Vasopressors- Critical Care RN's please help!

LadyTiger44 · Jul 3, 2008

I am a new grad nurse working in the SICU. I would love to help you with your questions but I have no idea. I have not been in a code yet. Doctors preferance maybe? I am truely not sure. Hopefully someone with more experience can answer!

mom2michael, MSN, RN, NP · Jul 3, 2008

Never heard of Cardizem being used in this situation, so I'm not any help there.

Most ER docs go with what they know. They know that fluids will fix low BP's d/t low fluids. They also know w/o fluids circulating, vasopressors won't work. 2L was pretty much the standard where I worked - if 2L didn't fix the problem, the docs starting looking further into the problem.

After that it really becomes Dr. driven and what they are comfortable with. We joked the Levophed is really called "leave them dead" and basically we used it as a last resort in our ER. If we pulled that stuff out, we knew we would be calling the code soon. Horrible to say but it was so very true.

He could've had an AMI and his Troponin hadn't had time to elevate or it could've been a PE. Did he run a fever (thinking sepsis here).

I had a similar code my last week of being an ER nurse and we tried for over 3 hours to save this guy and nothing we did fixed him.....it ended up being sepsis from a perforated bowel but we didn't know that right away.

schroeders_piano, RN · Jul 3, 2008

I have to agree that I haven't given Cardizem in this type of situation. I was wondering about your dopamine. I have never started someone at 25mcg of dopamine and then titrated up to 50mcg. The ICU/ER's I worked in 20-25 mcg was max dose and then you switched to Levophed.

Virgo_RN, BSN, RN · Jul 3, 2008

The Cardizem was most likely given to slow his rate. Was he in a rapid A-Fib? That would explain the "atrial kick" comment.

patwil73 · Jul 3, 2008

Hi everyone. I'm a new nurse coming up on one year of experience in a Level II Trauma Center Emergency Department and I need advice. This one patient stumped me.
He was crumping the minute paramedics brought into the department. Had a BP 84/52 and a HR 125. He was breathing 40/min and our ER MD decided to intubate. We started giving him IV fluids (NS X 2 liters). He didn't have any signs of CHF- despite the SOB his lung sounds were ok and he had no JVD/ pedal edema. His initial complaint was rapid onset of left sided paralysis. He had a history of left sided weakness from a prior CVA, but this paralysis was new. Anyway, after we started fluids on him, we took him to CT to R/O bleed. When we came back, his blood pressure hovered in the 80's systolic. At this point, his 2nd liter was halfway done.

So far so good - MAP is still above 60 - so fluids should have been a good choice. The new onset paralysis may have been caused by decreased blood flow to the area previously affected by the CVA (particularly if it was an embolic stroke)

I received an order to give Cardizem 10 mg IVP, to "Stimulate his atrial kick" according to the physician. I guess she was suspecting cardiogenic shock? My question however is "Why dump fluids into somebody if you're suspecting cardiogenic shock?" I advised the MD that the BP was low, she intructed to give it slow IVP and watch his BP, which I did. I slowly gave 5 mg of Cardizem and watched his BP go down to 64, then 54. I held the rest of the medication and notified the MD. She instructed to give more fluids.

My drug book indicates that cardizem is contradicted in cardiogenic shock - why would you give something known to cause hypotension? It also has a negative inotropic affect, so it would decrease contractility. Even if his HR was 125 afib I still would have held the cardizem because of the hypotension. Was his HR afib?

You can give fluids in cardiogenic shock although it is not the most desirable - the heart is damaged in some way so extra fluids most times will not help.

I ask "Any pressors?" I received an order to start the patient on Dopamine. I start the patient on Dopamine and titrate up. I started at 25 mcg, then titrated up to 50 mcg. This did nothing for his blood pressure and the MD wanted to then give dobutamine. At this point my patient brady'd down into the 40's and the physician stated to cancel dobutamine and start Levophed. While I'm preparing meds, the MD walks into the room and says she doesn't feel pulses and starts CPR.
Anyway, we code this guy. Initially he was in a PEA brady at 44. Then after rounds of medications and CPR, back and forth from Vfib to asystole, etc, pacing the guy, defibrillating, etc. The MD pronounces.
Not having any ICU experience besides the 13 week internship I had in school, my question is: Which vasopressor is chosen to be used at what time? Rather, which vasopressor is better for what patient? Dopamine, dobutamine, levophed? Are they the same as far as effect on BP/HR? Or are some more for HR vs. BP?

Dopamine is indicated for cardiogenic shock - it provides both pressor action and cardiac contractility. Levophed good for contractility and dilates coronary arteries to reduce workload. Dopamine increases HR, not sure if dobutamine or levophed does.

By the way, after my patient coded, we saw his labwork where his BNP was 120 and his troponin was negative. CT was negative for bleed. Do you think this guy was a PE?
ANY ADVICE/ETC WOULD BE GREATLY APPRECIATED!!

With the new onset paralysis - I would be concerned about embolic stroke - so yea PE would be a big concern of mine. What was his coags? Also CKMB - could indicate long-term damage. If nothing out of wack - assume acute precipitating event so no time for levels to change.

Finally the morbidity of cardiogenic shock is high - something like 80% I believe, so it is possible that even with everything you could have done he probably would have died. However, in the 20/20 hindsight I would seriously question any order to give cardizem again with such a low blood pressure.

Hope this helps

Pat

EricJRN, MSN, RN · Jul 3, 2008

Do you know if there was any talk of synchronized cardioversion initially?

Virgo_RN, BSN, RN · Jul 3, 2008

PEs can be hard to diagnose. I wonder what his chest xray, d dimer, and EKG looked like?

Dopamine works both on A1 and B1 receptors, increasing the rate and force of contraction of the heart, and increasing systemic vascular resistance. It also works on dopamine receptors, increasing renal perfusion. This action is dose dependent.

Dobutamine works on the B1 receptors, increasing the rate and force of contraction.

Levophed (norepinephrine) works on A1, A2 (not usually clinically significant), and B1 receptors, causing vasoconstriction and increasing the rate and force of contraction.

loopingrace · Jul 4, 2008

Wow, great feedback! I want to thank everybody that replied. Yes, he initially was in a rapid A-Fib. On arrival his rate was in the 120's but when the MD asked me to given Cardizem his rate was in the low 100's.

Dopamine at our institution can be given up to 50 mcg. I believe our ICU does differently; after 30 mcg, they will start Levophed.

I'm not sure about his clotting times. I didn't check them myself, but I don't believe the physician mentioned clotting times were significantly abnormal.

There was no talk about synchronized cardioversion intially because this patient had a history of CVA, HTN and heart disease, and his baseline EKG rhythm was unknown. The family members were horrible historians and the patient was altered and aphasic.

Virgo_RN, BSN, RN · Jul 4, 2008

The docs that I work with seem to like to get the rate under 100, so perhaps that's what the doc in your situation was shooting for. Even though Cardizem does act on the smooth muscle of the arterioles, it doesn't always significantly drop BP, at least, not what I have seen. Of course I have not seen it given IVP, but rather, as a continuous drip, where the patient would have gotten 10mg over an hour's time. It is contraindicated in cases of "severe" hypotension, but with the patient maintaining a MAP greater than 60 and in such dire condition, it sounds like the doc made the judgment call that it was more important to get that rate under control at that moment.

One of the things PE can cause is hypotension. Even if the patient had a history of A-Fib and was anticoagulated, he could still throw a clot.

That his BP was so low could be a result of a couple of things. One, his medications. Perhaps he had a cardiac history and was on an ace inhibitor and a beta blocker, perhaps a diuretic, and his BP ran low normally due to his medication regimen. When he went into the rapid A-Fib, this would decrease his BP further. The other cause could be decompensation. His condition had deteriorated to the point where his compensatory mechanisms were failing.

Both of those things could explain why his BP would be refractory to fluid replacement.

NsgChica · Jul 4, 2008

loopingrace,

he was crumping the minute paramedics brought into the department. had a bp 84/52 and a hr 125. he was breathing 40/min and our er md decided to intubate. we started giving him iv fluids (ns x 2 liters). he didn't have any signs of chf- despite the sob his lung sounds were ok and he had no jvd/ pedal edema. his initial complaint was rapid onset of left sided paralysis. he had a history of left sided weakness from a prior cva, but this paralysis was new. anyway, after we started fluids on him, we took him to ct to r/o bleed. when we came back, his blood pressure hovered in the 80's systolic. at this point, his 2nd liter was halfway done.

at this point, he may have been treated like a stroke patient. new onset of paralysis on a previous l sided weakness screams...reestablish blood flow with thrombolytics. but with changing diagnosis...it's hard to sort through.

i received an order to give cardizem 10 mg ivp, to "stimulate his atrial kick" according to the physician. cardizem is a ccb, which i am sure you know. it is used to selectively reduce tachycardias that involve the av node. it also slows ventricular rate in patients with rapid ventricular response during afib/aflutter. my guess is that if the patient went into afib, she wanted to slow the conduction to allow for an atrial kick, which would increase co and bp. however, cardizem will cause hypotension and cause bradycardia or complete heartblock. so to combat this...you give in combination with a pressor i.e. dopamine and plasma expanders and iv calcium gluconate/calcium chloride. this is asssuming patient isn't overloaded, chf, in which case you want an inotrope.

i guess she was suspecting cardiogenic shock? my question however is "why dump fluids into somebody if you're suspecting cardiogenic shock?"

there are two types of cardiogenic shock, systolic dysfunction and diastolic dysfunction. basically systolic dysfunction is the decreased ability of the heart to pump blood forward and it effects the left ventricle. diastolic dysfunction is an impaired ablility of the the ventricles to fill during diastole. so if the patient is having an increase heart rate with a low bp, the inital quick fix is volume. i advised the md that the bp was low (in some way you questioned the order), she intructed to give it slow ivp and watch his bp, which i did. i slowly gave 5 mg of cardizem and watched his bp go down to 64, then 54. i held the rest of the medication and notified the md. she instructed to give more fluids.

i ask "any pressors?" (great suggestion!!!) my thinking is that, this should have been done sooner. i received an order to start the patient on dopamine. i start the patient on dopamine and titrate up. i started at 25 mcg, then titrated up to 50 mcg. (this is the maximum amount of dopamine, at this does it is time to consider another pressor, like levophed.) or why not try epinephrine dose 0.01mcg/kg/min-0.1mcg/kg/min. this is a potent vasoconstrictor. it is used for cardiogenic shock. it can be used as inital treatment, it isn't only resevered for a code situation. epi, increases heart rate, contractility, cardiac output, systolic bp, and cvp. this drug decreases svr to some extent. this is benefical for patients in cardiogenic shock because an increase in svr (afterload) increases the workload of the heart, which is detrimental for a shock patient because increased workload will cause more myocardial damage. this drug would have been the first choice among the surgeons we work with. actually, one time we were coding this man. he eventually had a bp like 50's on dopamine at max dose. the surgeon saw the drug and sharply said that dopamine isn't going to help, get epi. which helped. this did nothing for his blood pressure and the md wanted to then give dobutamine. at this point my patient brady'd down into the 40's and the physician stated to cancel dobutamine and start levophed. while i'm preparing meds, the md walks into the room and says she doesn't feel pulses and starts cpr.

anyway, we code this guy. initially he was in a pea brady at 44. then after rounds of medications and cpr, back and forth from vfib to asystole, etc, pacing the guy, defibrillating, etc. the md pronounces. sounds like a rough night. sounds like you did all that you knew to do. you questioned what the doc and made suggestions.

not having any icu experience besides the 13 week internship i had in school, my question is: which vasopressor is chosen to be used at what time? if his pressures were low, he was probably tachy to compensate. if he was in afib..in theory correcting the afib with or without ventricular response would correct the low bp. cardiazem, however, i would have been weary of giving, which you were since it decrease bp. rather, which vasopressor is better for what patient? dopamine, dobutamine, levophed? all of these drugs are indicated for patient in cardiogenic shock. are they the same as far as effect on bp/hr? or are some more for hr vs. bp?

dopamine: increases hr, bp, co

[color=#a0522d]levophed: increases bp, map, not sure about hr

[color=#a0522d]epi: increases hr, bp, widened pulse pressure, contractility

[color=#a0522d]neo: increases hr, bp, svr, co

[color=#a0522d]dobutamine is a beta1 selective adrenergic stimulant, vasopressor, and inotrope. it will increase co and sv without increasing svr (it actually decreases svr), which increases the workload of the heart. therefore, you have a combination of effects working together to increase tissure perfusion without overworking the heart.

by the way, after my patient coded, we saw his labwork where his bnp was 120 and his troponin was negative. ct was negative for bleed. do you think this guy was a pe?

any advice/etc would be greatly appreciated!!

meandragonbrett · Jul 5, 2008

I would not have given the diltiazem. You mention that he was in A-Fib and was hypotensive....this is unstable a-fib and he should have had synchronized cardioversion.

As far as what is used when: 1)Patient situation 2)Physician preference 3)Past medical history.

Epi--Stimulates Alpha and Beta

Dopamine--Stimulates Alpha and Beta (had different affinities and different dosage ranges)

Norepi---More alpha stimulation than beta

Dobutamine--Major Beta 1 stimulation, arrythmogenic

NeoSynephrine--Alpha

Beta 1 is in the heart, beta 2 is in the lungs (1 heart and 2 lungs is the easy way to remember). Alpha receptors are vascular

If you stimulate beta 1 you are going to increase contractility and your rate which results in an increased CO/CI. Stimulating Alpha is going to cause vascular constriction= increased systemic vascular resistance=increased BP.

You must fill the tank (being the intravascular space) before you can press it (with pressors).

Renal dosing of dopamine is very controversial and is believed to be a figment of our imaginations. We start dopamine and UOP increases. Well of COURSE it's going to increase when you increase renal perfusion!