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If a patient has a septic shock requiring norepinefrine infusion and his HR is 130 can I use beta blockers? In general can we use beta-agonists and beta-blockers at the same time?
If a patient has a septic shock requiring norepinefrine infusion and his HR is 130 can I use beta blockers? In general can we use beta-agonists and beta-blockers at the same time?
If a patient has a septic shock requiring norepinefrine infusion and his HR is 130 can I use beta blockers? In general can we use beta-agonists and beta-blockers at the same time?
I actually encounter this frequently. Septic shock with an SVR in the toilet, pumping saline and still can't get a MAP above 60 so I have levophed rolling and often additional peripheral help with neo, but they're taching away at 150-160. However, I agree with above posters, it is almost never ST unless they have an underlying PE. Its most always AF with RVR in which case I do use Esmolol/metoprolol or sometimes diltiazem to drop the Hr down to 130. It allows for increased ventricular filling times and improves CO, often resulting in a slight bump in my abysmal MAP. But again, rarely ST. And even if it is, ST is always physiologic and a rate less than 130 we rarely intervene on.
If you have an SVT in the setting of septic shock and your patient is on levophed, you can try to transition to neo to see if the cardiac excitation abates. If it persists then you can use Amiodarone, which has a side effect of nodal blockade (without a drop in BP). If I am meeting my resuscitation goals during septic shock and SVT leads to significant hypotension - they get shocked.
Sinus tachycardia in the setting of septic shock is a compensatory mechanism to account for either an under filled ventricle combined with a low SVR OR sepsis-induced cardiomyopathy. Do not beta block sinus tach.
If you have an SVT in the setting of septic shock and your patient is on levophed, you can try to transition to neo to see if the cardiac excitation abates. If it persists then you can use Amiodarone, which has a side effect of nodal blockade (without a drop in BP). If I am meeting my resuscitation goals during septic shock and SVT leads to significant hypotension - they get shocked.
A prior poster suggested routine use of both leveophed and neo. That doesn't make a lot of sense at all given that both will be competing for the alpha receptor. Personally, I don't use more than two pressors. I usually use levo +/- vasopression OR neo +/- vasopressin (if tachyarrythmias are present) OR epi +/- vasopressin (RV failure)..This general approach does not take into account using inotropes like milrinone or dobutamine.
If patient is in PSVT and on levophed does it not then become unstable PSVT by definition and require cardioversion? Also what would be the role of adenosine in that scenario if cardioversion is not the option?