Case Study: Respriatory Distress - Fluid or Mucus? EKG+ABG!

[brentoli]

Fiz, pretend I am an EMT-B sitting in the back of the ambulance with you when you answer this question. I really don't know the answer, I need to go to medic school.

[hr:7856018d7e]

What made you decide to withold Lasix, and what would have been the implications of giving it?

[fiznat]

What made you decide to withold Lasix, and what would have been the implications of giving it?

I didn't give lasix because of the potential that this patient was suffering from pneumonia instead of CHF. The skin temperature was the biggest hint towards this, as well as the tachycardia (fast heart beat is typical in patients dealing with infections). Also I was pretty sure I heard rhonchi (mucus, typical of pneumonia) and not rales (fluid typical of CHF) in the lungs. While all of these aren't exactly enough to conclude that the patient definitely has pneumonia, it was enough to make me cautious.

Lasix is dangerous when given to pneumonia patients because it runs directly counter to the correct treatment for this condition. Patients with pneumonia are at high risk for sepsis, for which the first line treatment is almost always FLUID. This is because the peripheral vasculature tends to dilate, which drops blood pressure and decreases cardiac return (which also drops blood pressure). Also in these patients there is often a redistribution of fluid inside the body, which can also lead to low blood pressures. All in all, I imagine you can see why taking fluid away from these patients could potentially be a bad thing.

In addition, and this is a bit anecdotal, I have been told that rapid diuresis has a tendency to "dry out" pneumonia mucus within the lungs, causing it to be less mobile, more harsh, and effectively more obstructive. Lasix does nothing to change the amount of mucus within the lungs, but there is a potential there for that mucus to become even more dangerous than it was- which is another reason to avoid lasix if possible.

I'm sure there are other reasons why lasix is dangerous for these patients. If anyone has more to add, I would like to hear.

[tniuqs]

Well first off a great senario here, and presented quite nicely, but I do have just a few queries, before I hang my hat on a Pulmonary related sepsis. Ok was their a positive Babinskis sigh? LOL @ Hammer.

Lets recognize hammers advice Beta 2s are right on the money! Chuck in a little atrovent too what the heck, could prove to broncodilate and therefore improve oxygenation from the get go.

Also looks like a compensated respiratory acidosis. ...Borderline metabolic acidosis there, though, as the HCO3 is at the very high end of normal (top range is 26).

Hmmm: I did not check the site you provided but from a modicum of experience I find this ABG interpretation a bit odd a compensated respiratory acidosis you say?

There is a way, without having to go to a website to interpret ABGs, its a simple, yes simple way of understanding a weak acid base balance, So first off throw away the Bicarb measurement it is a "CALCULATED" value not "MEASURED" when you understand the relationship of PaC0 2 and PH it becomes rather apparent that bicarb is a touch high, and just my .002 cents not of real importance. Bicarb is usually "Measured" in Venous samples but lets no go there for now.

[align=center:505afbd12f]Now just memorize this simple relationship.

PaCO2 vs. PH

50 = 7.30

40 = 7.40

30 = 7.50

OK.... In a perfect world.[/align:505afbd12f]

This is the ventilation portion ONLY, so you have a PaCO2 of 53 (measured) so round it off to 50 just fer fun K?

Your expected PH SHOULD be 7.30....you follow so far? but it AINT its even lower so perhaps indicating a tiny bit of a metabolic of compensation but not the point of my ramblings.

So your measured PH is 7.295 so what is happening here ? This old gal is not moving enough AIR er CO2 absolutely right! so make it simple. Your ETC02 readings are telling you something here too. Her major component in ABG evaluation that concerns me is a Respiratory Acidosis (as defined by Shapiro..in passing the ultimate authority on ABG interpretation) AND is defined as VENTILATORY FAILURE, sorry for yelling....l :shock: .

Now in a hospital controlled environment or MICU these gasses would be quite seriously factual data that this Gal is circling the drain, she's crapped out dude and at her age VERY unlikely to compensate for very long, time to think about chewing on plastic !

Now on to another option "deep tracheal suctioning" this could tell you what was going on as well, Sputum tells you a LOT....pink foamy, vs. green/ yellow thick. Are you looking for a DX or treat the patient ? This Is what I am pointing at here, If you have enough experience/ confidence to shoot an NPT, and lots of Xylocaine (spray then viscous) deep tracheal suctioning this is done very frequently for DNRs in hospitals, oh yea did I mention am a mean SOB in the short run, long run I get kisses ! Personally I try to be less invasive as possible, as committing someone to an ICU stay I take VERY seriously, I love my NIPPV K now I am showing off ...bad bad squint!

Don't know if you RSI in your area? but if I had these gases at bedside and quite frequently I have an I-stat available flying this is just a teaching note persay: That is not really relevant in this scenario, the bedside sputum clinically findings after "shooting a tube" could support your choice to take immediate actions.

If this Gal had a huge pneumonia sure sounds like it from your presentation then clearing these thick GREEN goobers therfore her ventilation and oxygenation COULD improve, maybe consider some fluid in this case, perhaps staying off the dreaded tube, if you found Pink Foamy Stuff then time to consider BIPAP or CRAP and Lasix.

ps a side bar: The nursing / home care provider and history of a 30 minute onset is most likely crappola, perhaps just the last time she visited by her then multiply the number of other patients (dude be gentle on them, please accept that they are less educated and in most cases just doing there best too! tolerance of others is professionalism in part of those not putting down the other's) minus 1 on the dustdevil scale :twisted:

I suspect if patient is not a DNR than that is MOST likely "ETT" what they have done in the ER, please do a follow up for us .. ok.

Just saying here that we work in very different environments (and scopes of practice) and when transport time a truly excessive then one sometimes has to be far more aggressive, initially but don't get me wrong. I think transport L & S is way to go in an urban setting I am NOT suggesting you did anything wrong, just providing options is all.

Her initial SaO2, of 82% is life threating, it correlates to a MEASURED PaO2 of just for mental exercise on the Oxygen dissociation curve to about 50 or less and that alone could tell you she is in deep KA KA. this is most likely indicative of Shapiro's "RESPIRATORY FAILURE" sorry for yelling again, my bad? (ps thats oxygenation) and if it is correlating with pulse rate. BUT you treated that the field nicely and correcting this respiratory failure, after the fact ask yourself does she actually need to have a PaO2 of 200 + hmm another thread perhaps, could that be harmful ?

There is ONE question I have, now all things being equal how did you get a measurement of ETCO2 value of 59 is when measured ABG value is PaO2 is 53, it does not compute it does not take into account deadspace ventilation.

Granted patients do change but this too could be rationale to shoot that ETT too?

Yes I know her GCS was 15, do you have Versed and Fentanyl the "poor mans" RSI ?

THE BOTTOM LINE IS THIS GALL IS 95 y/o but without a clear written DNR one cannot look at age as a a means to limit treatment, thing is People actually do MOVE ON we are not IMMORTAL can't wrong you for ANY of your RX...really.

I had a very simmilar case study, although I do wear a few differnt HATS anyhow, Lady got TUBED by me in the ER and shaking my head at that time that we were NOT doing the right thing.....was I wrong .... yup, just 2 days after committed to a VENT, I got to extubate her as well, and (my friend) knowing that we had bought her the time to say goodby to her family was a big deal for me (she died 2 days after that) and seriously I did get a kiss from her.

IT was sweet!...K no tongue though :shock:

Like I never end my posts without making you laugh :twisted: :twisted: :twisted:

cheers

squint

[VentMedic]

The ABGs can be used to treat an immediate need as in oxygen or possibly clearing secretions by NT suctioning for more effective ventilations and watching quality of respirations. As tniuqs explained, much of the ABG is calculated. Getting serum (BMP) values to get also the anion gap, along with BNP, lactate level and of course, blood cultures will be the path to determine further action is taken. The ABG will not tell anything about tissure oxgenation as in the case of sepsis. They will just give some idea of V/Q mismatching. A CXR is also limited in adequately diagnosing all pulmonary and cardiac issues. A CT scan is actually more beneficial in diagnosing some PNAs. If the patient is still an alert 95 y/o and consents to informed therapies and diagnostic tests, then more definitive testing might be done if the lab work is inconclusive.

As for as lung sounds in PNA and CHF, I find listening to the heart sounds to be beneficial.

Checking urine output or the foley bag contents can also give a good direction to look for sepsis or renal failure. And yes, there will be pulmonary involvement if there is renal failure either acute or chronic.

Is the Lasix listed on the PRN/one time medication sheet or scheduled? I see it beside Lorazepam and ambien as well as the Lopressor. If the lasix is scheduled, the I&Os may have been monitored along with periodic weights. Is the lasix for cardiac or urinary output problems? Lopressor - renal insufficiency or CV or both for HTN?

There are so many different PNAs and etiologies of CHF that it is possible to have mixed. CHF by itself is not an end all diagnosis but rather a symptom of something else. However, which one to treat while not exacerbating the other is the tricky part.

Use of a beta-2 agonist would be questionable and probably of little use here. Administering a nebulizer via BVM, as mentioned earlier, may be difficult on an alert patient. You would take away their ability to breathe at their desired MV where the BVM 10 to 20 lpm flow may not be sufficient for their drive. You would also need perfect timing to trigger the valve in synch with the patient. Expecting a patient to trigger the BVM valve by himself requires an uncomfortably tight face mask seal and -20 cm H2O of pressure to open the valve. This will definitely increase the WOB especially with a nebulizer in line and tire the patient to failure quicker. If the patient is unresponsive, by all means, it is an excellent way to provide a nebulizer as long as you are assisting ventilations.

Atrovent, (anticholinergic, parasympatholytic) is not my favorite drug in the elderly especially if renal insufficiency is an issue which many times is in the older population.

[fiznat]

Wow...

Okay, I am on a computer at school right now so I can't get too in-depth, but to answer a few things:

The only reason I posted an ABG is because it was the only "lab work" done by the time I left the hospital. I felt it added an interesting component to the presentation as well. As far as values being calculated, I dont know much about ABGs but only one of the values there (SO2) is marked as "calculated." The others, by contrast I assumed are NOT calculated. Also keep in mind that the ABGs were done at the hospital, while the ETCO2 numbers I reported were on-scene and during transport on the LP12. The patient did evolve slightly between these two periods with my NRB O2, NTG, and proper positioning.

I will get followup tomorrow, including all of the lab works you guys could possibly desire.

The discussion about the utility of a neb treatment for this patient is an interesting one. People seem to be going both ways on it. I was worried about B1 effects with this tachycardic, ischemic, possibly failure patient.... although at the same time she may have benefited from a bit of bronchiodialation. Keep in mind though that a NRB alone brought the SPO2 up to almost 100% as it was.

The patient was in fact a DNR, and at the same time probably not a canidate for a tube. GCS 14-15, and we are neither allowed RSI nor sedated intubation.

Would you guys really have performed deep tracheal suctioning on this alert patient? I've never seen anyone do that, and also I doubt she would have tolerated it. There was nothing upper airway that I would have been able to reach-- I didnt even think about doing this.

I'll return with ED updates as soon as I can get them.

[VentMedic]

Would you guys really have performed deep tracheal suctioning on this alert patient? I've never seen anyone do that, and also I doubt she would have tolerated it. There was nothing upper airway that I would have been able to reach-- I didnt even think about doing this.

NT suctioning is often the first line of treatment in the hospital to "clean up the breath sounds" to hear what we're dealing with. Sometimes it just takes a tickle to get a good cough response and the patient does the rest. This is also how many sputum specimens are obtained for a nice "no spit" sample.

Of course, if the condition is obviously CHF and/or hemodynamically compromised, suctioning may be deferred while other airway stabilization may be considered.

NT suctioning is usually well tolerated, although, it is uncomfortable for about 15 seconds. Be sure you have been trained on good technique and care must also be taken not to damage to the soft tissues of the nose and throat. I usually do at least 2 NT suctions in the ER each morning for "CHF vs PNA" brought in by EMS crews. Usually, it's neither, just breakfast. Follow up will then be done for infections from the aspiration.

The 100% SpO2 on a non rebreather is deceiving. The PaO2 could be 90 or 400 mmHg. For this the ABG is useful in telling us that the A-a gradient is reasonable for a 95 y/o. Not great, but will suffice for the moment.

[fiznat]

Okay I met up with a friend in the ED today and got a print-out of the patient's chart. 23 pages, so I will try to summarize:

Tx in the ED

IV Rocephin

IV Zithromax

40 mg Lasix IVP

1 x Combivent Neb

650mg Tylenol PO

Labs

There is a lab bonanza. I will mark only the abnormal findings. All else normal:

WBC - 15.8 (high)

RBC - 4.03 (low)

MCH - 33.0 (high)

PLT - 133 (low)

LYMPH - 17.2 (low)

NEUTRO - 75.8 (high)

POTASSIUM - 5.6 (high)

BUN - 41 (high)

Creatinine - 1.4 (high)

BNP - 1830 (high)

Two blood culture studies were done, and both were negative for growth.

Radiology

A portable chest x-ray was done. Here is the report:

Findings: No previous films are available for comparison. Single frontal view of the chest was obtained. The study somewhat limited this patient is rotated. Increased density seen behind the left heart with blunting of left costophrenic angle which suggest pleural effusion and possible associated left lower lobe infiltrate. The remaining lung fields are clear. There is no pneumothorax. A calcified granuloma is seen in the right lower lobe. Findings suggest left pleural effusion and possible left lower lobe infiltrate.

Hospital Course

The patient was admitted to a floor and kept under observation for 2 days. The final discharge diagnosis was threefold:

1) Pneumonia

2) CHF + Cardiomyopathy

3) Dementia

Go figure. Both.

[spenac]

Sounds like the doctor didn't know what was real cause either. Just covered every possibility.

One of our medics went in recently. Doctors finally released with lots of meds. Asked them what was wrong they said not sure so we're covering all possibility's. Scary huh.

[CBEMT]

Fiz, as yo may have noticed nursing home patients have both ALL THE FREAKING TIME, which makes your plight one I have run into time and time again.

In the beginning of my ALS career, I mistook pneumonia for CHF and gave 40mg Lasix. The ER doctor, unfortunately for the patient, concurred with my diagnosis, and gave an additional 80. Days later I found out he'd been shipped to the ICU with a pneumonia diagnosis. I found out from the same ER doc, who looked as embarrassed as I felt.

The best advice I ever got on the subject was "If you think it's CHF, and they're hot, it's pneumonia." Honestly, the BP probably would've thrown me as it did you, I won't lie to you. Most of the time when I get these patients they are already septic, so the hypotension + skin temp is a dead giveaway for pneumonia.

There area always exceptions, but I've found the rule of thumb to be pretty accurate. Yeah, very often a patient is suffering from pneumonia AND an exacerbation of their CHF, as yours was. But I still don't consider that justification for throwing the CHF protocol at them- if they have both, I've found that CHF is almost never the main problem at that moment. It's not helping, certainly. But I feel treatment of secondary diagnosis in these cases is best left for the hospital.

Worst comes to worse, I play it conservative- O2/IV/Monitor/Transport. I only start pulling out drugs if I'm EXTREMELY confident that CHF is the issue. If I'm certain that pneumonia is the problem, I'll run a fluid bolus. Other than that I keep it simple.