Acute Coronary Syndrome Flashcards
What is included in ACS?
ACS basically covers acute presentations of IHD. There are 3 main types included:
- ST-elevated MI (STEMI)
- Non ST-elevated MI (NSTEMI)
- Unstable angina
What is the underlying pathophysiology of IHD?
- Initial endothelium dysfunction due to smoking, hypertension and hyperglycaemia
- Results in a number of changes in the endothelium –> proinflammatory, pro-oxidating, proliferative and reduced nitric oxide bioavailability.
- Fatty infiltration of subendothelial space by LDL particles
- Monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
- Smooth muscle proliferation and migration from the tunica media into the intima results in the formation of a fibrous capsule covering the fatty plaque.
What are the complications of atherosclerosis?
Once a plaque has formed a number of complications can develop:
- The plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
- The plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction
What are the risk factors for ischaemic heart disease? (modifiable and non-modifiable)
Unmodifiable risk factors
- Increasing age
- Male gender
- Family history
Modifiable risk factors
- Smoking
- Diabetes mellitus
- Hypertension
- Hypercholesterolaemia
- Obesity
- Sedentary lifestyle
- Cocaine use
Ischaemia vs Infarction?
Infarction –> Reduced blood supply ; reversible
Ischaemia –> process of cell necrosis/ death has begun. Presence of troponin markers
Symptoms of ACS
Acute chest pain lasting > 20 mins often associated with sweatiness, dyspnoea, palpitations.
Silent ACS –> ACS without chest pain. Seen in the elderly and diabetics
Signs of ACS
Distress, anxiety, pallor, sweatiness, sweatiness, pulse high or low, BP high or low, 4th heart sounds.
Signs of HF
Pansystolic murmur
Low grade fever
Pericardial friction rub or peripheral oedema may develop later
How is the diagnosis of ACS made?
- Increase in cardiac biomarkers (e.g. troponin) and EITHER:
2a. Symptoms of ischaemia
2b. ECG changes of new ischaemia
2c. Development of pathological Q waves
2d. New loss of myocardium
2e. Regional wall abnormalities on imaging
What investigations would you carry out for ?ACS? List them
- ECG
- CXR
- Bloods
- Cardiac enzymes
- Echo
ECG changes seen in STEMI?
Hyperacute (tall) T waves, ST elevation or new LBBB occur within hours.
T wave inversion and pathological Q waves over hours to days
ECG changes seen in NSTEMI/ unstable angina
ST depression, T wave inversion, non specific changes or normal
How may a CXR be useful in ACS?
May show cardiomegaly, pulmonary oedema or widened mediastinum
What bloods would you carry out for a patient with ?ACS
FBC U&Es Glucose Lipids Cardiac enzymes
What cardiac enzymes are measured in ACS?
Troponin T and I are most sensitive and specific markers of myocardial necrosis.
Give other differentials that could result in a raised troponin level.
Myocardial damage : myocarditis, pericarditis, ventricular strain
Non cardiac aetiology: massive PE causing right ventricular strain; subarachnoid haemorrhage, burns or sepsis; renal failure (common!!)
What are the differential diagnoses to chest pain?
Stable angina; ACS; pericarditis; myocarditis; aortic dissection; PE; oesophageal reflux/ spasm ; pneumothorax; MSK pain; pancreatitis
How would you manage a STEMI?
- Percutaneous coronary intervention (PCI) is first line - to revascularise myocardium => CATH LAB
Offer primary PCI to patients who present within 12 hours of onset of symptoms, if it can be delivered within 120 minutes of the time when fibrinolysis could have been given.
- Sublingual glyceryl trinitrate and intravenous morphine + metoclopramide should be given to help relieve the symptoms.
- Oxygen should only be given if the oxygen saturations are < 94%
- Aspirin 300mg should be given to all patients (unless contraindicated).
- A second antiplatelet is normally given, usually ticagrelor, clopidogrel or prasurgel (all are antagonists of the P2Y12 adenosine diphosphate receptor).
- Other treatments that may be given include bivalirudin (a direct thrombin inhibitor, usually given alongside aspirin + clopidogrel) and a form of heparin (either low-molecular weight or unfractionated).
What are the broad principles in the management of ACS?
- Symptom control
- Modify risk factors
- Optimise cardioprotective medications
- Revascularisation
- Manage complications
- Discharge plan
- General advice reg work and driving
How would you manage an NSTEMI?
All patients should receive:
- aspirin 300mg
- nitrates or morphine to relieve chest pain if required
- Antithrombin treatment. Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patients creatinine is > 265 µmol/l unfractionated heparin should be given.
- Clopidogrel 300mg should be given to all patients and continued for 12 months.
- Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.
- Coronary angiography should be considered within 96 hours of first admission to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically unstable.
MoA of aspirin
Antiplatelet - inhibits the production of thromboxane A2
MoA of clopidogrel
Antiplatelet - inhibits ADP binding to its platelet receptor
MoA of enoxaparin
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
MoA of fondaparinux
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
MoA of bivalirudin
Reversible direct thrombin inhibitor
