Ischaemic Heart Disease including ACS Flashcards
Define Stable Angina [3]
Discomfort in the chest and/or adjacent areas
Associated with myocardial ischemia
But without myocardial necrosis
Name 6 causes of Stable Angina
Think in terms of things that cause:
reduced coronary blood flow, reduced oxygen transport, increased myocardial demand
Obstructive Coronary Atheroma Coronary artery spasm Coronary artery inflammation Anaemia LVH Thyrotoxicosis
What are the risk factors for SIHD? [10]
Old - Race - Male - FH - Smoker
- Low exercise - Poor Diet-
Diabetes - Hypertension - Hypercholesterolaemia
Describe the site, character and radiation of Ischaemic heart pain? [3]
Retrosternal (Centre)
Tight band/pressure or heaviness
Radiates to neck, jaw and medial arms
What triggers [4] and relieves [2] symptoms of SIHD?
Triggered by Stress, exertion, cold weather and large meals
Relieved by rest & GTN spray
What could you see on an examination of a SIHD patient?
6 signs
4 findings of exacerbating/associated conditions
Tar Staining - smoker
Obesity
Tachycardia
Xanthalasma/Corneal Arcus - Hypercholesterolaemia
Hypertensive retinopathy - DM/HTN
Pansystolic murmur at mitral - Mitral Regurgitation
Ejection systolic murmur @ Aortic area - Aortic Stenosis
Associated conditions:
Pallor- Anaemia
Elevated JVP, basal crackles & peripheral oedema - Heart Failure
Hyperreflexia - thyrotoxicosis
Reduced peripheral pulses + abdominal bruit - AAA
How would you investigate suspected SIHD? [5]
What 6 blood tests will u request?
Bloods - FBC, lipid profile, Glc, U&Es , LFTs & thyroid function CXR ECG Exercise Tolerance Test (ETT) Myocardial Perfusion Imaging Coronary Angiography
What would an ECG show in a SIHD patient? [3]
Pathological Q waves indicative of a past MI [1]
High voltages [1], ST depression [1] - Strain pattern indicates LVH
Whats the use of an ETT in a SIHD patient? [1]
What will a positive test show [1]
Can confirm the diagnosis but unsuitable in those that cannot walk for 9 mins
A +ve test shows ST depression
Treatment approach to stable angina [3]
Rx: symptom relief (lower HR + vasodilation) [1] AND influence disease progression [1]
Revascularisation by PCI or CABG [1]
What meds treat the symptoms of angina? [7]
Lower HR: \+ B-blockers, CCBs Vasodilation: \+ Isosorbide Mononitrate \+ Long acting nitrate Influence disease progression: \+ Statins, ACEi, aspirin 75mg
What type of PCI is used in coronary revascularization?
Percutaneous Transluminal Coronary Angioplasty
What are the advantages of CABG over PCI? [2]
CABG is better in multi vessel disease [1]
Unlike PCI it can help prognostically [1] as well as the symptoms.
In what unusual way can SIHD present? [3]
What demographic is this atypical presentation most common? [2]
Without pain but with SOB on exertion, Excessive Fatigue OE and Near Syncope OE.
Usually in people with reduced pain sensation e.g. elderly & diabetics
What is the classification of angina stages? [4]
Canadian Cardiovascular Society scale of Angina Severity (CCS scale):
1 - Asymptomatic unless strenous acitvity
2 - Slight limitation e.g. walking >2 blocks or mu;tiple flights of stairs
3 - Marked Limitation e.g. i flight of stairs
4 - Cant really dress or wash etc
Which long acting nitrates are used? [3]
How are GTN sprays used? [4]
IVABRADINE, NICORANDIL or RANZOLAZINE monotherapy
GTN to prevent and treat angina episodes
- taken before planned exercise and on symptoms
- repeat dose after 5 mins if not resolved
- call ambulance if not resolved 5 mins after taking second dose
Define an ACS? [2]
Any sudden cardiac event [1] suspected to be related to occlusion of the coronary arteries [1]
What is an atypical ACS presentation? [3]
In people with reduced pain sensation such as the elderly, diabetics and women, ACS can present as: SOB
Signs of heart failure (i.e. pulmonary oedema, raised JVP etc)
Nausea/vomiting
But without the classic chest pain
What causes an ACS? [2]
Rupture of thin fibrous cap with exposed necrotic core, highly inflammatory and prothrombotic
Triggers (sub)occlusive thrombus
ACS investigations for diagnosis [2] What is needed for diagnosis of MI [4]
- ECG
- Cardiac biomarkers detect cardiac cell death
Positive cardiac biomarkers + ONE OF:
- Sx of ischemia >20 mins
- New ECG changes in 2 or more contiguous leads
- Evidence of coronary problem on coronary angiogram
- Evidence of new cardiac damage on another test
Initial management for STEMI
ASPIRIN 300 MG loading dose
- PCI +/- stenting, if within 12h of symptom onset and PCI available 120 mins of admission
- Thrombolysis if PCI not available in next 120 mins
- If still ST elevation after thrombolysis, then transfer for PCI if possible
Why cant streptokinase be used more than once? What will be used instead
Its bacterial so the patient will grow immune and may even have an allergic reaction to a 2nd dose. If treatment is needed for a 2nd MI then it will be rtPA.
If theres no ST elevation how do we distinguish between NSTEMI & UAP (unstable angina pectoris?
Blood Tests for biomarkers of myocardial necrosis- cardiac troponin (cTn), specifically type I & T (type C is present in blood anyway)
If present it indicates an NSTEMI & if absent its UAP.
How do we treat NSTEMI/UAP?
Think of the acronym - give egs for each [5]
Specialist things to prescribe [1]
- MONA - aspirin 300mg
- GRACE score estimates 6 month mortality
- Low risk <3% - conservative management: give ticagrelor
- High risk >3% offer PCI, if stable within 72h, give prasugrel or ticagrelor, give uH.
What is involved in secondary prevention of ACS?
4 lifestyle mods
Rx [6]
Lifestyle modification: - Smoking Cessation - Healthy limits for alcohol consumption - Daily Exercise & healthier diet (with weight loss if applicable)
Medication: -
- Aspirin 75mg + Clopidogrel for 1 year (dual anti-platelet therapy) then aspirin alone indefinitely
- Beta-blockers to reduce average O2 demand of heart (e.g. Metopolol/Atenolol)
- Statins to lower cholesterol & so reduce risk of atheroma
- ACEI/ARB to control BP (e.g. Ramipril/Losarten respectively)
- Mineralocorticoid receptor antagonist (EPLERENONE): if EF<40% and clinical signs HF or DM (assess with echo before discharge)
Why would thrombolytics be contraindicated? Name 5 instances
When theres any chance of bleeding due to injury elsewhere in the body as thrombolytics could impair clotting
Intercranial Haemorrhage - Malignant Intercranial Neoplasm - Ischaemic Stroke - Aortic Dissectoin - Bleeding diathesis (Coagulopathy)
How do GP2b3a receptor blockers work? [2]
The GP2a3b complex is a receptor found on platelets that activates in the presence of fibrinogen. By blocking the receptor platelets arn’t activated and so clotting doesn’t occur.
What do we give following PCI? [2]
Anti-platelets e.g. Aspirin and Clopidogrel for min 12 months
Plus GP2b3a receptor antagonist acutely (Abciximab)
Troponin is not specific to MI, what are other causes of a rise in troponin [4]
How long before you’d expect a rise in MI?
- Pulmonary embolism
- Sepsis
- Renal failure
- Sub-arachnoid hemorrhage
Elevated in MI within 3-12h after onset of chest pain
5 Types of MI
Describe the difference between Type 1 and 2
Type 1: Spontaneous MI
- Associated with ischemia and due to primary coronary event
- eg plaque erosion, rupture, fissuring or dissection
Type 2
- Due to imbalance in supply and demand of oxygen
- Result of ischemia but not ischemia from thrombosis of coronary artery
5 Types of MI
Describe the 2 classifications of Type 3 MI [2]
Describe the similarities of Type 4 and Type 5 MI [2]
SCD
Verified coronary thrombus by angiography or autopsy
Type 4 and 5 are iatrogenic
- Type 4 - MI associated with PCI
- Type 5- MI associated with CABG
Causes of Type 1 MI
Whats the usual or main cause [1]
Name 5 other causes
Usually - atherosclerosis
Other causes
- Coronary vasospasm eg cocaine, triptans, 5-FU
- Cocaine, triptans, 5-FU (chemotherapy)
- Coronary dissection
- Embolism of material downstream from coronary artery eg from AF
- Inflammation of coronary arteries (vasculitis)
- Radiotherapy to chest can cause fibrosis and stenosis of coronary arteries
NSTEMI VS STEMI - what does it mean in terms of damage to heart muscle?
NSTEMI = partial thickness damage of heart muscle
STEMI full thickness damage
Acute management of ACS [5]
Investigations [1]
Blood tests [4]
- Morphine 5-10mg IV + antiemetic metoclopromide
- Give O2 non-rebreathe (if SpO2 <94%)
- GTN Sub-lingual or IV (ROA)
- Aspirin 300mg
Investigations
- Serial ECGs
Blood tests
- Check not anaemic
- Kidney function
- Cholesterol
- Thyroid