Quick asthma question

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newEMT

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If you have an asthmatic with a severe exacerbation and their pulse ox is 100%. Why might that be?
 
Poor reading.

Anemia

They're maintaining their minute volume, even if using a lot of energy to do so.
 
Asthma is primarily a problem with ventilation, not oxygenation. It's not until late in the acute illness that hypoxia becomes a problem. By that point, the patient is well behind the 8 ball.
 
Because failure to oxygenate is one of the end stages of asthma exacerbation. Think about the mechanism of asthma and tell us why that is.
 
CO molecules bind just like O2 molecules. When treating CO poisoning your likely to see 100% on a pulse ox, but clearly the patient needs oxygen. This falls under the "treat the patient not the monitor" category. It's likely an asthmatic would hyperventilate during an attack, therefore not properly blowing of CO, hence the high reading.

This is merely my take on it. Some of the better experienced and more knowledgeable members will probably have a better explanation

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^
I believe you're confusing CO with CO2.
 
I think someone once told me that when an asthmatic is starting to crash, the wheezes stop (because they cannot generate enough force to get air out of their lungs) and their O2 sat may still be 100% (for some reason, which I forgot??)
 
Asthmatics have a problem with that exhale CO2. The pulse oximeter measures the proportion of CO2-laden red blood cells and takes it up against the number of 02-loaded cells. Hence it comes to the seizure onset is almost always to values ​​of 100%.
 
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newEMT said:
I think someone once told me that when an asthmatic is starting to crash, the wheezes stop (because they cannot generate enough force to get air out of their lungs) and their O2 sat may still be 100% (for some reason, which I forgot??)
Click to expand...

The wheezes stop because they are no longer moving air. This is a bad sign and you are WAY behind the curve. I doubt their sats will still be 100% at this point; if they are, it will be very short-lived.
 
I doubt their sats will still be 100% at this point; if they are, it will be very short-lived.
Click to expand...

In fifteen years as a medical provider (ten of those as a respiratory therapist) I've never seen an asthmatic "too tight to wheeze" who is still maintaining a sat above the low 90s.
 
I've never seen one shutting down who has scored about 93 either.

But all those I saw were either involved with heavy exercise and it came on, or they were hovering around the drain and it came on again, or they were smoking bad stuff and nearly ALL had a history of smoking bad stuff (Drano or Crack, your choice). None of them had garden variety asthma.
Wheeze can become difficult to hear or stop when the air stops moving either due to exhausted respiratory effort, or impending death. If the air stops moving, at that point there maybe be good absorption of O2 (air is under increased pressure due to asthmatic trapping) occurring but not for even a little long (versus "very long"). If someone slapped a dry cleaning bag with a reversed Heimlich valve across your mouth and nose, you would be able to suck in more air for one or less breaths, but not exhaust used air; O2 would still cross for a bit, but CO2 would be trapped, revving up respiratory drive and lowering pH. Asthma's a horrible way to die, and I've seen it three times.
 
newEMT said:
If you have an asthmatic with a severe exacerbation and their pulse ox is 100%. Why might that be?
Click to expand...

Even if you have a documented diagnosed hypoxic drive, oxygenation will never ever ever be the same as ventilation. SpO2 will only tell an approximation of how much oxygen a pt's blood has, not how well your pt might be ventilating.
 
Just to be difficult

If the point of respiration /ventilation is to boost the oxygen content of the RBC's and offgas CO2 and some other random stuff, why do I keep hearing this disconnect between effective ventilation and oxygenation? Not arguing it, I have sort of supported it her and in an earlier thread, but spell it out for those of us who didn't take the modern pathophysiology (i.e., evil spirits don't after all cause stuff to happen).
 
Well you just said it right there. Get O2 to the RBC's and you off gas CO2. It is literally that seperate.

When one inhales what happens? O2 is brought into the lungs, crosses the capillary membrane and connects Taking hemoglobin. What happens to the CO2? It's still being made inside the body. Does increasing FiO2 improve the CO2 being made inside the body? No.

Then what does? Improving the body's ability get said CO2 out of the body. By improving the body's ability to blow it of (ventilate).
 
Every time my Asthma gets bad; my sats always drop into the 80's. of course my normal is about 93%. The last major attack which put me in the hospital I got down to 68%; which the ED doc wasn't happy with. but came back up to 84% with more O2; so they didn't tube me, which I was happy with.

Took them 4 days to get me back up above 90% and stay there. (Asthma and pneumonia is a bad combo).
 
mycrofft said:
If the point of respiration /ventilation is to boost the oxygen content of the RBC's and offgas CO2 and some other random stuff, why do I keep hearing this disconnect between effective ventilation and oxygenation? Not arguing it, I have sort of supported it her and in an earlier thread, but spell it out for those of us who didn't take the modern pathophysiology (i.e., evil spirits don't after all cause stuff to happen).
Click to expand...

In hospitals that are considering organ donation, one of the tests for brain death is the apnea test where the tip of a suction catheter attached to 4 Lpm oxygen is placed at the carina. The patient is disconnected from the vent and serial ABG's are performed to watch for an increase in PCO2. After 5 minutes, if the PCO2 has risen to a determined level, the patient is considered apneic, supporting the determination of brain death (of course this is absence of any viewed sponatneous breaths on the patient's part).

During this procedure, the SpO2 cannot fall or the test is void. Essentially, the body absorbs the oxygen readily. I have always found this to be an excellent demonstration of how oxygenation and ventilation are separated. Yes, oxygen and CO2 transport is related, however our role is to treat a dysfunction in either if these two areas, which can have conflicting approaches. One example is using any one of the disposable CPAP devices which deliver 30% oxygen. The goal is to recruit alveoli using oxygen diluted with room air to create CPAP. Despite the lower FiO2, the alveoli are recruited, allowing CO2 to be exhaled while reducing the need for supplemental oxygen.

I hope that this addresses the question.
 
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