Case 1 - Chest Pain Flashcards
Differentials for chest pain
Describe their symptoms
ACS - tight, crushing chest pain, radiates to shoulder, neck, arms, jaw, sweaty and clammy. Lasts minutes to hours
Angina - as for ACS, but worsened on exertion, and relieved by rest/GTN
Aortic dissection - shearing, ripping pain, radiating to the back. Lasts minutes/seconds
GORD - indigestion, epigastric pain, associated with eating
PE - pleuritic chest pain and SOB
MSK/costochondritis - worse on touching, lasts hours to days. Achey pain
Pericarditis - central chest pain, relieved by sitting up
What is ACS?
Spectrum of disease from unstable angina > NSTEMI > STEMI
What is the definition of unstable/stable angina?
Stable angina meets all of:
- constricting chest/neck/jaw pain
- Worsened or precipitated by exertion
- Relived by rest/GTN within 5 minutes
Unstable angina only meets 2 of above
Pathophysiology of ACS
Atherosclerotic plaque Plaque ruptures Narrowed lumen in vasoconstriction Decreased blood flow through coronarys Ischaemia of tissues
Image of heart arteries
LAD R marginal L circumflex Posterior descending L marginal
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Image of heart veins
Coronary sinus
Great cardiac vein
Middle cardiac vein
Small cardiac vein
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Risk factors for ACS
Increasing age HTN Hyperlipidaemia Smoker Alcohol excess Poor diet Lack of exercise Psychosocial stress
Investigations for ACS
1) ECG
2) Troponins and other bloods
3) CT angiography
4) Non-invasive testing if CT angiogram is inconclusive e.g. echo
Potential ECG changes in ACS
A normal ECG does not rule out ACS
V1 and V2=Septal
V3 and V4=Anterior
V5 and V6 and leads I, aVL=lateral
Leads II, III and avF=inferior
May see STEMI and reciprocal depression - elevation=infarction, depression=ischaemia
Pathological (broad) Q waves may indicate previous MI
At what intervals should you perform an ECG?
At 0, 3, 6, 24 hours
What might troponins show in MI?
Troponins should be performed at baseline
Greater than 50% rise in 6 hours is diagnostic of MI
Start to rise at 2-4 hours post-MI, peak at 24-48 hours
Troponins I and T are cardio-specific, but rise could be due to a number of cardiac pathologies and therefore are not specific for MI
Unstable angina will not have a rise in troponin as there is no necrosis
What might CT angiography show?
When is it indicated?
Inject dye, and then can visualise the blood supply to the heart Can see areas of narrowing Indicated in: -angina -ST changes
What is the initial treatment for a STEMI?
Morphine for analgesia Oxygen if sats<96% ORA Nitrates ie. GTN Aspirin - 300mg loading dose Clopidogrel
What is the treatment for stable angina?
Stop exertion and rest Take GTN spray Wait 5 mins If symptoms not relieved, take a 2nd spray Wait 5 mins If symptoms not relives, call 999
What is the treatment for unstable angina and NSTEMI?
Loading dose of 300mg aspirin
Give fondaparinux unless CT angio planned within 24hours (clopidogrel instead)
Perform CT angiography in any patient above low risk
Consider stents, CABG, PCI etc.
Aspirin and ticagrelor for 12 months
Clopidogrel add on for higher risk
Glycoprotein inhibtiors add on for higher risk
What is the treatment for a STEMI?
Assess eligibility for coronary reperfusion
Give coronary angiography with PCI if:
-present within 12 hours of onset of symptoms
-PCI can be given within 2 hours of when fibrinolysis can be given
PCI could insert stents, aspirate thrombus etc.
Otherwise give alteplase, and coadminister anti-thrombin and reassess for PCI
Perform ECG at 60-90mins, if still in STEMI, perform coronary angio and PCI
Long-term drugs that might be given following ACS?
Beta blockers
Statins
ACE-i/ARB
Antiplatelets/anticoagulants
Complications of an MI
Death
Arrythmia - particular if infarct in RA
Rupture - if of ventricular wall could > tamponade
-if of papillary muscle > valvular inversion > regurgitation
-if of ventricular wall > mixing of blood > hypoxaemia > further damage
Tamponade
Heart Failure
Valvular disease Aneurysm Dresslers - a secondary pericarditis following autoimmune response Embolism Regurgitation
Describe the normal heart sounds and the anatomy they correspond to
Normal heart sounds are S1 and S2
S1 is start of systole
S2 is start of diastole
S1 is the closure of the mitral and tricuspid valves
S2 is the closure of aortic and pulmonary valves
Describe the features of aortic stenosis
An ejection click systolic murmur, as the blood initially flows very quickly through the valve and then decreases speed very quickly
Radiates to the carotids
2nd RICS
Describe the features of mitral regurgitation
5th LICS MCL Pan-systolic murmur Radiates to the axilla Causes: -rheumatic heart disease -IHD -Valvular vegetations -Physiological - due to dilated LA
Describe the features of tricuspid regurgitation
4th LICS
Pan systolic murmur
No radiation
Describe the features of pulmonary stenosis
Ejection click systolic murmur
2nd LICS
No radiation
How do you classify the intensity of a murmur?
Grade 1 - murmur only heard after a long period of auscultation
Grade 2 - faint murmur heard on auscultation immediately
Grade 3 - loud murmur heard immediately on auscultation but no thrill
Grade 4 - palpable thrill and loud murmur
How can you describe a murmur?
Intensity - as before Location where it is heard the loudest Any radiation Timing Shape - crescendo-decresndo etc. Response to manoeuvres Pitch Quality
What could be the reasons for murmurs?
Decreased blood viscosity e.g anaemia
Decreased diameter of vessel/valve/orifice
Increased viscosity through normal structures e.g. hyperthyroidism, sepsis
Regurgitation across incompetent valve
What manoeuvres could you perform to accentuate a murmur?
Leaning forwards accentuates aortic murmurs
Auscultation the carotids with breath held accentuates aortic stenosis
Leaning left accentuates mitral and tricuspid murmurs
What is the normal function of Troponins?
Prevent the cross- binding of myosin and therefore inhibit the contraction of muscle
As calcium concentration increases, the troponin is inhibited, so cross-binding can occur and the muscle can contract
