Treating Bipap Induced Hypotension

[Catticus11]

I had a patient who needed bipap for an elevated pCO2 in the 80s but compensated. He was on a Bumex gtt for an elevated BNP, and CXR which showed bilateral pleurel effusions. Patient had history of diastolic CHF. Per the H&P, no history of COPD.

Patient was transferred to the unit for possible precedex because he was agitated on the floor. No agitation witnessed by me upon initial assessment. We obtained an ABG, which showed compensated respiratory acidosis, pCO2 in 86.

We started Bipap and he tolerated it fine, I believe the settings were (20/5). Bumex gtt still going with adequate urine output. BP was still stable after hte initial Bipap placement, no significant changes. BP dropped to 70s/50s. So the RN initiated a Neo gtt.

I reviewed the patient's record, and he had a TEE that day or the previous day that showed severe pulmonary HTN.

Could I have adjusted the Bipap settings somehow, or was pressors the most appropriate way to address the hypotension?

[offlabel]

So breaking down the issues...

1. Hypotension presumably caused by a fall in venous return from the bipap.

2. Pulmonary hypertension that is exacerbated by the rise in PaCO2. If there was hypoxia present, that would contribute to the PHTN as well, but you don't mention that.

3. A relative hypovolemia from the diuretic.

4. Big potential for a struggling RV 2/2 the PHTN issue causing a fall in blood return to the LV causing a fall in MAP/CO causing a fall in coronary artery perfusion causing RV to struggle even further with the cycle repeating and worsening.

Options...

1. Back off the bipap a little until you restore aortic root pressure with a pressor and move it back up. It won't take that long and I don't think you lose to much ground with regard to his CO2. It is contributing to the hypotension, IMO, so I wouldn't decrease the bipap for too long as long as it is working.

2. Give a little volume.

3. I'd maybe choose vasopressin over phenylephrine as the former has less effect on PAP's than the latter. The idea is to increase coronary blood flow by increasing aortic root pressure, so some might argue that is just a style point. My opinion.

[PresG33]

More info on the TEE would be nice... if the RV was pumping like crap then I like dobutamine to increase RV contractility and decrease pulmonary vascular resistance then, like offlabel said, treat systemic hypotension with vasopressin to give a more pure systemic squeeze with less effect on PVR. Also stop diuretic because hypovolemia plus positive pressure is what gets you into trouble. Also, what was the time between putting on bipap and the hypotension? If it was a few minutes then the decreased venous return makes sense. Any longer and you may have seen a drop in BP because you dropped the CO2 (which is a SNS stimulant) and made the patient more comfortable, which caused him to chill out and stop releasing endogenous catecholamines. Have seen this type of post-bipap slump after an anxious patient is made more comfortable and they turn off all those nice fight or flight neurotransmitters.

[Catticus11]

More info on the TEE would be nice... if the RV was pumping like crap then I like dobutamine to increase RV contractility and decrease pulmonary vascular resistance then, like offlabel said, treat systemic hypotension with vasopressin to give a more pure systemic squeeze with less effect on PVR. Also stop diuretic because hypovolemia plus positive pressure is what gets you into trouble. Also, what was the time between putting on bipap and the hypotension? If it was a few minutes then the decreased venous return makes sense. Any longer and you may have seen a drop in BP because you dropped the CO2 (which is a SNS stimulant) and made the patient more comfortable, which caused him to chill out and stop releasing endogenous catecholamines. Have seen this type of post-bipap slump after an anxious patient is made more comfortable and they turn off all those nice fight or flight neurotransmitters.

When I asked the nurse about the BP following Bipap placement, she said the BP remained normal. I don't think she was measuring the BP more frequently than q30min at the time, so I'm not sure how fast the BP dropped.

So when the BP decreased, I should have asked to hold the Bumex gtt temporarily, and initiated vasopressin. That makes sense since he wasn't in much respiratory distress. I completely understand the thought behind the vasopressin, but would that cause any issues with the need to diurese him? Or would you say he was overdiuresed considering his BP dropped?

Also, would the PaCO2 have the same effect (i.e. pulm HTN) considering that the HCO3 had compensated?

Lastly, can you elaboate on "vasopressin to give a more pure systemic squeeze"...just so I can better understand the concept more.

[PresG33]

He may not have been so overdiuresed that his BP would drop on its own (that would take some major diuretic use) but positive pressure ventilation (bipap) is much more likely to collapse veins if they are under filled. So basically he was likely a bit dry, which normally is fine, but when the positive pressure was added the veins had less volume to keep them open and collapsed.

The lungs only care about the paCO2, not if there is any compensation. There are chemoreceptors in other areas that are affected by pH, but the lung vessels respond to high CO2 and low O2 in the same way: by constricting. There are a lot of other effects that acidosis will have but the effect on pulmonary HTN is independent of compensation by bicarbonate.

Vasopressin acts on V1 and V2 receptors. V2 receptors increase water reabsorption and this increases blood volume. The V1 receptors cause vasoconstriction. Interestingly, V1 receptors are almost completely located in the peripheral veins and arteries. Therefore there is very little vasoconstriction of the pulmonary vasculature (all other vasopressors act on alpha which are plentiful in the pulmonary system). So using phenylepherine is pretty much the worst choice in this situation because it increases the workload on the right heart without helping it pump at all. Of note is that there are V1 receptors in the coronaries, but there are alpha as well so it appears vasopressin has the same vasoconstrictive effect on the heart vasculature.

Vasopressin is great for patients with pulm HTN who need a vasopressor, but it has no inotrpy so it will increase left heart workload without any help to overcome this higher afterload.

[Catticus11]

Perfect, thank you so much!!

[pmath_RRT]

As an RT I would like to ask why they are starting biPAP on a person that is fully compensated? Unless this pt was tachypnic and they wanted it for WOB. You will blow off too much CO2 and the pt will become alkalotic which you don't want (obviously). What was the bicarb? I'm guessing high considering his PCO2 was in the 80's and fully compensated.

Secondly the settings are way to high. Start low like 8/5 and look at the tidal volumes. Make sure they are getting 6ml/kg of their IBW at least, and if not increase IPAP slowly because BiPAP's can decrease CO and drop BP's without even trying.

And third, is there an RT at your facility?

[HarleyGrandma, RN, EMT-B]

As a nursing student (I graduate in May) conversations like this are why I come to AllNurses -- thank you! It is so helpful to be able to read your thought process, and be able to hear the opinion of those with experience.

Back to lurking and learning... :-)

[Catticus11]

Yay, I'm so glad! You're always learning in this field, and this website's a great resource for new nurses like myself to discuss things with the more experienced RN, NPs, etc.

Best of luck! :)

[Catticus11]

As an RT I would like to ask why they are starting biPAP on a person that is fully compensated? Unless this pt was tachypnic and they wanted it for WOB. You will blow off too much CO2 and the pt will become alkalotic which you don't want (obviously). What was the bicarb? I'm guessing high considering his PCO2 was in the 80's and fully compensated.

Secondly the settings are way to high. Start low like 8/5 and look at the tidal volumes. Make sure they are getting 6ml/kg of their IBW at least, and if not increase IPAP slowly because BiPAP's can decrease CO and drop BP's without even trying.

And third, is there an RT at your facility?

Hi! I love that an RT is on here.

So yeah, when I was speaking with the cardiologist I asked the same thing, and he said his concern was from the fact that he has no history of COPD and that though compensated his CO2 was too high to just leave as is. He also assumed his sorta drowsiness was affecting his ability to blow it off and that's why needed to compensate. And I'm guessing his elevated CO2 was also contributing to the pulm htn/diastolic heart failure. But that lost part is just my conjecture based on what everyone has said so for.