fibrionolytic therapy for pts on anticoagulant

This is a part of a ACLS pre-class question. "A patient with ST-segment elevation MI has ongoing chest discomfort. Fibrinolytic therapy has been ordered. Heparin 4000 units IV bolus was administered, and a heparin infusion of 1000 units per hour is being administered."

Is this scenario right? I thought fibrionolytic therapy was contraindicated in pts on any anticoagulant.

Thanks Last edit by unsaint77 on Feb 12, '12 : Reason: need to be more specific on the title
Unfractionated Heparin infusion (Heparin gtt) is part of the treatment algorhythm for all types of ACS (STEMI, NSTEMI, UA). For STEMI, either fibrinolytic therapy (i.e., alteplase, tenecteplase, or reteplase) or percutaneous coronary intervention (i.e., angioplasty, stent) is recommended depending on the immediate availability of either services within a given hospital. Fibrinolytic therapy is not contraindicated in a patient on Heparin gtt. It is actually a Class I Recommendation as an adjunctive therapy to either form of reperfusion therapy. See: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction

Thanks for the help, juan de la cruz. I will have to explain where my question came from. The following is part of a fibrinolytic checklist from AHA stroke algorithm. (yes, stroke algorithm, not ACS algorithm) "[fibrinolytic therapy is contraindicated if...] Current use of anticoagulant (eg, warfarin sodium) that has produced an elevated international normalized ratio (INR) >1.7 or prothrombin time (PT) >15 seconds." INR 1.7 and PT 15 sec is considered normal in some situations. I think the fibrinolytic checklist in stroke algorithm exists because of the high risk of fibrinolytic's side effect. Therefore, shouldn't the same checklist also be used in ACS algorithm?

What happens during a stroke?What happens during an MI?You are just not thinking...

you are clear on the mechanisms of action of fibrinolytics and heparins?

Quote from unsaint77Thanks for the help, juan de la cruz. I will have to explain where my question came from. The following is part of a fibrinolytic checklist from AHA stroke algorithm. (yes, stroke algorithm, not ACS algorithm) "[fibrinolytic therapy is contraindicated if...] Current use of anticoagulant (eg, warfarin sodium) that has produced an elevated international normalized ratio (INR) >1.7 or prothrombin time (PT) >15 seconds." INR 1.7 and PT 15 sec is considered normal in some situations. I think the fibrinolytic checklist in stroke algorithm exists because of the high risk of fibrinolytic's side effect. Therefore, shouldn't the same checklist also be used in ACS algorithm?

OP, it's always pathophysiology first.What is going on. Visualize it happening to the organ/vessel/cell (whatever) with your "x-ray" vision.THEN what kind of thing do you you need to treat it. Look at your "tools of the trade" you got this thing and that thing you can use. What makes you choose one of those things over the other?

I understand clearly that heparin is used in ACS. My question is this.. why is the bleeding risk of thrombolytics heavily weighed in stroke cases, but not in ACS?

Your questions seem pretty straightforward, although from reading the other responses I'm thinking I may not be understanding them properly so please correct me if I'm wrong. The basic processes involved in an AMI and a CVA are very similar; vessel blockage (usually due to some form emboli) causes tissue ischemia. Because of this fibrinolytics can be used to treat both. So then why is heparin contraindicated after TPA for stroke but is typically given following fibrinolytics for MI? There are two very different risks following treatment of the emboli in a CVA vs an MI. In CVA's "hemhorragic transformation" can occur. This is where as a result of the natural process of an embolic CVA, the blockage becomes a bleed. This can occur without the use of any fibronlytics or anti-coagulants at all, but the risk is much higher when anti-coagulants are used within 24 hours of of the event, particularly following fibrinolytics.A significant concern with AMI on the other hand is essentially the opposite; reclotting. For this reason heparin and or integrilin, bivalarudin, etc is standard therapy even after the emboli is cleared. Very good questions, hope I've helped.

So, can you explain or point me to why the different progressions between CVA clot and MI clot?

It has everything to do with the type of clot, what kind of stroke and where and the characteristics of the response of the brain to insult versus the heart. Sometimes it's just the efficacy of giving the med doesn't warrent the use of one medicine versus another.I know it's wiki.....but it explains parets of what you are looking for.Stroke - Wikipedia, the free encyclopedia