Angina, ACS and arrythmias Flashcards

(36 cards)

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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Angina - causes

A

Usually atheroma but rarely anaemia, aortic stenosis, tachyarrhythmias or hypertrophic CM.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

STEMI management

A
  • 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 perfusionPCI 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.
18
Q

ACS management

A
  • 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
19
Q

TIMI score and GRACE

A
  • 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.
20
Q

MI or ACS - subsequent management

A
  • 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.
21
Q

Post MI complications

A

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.

22
Q

Arrhythmias - definition

A

A disturbance in heart rhythm - usually benign and intermittent but can lead to cardiac compromise.

23
Q

Arrhythmia’s - causes

A
  • 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.
24
Q

Arrhythmia’s - history

A

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.

25
Q

Arrhythmia’s - investigations

A
  • 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.
26
Narrow complex tachycardia - definition
ECG shows a rate of \>100 bpm and the QRS complex duration of \<120ms (3 small squares).
27
Narrow complex tachycardia - DD
* ***Sinus tachycardia*** – normal P wave is followed by a normal QRS complex but rate is \>100 bpm. * ***Supraventricular tachycardia*** – the P wave is absent or inverted after the QRS complex. * ***Atrial fibrillation*** – absent P waves and irregularly irregular QRS complexes are present. * ***Atrial flutter*** – the atrial rate is usually \>300 bpm and the ECG has a ‘sawtooth’ appearance. * ***Multifocal atrial tachycardia*** – 3 or more P waves morphologies and irregular QRS complexes. * ***Junctional tachycardia*** – P waves are buried in QRS complexes or occur after them. These include AV re-entry tachycardia (e.g. WPW syndrome) and AV node re-entry tachycardia.
28
Narrow complex tachycardia - management
* Give ***O2*** if SaO2 is \<95%. * Continuous ***ECG monitoring*** – if it is irregularly irregular treat as AF if regular continue below. * If the patient is compromised use ***DC cardioversion*** – 100J, then 150J and then 200J. * ***Vagal manoeuvres*** – carotid sinus massage and the Valsalva manoeuvre. * Give ***6mg adenosine*** bolus injection (repeat 6mg once and then give 12mg if required) (lower dose if patient on dipyridamole) * Monitor for ***adverse effects*** e.g. SBP \<90 mmHg, heart failure, impaired consciousness or HR \>200 bpm. * If adverse effects use ***DC cardioversion*** – 100J, then 150J and then 200J. * If no adverse effects use one of the following – 5-10mg IV ***verapamil*** over 2 mins, 40mg IV ***esmolol*** over 1 min followed by IVI, 500μg IV ***digoxin*** over 30 mins or 300mg IV ***amiodarone*** over 1 hour.
29
Broad complex tachycardia - definition
The rate is ***\>100bpm*** and duration of the QRS complexes is ***\>0.12 secs*** (or \>3 small squares).
30
Broad complex tachycardia - DD
Most common cause is ***ventricular tachycardia*** (including torsade de pointes) but could also be ***supraventricular tachycardia*** with aberrant conduction e.g. AF or atrial flutter.
31
Broad complex tachycardia - management
* **Oxygen –** **give high flow O2, connect to cardiac monitor and gain IV acces****s****.** * **Are there adverse signs** – SBP \<90mmHg, chest pain, heart failure or heart rate \>150bpm. * If yes ***sedate*** the patient and ***perform DC cardioversion*** – 200J, 300J and finally 360J shock. * After shock or if no adverse signs – give ***300mg Amiodarone IV*** in 20-60 mins then 900mg in 24 hours. * If the arrhythmia ***does not resolve*** and not yet done sedate the patient and ***perform DC cardioversion***. * Correct ***hypokalaemia*** and ***hypomagnesaemia*** – with 60mmol KCl and 50% magnesium sulphate. * Consider ***maintenance anti-arrhythmic*** with sotolol if good LV function or amiodarone if not.
32
Atrial fibrillation - definition
* An ***irregular*** atrial rhythm at 300-600 bpm to which the AV node and ventricles responds intermittently. * When the ventricles are not primed reliably by the atria ***cardiac output falls*** by between 10 and 30%. * The main risk is ***embolic stroke*** – warfarin (INR range 2-3) reduces the risk from 4% to 1% per year.
33
AF - causes
Caffeine, alcohol, post-operatively, hypertension, MI or cardiac ischaemia, heart failure, mitral valve disease, pulmonary embolism, pneumonia, hyperthyroidism, hypokalaemia, hypomagnesaemia.
34
AF - clinical features
* ***Symptoms*** – can be asymptomatic or can cause chest pain, palpitations, dyspnoea or syncope. * ***Signs*** – irregularly irregular pulse rate, variable intensity of the 1st heart sound and signs of LV failure.
35
AF - investigations
* ***ECG*** – will shows absent P waves and irregularly irregular QRS complexes. * ***Bloods*** – for Us and Es (K+ and Mg+), cardiac enzymes (e.g. troponin) and thyroid function tests. * ***Echo*** – to look for left atrial enlargement, mitral valve disease or poor left ventricular function.
36
AF - acute management
* If patient is ***haemodynamically unstable*** – give oxygen and IV sedation or GA and perform ***emergency cardioversion*** at 100J, then 150J and 300J. If DC cardioversion unavailable give IVI (5mg/kg over 1 hour) or PO (200mg tds) ***amiodarone*** or IV ***flecanide*** (2mg/kg) over 30 mins . * ***Control ventricular rate*** – 1st line treatment is a β-blocker e.g. ***metoprolol*** (50mg bd) or a CCB e.g. ***diltiazem*** (60mg tds) or verapamil (40mg tds). 2nd line is digoxin or amiodarone. * ***Anticoagulation - ***use ***LMWH*** until an assessment for emboli has been made. If patient is high risk (previous stroke, TIA or emboli) then ***warfarin*** should be started (INR target range is 2-3). * In addition to the above look for ***associated illness*** e.g. MI or pneumonia and treat accordingly.
37
AF - chronic management
* ***Rate control*** – 1st line treatment is a β-blocker e.g. ***metoprolol*** (50mg bd) or a CCB e.g. ***diltiazem*** (60mg tds) or verapamil (40mg tds). 2nd line is digoxin followed by amiodarone. * ***Anticoagulation*** – give ***warfarin*** (INR target range of 2-3) or 300mg ***aspirin*** OD if warfarin contraindicated or risk of emboli is very low. An alternative is ***dabigatron*** (direct thrombin inhibitor) – no need for monitoring or dose adjustment and less bleeding but expensive. * ***Rhythm control*** – if symptomatic, congestive cardiac failure, young patient or first presentation. Use ***DC cardioversion*** with 4 weeks pre-treatment with sotalol or amiodarone or ***medical cardioversion*** with flecanide (if no structural heart disease) or amiodarone.