Cardiology: Ischaemic Heart Disease I Flashcards
How does angina typically present? [4]
Chest pain:
- Left sided
- Tight / squeezing
- Pressure like pain
- Associated SOB
- Radiates down left arm or back
Pain worse with exercise or cold weather
Pain relieved with rest
Pain relieved with GTN
Describe what is meant by cresendo angina [1]
Describe the clinical consequence of this [1]
Recent progressive drop in exercise tolerance
Suggests narrowing is getting tighter and vulnerable atherosclerotic plaque may occur
If pain at rest: unstable angina
NICE define anginal pain as what? [3]
NICE definition:
1. Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. Precipitated by physical exertion
3. Relieved by rest or GTN in about 5 minutes
Interpretation:
* Patients with all 3 features have typical angina
* Patients with 2 of the above features have atypical angina
* Patients with 1 or none of the above features have non-anginal chest pain
How long does it take for GTN to provide symptomatic relief of angina? [1]
~ 2mins
If more: then not GTN
What are the different causes of angina? [3]
Coronary Atherosclerosis
- Predominant cause
Also:
Coronary artery vasospasm:
- Constriction of the coronary arteries, leading to transient ischemia.
Microvascular dysfunction:
- Impaired function of the coronary microvasculature, leading to inadequate blood supply to the myocardium.
Extracoronary factors: which increase myocardial oxygen demand or decrease supply.
- Aortic stenosis
- Aortic regurgitation
- hypertrophic cardiomyopathy
- significant anemia
Why does AS and AR cause angina? [1]
Coronary arteries emerge just above the aortic valve: so get impeded blood flow
What is the name of this sign when asked for description of chest pain? [1]
Levine’s sign
What is decubitus angina? [1]
Form of stable angina where get pain when lying down without any apparent cause
What is meant by Prinzmetal’s or variant angina? [1]
When you get transient ST elevation due to coronary vasopasm (artery isn’t blocked, but muscle is in spasm)
What is meant by cardiac syndrome X? [1]
St depression on excerise ECG but normal angiogram
Sign of microvascular angina
What is meant by St Vincent’s angina? [1]
Not actually angina: pharyngitis due to ulcerative ginigivitis
What is the name for this sign of hyperlipdaemia? [1]
corneal arcus lipid deposits that appear as rings on the outer region of the cornea
NICE:
What investigations are used to investigate angina? [3]
1st line:
- CTCA (+calcium score)
2nd line:
- Non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line:
- Invasive coronary angiography
Describe how invasive coronary angiography occurs [3]
A catheter is inserted into the patient’s brachial or femoral artery
Directed through the arterial system to the aorta and the coronary arteries under x-ray guidance
Contrast is injected to visualise the coronary arteries and identify any areas of stenosis using x-ray images
This is considered the gold standard for determining coronary artery disease
What function investigations can you conduct for borderline cases of angina / need further investigations? [4]
- Exercise or stress ECHO
- Nuclear medicine: myocardial perfusion scan
scans use a small amount of radioactive substance to create images which show blood flow to the heart muscle - Cardiac MRI with stress perfusion
- Exercise ECG
What advice do you give when giving GTN spray? [1]
Why? [1]
Can cause dizziness: due to veno-dilatation and BP to drop
All patients with angina should be prescirbed which drugs? [2]
Aspirin 75mg (prevent risk of MI)
Statin (reduces cholesterol)
Describe the treatment algorithm for stable angina patients [5]
Sublingual glyceryl trinitrate to abort angina attacks
All patients:
- Aspirin 75 mg
- Statin
1st line:
- Beta blocker: e.g. metoprolol
- CCB: e.g. Amlodopine
- If there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od)
- If a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa
2nd line:
- a long-acting nitrate: Isosorbide mononitrate
- ivabradine
- nicorandil
- ranolazine
3rd line:
- CABG
- PCI
Beta blockers shouldn’t be prescribed alongside which angina medication? [1]
Why? [1]
Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
Coadministration of verapamil and β-blockers results in additive negative inotropic, chronotropic and dromotropic (conduction properties) effects on the heart.
If a CCB is being used as first line tx for stable angia, what type should be used? [1]
Give two examples [2]
If a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used.
What do you need to consider about nitrate therapy for stable angina? [1]
How do you modifiy treatment to allow for this? [1]
Nitrate tolerance can occur
The BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness
Describe the MoA of ivabradine [1]
** pacemaker current inhibitor**: slows the HR down (not a Beta blocker)
Describe the MoA of ranolizine [1]
Late Na current blocker
Nicorandil has a rare AE of ? [1]
GI ulceration
How can you remember the drugs used for secondary prevention of stable angina patients? [4]
4 As:
A – Aspirin 75mg once daily
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
A – Already on a beta blocker for symptomatic relief
Why do you get nausea, anxiety or sweating when have ACS? [1]
Undergoing adrenaline surge:
Due to severe ischaemia; causes necrosis; negative feedback loop causes huge amount of adrenaline released
Describe the pathophysiology of ACS ]3
Myocardial damage secondary to ischaemia
Generally occurs after following steps:
Step 1 - endothelial dysfunction
* Endothelial injury causes a local inflammatory response.
* If the injury recurs or healing is incomplete, inflammation may continue leading to the accumulation of low-density lipoproteins (LDL).
* These become oxidised by local waste products creating reactive oxygen species (ROS).
Step 2 - plaque formation
* In response to these irritants, endothelial cells attract monocytes (macrophages).
* These engulf (phagocytose) the LDLs swelling to become foam cells and ‘fatty streaks’.
Step 3 - plaque rupture
* Continued inflammation triggers smooth muscle cell migration.
* This forms a fibrous cap, which together with the fatty streaks, develops into an atheroma.
* The top of the atheroma forms a hard plaque.
* This may rupture through its endothelial lining exposing a collagen-rich cap.
* Platelets aggregate on this exposed collagen forming a thrombus that may occlude or severely narrow the vessel.
* Alternatively, the thrombus may break lose, embolising to infarct a distant vessel.
How do you assess ACS patient? [4]
ABCD
Airway:
- Patent?
Breathing:
- RR?
- Saturations?
- Pulmonary oedema due to LV impairment can cause hypoxia
Circulation:
- HR
- BP
Disability:
- GCS
DONT FORGET GLUCOSE
ACS causing bradycardia can indicate MI in which part of heart? [1]
Why? [1]
Inferior MI
Right coronary artery perfuses the sinoatrial node, heart block and bradycardia may occur
go over heart anatomy & SALI
What is LDL target for secondary prevention of MI? [1]
< 1.4
What are target times for coronary angiography for:
STEMI [1]
NSTEMI [1]
STEMI: < 6 hours
NSTEMI: < 72 hours
In cases of primary PCI, which is the first line P2Y12 inhibitor? [1]
Why? [1]
Ticagrelor: most rapidly acting
What is the difference between myocardial infarction and myocardial injury? [2]
Myocardial injury = trop > 99% percentile ULN
Acute MI = Injury +
- Symptoms
- ECG changes
- Imaging showing loss of viable myocardium
- Evidence of coronary aetiology
Implies ischaemia
