Angina Flashcards
Angina is caused by…?
Narrowing of coronary arteries that supply the heart with blood + oxygen
This reduces blood flow to myocardium
e.g. during high demand such as exercise there is insufficient blood (supply) to meet demand, which causes (reversible) myocardial ischaemia
Symptoms of angina
Constricting central chest pain
May radiate to jaw/arms
Associated with SOB and/or nausea, sweating, feeling faint
Aggravated by exertion or emotional stress, cold weather, hills
Relieved by GTN and rest
Define stable angina
Symptoms relieved by rest or GTN
Define unstable angina
Symptoms come on at rest
Part of acute coronary syndrome
Gold standard investigation for stable angina
Gold standard = CT coronary angiography (with contrast)
What to look for on examination?
Heart sounds - structural or valvular disease
Signs of heart failure e.g. oedema, crackles
Measure weight and waist circumference (risk factors for CVD)
Baseline investigations for angina
ECG - look for old ischaemic changes FBC - look for anaemia U+E - useful before starting ACE-i LFT - useful before starting statins Lipid profile (modifiable risk factor) TFTs (hyper/hypothyroid can be linked to angina) HbA1c
Overview of management of stable angina
Refer to SPECIALIST CHEST PAIN SERVICE/cardiology (urgently if unstable angina)
Advise about diagnosis and management, inc when to call ambulance
Treat medically
Options for surgical interventions
First line medical management of stable angina
1) Immediate relief of symptoms - glyceryl trinitrate spray
2) Prevent symptoms - beta blocker (bisoprolol 5-10mg OD) or CaB (verapamil or diltiazem)
- If poor response, increase to max tolerated dose
- If poor response to monotherapy, add the other drug. If using combo, should use nifedipine as CaB as verapamil + BB can’t be co-prescribed due to risk of complete heart block.
3) Secondary prevention for CVD - aspirin 75mg OD, atorvastatin 80mg OD, ACE-i (e.g. ramipril)
How does GTN work/how to use/side effects?
Use with symptoms
Causes systemic vasodilation so reduces LV wall stress and oxygen demand, and also increase coronary flow by coronary vasodilation
Take GTN + rest - if symptoms persist after 5 mins, repeat dose
If still in pain after another 5 mins, call ambulance
SE: headaches, low BP
Other medical options for angina if BB and CaB don’t work
- initiated by specialist
Long acting nitrates (isosorbide mononitrate)
Ivabradine
Nicorandil
Ranolazine
If taking BB and CaB, only add a third drug whilst the patient is awaiting assessment for PCI/CABG.
Surgical/procedural options
Percutaneous coronary intervention with coronary angioplasty - offered with proximal or extensive disease on CT angiography or CABG (coronary artery bypass graft) - offered if severe stenosis
Atherosclerosis - what is it
Fatty deposits in artery walls and sclerosis (hardening/stiffening) of the vessels
Affects medium and large arteries in the body
Pathophysiology of atherosclerosis
Caused by chronic inflammation and activation of immune system in the artery wall
Causes deposits of lipids in artery wall, followed by development of fibrous atheromatous plaques
Plaques cause stiffening of artery wall –> hypertension as it causes strain on heart trying to pump blood against artery wall that won’t expand with the extra pressure
Plaques also cause stenosis, reducing blood flow e.g. in angina
Plaques can also rupture and give off a thrombus, with can travel and block off distal part of vessel, causing ischaemia e.g. in ACS
Modifiable risk factors for atherosclerosis
+ how to modify for angina patients
Smoking, alcohol –> smoking cessation, alcohol advice
Poor diet, low exercise, obesity –> dietary advice, help with weight loss, exercise
Poor sleep
Stress
Diabetes –> optimise control
Hypertension –> measure BP, target 130/80, optimise control, on ACE-i
CKD
Inflammatory conditions e.g. RA
Atypical antipsychotics
Hyperlipidaemia –> atorvastatin 80mg OD
Also given aspirin 75mg OD for prevention
Non-modifiable risk factors for atherosclerosis
Older age, family history, male, ethnicity
How are plaques formed?
Injury to endothelial lining
Aggregation of platelets + release of platelet-derived growth factors
Inflammatory cells recruited
Inflammation + oedema
Inflammatory cells infiltrate cells in the intima
Smooth muscle cells proliferate and produce collagen
Plaque bulks up + narrows lumen
Macrophages and smooth muscle cells recruit circulating lipids into the plaque
Plaque gets necrotic with calcified liquid mass in centre Plaque ruptures, collagen is exposed + coagulation cascade is activated
Causes of angina
Decreased myocardial oxygen supply
- Coronary artery disease (atherosclerosis, spasm, vasculitic disorders, post-radiation therapy)
- Severe anaemia
- Hypoxia
Increased myocardial oxygen demand
- LVH – hypertension, aortic stenosis, aortic regurg, hypertrophic cardiomyopathy
- RVH – pulmonary hypertension, pulmonary stenosis
- Rapid tachyarrhythmias
- Thyrotoxicosis
Differentials for retrosternal chest pain - cardiac
Acute coronary syndrome Stable angina Dissecting thoracic aneurysm Pericarditis/cardiac tamponade Acute congestive cardiac failure Arrhythmias
Differentials for retrosternal chest pain - resp
Pulmonary embolism Pneumothorax or tension pneumothorax Community-acquired pneumonia Asthma Lung or lobar collapse Lung cancer Pleural effusion
Differentials for retrosternal chest pain - other
Acute pancreatitis Oesophageal rupture Peptic ulcer disease, gastro-oesophageal reflux, oesophageal spasm, or oesophagitis Acute cholecystitis Rib fracture Costochondritis Spinal disorders (disc prolapse, cervical spondylosis, facet joint dysfunction) Psychogenic or non-specific chest pain
What is typical angina?
Needs to be:
Precipitated by physical exertion.
AND
Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms.
AND
Relieved by rest or glyceryl trinitrate (GTN) within about 5 minutes.
What is atypical angina?
TWO OF:
Precipitated by physical exertion.
OR
Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms.
OR
Relieved by rest or glyceryl trinitrate (GTN) within about 5 minutes.
How to confirm stable angina?
Refer to specialist chest pain service
Resting 12-lead ECG ASAP - pathological Q waves, LBBB, ST segment and T wave abnormalities (indicate ischaemia or previous MI)
Bloods - FBC, U&E, LFTs, TFTs, lipids, HbA1c
Diagnostic testing - exercise ECG, single photon emission CT (SPECT), MRI myocardial perfusion imaging, stress echo (dobutamine), CT calcium score + CT coronary angiography, invasive coronary angiogram (used if CAD more likely)
Mechanism of BB in angina
+ SEs
Decrease HR, LV wall tension, and contractility.
SE: fatigue, cold peripheries, diarrhoea, nausea
Mechanism of CaB in angina
+ SEs
Decreases LV wall tension and contractility, increases coronary flow
SE: flushed face, headaches, dizziness, tiredness, skin rashes, peripheral oedema
Isosorbide mononitrate SEs
SE: headache, flushed face, hypotension.
Mechanism = vasodilation.
Ivabradine mechanism and SEs
*Patient has to be in sinus rhythm.
SE: temporary flashes of brightness in field of vision, bradycardia, AF.
Mechanism – If channel blocker, reduces pacemaker activity so reduces HR.
Ranolazine mechanism + SEs
Inhibits Na+ current, decreases ventricular diastolic tension
SE: constipation, dizziness, feeling weak, prolongs QTc.
Nicorandil mechanism + SEs
Potassium channel activator, increases coronary flow, decreases LV wall tension
Contraindicated in acute pulmonary oedema, severe hypotension, hypovolaemia, LV failure.
SE: dizziness, headaches, nausea and skin, mucosal, eye and GI ulceration.
Indications for referral to specialist cardiology service
- New onset angina
- Exclusion of angina in high risk individuals with atypical symptoms
- Worsening angina in patient with previously stable symptoms
- New or recurrent angina in patient with history of MI or coronary revascularisation
- Assessment of occupational fitness (e.g. airline pilots)
Define unstable angina
New onset angina or abrupt deterioration in previously stable angina, often occurring at rest
Requires immediate admission or referral to hospital
Part of acute coronary syndrome
How does unstable angina differ from MI?
Thrombus breaks down before infarction occurs (<20 minutes) so there are no raised cardiac markers
Symptoms and signs of unstable angina
Retrosternal chest pain radiating to jaw, arm or neck. Sweating, nausea, breathlessness, and tachycardia.
Prolonged (>15 minutes)
May be new or deterioration of stable angina (e.g. more frequent, at rest)
Haemodynamic instability
Investigations for chest pain (unstable angina)
ECG
High-sensitivity troponin I or T measurement (not elevated in angina)
Glucose, lipids, U+E (for CVD risks)
FBC (anaemia can exacerbate angina)
Thyroid function tests
LFTs and amylase — for differentials (cholecystitis and pancreatitis)
CRP and ESR — for infection or inflammation.
CXR — rule out heart failure and pulmonary pathology (not routine)
May do other investigations if ECG inconclusive e.g. echo, myocardial perfusion study, coronary angiography
ECG findings that indicate ischaemia or previous MI
Pathological Q waves
Left bundle branch block
ST-segment and T-wave abnormalities (for example T-wave flattening or elevation, or T-wave inversion)
Initial management of unstable angina
Morphine 2-5mg IV every 5-30 minutes when required (+ metoclopramide)
Oxygen (if needed)
Nitrates - GTN 0.3-0.6mg sublingually every 5 minutes or 1-2 sprays every 2-5 minutes (max 3 in 15 mins)
Aspirin - 300mg
Beta blockers (or diltiazem/verapamil)
Clopidogrel - 300mg
Heparin (unfractionated), LMWH, or fondaparinux - if angiography planned within 24 hours
Beta blockers (or diltiazem/verapamil)
Glycoprotein IIb/IIIa inhibitors e.g. eptifibatide, tirofiban, abciximab
Revascularisation procedures or conservative management if mortality 3% or less
When are glycoprotein IIb/IIIa inhibitors added in unstable angina?
If 6 month mortality above 3% or scheduled to undergo angiography within 96 hours or as adjunct to PCI
When is clopidogrel used in unstable angina?
if undergoing PCI within 24 hours or 6 month mortality of more than 1.5%
Secondary prevention for ACS
AS ABC:
ACE inhibitor
Statin
aspirin
beta-blocker
clopidogrel
Indications for immediate invasive strategy
coronary angiography + PCI if needed
- Haemodynamic instability
- Pain refractory to medical treatment
- Life-threatening arrhythmias or cardiac arrest
- Mechanical complications of MI
- Acute heart failure with refractory angina or ST deviation
- Recurrent dynamic ST or T wave changes, particularly with intermittent ST elevation
Indications for early invasive strategy
coronary angiography + PCI if needed within 24 hours
Rise or fall in troponin
Dynamic ST or T wave changes
GRACE score >140
Indications for invasive strategy within 96 hours
Predicted 6 month mortality above 3%
Heparin mechanism and side effects
Activates antithrombin III
Side effects - bleeding
thrombocytopenia,
osteoporosis, hyperkalaemia
Beta blockers mechanism and side effects
Block β1 receptors in the heart
Decrease HR, contractility, and AVN conductivity
Side-effects bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction
Clopidogrel mechanism
antagonist of the P2Y12 (ADP) receptor, inhibiting the activation of platelets
Aspirin mechanism and side effects
Blocks COX1 AND 2 (reduces ability of platelets to aggregate)
S/Es -
dyspepsia; haemorrhage
CAN GET BRONCHOSPASM, ASTHMA ATTACK
GTN mechanism and side effects
Systemic + coronary vasodilation
SE: headaches, low BP
Morphine mechanism and side effects
Arrhythmias; confusion; constipation; dizziness; drowsiness; dry mouth; euphoric mood; flushing; hallucination; headache; hyperhidrosis; hypotension (with high doses); miosis; nausea (more common on initiation); palpitations; respiratory depression (with high doses); skin reactions; urinary retention; visual impairment; vomiting (more common on initiation); withdrawal syndrome
Fondaparinux mechanism and side effects
Inhibits activated factor X
Common S/Es = anaemia; haemorrhage
ACE inhibitors mechanism and side effects
Inhibit conversion of angiotensin 1 to 2 and so reduce sympathetic activity + vasoconstriction
Common S/E = dry cough, dizziness, headaches, diarrhoea, vomiting, skin rash, blurred vision, renal impairment
Serious S/Es = hepatitis, pancreatitis, agranulocytosis and other blood disorders, MI
Statin mechanism and side effects
Inhibit HMG-CoA reductase
S/Es = myopathy, liver impairment, increased risk o f intracerebral haemorrhage in those who have had a stroke
Indications for CABG
Severe stenosis (>70%) with left main stem or triple vessel disease >50% stenosis + unresponsive severe angina, marked ST depression on exercise ECG, LMS stenosis, severe 3VD, or angina with LV dysfunction.
