CVS 9 Chest Pain + Acute Coronary Syndromes Flashcards
Areas which can cause chest pain
Cardiac- cardiac muscle + pericardial sac
Respiratory - lungs + pleura
Gastro-intestinal - Oesophagus + Peptic ulcer disease
Vascular - Aortic dissection
MSK - muscle, bone, costochondritis, cartilage
Skin
What could a patient with a respiratory condition present with that a patient with acute contrary syndrome wouldn’t?
Coughing
Fever
Difference in location of chest pain caused by cardiac vs respiratory issues?
Cardiac - central
Respiratory - antero-lateral
Features of pleuritic chest pain
- Sharp, well localised
- Antero-lateral
- Worsening with breathing in or coughing
- Indicates involvement of structures with somatic innervation e.g. lung pleura, MSK structures, pericardial sac
What nerves innervate cardiac chest pain?
Visceral nerves
What nerves innervate pleuritic chest pain?
Somatic nerves
Features of cardiac chest pain
Dull/heaving
Poorly localised
Central
Can radiate to jaw, neck, shoulder + arm
Worsens with exercise
Indicates involvement of heart muscle (visceral nerves)
Why is cardiac chest pain felt centrally (+ radiation to arm)?
- Cardiac ischaemia stimulates visceral nerve endings
- signals sent to spinal cord segments T1-T4/5
- sensory afferent from T1-T4/5 Dermatomes of skin
- brain interprets pain as arising from skin
- pain perceived as arising from chest (+ limbs innervated by T1-T4/5)
What Dermatomes are involved in cardiac chest pain?
T1-T4/5
Cardiac causes of chest pain
Pericardium - pericarditis
Cardiac muscle - stable angina
- acute coronary syndromes
Typical history of pericarditis
Male > female
Often virally caused
Previous viral infection
Eased with sitting forwards
Worsened when lying supine/flat
What worsens the pain of pericarditis?
Lying supine/flat
What eases the pain of pericarditis?
Sitting forwaeds
ECG of pericarditis
Saddle shape ST elevation
PR depression
Widespread - across all leads
management of pericarditis
- treat underlying cause
- avoid strenuous activity until symptoms + inflammatory markers are resolved
- NSAIDs or colchicine
What is dressler’s syndrome?
- post MI syndrome
- occurs 2-3 weeks after acute MI
- causes pericarditis
Presentation of dressler’s syndrome
- presents 2-3 weeks after acute MI
- pleuritic chest paim
- low grade fever
- pericardial rub
Diagnosis of dressler’s syndrome
- ECG - ST elevation + T wave inversion
- echo - pericardial effusion
- raised CRP + ESR
Management of dressler’s syndrome
- NSAIDs
- steroids if more severe
- pericardiocentesis if pericardial effusion
What causes ischaemic heart disease?
Insufficient blood supply to heart muscles due to atherosclerotic disease of coronary arteries
Risk factors of acute coronary syndrome
Age
Gender
Smoking
Hypertension
Diabetes mellitus
Alcohol
Infection
Obesity
Lack of exercise
Hyperlipidaemia
Describe the plaque in stable angina
Plaque is fixed - stable occlusion
What happens if an atherosclerotic plaque ruptures in a stable occlusion in stable angina?
Thrombus formation
Sudden increased occlusion
Acute coronary syndrome occurs
Describe a thrombus in a STEMI
Complete conclusion of vessel
What eases stable angina pain?
Relieved by rest
Key differential between stable angina and acute coronary syndrome
Stable angina - pain relieved by rest
ACS - pain at rest
Are there any associated autonomic features with stable angina?
No
Similarities between pains of acute myocardial infarction + pericarditis
Felt centrally
Differences between pains of acute myocardial infarction + pericarditis
MI - pain radiates to left arm + jaw
Pericarditis - worsens on lying down
- eases when leaning forward
Differences between ECGs of STEMI + pericarditis
STEMI - ST elevation
Pericarditis - widespread saddle shaped ST elevation
ECG in unstable angina
ST depression
T wave inversion
ECG in NSTEMI
ST depression
T wave inversion
What distinguishes between unstable angina and NSTEMI
Both have ST depression + T wave inversion
Unstable angina - normal troponin
- no autonomic feature
NSTEMI - raised troponin
- associated autonomic features
What is stable angina characterised by?
Cardiac sounding pain only on exertion
Relieved by rest
Pain settles <15 minutes
What are acute coronary syndromes characterised by?
Cardiac sounding chest pain at rest
Pain >15 mins
Possible associated autonomic features
Pathology of an acute coronary syndrome
Atheromatous plaque rupture
Thrombus formation
Partial or full occlusion
What causes a type 1 myocardial infarction?
Atherosclerotic plaque rupture, ulceration, erosion or dissection > thrombus in coronary arteries > decrease in blood flow / distal embolisation > myocardial necrosis > myocardial infarction
What is type 2 myocardial infarction?
A condition other than coronary plaque instability contributes to decreased myocardial O2 supply
e.g.
Coronary artery spasm
Coronary endothelial dysfunction
Tachyarrthymias, bradyarrthymias
Anaemia
Respiratory failure
What is GTN?
Glyceryl trinitrate
Vasodilator
What is used to treat angina?
GTN
What does a ST elevation imply?
Sudden occlusion
What does a T wave inversion imply?
Under supply of blood to myocardium
Not sudden occlusion
What does a ST depression imply?
Under supply of blood to myocardium
Not sudden coronary occlusion
Blood test for NSTEMI
Troponin - raised
Cholesterol
Renal function
HbA1C (blood glucose)
Haemoglobin (anaemic?)
How is troponin measured?
Immunoassay
When is troponin raised after cardiac muscle death?
3 hours
How long does troponin remain elevated for after cardiac muscle death?
2+ weeks
General management of ACS
- chewable aspirin 300mg
- O2 if <94%
- morphine if severe pain
- IV or sublingual nitrate (not if pt is hypotensive)
Management of STEMI
- IV morphine with metoclopramide
- Chewable aspirin 300mg > 75mg od for life
- aspirin + clopidogrel + heparin
- if PCI possible within 2 hours > give praugrel + UFH
- if not possible > fibrinolysis + dabigatran | ticagrelor after procedure
- repeat ECG
Management of NSTEMI/unstable angina
- pain relief morphine
- aspirin 300mg loading dose > 75mg od
- LMWH if no immediate PCi planned
- repeat ECG
- estimate 6 month mortality e.g. GRACE
- if high risk (>3%) > PCI + prasugrel + UFH
- if low risk > ticagrelor
When is urgent PCI needed in NSTEMIs?
if patients estimated 6 month mortality if high risk >3%
If patient has ongoing CP with dynamic ECG changes
If patient develops arrhythmias with compromise
Management of acute coronary syndromes
Lifestyle changes - low fat + salt diet, regular exercise
Dual anti platelets for 12 months
Aspirin for life
Statins to lower cholesterol
Bisoprolol
ACE inhibitors
Why does chest pain in a patient with stable angina come on with exercise?
Blood flow through the left coronary artery is compromised due to shorter diastole + O2 demand has increased
What is the primary mechanism by which GTN spray alleviates myocardial ischaemia in a patient with stable angina?
Dilation of systemic veins
Why is cardiac chest pain poorly localised whereas pleuritic chest pain is well localised?
- Cardiac chest pain is innervated by visceral nerves which arises from splanchnic part of lateral plate mesoderm
- whereas pleuritic chest pain is somatic nerves
What order of ADP receptor antagonist should be given in management of STEMIs?
What loading dose for each?
Prasugrel 60mg
Clopidogrel 600mg
Ticagrelor 180mg
Why are ACEi given in STEMI management?
To prevent muscle over damage
Causes of non-cardiac chest pain
- costrochondritis
- GORD
- PE
- pneumonia
- pneumothorax
- shingles
Investigations of angina
- physical exam
- ECG
- FBC + U&Es
- LFTs + lipid profile
- thyroid function test
- HbA1C + fasting glucose
Management of stable angina
RAMPS
- Refer to cardiology
- Advise about diagnosis + managment
- Medical treatment - GTN + B blockers
- Procedural or surgical interventions: PCI or CABG
- Secondary prevention - aspirin
Medical management of stable angina
- sublingual glycerol trinitrate
- beta blocker +/- CCB e.g. Diltiazem or verapamil (both avoided in HFrEF
Surgical interventions of stable angina
- percutaneous coronary intervention (balloon + stent)
- coronary artery bypass graft
What are the 3 main options for graft vessels in a coronary artery bypass graft?
Saphenous vein
Internal thoracic artery
Radial artery
What is involved in a coronary artery bypass graft?
- midline sternotomy incision to open chest along sternum
- graft vessel is attached to affected coronary artery > bypasses stenotic area
- options for graft vessels: saphenous vein, internal thoracic artery or radial rtery
Compare PCI vs CABG scars
- PCI: brachial or femoral artery access
- CABG: midline sternotomy, scar on inner leg (saphenous vein harvesting)
Causes of raised troponin
- NSTEMI/STEMI
- chronic kidney disease
- myocarditis
- sepsis
- aortic dissection
- PE
Complications of myocardial infarction
- death
- rupture of heart septum or papillary muscles
- heart failure
- arrhythmias + aneurysm
- Dressler’s syndrome
Types of myocardial infarction
- type 1: traditional MI - sudden occulsion of vessel
- type 2: ischamia secondary to increased demand or reduced supply of O2
- type 3: sudden cardiac death or caridac arrest suggestive off ischaemic event
- type 4: MI assocaited with procedures such as PCI, CABG… (iatrogenic)
What is percutaneous coronary intervention?
- putting a catheter into patients radial artery
- fed to coronary arteries via angiography guidance
- angioplasty (balloons) used to widen lumen
- stent left in place
- then dual antiplatelet for 1 year - aspirin + clopidogrel then drop one
what is thrombolysis
injecting fibrinolytic agent e.g. streptokinase or alteplase
breaks down fibrin in blood clots
