Case Review: Patient with pulmonary hypertension with deteriorating hemodynamics

CCU BSN RN · Dec 9, 2016

Neo is an alpha 1 agonist, increases PA pressures and worsens RV function. Hence why it's not indicated for this patient. Levo is the pressor of choice in these instances because as an alpha 1 and 2 agonist, it increases SVR and increases CO

I think the question you're really getting at is 'what should have been done differently for this patient?' and that's a great thing to ask, always. Without full chart review, the things that I would be concerned about:

1. This patient was admitted with a cardiac problem. Why was cardiology not consulted until after she coded? Who was attending this patient, and a follow up, why not a cardiologist?

2. She was sent to the ICU initially, but not the cardiac ICU?

3. Did anyone work up the etiology of her symptomatic bradycardia? Did she have tachy-brady? Intermittent heart block? Need a PPM/AICD? Or just good old-fashioned cardiogenic shock.

4. I see a lot of repeatedly giving someone fluid who could've probably used vasopressor support.

5. Overall I see very little about what the treatment plan is/was supposed to be for the PAH/R sided heart failure? She got a couple of doses of Bumex on tele last week? That's it? Idk Dobutamine or Milrinone would have been cool to start early. Levo for hypotension, not 3L of saline.

6. Would've intubated sooner. Bipap increases thoracic pressures in PAH patient and can worsen preload

7. Would've cardioverted to NSR instead of BB (Metoprolol) or CCB (Dilt) to prevent cardiogenic shock

Catticus11 · Dec 9, 2016

Neo is an alpha 1 agonist, increases PA pressures and worsens RV function. Hence why it's not indicated for this patient. Levo is the pressor of choice in these instances because as an alpha 1 and 2 agonist, it increases SVR and increases CO
I think the question you're really getting at is 'what should have been done differently for this patient?' and that's a great thing to ask, always. Without full chart review, the things that I would be concerned about:
1. This patient was admitted with a cardiac problem. Why was cardiology not consulted until after she coded? Who was attending this patient, and a follow up, why not a cardiologist?
2. She was sent to the ICU initially, but not the cardiac ICU?
3. Did anyone work up the etiology of her symptomatic bradycardia? Did she have tachy-brady? Intermittent heart block? Need a PPM/AICD? Or just good old-fashioned cardiogenic shock.
4. I see a lot of repeatedly giving someone fluid who could've probably used vasopressor support.
5. Overall I see very little about what the treatment plan is/was supposed to be for the PAH/R sided heart failure? She got a couple of doses of Bumex on tele last week? That's it? Idk Dobutamine or Milrinone would have been cool to start early. Levo for hypotension, not 3L of saline.
6. Would've intubated sooner. Bipap increases thoracic pressures in PAH patient and can worsen preload
7. Would've cardioverted to NSR instead of BB (Metoprolol) or CCB (Dilt) to prevent cardiogenic shock

Thank you so for responding. What was throwing me off about Neo was the information I had about neo telling me that it was pure alpha stimulation = peripheral vasoconstriction,â€ and so I understood that vasoconstriction of vessels outside the pulmonary and cardiac circuits. But by peripheral vasoconstriction, it's referring to all vessels outside the heart?

I

1. Originally cardiologist was consulted, and they were the ones who originally ordered the IVP bumex upon her manifestation of HF symptoms and RV dysfuntion noted on the echo. However, they never did quite much of anything until after the code. An inotrope was mentioned up before the code, but nothing was ever ordered by them.

2. In terms of originally being sent to the ICU, that's a good question.

3. The bradycardia confused me initially but nobody noted anything of it. Originally I thought it could be a result of the Optimist, because it never recurred again (with the exception of when we started the Precedex). Could it be from the cardiogenic shock?

4. When I was getting report from the ICU nurse transferring her to me, she kept mentioning all this fluid she gave her. I understand the concept of a fluid challenge, but would that still work with severe RV dilation?

5. That's what I was wondering. She was coming to my flood with severe pulmonary hypertension, and she was only on a pressor and hiflo. I understand she came in with hypotension and was being maintained on Neo at the time. After the day she was intubated and coded, I learned that night she was started on Nitric Oxide. Was there anyting sooner we could have done specifically for the pulmonary hypertension? Or would an inotrope have corrected that?

6. That's true about the Bipap. Originally I was just pushing for intubation after I saw her labored breathing and her metabolic acidosis on ABG.

7. The day after the code, the cardiologist stopped by suggested amiodarone gtt however was concerned for her already elevated LFTs, and suggested possible cardioversion, but noted that a TEE would have to be done and didn't want to do one with INR that was so elevated. So basically nothing was done really to control her afib.

offlabel · Dec 9, 2016

Good case study with a lot to unpack...good thoughts by CCUBSNRN...here's mine. First off, what is Optimist? That aside...the issues that I see.

11/29 -- She became hypotensive again went into a hypercarbic respiratory failure per ABG analysis. She was unresponsive to fluid resuscitation and she was transferred back to the ICU. She was started on a Bipap She was given a total of 3 L of NS, 1 unit of albumin and finally started on a Phenylephrine gtt. Her afib HR increased while at rest, and she was started on a Cardizem gtt.

This is what did her in, IMO. The huge problem with PHTN is the effect it has on the right ventricle. If the RV doesn't work, nothing gets to the LV and a vicious cycle sets in. Hypercarbia and hypoxia dramatically and acutely worsen PHTN and that would further impair RV function. Blasting her with volume and then adding insult to injury with phenylephrine pretty much guaranteed she'd not do well. Really sounds like PHTN was causing all of this and the interventions made it worse.

So, OP, you're right about the RV failure and it sounds like you're on the right track thinking about having started NO sooner. Did she have an echo during the 11/29 event? That would have been a good guide for determining inopressor/inotrope. NE is good for PHTN, but when the RV is failing like that sometimes a phosphodiesterase inhibitor with NE or vasopressin is required. Epi would be a last choice as it can drive the pulmonary pressures as well.

good discussion

ps...I'm skeptical that cardioversion would have done anything for her afib as the PHTN probably had a lot to do with it.

CCU BSN RN · Dec 11, 2016

Follow up thoughts.

Yeah I would've liked Amio for cardioversion as opposed to electrical because it would probably have a more sustained effect.

Agree that 4L of IVF was probably the single action here that caused the most irreversible harm. Small boluses of crystalloids may have been indicated for intravascular volume depletion, but I'm talking about 250cc NS boluses, not a 3-4L IVF challenge. That can be a side effect of having an attending from any other specialty.

I would say that if this were my family member, I would've pushed for a cardiology attending, and not wanted her in any ICU except CICU with this issue. There may have been times where she was appropriate for telemetry/step down, but she definitely needed a cards attending way before she coded. When someone is consulting it's fairly easy for the attending to not heed their advice, which seems like it happened to some extent here.

As for Neo, a follow up, it's important not only to know that it's an alpha 1 agonist, but also HOW STRONG its alpha 1 agonist properties are, which is what trips a lot of people up. So keep that in mind for future analysis of pressor-appropriateness, just as a general FYI.

Cardiogenic shock is my best guess for the bradycardia, which is what made me initially feel she should've started out her hospital stay in the CICU.

An inotrope is the treatment here, yes, so Dobutamine or Milrinone or some combination thereof, would've been what I wanted to see as treatment for the actual PAH issue, with levo for a pressor if BP did not initially tolerate instead of IVF.

Avoiding intubation should always be the goal until it is absolutely necessary, but with PAH you need to be really careful of positive pressure ventilation actually making things worse, believe it or not. That might have something to do with why they chose Hi-Flow instead of BiPap during certain periods.

I agree, *** is Optimist? I assume from the 'mist' that this is an inhaled vasodilator, but yeah I didn't address it because I have no idea which of the many PAH meds it is.

I'm going to toss in a link that I think goes over the treatment plans and rationale for this issue really well, helped me quite a bit when I was trying to figure out the same concepts on orientation several months ago. Overall this is a great discussion and I hope to see more like it in the future!

The Crashing Pulmonary Hypertension Patient - emdocs

offlabel · Dec 12, 2016

Cardiogenic shock is my best guess for the bradycardia...

Yeah...spot on...goes along with her RV failure and RCA perfusion.

Catticus11 · Dec 12, 2016

Yeah...spot on...goes along with her RV failure and RCA perfusion.

So right ventricular failure can cause bradycardia?

Catticus11 · Dec 12, 2016

Great article!

offlabel · Dec 12, 2016

So right ventricular failure can cause bradycardia?

It's part of the downward cycle...as the RV fails, return to the LV falls and so does CO/MAP. The RCA is perfused over systole as well as diastole (as opposed to the LV being perfused over diastole) As SBP falls so does RCA perfusion which is associated with bradycardia and RV failure gets worse, perpetuating the cycle.

tcvnurse, BSN, RN · Dec 13, 2016

Wow, in my unit she would not have gotten all the normal saline (too much sodium, we use plasmlite instead) and probable on flolan, milrinone and epinephrine, with a Mac and a PA cath to monitor cardiac indices. Also cardizem AND precedex? ABSOLUTELY that would cause bradycardia. They needed to lower the PA pressure and improve RV function in order to get the liver back into some shape. It's the blood backing up into the liver from the RV failure that causes the liver failure. Renal failure, easy- not much forward flow due to blood unable to be pumped across from the RV.

Some serious mishandling here. On the part of all involved.

offlabel · Dec 14, 2016

Some serious mishandling here. On the part of all involved.

It's pretty easy for us to Monday morning quarterback. We have a very black and white presentation in the comfort of our downtime here with all of the pertinent facts presented to us very clearly.

Very different from a running resuscitation of a patient that is an unknown quantity. Way harder to do that than have a case discussion on an anonymous forum.

Lev, MSN, RN, NP · Dec 15, 2016

77 y.o. female arrived to ED with bradycardia and hypotension with c/o weakness and fatigue. She was found to have been just diagnosed of pulmonary hypertension after years of symptoms and was started on Optimist recently (though actual date is unclear).
Past Medical History: Pulmonary Hypertension, HLD, chronic atrial fibrillation and on coumadin.
Course of Stay:
11/24 -- The Optimist was discontinued, and she was transferred to the ICU where she was started on a dopamine gtt and started on fluids. She responded very well to both. Echo was performed which showed elevated pulmonary pressures and a severely dilated right ventricle. However LVEF was >70%.
11/27 -- She was then transferred to a medical floor. She was edematous and was being maintained on supplementary oxygen. She was started on IVP Bumex and started on PO Lopresser for the HF.
11/29 -- She became hypotensive again went into a hypercarbic respiratory failure per ABG analysis. She was unresponsive to fluid resuscitation and she was transferred back to the ICU. She was started on a Bipap She was given a total of 3 L of NS, 1 unit of albumin and finally started on a Phenylephrine gtt. Her afib HR increased while at rest, and she was started on a Cardizem gtt.
11/30 -- She was changed to 20 L of HiFlo. She was noted to not be producing any urine. She was transferred to the cardiac ICU. Swan catheter was placed which showed elevated PA and CVP pressures. PAOP unable to be obtained. SVR normal. MAP maintained on Neo gtt. HR controlled.
12/1 -- Her BUN/Cr and LFTs had increased. Patient still producing little urine. Upon assessment, patient demonstrated increased confusion, RR was elevated, and O2 saturation was variable 88% to 92%. She was placed on Bipap which appeared to help. ABG was performed showed metabolic acidosis. CRRT initiated per Renal consult. Pulmonary also chose to intubate.
Patient was started on a Fentanyl and Precedex gtt was started for sedation. Patient developed bradycardia so precedex and cardizem gtt were stopped. Later in the shift, patient was being boosted up in bed when she appeared to go into a PEA arrest. CPR was initiated, and 1 amp of Epi was administered before ROSC. CRRT discontinued. Cardiologist on consulted changed the patient from Phenylephrine to Norepinephrine gtt and Milrinone. Cardiologist also made a point that "Neo was the last thing you wanted her on." Patient then became tachycardic, HR in 140s-160s. Milrinone was discontinued.
12/2 -- CXR revealed pulmonary infiltrates, thought to be PNA. Patient started on Zosyn. CRRT restarted. Patient remained tachycardic with a HR in 140s-160s, Levophed titrated as much as possible.
12/4 -- Patient terminally extubated.
My issues:
Should she have been started on a Cardizem gtt in the first place?
Also, why did the cardiologist say Neo was the last thing she needed to be on?
Did we put her into a Left sided heart failure as well with the Neo?

I think at around 11/27 is when things started going south. She had right sided heart failure as evidenced by that severely dilated right ventricle. The dopamine drip was maintaining her. That was probably discontinued when she went the medical floor.

bumex+ lopressor= hypotension. But she probably still fluid overloaded so went into hypercarbic respiratory failure from ineffective ventilation. How low was her albumin? Did they check her BNP when this was happening?

Why did they choose phenylephrine(neosynephrine)? Why not levophed or back on dopamine? Phenylephrine (neosynephrine) can increase pulmonary vascular resistance and thereby worse the pulmonary hypertension. It actually decreases renal perfusion which could be why she stopped producing urine. That and the bumex IVP put her into renal failure She then developed metabolic acidosis from the renal failure.

She aspirated when she coded and developed PNA. She then became septic and died. Or she was septic as far back as "Increased LFTs" and "increased confusion." Were blood culture drawn at any time prior to the intubation? She may have developed a central line infection.

Definitely a very complicated patient.

If you think about right sided MI, this may give a clue about how this patient should have been handled. We don't give nitro so we don't drop their pressures and we don't pump them too full of fluids because they can't handle (or need) the volume. Those patients are sick. And can be hypotensive and bradycardic.

Acute Right Ventricular Failure in the Setting of Acute Pulmonary Embolism or Chronic Pulmonary Hypertension: A Detailed Review of the Pathophysiology, Diagnosis, and Management

Management of Acute Right Ventricular Failure in the Intensive Care Unit