PBL 3: MIchael O'Conlan Flashcards
What is angina?
A clinical syndrome caused by transient myocardial ischaemia
What are the 3 features of angina?
- chest, jaw, shoulder, back and arm pain
- exertion
- relieved by rest and nitrate sprays
What are the main causes of angina?
Ischemia due to either reduction in supply or less commonly a uncompensated increase in oxygen supply
What are the causes for a reduction in supply of oxygen?
- coronary artery disease is the common
- severe anaemia
What causes coronary artery disease?
- most commonly atherosclerosis
- arterial spasms
- vasculitis
- radiation
Why might oxygen demand increase?
- left ventricular hypertrophy
- right ventricular hypertrophy
- tachycardias
What may be the cause of left ventricular hypertrophy?
Aortic stenosis or regurgitation
Hypertension
What may be the cause of right ventricular hypertrophy?
Pulmonary hypertension
Pulmonary stenosis
What is the most important diagnosis method?
HISTORY
- where is the pain? = central chest
- what provokes it? = exertion
- what is its character? - constricting tightness
- where does it radiate to? - left arm, right arm, jaw, face, shoulders, neck
- what alleviates it? - rest/GTN spray
- how long does it last? - a few minutes post exercise
- what exacerbates it? - cold weather
What are the different types of angina?
Stable and unstable
What is the difference between stable and unstable angina?
Unstable - unpredictable attack and may not have a trigger, may continue after rest medical emergency, acute coronary syndrome, partial rupture of a plaque
Stable - predictable, brought on by a trigger (stress or exercise), stops when you rest, due to atherosclerotic plaques restricting vessel lumen
What type of angina does Michael have?
Stable as occurs after exercise
How can atherosclerosis cause angina?
Narrows the coronary arteries due to the lipid plaque build up
This means less oxygen is supplied to the heart via these coronary arteries resulting in myocardial ischaemia
At rest blood flow is still enough however during exercise demand increases (exercise induced myocardial ischemia)
Pain therefore usually stops 3-10 minutes after begin rest
May get transient breathlessness
What are the risk factors of angina?
Smoking, diabetes, obesity, high cholesterol, hypertension
First degree family history of MI, sedentary lifestyle
How is angina diagnosed?
Anatomical tests look for coronary artery disease = angiography (CT or invasive)
Functional tests look for ischemia evidence = stress echo/MRI scan, perfusion scans, ECG
First line is CT coronary angiography
What would you see on ECG?
When exercise - ST depression, if depression starts prior to exercise this is a poorer prognosis
Pathological Q waves and left bundle branch block indicative of coronary artery disease
What features would not suggest a stable angina?
- continuous/prolonged chest pain
- chest pain unrelated to activity
- pain brought on by breathing
- pain associated with dizziness, palpitations, tingling, swallowing difficulty
How are symptoms managed?
- GTN (glyceryl trinitrate spray) taken sublingually (first line)
- Beta blocker or CCB - vasoconstriction of coronary arteries and negative ionotropic effects to slow down heart activity (first line)
- second line = long acting nitrate, ivabradine, nicorandil, ranolazine
- if these do not work = PCI, CABG
What are PCI and CABG?
PCI - percutaneous coronary intervention = non-surgically open up narrowed vessels with a stent
CABG - coronary angiography bypass graft = replace damaged vessel with saphenous vein/artery
How is angina prevented?
Aspirin - antiplatelet and anti-inflammatory drug decreases the chance of clot formation in atheromatous coronary arteries
Statins - inhibit hMG-coA-reductase to prevent cholesterol synthesis in the blood contributing to atherosclerosis
ACE inhibitors - hypertension/diabetes mellitus
P2Y12 receptor antagonist - after PCI or if intolerant to aspirin, receptor involved in platelet aggregation
What is acute coronary syndrome?
Myocardial Infarction and unstable angina
How does myocardial infarction occur?(pathogenesis)
Atherosclerotic plaques form in coronary arteries
If a plaque is unstable the fibrous cap can rupture -> thrombus formation -> occlusion of coronary artery -> no blood or oxygen supply to myocardium which stops contracting and cardiomyocytes die -> troponin released
What is the difference between a STEMI an a NSTEMI?
STEMI = ST elevation where there is a sudden complete blockage of a coronary artery, transmural involving whole thickness of ventricular wall
NSTEMI = severely narrowed artery but not completely blocked so no ST elevation, subendocardial confined to the inner part of myocardium
What risk factors are associated with which type of MI?
Aspirin increases risk of NSTEMI
Smoking increases risk of STEMI
What is the difference in an ECG from angina and from MI?
Angina - ST depression
MI - ST elevation if STEMI or ST not affected/ST depression if NSTEMI
What are the signs of an MI?
Tachycardia
4th heart sound (late diastolic, before S1)
Low grade fever
What are the symptoms of MI?
Chest pain - acute crushing central/left sided, lasts more than 20 minutes, radiates to jaw/left arm/epigastric region
Autonomic disturbances (sweating, nausea, vomiting)
Dyspnoea
Syncope
What are the risk factors of MI?
Unmodifiable = old age, male, family history of ischemic heart disease
Modifiable = smoking, hypertension, diabetes mellitus, hyperlipidaemia, obesity
How is an MI diagnosed?
ECG
Cardiac enzymes - creatine kinase, LDH, aspartate transaminase
Intracellular proteins - troponin I and T when myocytes necrosis occurs
How would an ECG differ between STEMI and NSTEMI?
STEMI - ST elevation, tall T waves, left bundle branch block
NSTEMI - ST depression, T wave inversion, or normal
Why is an ECG important in an MI?
Can localise the MI
Can determine if it is a STEMI or NSTEMI
When would troponin I and T be released and when would levels decrease?
Released 2-4 hours following MI
Remain elevated for up to 2 weeks
When would creatine kinase be released and when would levels decrease?
Rises 3-12 hours after MI
Returns to baseline within 48 hours
What is the immediate emergency management of an MI?
If ACS suspected:
brief history, quick physical exam, ECG
MONA - morphine, oxygen, nitrates, aspirin
How would a STEMI be managed?
- antiplatelet aspirin
- reperfusion (PCI is gold standard, then thrombolysis - streptokinase IV up to 12 hours after or TPA)
- act quick as more greater degree of necrosis for greater length of time
How is thrombolysis carried out?
Administrate tissue plasminogen activator to produce active plasmin enzyme to degrade fibrin clots restoring blood flow
What are the 5 medications patients take home?
Aspirin Statins Beta blockers ACE inhibitors Second antiplatelet agent
What are some complications of MI?
Arrhythmias - tachycardia, ventricular fibrillation
Heart failure
Pericarditis
Thromboembolism
What does aspirin do?
- COX inhibition of thromboxanes
- needed for platelet activation and aggregration
What is clopidogrel?
P2Y12 receptor antagonist
- blocks this receptor on platelets for ADP which is required for platelet aggregation and fibrin cross linking
- antiplatelet
What are the indications for special referral with angina?
- new onset
- worsening in patient with previously stable symptoms
- new/recurrent angina in patient with history of AMI/coronary revascularisation
What do you give for an NSTEMI?
- antiplatelet aspirin
- antiplatelet clopidogrel
(ANTIPLATELETS)
What is variant angina?
Also called Prinzmetal’s angina
Comes in waves due to vasospasm rather than exertion
So can happen at night/rest in coronary arteries
What is microvascular angina?
In small arteries coming off coronary arteries
