acute coronary syndrome Flashcards
what are some causes of chest pain?
broken rib collapsed lung nerve infection (shingles) "pulled" muscle infection heart burn (hernia) pericarditis blood clot in the lungs (PE) Angina Myocardial infarcation
Someone comes with chest pain= ECG, take blood + look for markers- if it is an MI= troponin t and troponin I released into the blood
why is it important to define the type of ischaemic heart disease (IHD)?
For treatment, prognosis and management
Stable angina vs acute myocardial infarction – treatments and severity differ
Stable angina= not life threatening
Acute MI= life threatening and need to work quickly to get that patient restored blood flow back to the part of the affected heart.
how is IHD assessed?
- Medical history
- Risk factors
- Presenting signs and symptoms
- ECG
- Biomarkers
- Imaging/scans (to identify where the occlusion might be)
coronary heart disease can either be chronic ischaemic heart disease or acute coronary syndromes. Describe what acute coronary syndromes can lead to
unstable angina
Non ST-segment elevation MI
ST-segment elevation MI
Based on ECG results, can have a non ST-segment elevation MI and an ST-segment elevation MI.
describe the characterisation of acute coronary syndromes
plaque disruption or erosion–> thrombus formation with or without embolism–> acute cardiac ischaemia:
a) no ST segment elevation:
markers of myocardial necrosis not elevated- unstable angina
OR
elevated markers of myocardial necrosis- non-ST segment elevation myocardial infarction (Q waves usually absent)
b) ST segment elevation: elevated markers of myocardial necrosis- ST segment elevation myocardial infarction (Q waves usually present)
what is the lumen of someone with unstable angina like?
- Enough lumen diameter= enough blood flow = still have enough oxygen reaching the part of the heart that are fed by the vessel= don’t have a significant enough ischaemia that will warrant it as an MI
- Ongoing thrombosis and the underlying core of the atherosclerotic lesion= unstable
what is the lumen of someone with Non-STEMI like?
- Don’t get full occlusion of the vessels= still some lumen present= still some blood flow that allows oxygen to get to the parts of the heart that is fed from the blood vessel
- Necrotic core= thrombosis
- Platelet activation due to ongoing haemostasis and coagulation
what is the lumen of someone with STEMI like?
full occlusion of vessel
what are the treatment aims?
- Relieve symptoms
- Improve survival
- Minimise cardiac risk
Major aim of treatment should be to facilitate a return to normal activities depending of severity of MI
what are the treatment methods for recanalisation for acute myocardial infarcation
Thrombolytic treatment or primary angioplasty.
If thrombolytic agents are used and the infarct artery is not recanalised: rescue angiplasty can be done (1-2 hours after failed thrombolysis) or elective angioplasty (if continued ischaemia)/
If thrombolytic treatment is used and the infarct artery is recanalised but with signant residual stenosis, adjunctive angioplasty or deferred angioplasty can be done (1-7 days after thrombolysis)
Imaging plays a vital role in a lot of the interventional treatment (Stenting and angiography)
what are the surgical intervention treatments of acute coronary syndromes?
- Balloon angioplasty
- Stent
- Coronary bypass
Catheter inserted into vessel where plaque is:
Open up a balloon to reopen that vessel and push back the occluded plaque= can leave a stent in place.
what is the pharmacological treatment of acute coronary syndromes?
Initial pharmacological approach:
• O2 (2-4 L/min) if short of breath
• IV diamorphine with IV anti-emetic (metaclopramide or cyclizine)
• Aspirin (painkiller) and Clopidogrel (Antiplatelet)
• IV beta adrenergic antagonists (beta blocker)
• GTN (glycerine trinitrate–> vasodilatory agent)
Thrombolytics/Fibrinolytics:
•Streptokinase (SK)
•Urokinase
-Found in urine and also secreted by a lot of different cell type
-Broad role aside from activating plasminogen
•Tissue plasminogen activators (secreted from endothelial cells and present naturally)
describe tissue plasminogen activator-mediated thrombolysis
- plasmin – potent proteolytic enzyme, chews up a lot of fibrin and proteins, need a specific activity for clot- don’t want a systemic plasminogen activation. THEREFORE
- TPA is kept in a complex where its inhibitor (TPA-PAI-1) prevents plasminogen activation – do not want to unnecessarily generate a lot of plasmin
- TPA is a plasminogen activator –> activates plasminogen to plasmin
- TPA has a greater affinity for plasminogen than its inhibitor–> will dissociate from inhibitor and bind to plasminogen to activate plasmin–> allow degradation of fibrin
UPA can do the same job it is generally TPA secreted from endothelial cells that will result in the majority of the plasminogen activation that we see on a thrombus within an occluded vessel.
Fibrin degradation products= useful measures for ongoing plasminogen activations
describe streptokinase
SK is bacterial (beta-haemolytic streptococci); Possible immune recognition as it is foreign= generate immune response
- Can generate antibodies to first dose + then second dose can cause an allergic reaction in some patients
- SK will bind to circulating plasminogen not associated with fibrin – generalised plasmin generation
- Too much fibrinolysis= too much bleeding
compare the mechanism of action of tPA to SK
- tPA is a plasminogen activator
- Catalyst
- Fibrin selectivity
- Activates plasminogen to plasmin
- SK binds with free circulating plasminogen/plasmin
- Not a classic plasminogen activator like tPA
- Forms an active complex that can convert additional plasminogen to plasmin
