Angina, ACS and arrythmias Flashcards
2
Q
Angina - definition
A
- Myocardial ischaemia causes central chest tightness which may radiate to the jaw, teeth, neck or one or both arms.
- Associated symptoms can include dyspnoea, nausea, sweatiness or fainting.
- It is usually brought on by exertion, emotion, cold weather and heavy meals and is relieved by rest.
3
Q
Angina - causes
A
Usually atheroma but rarely anaemia, aortic stenosis, tachyarrhythmias or hypertrophic CM.
4
Q
Angina - 4 types
A
- Stable angina – only induced by significant exercise and always relieved by rest.
- Unstable or crescendo angina – increases in severity and occurs with minimal exertion or rest.
- Decubitus angina – chest pain and dyspnoea that is precipitated by lying flat e.g. at night.
- Variant or Prinzmetal’s angina – a rare form of angina that is caused by coronary artery spasm.
5
Q
Angina - ECG changes
A
- ECG – shows ST depression (ischaemia), flat or absent T waves or evidence of a previous MI.
- If resting ECG normal consider exercise ECG, thallium scan, cardiac CT or coronary angiography.
6
Q
Angina - conservative management
A
- Modify risk factors – encourage to lose weight, exercise and stop smoking. Ensure HTN and diabetes are well controlled.
- If serum cholesterol >4 mmol/L - simvastatin 40mg OD at night.
7
Q
Angina - medical management
A
- Aspirin 75 mg OD – reduces cardiac mortality.
- Atenolol 50-100mg OD – to reduce symptoms but has contraindications – respiratory diseasem LVF, bradycardia or Prinzmetal’s angina.
- Isosorbide mononitrate 20-40 mg BD for prophylaxis or symptomatic relief with sublingual GTN.
8
Q
Angina - additional medical management
A
- Diltiazem or verapamil – calcium antagonists for patients with contraindications for β blockers.
- Dihydropyridine – e.g. amlodipine - L-type calcium antagonists that can be added to β blocker.
- Nicorandil 10-30mg BD – potassium receptor activator used for angina that is still not controlled.
- Ivabradine – inhibits the pacemaker ‘funny’ current in the SA node and therefore reduces heart rate. It is useful in those that cannot take β blockers and has a similar efficacy.
- Ranalozine – inhibits the late Na+ current and so prevents calcium overload and ischaemia.
- Trimetazidine – inhibits fatty acid oxidation - myocardium uses glucose which is more efficient.
9
Q
Angina - PTCA
A
- Indications – poor response or intolerance to medical therapy, previous CABG or post thrombolysis with severe stenosis, symptoms or a positive stress test.
- Complications – restenosis (30% in 6 months), emergency CABG (3%), MI (2%) or death (0.5%).
- Stenting – NICE recommends PTCA is accompanied by stenting in 70% of patients. Combined therapy with aspirin and clopidogrel will reduce the risk of subsequent stent thrombosis.
- IV Glycoprotein IIb/IIIa inhibitors – e.g. eptifibatide can reduce rate of procedure related ischaemic events by preventing platelet aggregation and thrombus formation.
10
Q
Angina - CABG
A
- Indications – to improve survival (left main stem disease or triple vessel disease) or to relieve symptoms (if unresponsive to drugs, unstable angina or if angioplasty unsuccessful).
- Procedure – the heart is stopped and put onto cardiac bypass. The patient’s own saphenous vein or internal mammary artery (last longer) is used.
- Prognosis – If angina persists or reoccurs restart anti-anginal drugs and consider angioplasty. It is known that >50% of grafts will close within 10 years but this can be prevented with low dose aspirin.
11
Q
ACS - definition
A
- Common pathology is rupture or erosion of a coronary artery plaque leading to thrombosis. The resulting syndrome depends on whether the coronary artery is totally, partially or transiently occluded:
- STEMI - ST elevation and +++ troponin.
- Non- STEMI - no ST elevation and + troponin.
- Unstable Angina - ST depression or T wave inversion and no or trivial rise in troponin.
12
Q
ACS - risk factors
A
- Non-modifiable – increasing age, male gender and family history of ischaemic heart disease.
- Modifiable – smoking, hypertension, diabetes, hyperlipidaemia, obesity or sedentary lifestyle.
13
Q
ACS - diagnosis
A
Criteria include a rise and then fall in cardiac biomarkers e.g. troponin, symptoms of cardiac ischaemia, ECG changes, development of pathological Q waves and loss of myocardium on imaging.
14
Q
ACS - symptoms and signs
A
- Symptoms – central chest pain for >20 mins with nausea, sweatiness, dyspnoea and palpitations.
Can be silent in elderly and diabetics – syncope, pulmonary oedema, epigastric pain, vomiting, post-operative hypotension, oliguria, an acute confusional state, stroke or diabetic hyperglycaemia states.
- Signs – distress, anxiety, pallor, sweatiness, increase or decrease in pulse and blood pressure, 4th heart sound, signs of heart failure, pansystolic murmur (papillary rupture or VSD) or a low grade fever.
15
Q
ACS - investigations
A
- ECG – hyperacute (tall) T waves, ST elevation and new onset left bundle branch block within hours of an infarction. Within days T wave inversion and pathological Q waves will develop.
- CXR – to look for cardiomegaly, pulmonary oedema or a wide mediastinum in aortic rupture.
- Bloods – measure FBC, Us and Es, glucose, lipids and serial levels of cardiac enzymes.
16
Q
ACS - cardiac enzymes
A
- Cardiac troponin - most sensitive and specific marker of myocardial necrosis. Levels rise within 3-12 hours from onset of chest pain, peak at 24-48 hours and return to baseline over 5-14 days (if normal after 6 hrs and ECG normal chance of missing MI is 0.3%).
- Creatinine kinase – there are 3 isotopes (MM, BB and MB) – CK-MB levels rise within 3-12 hours of onset of chest pain, reach a peak at 24 hours and return to normal by 48-72 hours.
