theres any chance of bleeding due to injury elsewhere in the body that could be ‘de-clotted’ by the thrombolytics:
Intercranial Haemorrhage - Malignant Intercranial Neoplasm - Ischaemic Stroke - Aortic Dissectoin - Bleeding diathesis (Coagulopathy)
How do GP2b3a receptor blockers work?
The GP2a3b complex is a receptor found on platelets that activates in the presence of fibrinogen.
By blocking the receptor platelets arn’t activated and so clotting doesn’t occur.
What is the treatment given at the door to ACS patients?
“MONA greets chest pain at the door”
Morphine - Oxygen - Nitroglycerin - Aspirin
Not necessarily all given or in that order.
