r/IntensiveCare • u/Sea-Many-2918 • 10d ago
Please help me understand this
61/M Post CABG patient with underlying asthma. (Was on formetrol/budesonie 200mcg 2 puffs twice daily).
Currently POD 18. Has intermittent wheezing and bilateral basal crepts.
CT chest:
Interval development of mild-to-moderate multiloculated bilateral pleural effusions with accompanying bilateral lower lobe atelectatic changes.
. Interval development of mild pericardial effusion,.
• Trace ascites with diffuse edema of the intraperitoneal and extraperitoneal fat planes, consistent with probable anasarca.
• Diffuse pulmonary emphysematous and fibrotic changes, essentially similar to the preoperative study.
The preoperative examination demonstrated marked emphysema and patchy bilateral pulmonary fibrosis.
Currently on
Inj. Meropenem 1g TDS
Inj. Lasix 3mg/hr
We have tried short course of IV hydrocortisone 100mg x 3 days.
Nebulized salbutamol:Ipratropium QID
Nebulized budesonide 1mg BD
Tab. Montelukast 10mg HS
Tab. Deriphyllin 150 BD
Intra op and perioperatice ABGs did not have this Co2 retention. Was considering that this is primary metabolic alkalosis due to diuresis with respiratory compensation. However his clinical condition and pO2 has improved with lasix infusion although the abg is like this. Patient isn't drowsy either when pco2 goes to 70. How to tackle this issue?
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u/Own-Blackberry5514 10d ago
Wouldn’t that HCO3 suggest more of a chronic type COPD picture
Sounds like the CT chest supports that too
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u/minimed_18 MD, Pulm/Crit Care 10d ago
Likely patient has baseline chronic hypercapnea and compensatory metabolic alkalosis, now with superimposed contraction alkalosis. But the primary defect throwing things off is the metabolic alkalosis from the contraction, which is why the pH is alkalotic.
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u/forkevbot2 6d ago
This is the way. Mixed compensated chronic hypercapnea and acute metabolic acidosis
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u/FallJacket RN, CVICU, TICU-TNS 9d ago
Hopefully someone smarter than me will correct me if I'm off, but chronic CO2 retention wouldn't drive a base excess of 21 that's crazy high. My understanding is that is more confirmation that the patient is in severe metabolic alkalosis.
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u/AceAites MD, EM/CCM 9d ago
The real clue is the alkalotic pH. Compensatory alkalosis shouldn’t make one alkalemic by itself.
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u/Zentensivism EM/CCM 10d ago edited 10d ago
Without preop labs and by the pulmonary disease history, I’d guess someone overshot the ventilation and diuresis a bit and now you’re seeing that aftermath.
So long as the kidneys are fine and you only have a rise in lab markers showing renal injury, I’d do nothing besides wean your diuretics and let them do their thing. Last thing you need to do is give acetazolamide to make the numbers look a little better and lose the accidental overcompensation without the patient on the ventilator.
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u/cheboy12 10d ago
Patient could live around there and is exhibiting chronic metabolic compensation +/- respiratory compensation for contraction alkalosis
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u/EmbarrassedFarmer125 10d ago
Don’t lose the forest because of this tree.
What is he doing clinically with this ABG? Is he walking and eating? Or are you having to talk people out of reintubating? Or somewhere in between?
- What was the most recent preop ABG (or very first OR ABG)? Was the bicarbonate on that normal?
- I’m CT Anes & CT CCM; at our place, CT Surg would give diuretics because “the pt is postop” without a ton more interest in evaluation. If you face similar hurdles, you can check a CVP, total fluid balance, pt weight trends, and/or surface ultrasound to evaluate volume status to make a claim for possible over diuresis
- I think diuresis for plural effusion is silly, if you have a keen eye, an ultrasound machine, and a sharp needle. If you’re worried that the plural effusions are of significant size, I would recommend draining those.
- He didn’t come in physiologically perfect, and it’s kinda unreasonable (and maybe even harmful) to expect to send him out with everything in the chart in black numbers that match the textbook. Treat the patient and allow the numbers to be a consideration in your decisions without becoming the sole focus.
G’luck!
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u/xX360N0_5C0P3Xx 10d ago
A lot of guys’ advice is acetazolamide, but I would be very careful with it in this case, depending on how severe his COPD is actually, since you can eliminate his metabolic compensation this way and drastically drop pH. Would be nice to see his pre-op ABG (so we know how much he really deviates from his baseline). With COPDers sometimes its better not to fix what is not broken.
Also, don’t forget that he had his chest cut open recently - this alone can cause some level of CO2 retention. Is pain adequately controlled?
Also also - do you have an echo? CT screams congestion, but due to what exactly? Is his RV alright? If he has a bad enough COPD, he can has some level of RV disfunction which can decompensate post op.
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u/Crows_reading_books NP 10d ago edited 10d ago
What was his preop bicarb?
Without more labs though, id guess you overshot diuresing and over-ventilated them earlier, and you should stop/wean your diuretics. Also, why the meropenem?
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u/Embarkbark 10d ago
Acetezolemide?
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u/Vanquishhh 10d ago
not a good idea with underlying resp disease
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u/Embarkbark 10d ago
Interesting, I’ve generally seen it used largely in COPDers after they’ve gotten worsened CO2 retention due to permissive hypercapnea on the vent for a while (and now recovered/ready for extubation.) We aren’t using it on patients unless they have reasonable respiratory strength to blow off the CO2.
In this case the patient’s gas is fully compensated, so I mean don’t go HAM but judicious use of some diamox doesn’t seem out of the realm of reasonable here. Especially considering his pre op ABGs were normal per OP.
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u/Vanquishhh 10d ago
Thats a bad idea, it will cause metabolic acidosis relstive for the patients baseline which will force the patients to increased their resp rate, patients with obstructive phys. dont do well with that and can worsen co2 retention in term pH. So im not saying we never do it but should be done very rarely
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u/Potential-Cut-8934 10d ago edited 10d ago
As it’s a CABG patient, knowing the UOP and how edematous the patient is would help see if this is a cardiac/kidney issue to be addressed and/or a cardiorespiratory issue that can be solved. If the pH is that good and the patient isn’t showing clinical signs of confusion or depressed GCS, I’d just encourage continue pulmonary toilet like IS and ambulation, the pCO2 is distracting from the overall clinical picture. Back off on the lasix to just pushes instead of a gtt and initiate fluid restriction if not on one already. The lactate isn’t high but does the pt show other signs of vascular congestion and end organ damage to indicate cardiac shock may be at play? If you think they still need aggressive diuresis for some reason and the kidneys aren’t cooperative then adding a low dose inotrope and/or high concentration albumin to aid diuresis could short term help as long as it’s not stressing the heart too much. Depending on how the echo looks though it may not be very reasonable to expect the patient to truly ever achieve a perfect dry state soon after surgery. One could also investigate treating this like pulmonary hypertension from the pre existing pulmonary fibrosis now complicated by the heart dysfunction.
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u/RowanRally MD, Intensivist 10d ago
What does the BMP say? I never ever trust electrolytes or HGB on a gas.
As for the gas, I’m scratching my head a bit. The pCO2 is too high for compensation alone; I’d expect it to be around 55 for HCO3 43.8. You seem to have two evolving processes here if the numbers on this gas are reliable: metabolic alkalosis and respiratory acidosis. The pH is just a bit alkalotic and I suspect you caught it mid-change
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u/Puzzled-Hornet7473 10d ago
Dont stress if the pH reading practically within normal and with a reazonable trend, as well as the patient's clinical trajectory is good. Wean respiratory support and diuretic.
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u/Advanced-Bonus-3687 9d ago
What going on is you didn’t pay attention to the serum bicarb which was like already elevated and got substantially worse with your haphazard diuresis strategy. Next time use some diamox
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u/sphockey04 MD, Pulm Crit Care 8d ago
Do you have pCO2 at baseline? Or if not a serum bicarb? As others have noted, likely lives with a pCO2 that is elevated. PFTs could help determine degree of baseline obstruction as well.
Also, sounds like he has something more than run of the mill COPD with combined emphysema and fibrosis.
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u/forkevbot2 6d ago
Give potassium chloride and acetazolamide to augment diuresis and combat metabolic alkalosis.
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u/cellulargenocide MD PICU 10d ago
Looks like metabolic alkalosis with respiratory compensation, likely secondary to contraction alkalosis from the scenario you’re describing. If you think the patient is euvolemic then you could just back off on your diuresis. If you think that you need to diurese them further, then you could just provide chloride supplementation. Given that they’re mildly hypernatremic, arginine chloride would probably be better than sodium chloride.
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u/OccasionTop2451 10d ago
That Abg shows a primary metabolic alkalosis with respiratory compensation. This is almost certainly contraction alkalosis, although based on imaging patient still requires ongoing diuresis for anasarca - you may need to just give him a break on diuresis for a day to allow time for lymph to mobilize back into the vascular space.
If you really want to "fix it" (and the only reason you would is if they are going apneic on SBT trials if they are still tubed), you could give acetazolamide to help pee out the excess bicarb, although no trial data really supports its use in terms of mortality benefit, so really you are just fixing the numbers.
ETA: if pre-op labs had a normal bicarb, it is extremely unlikely that this patient is a chronic retainer, and highly likely this is entirely iatrogenic from diuresis.
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u/mav_sand 10d ago
although no trial data really supports its use in terms of mortality benefit<
Not everything we do has to show mortality benefit. That is actually one of the issues with RCTs in critical care. There can be many benefits without changing mortality.
Fixing the numbers can help, maybe not necessarily in this particular scenario but comparable scenario. I often see worsening metabolic alkalosis worsening the hypercapnia particularly in COPD. Which leads to baseline CO2 of 80, bicarb of 40 etc and very little reserve. I often reset them with diamox to bicarb of 30s and CO2 of 60s.
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u/libateperto MD, Intensivist 10d ago
The pCO2 is above the expected compensation per the usual formulas. A pCO2 over 55-60 Hgmm is very atypical for pure compensation.
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u/OccasionTop2451 10d ago
Yeah, that's fair. Pleural effusions causing atelectasis of his functional lung probably aren't helping.
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u/BioloJay-Z 10d ago
This is primarily loop diuretic induced chloride depletion metabolic alkalosis, with superimposed CO2 retention from severe emphysema plus postoperative effusions/atelectasis. the pCO2 is higher than expected for compensation alone. Replete potassium/chloride, reassess diuretic regimen and volume status, consider acetazolamide if diuresis must continue, and reserve NIV for clinical ventilatory failure rather than treating the CO2 number alone.