Wheezing questions

[Grizzlyadamz]

Hey everyone, looking to absorb some experience while I'm working on my paperwork.

I had a middle-aged patient recently who came in complaining of SOB. RR & HR were elevated, spO2 was low and they had a loud expiratory wheeze (audible in all 5 lobes). Over about 8 hours the patient was on O2 at 2L NC & received at least one duoneb, (which brought their sat up from 90 to 95%).

ABGs came back halfway through their stay with mild hypercapnia/hypoxemia.

At the end of the 8 hours the patient wasn't showing signs of distress & their RR had come down, but it was still greater than 20 & SpO2 was holding steady in the low 90s.

Wheeze was still present x5.

Patient has an occasional productive cough w/ green sputum.

CXR found 'No acute pulmonary diseases'.

The patient stated the wheezing started either a week ago or a couple months ago, (preceptor got 'a week ago', but the patient told me it had been 'a few months').

So, does my patient have an excess of secretions in the lower respiratory tract? I figure the CXR would pickup any inflammation/edema, if that were a contributing factor. But would it spot excessive secretions in largish airways?

Can patients usually expectorate secretions all the way up from the bronchioles? Or is the patient's sputum related to something else? (patient is positive for influenza)

Here's my working primary ND:

Ineffective airway clearance r/t secretions in the bronchi a/e/b audible expiratory wheezes, tachypnea, elevated CO2 & hypoxemia, dyspnea, sputum production.

[Grizzlyadamz]

Also, if mucolytics & drainage aren't advisable (patient has HTN & is being watched for possible sepsis, so I'm guessing it might go uncontrolled), would a cough suppressant be a bad idea? The patient stated that they had difficulty sleeping due to the cough & chest pain associated with it, but there has been some sputum production & they're sat'ing rather low.

-e

Hmm, looked closer at the forum, seems this should go in the 'assistance' section.

[bgxyrnf, MSN, RN]

Green sputum is clinically indicative of pneumonia which is supported by them "being watched for possible sepsis." The initial tachypnea and tachycardia would meet the SIRS criteria. They'd almost certainly have a lactate drawn in addition to the other labs. Do you know what those values were?

To answer your question, "no, you would not see the airway secretions on the cxr." The patient's sputum production is likely from a developing pneumonia.

[Grizzlyadamz]

Lactate was normal but they suspected a false low due to 'NAPQI & NAC'. (something about acetaminophen poisoning?)

[bgxyrnf, MSN, RN]

This is what makes it so hard to troubleshoot case studies in a vacuum; there are far more questions than answers thus far.

Why were they concerned about acetaminophen toxicity? Typically, unless there was something in the HPI to point them in that direction, you wouldn't draw an APAP level.

The normal lactate only indicates that they've got adequate tissue perfusion and don't need fluid resuscitation. The hypercarbia/hypoxia indicate insufficient pulmonary gas exchange which is why they are tachypneic.

The patient evidently has pneumonia and needs to be admitted for supportive care and treatment with antivirals and antibiotics.

[Grizzlyadamz]

So does lactate only really rise with inadequate perfusion, or can an anaerobic septicemia cause it as well?

Also, do blood cultures always catch the bacteria causing the SIRS, (assuming it's not viral), or can they (the bacteria) remain relatively localized?

...Are these questions I should direct to my instructors?

case studies in a vacuum

Yeah I understand, kind of (I haven't gone around on the forums trying to help others yet so I can't really say I do), so thank you for hanging around and answering questions despite the issues- it's really appreciated!

[bgxyrnf, MSN, RN]

There are other things that can cause the lactic acid level to rise (for example, the acetaminophen poisoning) but in the context of SIRS and sepsis, it means inadequate perfusion.

If the bacteria are isolated then they're not systemic, right? Hence, no Systemic Inflammatory Response Syndrome and no bacteremia.