Anyone know of any research to indicate for our against giving a rate reducing rx in sinus tachycardia in the critically ill provided their BP and oxsat can handle a rate reduction?
Why? Unless they are in Afib w RVR and or having a hard time filling because the HR is too high.Anyone know of any research to indicate for our against giving a rate reducing rx in sinus tachycardia in the critically ill provided their BP and oxsat can handle a rate reduction?
Esmolol and Heart Rate Control in Septic Shock
To determine whether treating critically ill patients with severe septic shock with esmolol, a short-acting β-blocker, to reduce their heart rates, Morelli and coauthors conducted an open-label, randomized phase 2 study, involving 154 qualifying patients treated at a university hospital intensive...jamanetwork.com
I have always found this to be an interesting line of research. Keep in mind that your mileage may vary, especially if you don't have Levosimendan to "rescue" as they put it. I think this may have more to do with blunting adrenergic effects generally than particularly preventing people from being tachycardic. Looking forward to what the CCM boarded folks post here
Anyone know of any research to indicate for our against giving a rate reducing rx in sinus tachycardia in the critically ill provided their BP and oxsat can handle a rate reduction?
What’s IST?I'd need a compelling reason to rate control sinus tachycardia (eg dissection). Unless it's IST, it's happening for a reason - target that
What’s IST?
IST is an outpatient diagnosisInappropriate sinus tach
their rate control is resuscitation (eg antibiotics, anticoagulation, fluids, blood, etc etc).Anyone know of any research to indicate for our against giving a rate reducing rx in sinus tachycardia in the critically ill provided their BP and oxsat can handle a rate reduction?
My favorite part of this study:Esmolol and Heart Rate Control in Septic Shock
To determine whether treating critically ill patients with severe septic shock with esmolol, a short-acting β-blocker, to reduce their heart rates, Morelli and coauthors conducted an open-label, randomized phase 2 study, involving 154 qualifying patients treated at a university hospital intensive...jamanetwork.com
I have always found this to be an interesting line of research. Keep in mind that your mileage may vary, especially if you don't have Levosimendan to "rescue" as they put it. I think this may have more to do with blunting adrenergic effects generally than particularly preventing people from being tachycardic. Looking forward to what the CCM boarded folks post here
I’ll treat sinus tach so the surgeon feels comfortable with the patient going to the floor from SICU...
Agreed. The number of times I’ve had to treat a number just to get a patient out of SICU is too gosh darn high!That sounds like a bad idea....
I've seen a few mortalities from beta blocking sinus tach. Depending on the underlying cause, ST can be a response to low cardiac output. Blocking this backup defensive mechanism can suddenly drop CO with resultant cardiac arrest. Especially problematic in PE, cardiogenic shock, tamponade, PTX, hypovolemia etc.
Find the underlying cause and treat if possible. Otherwise leave it alone unless patient is dependent on diastolic filing time.
It makes me slightly worried that more that half the articles aren't in English, not that good studies can't be done in other countries, but there clearly was a reason they didn't publish in an English speaking journal given the ubiquitous access to language services for publications nowadays. The lack of clear data on baseline characteristics makes it also challenging to interpret. I mean, Dopamine used be a front-line agent for sepsis, but fell out of favor in adults (then pediatrics) related to the tachyarrhythmias it induced. If you're septic and prone to a tachyarrhythmia, could rate control actually be helpful? I mean, it seems like the answer would be yes. I suspect that is what they are seeing (in fact, that's what the Lancet Resp. Med article shows). Now, does that mean it should be extrapolated to every patient with tachycardia irrespective of their arrhythmia risk? I would guess no. But I say that knowing that we give out Propranolol like water to burn patients because of perceived inappropriate tachycardia. Of course, the effect on outcomes isn't mortality but visceral fat, but is there a role for short acting B-blockade? Maybe. Clearly this question needs to be answered in a better fashion.Effect of Ultrashort-Acting β-Blockers on Mortality in Patients With Sepsis With Persistent Tachycardia Despite Initial Resuscitation: A Systematic Review and Meta-analysis of Randomized Controlled Trials - PubMed
UMIN Clinical Trials Registry; No.: UMIN000040174; URL: https://www.umin.ac.jp/ctr/index.htm.pubmed.ncbi.nlm.nih.gov
More evidence on this topic, a meta-analysis of seven RCTs with a pooled sample size of 613 patients. I don't disagree with anything anyone wrote in response to the earlier paper I posted, but it's an interesting question I think -- perhaps there is benefit in modulating adrenergic tone after appropriate resuscitation, maybe it's just the heart, maybe it's something else. Not something I intend on incorporating into my practice, but I think it's cool to think about the potential mechanisms.
beta blocker plus dopamine is just phenylepi in a roundabout wayIt makes me slightly worried that more that half the articles aren't in English, not that good studies can't be done in other countries, but there clearly was a reason they didn't publish in an English speaking journal given the ubiquitous access to language services for publications nowadays. The lack of clear data on baseline characteristics makes it also challenging to interpret. I mean, Dopamine used be a front-line agent for sepsis, but fell out of favor in adults (then pediatrics) related to the tachyarrhythmias it induced. If you're septic and prone to a tachyarrhythmia, could rate control actually be helpful? I mean, it seems like the answer would be yes. I suspect that is what they are seeing (in fact, that's what the Lancet Resp. Med article shows). Now, does that mean it should be extrapolated to every patient with tachycardia irrespective of their arrhythmia risk? I would guess no. But I say that knowing that we give out Propranolol like water to burn patients because of perceived inappropriate tachycardia. Of course, the effect on outcomes isn't mortality but visceral fat, but is there a role for short acting B-blockade? Maybe. Clearly this question needs to be answered in a better fashion.
Funny you should mention this. When I was a bit of a newbie I had a septic patient with Afib RVR that I was giving Norepi and lots of fluid to in the OR. Had to be perforated viscus or something like it. I gave lots of fluid as source control was happening but, I couldn't slow the rate down. I remember texting my partner about either the surgeon or RN suggesting a beta blocker, but of course, I declined knowing that if I fixed the acidosis I would fix the problem. My 65 year old partner said, "well a beta blocker isn't a contraindication in case like this". Of course I never did as I texted after the fact and I don't remember what happened to the patient.It makes me slightly worried that more that half the articles aren't in English, not that good studies can't be done in other countries, but there clearly was a reason they didn't publish in an English speaking journal given the ubiquitous access to language services for publications nowadays. The lack of clear data on baseline characteristics makes it also challenging to interpret. I mean, Dopamine used be a front-line agent for sepsis, but fell out of favor in adults (then pediatrics) related to the tachyarrhythmias it induced. If you're septic and prone to a tachyarrhythmia, could rate control actually be helpful? I mean, it seems like the answer would be yes. I suspect that is what they are seeing (in fact, that's what the Lancet Resp. Med article shows). Now, does that mean it should be extrapolated to every patient with tachycardia irrespective of their arrhythmia risk? I would guess no. But I say that knowing that we give out Propranolol like water to burn patients because of perceived inappropriate tachycardia. Of course, the effect on outcomes isn't mortality but visceral fat, but is there a role for short acting B-blockade? Maybe. Clearly this question needs to be answered in a better fashion.