When to Neb.

Respiratory distress -> Respiratory arrest -> cardiac arrest...

Why risk it? If they refuse after the treatment and you get chewed out for it, that manager needs to be talked to, we are patient advocates.
 
Ya know, considering that albuterol takes a good 15-20 minutes to reach peak effectiveness, are you sure there weren't medics at your service who were giving the neb then sitting onscene waiting for the refusal?

There's a few cases where treat and release after albuterol may be appropriate (the healthy teen who forget their inhaler), but most asthma and COPD exacerbations that the patient can't control with their home medications need to be transported to evaluate the need for admission.
 
Last edited by a moderator:
anyone care to discuss the use of etco2 to identify bronchospasm in these "maybe respiratory/maybe cardiac" patients?
 
anyone care to discuss the use of etco2 to identify bronchospasm in these "maybe respiratory/maybe cardiac" patients?
"Shark tooth" waveform indicates bronchospasm, but again, it's not really that simple. One condition often precipitates the other. You could somewhat expect to see decreased ETCO2 initially with CHF due to the increased minute volume, however in my anecdotal experience this isn't a reliable enough indicator to be a serious distinguishing factor.

Being a good historian as well as knowing the concurrent signs and symptoms for each condition is important. Trying to make the patient fit a protocol rather than the other way around is a good way to do these patients a disservice.
 
Last edited by a moderator:
"

Being a good historian as well as knowing the concurrent signs and symptoms for each condition is important. Trying to make the patient fit a protocol rather than the other way around is a good way to do these patients a disservice.

^This.
 
There's a few cases where treat and release after albuterol may be appropriate (the healthy teen who forget their inhaler), but most asthma and COPD exacerbations that the patient can't control with their home medications need to be transported to evaluate the need for admission.

I absolutely agree. I work on a college campus (for a BLS service), and we do a about a neb a month on an otherwise healthy college-aged patient who has run out of their albuterol MDI. Our protocol requires we roll an ALS ambulance when we start the neb, but unfortunately, the medics would rather transport than get a refusal from many of these patients. For most, it's a straightforward asthma attack (determined by history, we even have some frequent fliers), with no other symptoms or conditions. The patients rarely get any treatment in the truck (or ED), symptoms have completely subsided by the time we transfer care, and the patients are often discharged from the ED within 45 minutes.

Unfortunately, for the private service that transports our patients, from a billing (and paperwork) perspective, it's easier just to do the transport then try to get a refusal (per company protocol, all need to be medical-control approved), and the paperwork is more complicated than that of a transport.

From my perspective, I can't justify giving what is otherwise ALS medication without calling for an ALS truck, and my medical director would prefer medics get the medical control refusal.

Side question: For a respiratory arrest that we know to be induced by broncospasm/asthma, is there a way to connect a SVN to a BVM, or otherwise provide positive pressure ventilation with albuterol? Are we better off just ventilating with oxygen?
 
Side question: For a respiratory arrest that we know to be induced by broncospasm/asthma, is there a way to connect a SVN to a BVM, or otherwise provide positive pressure ventilation with albuterol? Are we better off just ventilating with oxygen?

Yes. We have an adapter that lets us bag in a neb, or we can attach a neb to our CPAP.
 
You could somewhat expect to see decreased ETCO2 initially with CHF due to the increased minute volume

Or decreased EtCO2 as an indicator of poor cardiac output in CHF with say cardiogenic shock.
 
i had a good patient the other day like this...

70ish y/o female started having SOB about 3 hours prior with a brreif period of chest pain.

Hx= COPD, and CHF

Moderate Dyspnea, RA SPO2 82% increased with NRB by 1st responders. They thought they heard wheezing to bilat bases. wanted to start a neb (its a BLS skill here) as we were walking in. We put her on ETCO2, great bronchospastic waveform @ about 50. BUT she was hypertensive (not tachy, but was on Atenolol). MD had dc'd her Lasix about 3 weeks ago. We listened to her and heard good air movement and rales to bilateral bases.
ECG was okay with a... (if i remember correctly) only a 1st degree blcok.

Clinically she had CHF, but ETCO2 showed COPD exacerbation...

We treated with ASA, NTG paste, NTG sublingual q 5 minutes for pretty much the entire transport. We lowered her O2 to NC and remained 99ish% on 4 lpm. She remained hypertensive so we gave her Enalapril also. Her dyspnea improved and her BP came down slightly. I dont knwo for sure, but i would imagine that this lady was having both a COPD and CHF exacerbation...

ETCO2 is a tool and should HELP you make a decision, but it shouldnt make you treat patients a certain way... Its a tool. A peice to the puzzle.
 
Or decreased EtCO2 as an indicator of poor cardiac output in CHF with say cardiogenic shock.

Yes, sorta, but not in any way reliable enough to use as a sole diagnostic indicator for cardiogenic shock. Chalking that low ETCO2 up to cardiogenic shock in your patient who's circling the drain may be ignoring severe bronchospasm, increased minute volume due to sepsis, ect.

You've really got to know a little about what ETCO2 is measuring, hemodynamics, pulmonary physiology, pathophysioloy of shock states and how to corelate them clinically before you start using ETCO2 as a diagnostic tool. Not saying you don't, just want everyone to proceed with caution and realize there aren't any simple rules or pearls here.
 
You could somewhat expect to see decreased ETCO2 initially with CHF due to the increased minute volume

....or elevated ETCO2 because of decreased minute ventilation as a result of the pulmonary edema. Remember guys, just because they are tachypneic, does not mean they have an increased minute ventilation. More often than not, you're going to see an elevated CO2 level in these folks because of the "backup" of CO2 that isn't getting offloaded.
 
Last edited by a moderator:
Do any of the services in the U.S give nebulised adrenaline (epinepherine) to croup with stridor?
 
....or elevated ETCO2 because of decreased minute ventilation as a result of the pulmonary edema. Remember guys, just because they are tachypneic, does not mean they have an increased minute ventilation. More often than not, you're going to see an elevated CO2 level in these folks because of the "backup" of CO2 that isn't getting offloaded.
My anecdotal experince only. Most of the CHF'ers I take care of have decreased ETCO2. The ones that have turned the corner to hypercarbia are headed downhil and it's usually a fight to keep from tubing them.
 
EtCO2 is more reflective of perfusion state when ventilation is relatively normal. Several studies have shown this. EtCO2 is not a "tell all" but does tell a lot about perfusion and not just ventilation.

EtCO2 has also been shown to have predictive value with cardiac arrest and can be a direct indicator of CPR quality and ROSC.
 
Back
Top