ACS Flashcards
initial treatment for STEMI
300mg aspirin
if going to receive PCI-> prasugrel or clopidogrel if already on anticoagulant
during PCI
radial access: UFH with glycoprotein IIb/IIIa inhibitor (eptifibatide and tirofiban)
femoral access: blilvardin with same glycoprotein thing
if not treating STEMI with PCI
ticagrelor as dual treatment with aspirin
if high bleeding risk -> clopidogrel
treatment for MI
Initial: MONA • Morphine • Oxygen (If SPO2 < 94%) • Nitrate : GTN spray • Antiplatelet (aspirin and P2y12 inhibitor) & antiemetic
After: BASH • Beta blocker ○ Calcium channel if asthma • ACE inhibitor • Statin • Heparin if NSTEMI: 3 days • + aspirin and clopidogrel ○ Clopidogrel continues for a year ○ Aspirin forever
NSTEMI
B – Beta blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
M – Morphine titrated to control pain
A – Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
Give oxygen only if their oxygen saturations are dropping (i.e. <95%).
which Ca channel blocker for those with reduced EF post MI
amlodipine dont use verapamil, diltiazem and short acting dihydropyridine agents
Complications of MI
(Heart Failure DREAD)
D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
factors that affect prognosis of MI
- Comorbidities such as hypertension, chronic kidney disease, anaemia, and diabetes
- Site of the infarction. For example, a STEMI in the anterior part of heart has a less favourable prognosis than one in the inferior part of the heart
- Depression, particularly treatment-resistant and insufficiently treated depression
- Older age and female sex
MI can cause impairment of NA-K ATPase due to impaired ATP production
○ Increased intracellular Na → intracellular edema
○ Increased extracellular K → alteration in transmembrane potential → electrical instability and susceptibility to arrhythmias
○ Increased intracellular Ca → activation of degradative lipases and proteases → tissue necrosis
secondary prevention
6A's aspirin antiplatelet Atorvastatin ACE inhibitor atenolol aldosterone antagonist (for clinical heart failure - eplerenone)