What is a good sedative for a hypotensive patient?

Specialties CCU

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I had a patient that was dropping her pressure on propofol, switched her to ativan and fentanyl drips, and it was just as bad. She was on 20 mcg dopamine and 250 mcg of neosynephrine, definitely was not hypovolemic. Would you try ativan alone, or fentanyl alone, or something else? I know ativan and fentanyl work synergistically to create sedation, do they do the same to blood pressure when they are combined?

Specializes in Critical Care.

I've found versed to be the best, but you said your facility doesn't use it. That's too bad; it works great. Fentanyl typically works well too. Also, 250cg of Neo is over the max dose! Yikes! I'm also curious about why you said pt wasn't hypovolemic- what were their numbers?

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Specializes in SICU.

Dex drops BP and HR just as much as propofol and ativan.

Was the patient too sedated? Some places seem to like patients near comatose, others want them more awake. If you want them totally snowed you will most likely have to use pressors. I could be wrong, but I don't know of any sedative that doesn't drop BP.

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Specializes in Nurse Anesthesiology.
Dex drops BP and HR just as much as propofol and ativan.

Was the patient too sedated? Some places seem to like patients near comatose, others want them more awake. If you want them totally snowed you will most likely have to use pressors. I could be wrong, but I don't know of any sedative that doesn't drop BP.

Sorry to tell you, but dexmedetomidine does not drop BP nearly like propofol or ativan. Dex is an alpha 2 agonist. Propofol works on GABA receptors and is totally different than dex. Ativan is a benzo and also acts on GABA receptors in a different manner.

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dexmedetomidine does not drop BP nearly like propofol or ativan..

While it might not be as acute of a drop in BP and initiation bradycardia.......

-dexmedetomidine has similar pharmacological effects to clonidine, another alpha2-adrenoceptor agonist.

-its use may require vasopressor and/or anticholinergic support to maintain blood pressure and heart rate goals.

-Dexmedetomidine is a relatively selective, centrally acting, alpha2-adrenoceptor agonist with sympatholytic, sedative, and analgesic properties but without significant ventilatory effects. Selectivity for the alpha2-receptors is observed in animals following slow intravenous (IV) infusion of dosages ranging from 10—300 mcg/kg. Both alpha1 and alpha2 activity is observed following slow IV infusion of very high doses (>=1000 mcg/kg) or with rapid IV administration. Sedation and analgesia occurs following stimulation of central alpha2-adrenergic receptors, which inhibit sympathetic outflow and tone.

-Consistent with alpha2-adrenoceptor agonism, hypotension and bradycardia occur frequently during dexmedetomidine administration.

9443. DeWolf AM, Fragen RJ, Avram MJ, et al. The pharmacokinetics of dexmedetomidine in volunteers with severe renal impairment. Anesth Analg 2001;93:1205—9.

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Specializes in Nurse Anesthesiology.

I understand how dex works. That's why I said it's an alpha2 agonist. Initially when you give dex it will work peripherally and can cause an increase in BP because of the alpha1 effects it causes on the peripheral venous system. Once it reaches centrally that is where you will see the drop in BP, but what I was saying is the effects are not like Propofol. Propofol can cause a 15-25% drop in SVR and you can see a drop in your BP by as much as 25-40% with an induction dose.

While it might not be as acute of a drop in BP and initiation bradycardia.......

-dexmedetomidine has similar pharmacological effects to clonidine, another alpha2-adrenoceptor agonist.

-its use may require vasopressor and/or anticholinergic support to maintain blood pressure and heart rate goals.

-Dexmedetomidine is a relatively selective, centrally acting, alpha2-adrenoceptor agonist with sympatholytic, sedative, and analgesic properties but without significant ventilatory effects. Selectivity for the alpha2-receptors is observed in animals following slow intravenous (IV) infusion of dosages ranging from 10--300 mcg/kg. Both alpha1 and alpha2 activity is observed following slow IV infusion of very high doses (>=1000 mcg/kg) or with rapid IV administration. Sedation and analgesia occurs following stimulation of central alpha2-adrenergic receptors, which inhibit sympathetic outflow and tone.

-Consistent with alpha2-adrenoceptor agonism, hypotension and bradycardia occur frequently during dexmedetomidine administration.

9443. DeWolf AM, Fragen RJ, Avram MJ, et al. The pharmacokinetics of dexmedetomidine in volunteers with severe renal impairment. Anesth Analg 2001;93:1205--9.

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Specializes in Critical Care Nursing AKA ICU.
Fentanyl has less histamine release than other narcotics and is the textbook answer for that class.

You will need a combo for adequate sedation in most.

Dexmedetomidine is another choice.

agree...

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While maybe not the best drug (can cause very vivid halucinations) ketamine will cause the release of endogenous catecholamines and usually won't drop your pt's pressure as much as midaz or loraz...tho it is still a partial cardiac depressant.

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