Use of clot busting drugs in cardiac arrest
- Thread starter Rialaigh
- Start date
No references handy, but I'm pretty sure there's zero evidence to support their routine use in arrest, in or out of hospital. And TPA is too expensive to use and has far too many side effects to use without good evidence. Even the evidence in CVA isn't great.
I was having trouble finding anything good online but based on how clot busters work I have trouble believing that there is no place for them in improving the resuscitation rate as well as improving outcomes in cardiac arrests that fall under XYZ conditions.
Anyone want to talk me through the pathophysiology side and get some theory going here.
I would probably agree off the bat though that routine use in cardiac arrests is not warranted.
NYMedic828
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Queue Veneficus noble prize worthy response...
From my feeble mind, I believe the main reason for the lack of their use is that the medication doesn't neccesarily reach the site. It has a systemic effect which is a double edged sword. It has potentially more negative than positive effects.
You wouldn't pour draino into your shower drain to unclog your kitchen sink. The same concept applies.
Select hospitals have the capability to directly administer the tPa into the insulted vessel. Pouring draino into your sink, to unclog your sink, is the way to do things.
From my feeble mind, I believe the main reason for the lack of their use is that the medication doesn't neccesarily reach the site. It has a systemic effect which is a double edged sword. It has potentially more negative than positive effects.
You wouldn't pour draino into your shower drain to unclog your kitchen sink. The same concept applies.
Select hospitals have the capability to directly administer the tPa into the insulted vessel. Pouring draino into your sink, to unclog your sink, is the way to do things.
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ah2388
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That is my understanding as well.
I could be mistaken, but I recall regarding a study at one point that concluded it was unclear whether medication administered through a peripheral IV ever actually reached the heart.
I could be mistaken, but I recall regarding a study at one point that concluded it was unclear whether medication administered through a peripheral IV ever actually reached the heart.
JPINFV
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JPINFV
Gadfly
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To the OP, the assumption that cardiac arrests are only linked to MIs is a very bad assumption.
Thrombolysis during Resuscitation for Out-of-Hospital Cardiac Arrest
Bernd W. Böttiger, M.D., Hans-Richard Arntz, M.D., Douglas A. Chamberlain, M.D., Erich Bluhmki, Ph.D., Ann Belmans, M.Sc., Thierry Danays, M.D., Pierre A. Carli, M.D., Jennifer A. Adgey, M.D., Christoph Bode, M.D., and Volker Wenzel, M.D., M.Sc. for the TROICA Trial Investigators and the European Resuscitation Council Study Group
N Engl J Med 2008; 359:2651-2662
Abstract
Article
References
Citing Articles (57)
Background
Approximately 70% of persons who have an out-of-hospital cardiac arrest have underlying acute myocardial infarction or pulmonary embolism. Therefore, thrombolysis during cardiopulmonary resuscitation may improve survival.
Methods
In a double-blind, multicenter trial, we randomly assigned adult patients with witnessed out-of-hospital cardiac arrest to receive tenecteplase or placebo during cardiopulmonary resuscitation. Adjunctive heparin or aspirin was not used. The primary end point was 30-day survival; the secondary end points were hospital admission, return of spontaneous circulation, 24-hour survival, survival to hospital discharge, and neurologic outcome.
Results
After blinded review of data from the first 443 patients, the data and safety monitoring board recommended discontinuation of enrollment of asystolic patients because of low survival, and the protocol was amended. Subsequently, the trial was terminated prematurely for futility after enrolling a total of 1050 patients. Tenecteplase was administered to 525 patients and placebo to 525 patients; the two treatment groups had similar clinical profiles. We did not detect any significant differences between tenecteplase and placebo in the primary end point of 30-day survival (14.7% vs. 17.0%; P=0.36; relative risk, 0.87; 95% confidence interval, 0.65 to 1.15) or in the secondary end points of hospital admission (53.5% vs. 55.0%, P=0.67), return of spontaneous circulation (55.0% vs. 54.6%, P=0.96), 24-hour survival (30.6% vs. 33.3%, P=0.39), survival to hospital discharge (15.1% vs. 17.5%, P=0.33), or neurologic outcome (P=0.69). There were more intracranial hemorrhages in the tenecteplase group.
Conclusions
When tenecteplase was used without adjunctive antithrombotic therapy during advanced life support for out-of-hospital cardiac arrest, we did not detect an improvement in outcome, in comparison with placebo. (ClinicalTrials.gov number, NCT00157261.)
Bernd W. Böttiger, M.D., Hans-Richard Arntz, M.D., Douglas A. Chamberlain, M.D., Erich Bluhmki, Ph.D., Ann Belmans, M.Sc., Thierry Danays, M.D., Pierre A. Carli, M.D., Jennifer A. Adgey, M.D., Christoph Bode, M.D., and Volker Wenzel, M.D., M.Sc. for the TROICA Trial Investigators and the European Resuscitation Council Study Group
N Engl J Med 2008; 359:2651-2662
Abstract
Article
References
Citing Articles (57)
Background
Approximately 70% of persons who have an out-of-hospital cardiac arrest have underlying acute myocardial infarction or pulmonary embolism. Therefore, thrombolysis during cardiopulmonary resuscitation may improve survival.
Methods
In a double-blind, multicenter trial, we randomly assigned adult patients with witnessed out-of-hospital cardiac arrest to receive tenecteplase or placebo during cardiopulmonary resuscitation. Adjunctive heparin or aspirin was not used. The primary end point was 30-day survival; the secondary end points were hospital admission, return of spontaneous circulation, 24-hour survival, survival to hospital discharge, and neurologic outcome.
Results
After blinded review of data from the first 443 patients, the data and safety monitoring board recommended discontinuation of enrollment of asystolic patients because of low survival, and the protocol was amended. Subsequently, the trial was terminated prematurely for futility after enrolling a total of 1050 patients. Tenecteplase was administered to 525 patients and placebo to 525 patients; the two treatment groups had similar clinical profiles. We did not detect any significant differences between tenecteplase and placebo in the primary end point of 30-day survival (14.7% vs. 17.0%; P=0.36; relative risk, 0.87; 95% confidence interval, 0.65 to 1.15) or in the secondary end points of hospital admission (53.5% vs. 55.0%, P=0.67), return of spontaneous circulation (55.0% vs. 54.6%, P=0.96), 24-hour survival (30.6% vs. 33.3%, P=0.39), survival to hospital discharge (15.1% vs. 17.5%, P=0.33), or neurologic outcome (P=0.69). There were more intracranial hemorrhages in the tenecteplase group.
Conclusions
When tenecteplase was used without adjunctive antithrombotic therapy during advanced life support for out-of-hospital cardiac arrest, we did not detect an improvement in outcome, in comparison with placebo. (ClinicalTrials.gov number, NCT00157261.)
I don't have it handy right now, but there was a European Study, I believe out of Denmark or Netherlands that came to the same conclusion.
(sorry, I read 3-5 studies a day and I don't always remember exactly where everyone is.)
mycrofft
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Hurrah for intelligent studies and citations!
That said, it may be that one factor in all that is that it isn't the clot per se but the subseqent infarct and metabolic cascades leading to shock which actually kill you dead. Once done, the clot is unnecessary for death, the damage has gone systemic (hypoperfusive anoxia, shock).
One could say a patient in asystole is becoming one big infarct.
That said, it may be that one factor in all that is that it isn't the clot per se but the subseqent infarct and metabolic cascades leading to shock which actually kill you dead. Once done, the clot is unnecessary for death, the damage has gone systemic (hypoperfusive anoxia, shock).
One could say a patient in asystole is becoming one big infarct.
I appreciate the responses. I was not under the assumption that all cardiac arrests are MI related. However for the cardiac arrests that are not MI related I was guessing that giving a clot buster would do no harm at all because the survival rate for PE's and traumatic arrests is so low.
I was trying to find a study or research that pointed one way or another. Thanks guys
I was trying to find a study or research that pointed one way or another. Thanks guys
Brandon O
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I've seen it done but never with any expectation it'd work.
It's not hard to imagine why. Most arrests already come in with low expectation of survival; these are very sick people, natch. Even with PCI they'd be expected to have high mortality. We know that thrombolytics have significantly greater complications than angioplasty, so we're narrowing the benefit even more. Plus we're increasing the chance of bleeding in a patient whose chest we've been hammering on (isn't recent CPR considered a relative contraindication for lytics?). And the time to peak effect isn't particularly quick for this stuff anyway -- never mind the added delay from the poor circulatory state. And, as stated, many of these people don't have an occlusion at all, so in many cases there's not even a potential for benefit.
It's not hard to imagine why. Most arrests already come in with low expectation of survival; these are very sick people, natch. Even with PCI they'd be expected to have high mortality. We know that thrombolytics have significantly greater complications than angioplasty, so we're narrowing the benefit even more. Plus we're increasing the chance of bleeding in a patient whose chest we've been hammering on (isn't recent CPR considered a relative contraindication for lytics?). And the time to peak effect isn't particularly quick for this stuff anyway -- never mind the added delay from the poor circulatory state. And, as stated, many of these people don't have an occlusion at all, so in many cases there's not even a potential for benefit.
mycrofft
Still crazy but elsewhere
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I appreciate the responses. I was not under the assumption that all cardiac arrests are MI related. However for the cardiac arrests that are not MI related I was guessing that giving a clot buster would do no harm at all because the survival rate for PE's and traumatic arrests is so low.
I was trying to find a study or research that pointed one way or another. Thanks guys
Non-MI and non-PE related arrests: electrocution, poisoning, strangulation, anaphylaxis, drowning...none really expected to be helped by anti-embolics, and some may have contraindications to using them responders would not necessarily know about. But the vast majority are MI related.
Any thoughts on clot busters showing results that improve outcomes when used in Witnessed arrests with Autopulse or Lucas (Mechanical CPR) thus improving circulatory flow considerably? I'm just wondering if the benefit (if any) of these drugs is just not able to be utilized in MI situations because of poor CPR, or other factors that could be changed and improved upon. Again, I understand now that given the current system (in most areas) there would be no benefit but hypothetically could this produce a positive result?
mycrofft
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Thrombolytics won't bring back infarcted tissue. I'm betting ....
Thrombolytics won't bring back infarcted tissue. I'm betting ....
Yeah but will it reduce the amount of blockage during CPR allowing more oxygen to the brain to allow for more neuro intact survivors?
mycrofft
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But with a lethal infarct, often the only Tx is cardiopulmonary bypass until a transplant can be arranged, if it is feasible at all. CPR is a finger in the hole of the boat between you and Jaws, and the hole is as big as your elbow.