Acute coronary syndrome Flashcards
what is the initial management of a patient who presents with ACS?
morphine
oxygen if Sp02 < 94%
nitrate (GTN spray)
aspirin 300mg
what is the long term management after an MI?
beta blocker
ACE inhibitor
statin
dual anti platelet (aspirin + clopidogrel/ticagrelor/prasugrel) for 1 year followed by aspirin indefinitely
aldosterone antagonist (i.e. spironolactone) if HF and LVSD
describe the management of STEMI.
immediate;
- morphine, oxygen, GTN, dual anti platelet
PCI - if symptom onset < 12 hrs and available within 120 mins
thrombolysis if PCI unavailable within 120 mins
Medical management is thrombolysis unsuitable and/or onset > 12 hrs
+ anticoagulant
- LMWH e.g. dalteparin
- IV unfractionated heparin
describe the management of NSTEMI.
immediate;
- morphine
- oxygen
- GTN
- aspirin + clopidogrel / ticagrelor / prasugrel +/- glycoprotein IIb/IIIa receptor inhibitor (3rd option)
if high risk / clinical unstable - immediate coronary angio
within 92hrs if intermediate and conservative if low risk
anticoagulants;
- fondaparinux
- IV unfractionated heparin (if angio within 24hrs + creatinine > 265)
how is prognosis after ACS classified?
killip class; (3 month mortality)
I - no signs of HF (6%)
II - lung cradles, S3 (17%)
III - frank pulmonary (38%)oedema
IV - cariogenic shock (81%)
what are complications of ACS?
acute complications (< 2 weeks) - death - arrhythmia - VSD mitral regurgitation - ventricular wall rupure - pericarditis - acute pulmonary oedema
long term complications (> 2 weeks)
- dressler’s syndrome
- heart failure
- ventricular aneurysm
what is dressers syndrome?
inflammation of the pericardium which occurs > 2 weeks after an MI
autoimmune reaction
differs from pericarditis which can occur due to other aetiologies such as viral infection - pericarditis also occurs < 2 weeks of MI
what are risk factors for ACS?
modifiable;
- diabetes
- hypertension
- hyperlipidaemia
- smoking
- AF
non-modifiable
- age
- male
- family history
occlusion of what artery would show on leads II, III and aVF on ECG?
right coronary artery (inferior MI)
occlusion of what artery would show on leads V1, V1, V3 and V4 on an ECG?
left anterior descending (septal/anterior MI)
occlusion of what artery would show on leads I, aVL, V5 and V6?
left circumflex artery (lateral MI)
how would you identify a posterior MI?
if ST depression in septal/anterior leads - V1, V2, V3, V4) position these leads on the back to record posterior MI
(they will then be termed V7, V8, V9)
tall R waves on V1 and V2
describe the pathophysiology of ACS.
endothelial damage due to factors such as smoking, hypertension, hyperlipdaemia.
results in pro inflammatory, pro oxidative, proliferative and reduced nitric oxide bioavailability of the endothelium
infiltration of LDL into endothelial space
monocytes migrate to the area and become macrophages
macrophages phagocytose LDL forming foamy cells
smooth muscle proliferation and migration of tunica media into tunica intima results in formation of fibrous capsule covering fatty plaque
narrows vessel lumen
plaque may rupture causes complete occlusion = MI
why might glycoprotein IIa/IIIb be required as a 3rd anti platelet in the management of NSTEMI?
- if the patient is at high risk of adverse CV event and receiving coronary angio within 96 hours
why is IV unfractionated heparin proffered over fondapariux in the management of NSTEMI?
if creatinine > 265
receiving coronary angio within 24 hours
high risk of bleeding
