Acute Coronary Syndromes II Flashcards
Paradigm for treating STEMI
“Time is muscle” Goal is immediate restoration of blood flow to occluded vessel.
Therapy that all MI patients get
Anti-coagulation, anti-platelet, anti-ischemic, adjunctive
Anti-ischemic Rx
Beta-blockers (relieve ischemic pain by decreasing cardiac work and oxygen demand. Reduce infarct size and arrhythmias. Mortaility benefit.)
Nitrates (enhance blood flow by coronary vasodilation and decrease preload. But don’t give to STEMI patients early, or with RV infarct)
CCB (NonDHP’s reduce HR and contractility. No mortality benefit in ACS.)
Antithrombotic therapy
Antiplatelets and anticoagulants.
Antiplatelets decrease platelet aggregation and are effective in arterial circulation.
Anticoagulants limit blood from clotting.
Aspirin
Effective across entire spectrum of ACS. Should be given as soon as possible to all patients with suspected ACS. Has rapid anti-platelet effect and reduces coronary occlusion and recurrent ischemic events after fibrinolytic therapy.
Clopidogrel/Prasugrel
Thienopyridine derivative that is an IRREVERSIBLE inhibitor of the P2Y12 Receptor. Indicated in all patients with USA/NSTEMI unless surgery planned. Takes 5 days to recover.
Prasugrel has more even effect. Newer generation.
Lots of interindividual variability in response to clop.
Glycoprotein IIb/IIIa inhibitors
Super potent, inhibit the final common pathway of platelet aggregation, but use has declined with antiplatelet drugs.
Anticoagulation therapy
Heparin
Bivalirudin
Factor Xa inhibitor
Heparin
Standard anticoagulant
Bivalrudin
Direct thrombin inhibitor. Can be used instead of heparin
Factor Xa inhibitor
Similar efficacy to LMWH but less bleeding
How does heparin work?
Unfractionated heparin: Binds to antithrombin, causes conformational change that causes it to bind to thrombin more avidly, also factor Xa.
LMWH: Binds to antithrombin, binds to just factor Xa more avidly.
Conservative treatment of USA/NSTEMI patients
Medications alone with angio/revasc only if clinical worstening or evidence of ischemia
Invasive treatment of USA/NSTEMI patients
Urgent cardiac cath.
How to determine risk of USA/NSTEMI
TIMI risk score. Risk of adverse outcomes increases with each point
What is ideal time to start PCI with STEMI?
<90 minutes.
Can lytic agents be used for coronary artery occlusion
Yeah! TPA is good.
What is better for STEMi in high risk patients: PCI or Fibrinolysis?
PCI
When is fibrinolysis preferred to PCI for STEMI?
If there is a huge delay to get to a cath lab.
If presentation is < 3 hours and there is no delay to an invasive strategy, what should be done?
No preference for either.
Why are ACEi given in MI
Prevent ventricular remodeling.
Greatest benefit in anterior MI and systolic dysfunction
What is a major complication of MI?
Arrhythmias.
VFIB
Can cause sudden cardiac death early in MI, but can be aborted with rapid defibrillation. Take to CCU
Supraventricular arrhythmias
Bradycardia, tachycardia, afib
Pseudoaneurysm
Hole causes blood to pool outside LV. Communication between LV and pericardium
True aneurysm
Develop months to weeks after MI. No communication between LV cavity and pericardium. Can cause arrhythmia. Tissue bulges
Papillary muscle rupture
If RCA occluded, papillary muscle can rupture.
Pericarditis after MI
Acute can occur if inflammation extends from myocardium to pericardium
Dressler syndrome
Autoimmune process that happens 6-8 weeks post MI. Causes pericarditis,
