cardiology Flashcards
Angina - definition
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.
Angina - causes
Usually atheroma but rarely anaemia, aortic stenosis, tachyarrhythmias or hypertrophic CM.
Angina - 4 types
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.
Angina - ECG changes
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.
Angina - conservative management
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.
Angina - medical management
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.
Angina - additional medical management
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.
Angina - PTCA
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.
Angina - CABG
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.
ACS - definition
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.
ACS - risk factors
Non-modifiable – increasing age, male gender and family history of ischaemic heart disease. Modifiable – smoking, hypertension, diabetes, hyperlipidaemia, obesity or sedentary lifestyle.
ACS - diagnosis
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.
ACS - symptoms and signs
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.
ACS - investigations
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.
ACS - cardiac enzymes
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.