Angina, ACS and arrythmias Flashcards
(36 cards)
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.
STEMI management
- Give oxygen – 2-4L aiming for SaO2 of >95% (use caution in patients with COPD).
- Give 300mg aspirin PO and 300mg clopidogrel OD (unless given by GP or paramedics).
- Give analgesia – 5-10mg morphine IV with 10mg metoclopramide IV.
- Give GTN – either 2 puffs or 1 tablet sublingually as required
- Restore perfusion – PCI is the choice within 12 hours. Where PCI is unavailable consider thrombolysis within
- 5mg atenolol IV unless contraindication and 5mg lisinopril (where SBP >120mmHg) within 24 hours.
ACS management
- Give 2-4L of oxygen – aim for SaO2 of >95% (caution in COPD).
- Give analgesia – 5-10mg IV morphine and 10mg IV metoclopramide.
- Give nitrates – GTN spray or sublingual tablets as required
- Give Low molecular weight heparin – 1mg/kg enoxaparin BD or fondaparinux (factor X inhibitor).
- Give β-blockers – 50-100mg OD metoprolol tds (if contraindicated 60-120mg OD diltiazem tds).
- Give IVI nitrates if pain continues – 50mg GTN in 50ml 0.9% saline at 2-10mL/hour.
- Do an ECG and bloods – if ischaemia, raised troponin or diabetes patient is high risk – do angiography
TIMI score and GRACE
- Thrombolysis in myocardial infarction (TIMI) score – A – age >65 years, aspirin taken within 7 days or angina >2 times within 24 hours, B – biomarkers e.g. troponin are raised, C - CAD risk factors - >3 present, D – diagnosis of CAD and E – ECG changes - >0.5mm ST elevation.
- GRACE (global registry of acute coronary events) risk score – this is recommended by NICE.
MI or ACS - subsequent management
- Bed rest for 48hrs – daily 12 lead ECG should be performed and heart, lungs and legs examined.
- Address risk factors – stop smoking, encourage exercise, treat HTN, DM and hyperlipidaemia.
- Aspirin – 75mg OD reduces the risk of vascular events e.g. MI and stroke by 29%.
- Β-blockade – give 50-100mg metoprolol tds to decrease pulse to
- ACE inhibitor – 2.5mg lisinopril OD should be given to all patients post MI.
- Statin – even is cholesterol is normal give 40mg simvastatin OD to all patients post MI.
Post MI complications
Cardiac arrest, cardiogenic shock, bradycardia or heart block, tachyarrhythmia’s, ventricular failure, pericarditis, DVT and PE, cardiac tamponade, mitral regurgitation, ventricular septal defect, Dressler’s syndrome or a left ventricular aneurysm.
Arrhythmias - definition
A disturbance in heart rhythm - usually benign and intermittent but can lead to cardiac compromise.
Arrhythmia’s - causes
- Cardiac – myocardial infarction, coronary artery disease, left ventricular aneurysm, mitral valve disease, cardiomyopathy, pericarditis, myocarditis or abnormal conduction pathways.
- Non-cardiac – caffeine, smoking, alcohol, pneumonia, drugs (β2 agonists, digoxin, L-dopa or tricyclics), metabolic disturbance (K, Ca, Mg, hypoxia or hypercapnia) or phaeochromocytoma.
Arrhythmia’s - history
Ask about palpitations – onset and offset, nature (fast or slow and regular or irregular), duration and associated symptoms - chest pain, syncope, hypotension or pulmonary oedema.
Arrhythmia’s - investigations
- Bloods – FBC, Us and Es, glucose, Ca2+, Mg2+ and thyroid function.
- ECG – look for signs of ischaemic heart disease, atrial fibrillation, short PR interval (in WPW), long QT (metabolic disturbance, congenital or drugs) or additional U waves (hypokalaemia).
- 24 hour ECG monitoring – several recordings are needed as arrhythmia may be intermittent.
- Echocardiography – to look for structural heart disease e.g. mitral stenosis or hypertrophic CM.
- Provocation tests – exercise ECG, cardiac catheterisation or electrophysiological studies.