why is aspirin given after heart attack:confused:
Aspirin can help dissolve blood clots. Many heart attacks are caused by blood clots cutting off blood flow and oxygen to the cardiac muscle. This will cause the muscle to die, causing the heart to be permanently damaged. If you can bust the clot fast enough, you can restore blood flow and prevent permanent damage.
After heart attacks, aspirin and other “blood thinners” can prevent future heart attacks by keeping small blood clots from forming.
Aspirin doesn’t dissolve clots, but it does make platelets (which form clots) less ‘sticky’ and can keep the clots from growing further. So if a person is not taking aspirin regularly, and they appear to be having an acute heart atttack, it’s often advised to have the patient chew an aspirin, to try to minimize clot growth.
And taking it regularly may reduce the chance of new clots forming.
Of course, taking low dose aspirin regularly does increase the risk of hemorrhage, so one must decide if the treatment is worth the risk.
Thanks for the clarification- I was going for familiar colloquialisms (clot buster, blood thinner, clot dissolver etc), but you found the familiar term (less sticky) I couldn’t think of.
I’m on warfarin, a blood thinner, and I’m not supposed to take aspirin for pain, only non-aspirin pain relievers because of its blood thinning properties.
The term “blood thinner” is really not at all accurate, and warfarin and aspirin work in completely different ways. But taking them together does substantially increase the risk of having a hemorrhage, well beyond the risk of using them separately.
Aspirin suppresses thromoboxane, which makes platelets less ‘sticky’ and reduces their effectiveness in stopping a hemorrhage. At the same time, aspirin also inhibits prostaglandin production, which means that the stomach lining is less protected against the acid in the stomach, and the risk for bleeding erosions is hence increased.
Warfarin inhibits production of several different proteins called clotting factors, hence making clots more slow to form in the first place.
Neither medication actually changes the viscosity of the blood.
How did those become the common euphemisms for what anticoagulants and thromboxane inhibitors actually do? (Used by many doctors and nurses talking to patients too.)
QtheM does ASA do much good in the acute phase, or is it more to prevent the future MI?
No idea bout the first.
As for the 2nd, my sources (UpToDate) show definite benefit from ASA use early during Acute ST elevation MI, and in unstable angina. Lowered mortality rates, fewer early reinfarctions, and less extensive initial infarctions.
As always, the good doctor Qadgop is spot on. I just wanted to add that aspirin given in the “acute phase” after a stroke, i.e. given immediately upon presentation, is also of benefit (with fewer downstream deaths and recurrent strokes).
Thanks to both of you for the answer. I have also found this ACC/AHA guideline, also stating the same spot on information, including the chewing bit, as buccal absorption is faster.
I did not know that.
I’m still curious about the origin of the phrase. The best speculation I can find so far is a reference to measuring clotting time in a tube, a circumstance in which faster clotting blood became more viscous (thicker) sooner, as opposed to more slowly clotting blood which stayed less viscous (thinner) longer. Nothing authoritative though.
As someone who has on occasion had to stick needles into people on aspirin, warfarin etc, my feeling about “blood thinner” is this:
When someone on a “blood thinner” is bleeding, the blood doesn’t clot, it doesn’t go thick and tacky and form clots the way blood usually does when someone bleeds. It continues to flow for much longer, usually requiring a lot of pressure for a prolonged time to stop.
So in a “normal person” the blood will coagulate and clot quickly, and someone on aspirin or warfarin the blood will stay liquid for longer- hence “thinner”.
This borders on a quibble but anticoagulants probably do affect blood viscosity at least a tiny bit. Heparin is probably the one that has been most thoroughly studied but aspirin may affect it a bit too.
As for the etiology of the term, as soon as the blood leaves the vessel, it actually does noticably change in viscosity. Oozing blood from a cut surface will gradually thicken and harden on its own without your intervention the majority of the time. Even a fair sized artery spraying blood will start to clot fairly quickly (though that’s a relative term, I suppose). Blood progresses from watery, to thick, to sticky, to firm, all the way to difficult to remove from the underlying tissue in a matter of seconds to minutes. If you are operating in a cavity significant amounts of blood will often partially solidify before you are finished, at times becoming difficult to remove with simple suction.
When the subject at hand is on blood thinners, that progression is greatly delayed, and blood will remain thin and watery for an extended period. As opposed to a normal patient, continued bleeding will disrupt the coagulating blood before it can set up as a firm clot, and what would otherwise be trivial oozing will continue indefinitely (or at least for an annoyingly long time) unless it is controlled by other means. Pooling blood will remain liquid for much longer and surfaces are not as sticky. It actually flows differently as it bleeds. For fully anticoagulated patients the difference is very noticable.
By the way, I wish you’d stop cluttering up the boards with all your posts! It seems I run into one of your contributions at least every . . . every . . . two or three years.