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| |  Vasopressors- Critical Care RN's please help!
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.
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.
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?
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!!
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Jul 02, 2008, 07:54 PM
Re: Vasopressors- Critical Care RN's please help!
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.
| | No. 5 |
Jul 03, 2008, 01:57 AM
Re: Vasopressors- Critical Care RN's please help! Originally Posted by loopingrace  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) Originally Posted by loopingrace 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. Originally Posted by loopingrace 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. Originally Posted by loopingrace 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
| | No. 7 |
Jul 03, 2008, 04:43 AM
Re: Vasopressors- Critical Care RN's please help!
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.
| | No. 8 |
Jul 04, 2008, 10:30 AM
Re: Vasopressors- Critical Care RN's please help!
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.
| | No. 9 |
Jul 04, 2008, 02:06 PM
Re: Vasopressors- Critical Care RN's please help!
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.
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