Case Review: BP and Urine Output

Specialties Critical

Published

I had a patient who was s/p Thoractomy with CT draining 100 cc over 8 hours. He was slightly confused and agitated but I was told that was him at baseline. He appeared jaundiced. He was afib and VPaced, however his HR was elevated in 120s-130s. He managed to control his HR after 5mg of IVP Lopressor, and 500 mcg of Digoxin over the course of the shift, and his Neo was titrated was titrated up as needed to control the effect on BP. Per the surgeons order, she specificially wanted his MAP between 70-80 being monitored via Arterial Line.

Patient had history of Hypertrophic CM with an EF 25%. Other history includes CKD III, Glibert's Dx, HTN, and Colon Ca.

He arrived from the PACU receiving 20 mL of NS until patient could tolerate PO. Patient also recieving Vasopressin at 0.1 units/min and Neo at 0.5mcg/kg/min, usually amounting to 100 mL an hour.

The problem was his lack of urine output over the course of my shift. Originally we tried Albumin 5% 500 cc over an hour. Then a couple hours later a Albumin 5% 250cc over an hour. He had a total input of over 2 L and only made 65 mL of urine over the course of the night. The surgeon was made aware who came to see the patient after the BP started to become more stable, and she got upset that he was on so much pressor therapy. MAP was in the high 70s at the time. SBP was in the 100s, DBP was in 60s. I explained to her that I was planning on titrating down soon since his BP and HR just became stable, and that her order did say MAP between 70-80mmHg. But she remained upset saying that the high MAP was "clamping down" on the kidneys so she ordered I wean the Neo off, and then once the neo was off, to wean the vasopressin.

He tolerated weaning well over the course of my shift. Neo was off and vasopressin was almost off by the time I left. Urine picked up to 45 mL/hr by the time my shift ended.

I understand I could have weaned the vasopressors, I had every intention to before she arrived, but my concern was whether that or not the MAP of 70s was actually "clamping down" on the kidneys. And if so, can someone elaborate on the concept.

Or was it the max dose of vasopressin that hindered the urine output. Or did the albumin assist with UO.

Sorry, I just left the shift sorta unclear about the situation.

Specializes in Critical Care.

Vasopressin = ADH

1. After any kind of surgery there is a stress response release of ADH and unrine output can drop despite adequate kidney perfusion. Low UO by itself is neither a sensitive nor specific measure of perfusion. Low UO with climbing creatinine and markers of impaired perfusion (rising lactate, low Svo2, no peripheral pulses/cap refill) is a marker of bad perfusion and is a bad thing.

2. It is important to know exactly how each vasopressors works. Both phenylephrine and vasopressin are pure peripheral vasoconstrictors which add afterload. In this case, with someone with a poor EF, adding afterload is the opposite of what you need because the heart already sucks at ejecting blood and needs as little to push against as possible. Having lower afterload with increased inotropy (milrinone or dobutamine if BP can tolerate; low dose epinephrine if BP is marginal) will mean more flow to kidneys.

3. This is a great example of why blood pressure is not a great measure of perfusion. What we really care about is flow, not pressure. However we have a difficult time measuring flow so we use pressure as a surrogate. In this case a peripheral vasoconstrictor clamped down on vessels which led to less flow at higher pressure and gave everyone a BP number that looked nice but wasn't helpful for the patient.

4. With his specific case the albumin probably helped with volume resuscitation. In every pt think about if they need help with preload, afterload, and/or contractility. All in all this is just a sick dude; but most of his problems probably could have been helped by helping the heart pump better (both by increasing preload which you did with albumin and maybe with an inotrope) but not with increasing afterload.

Thank you, very helpful!

Specializes in Cardiac/Transplant ICU, Critical Care.

Did you have a SWAN in? If so, how was the CI and SVO2? How was your CVP? How was your Base excess/deficit on the gas? Did you choose those drips? There are a lot of questions that would help paint a better picture.

If it were me I would say "These are the drips that were ordered, your orders were to keep maps in the 70s-80s, I followed those orders, please change them as you see fit". It sounds like she did just that, but don't be worried that she was pissed off at her own mistake.

In a pt with a EF nearing VAD implantion territory I would have recommended a pressor that has B1 properties (Epi, Dob) and then Norepi for BP because it would also stimulate A1, A2, and B1 receptors. Next time just ask for clarification, ask them the theory and physiology behind it, and thank them for teaching you. Attendings can lash out over weird things, don't let it get to you

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