Hyperventilation question

[HERBIE1]

Take home message:

You will have to go beyond your EMT book to adequately understand "hyperventilation".

Exactly true. When asking questions like this, you need to consider the target audience. Like many times, someone who may have a more in depth knowledge of a subject could read into a question and challenge many answers. Just as if you have someone with CO poisoning, if you simply look at their pulse oximetry values, they may say the patient is saturating at 100% when they are actually severely hypoxemic. In other words, like many things in medicine, very few things are black and white.

Point being, instructors need to vett their questions thoroughly to avoid potentially ambiguous answers.

[Matt B.]

Wow! Thanks for all of the great replies! Just wanted to let you all know I'm getting my test back on Thursday 4/16 so I will be sure to let you know if I got that question right. I did put A as the answer.

[ladybear]

My EMT instructor was going over questions for the upcoming test the other day and he gave us this one:

1) Which of the following statements about hyperventilation is false?

a. Hyperventilation is almost always due to psychogenic stress.

b. Hyperventilation frequently causes numbness and or tingling and spasms in the hands and fingers.

c. Hyperventilation may be a sign of head injury or diabetic problem or overdose.

d. Psychogenic hyperventilation rarely causes cyanosis.

He claimed that he thought the correct answer was C but after going over my notes it seems like the answer should be A. Could I get your opinion on this? Which answer do you think is right?

A would be the correct answer.

There are too many reasons for hyperventilation to state that it is "almost always" caused by psychogenic stress.

D is a true response because most patients who hyperventilate due to anxiety finally slow down their own breathing by going to sleep.

It's too much work for them to keep up that level of work. Poor babies.

For the OP, if your instructor says C is the correct answer.. they need to re-educate themselves. This CAN and does happen, even though usually hypo-ventilation is the norm, Hyperventilation CAN and does occur. Not all OD's are narcotics. There are other substances that can cause people to hyperventilate.

[wrmedic82]

When we hyperventilate, we breathe rapidly. We breathe so fast we can't get full tidal volume into our lungs. We breathe in a small out of o2 and retain more CO2, thus making us more acidiotic. Having more co2 and less o2 in your system being circulated, will lead to cyanosis, which is a lack of oxygen.

I hate to disagree with you there bud, but you actually blow off all your CO2 and have an over abundance of O2 when a person hyperventilates. That is why you will see when you place the person on SpO2 and ETCO2 monitors that the person's SpO2 will be 100% and their ETCO2 will be 19 or lower.Thus making the patient alkalotic, not acidotic. Its again important to evaluate the patient, because if they are hyperventilating secondary acidosis( Example DKA ), we do not want to coach the patient into slowing their respiration.

Worst comes to worst, the person passes out, and resumes normal breathing. Or they continue to breath fast to compensate.

Edited April 15, 2009 by wrmedic82

[VentMedic]

I hate to disagree with you there bud, but you actually blow off all your CO2 and have an over abundance of O2 when a person hyperventilates.

No. If a person has a Pulmonary Emboli, they will be tachcypneic with a measured low PaCO2 and not have an abundance of O2.

That is why you will see when you place the person on SpO2 and ETCO2 monitors that the person's SpO2 will be 100%

You also do not know their carrying capacity for O2 such as Hb, CO exposure and MetHb from some nitrates.

and their ETCO2 will be 19 or lower.Thus making the patient alkalotic, not acidotic.

No, not necesssarily. You do not kow the PaCO2/PetCO2 gradient.

There are several causes for a low ETCO2. Air entrainment by tachypnea will dilute the ETCO2 measurement.

Deadspace ventilation, low tidal volume ventilation, hypovolemia, hypothermia, lung parenchymal destruction and low cardiac output will give a low ETCO2. Of course you can always have the issue with poor equipment maintance and failure to calibrate.

This is often the mistake some who don't understand V/Q mismatching will make on CCT when they try to "normalize" the PaCO2 of a ventilator patient by just looking at the ETCO2. Thus, the rec'g hospital ends up with a very acidotic patient.

A DKA and some sepsis (or whatever metabolic acidosis) patients can get their PaCO2 into the single digits and still be very acidotic.

Its again important to evaluate the patient, because if they are hyperventilating secondary acidosis( Example DKA ), we do not want to coach the patient into slowing their respiration.

This I definitely agree with. I will do a thorough assessment for organic problems of the patient before I write them off as anxiety and it is doubtful if I will even assume it then until all lab data is in. We have had many young people with new onset diabetes and their body will not let them slow down. One should consider an organic cause quickly during the initial examine and move on with further assessment to find the organic cause.

Edited April 15, 2009 by VentMedic

[wrmedic82]

No. If a person has a Pulmonary Emboli, they will be tachcypneic with a measured low PaCO2 and not have an abundance of O2.

You also do not know their carrying capacity for O2 such as Hb, CO exposure and MetHb from some nitrates.

No, not necesssarily. You do not kow the PaCO2/PetCO2 gradient.

There are several causes for a low ETCO2. Air entrainment by tachypnea will dilute the ETCO2 measurement.

Deadspace ventilation, low tidal volume ventilation, hypovolemia, hypothermia, lung parenchymal destruction and low cardiac output will give a low ETCO2. Of course you can always have the issue with poor equipment maintance and failure to calibrate.

This is often the mistake some who don't understand V/Q mismatching will make on CCT when they try to "normalize" the PaCO2 of a ventilator patient by just looking at the ETCO2. Thus, the rec'g hospital ends up with a very acidotic patient.

A DKA and some sepsis (or whatever metabolic acidosis) patients can get their PaCO2 into the single digits and still be very acidotic.

This I definitely agree with. I will do a thorough assessment for organic problems of the patient before I write them off as anxiety and it is doubtful if I will even assume it then until all lab data is in. We have had many young people with new onset diabetes and their body will not let them slow down. One should consider an organic cause quickly during the initial examine and move on with further assessment to find the organic cause.

With a patient with a PE, wouldn't the SpO2 be low?? Case and point I'm going to make is I had a patient who was later confirmed to have 4 PE's have a SpO2 of 64 and ETCO2 56. As far as the other stuff there is nothing for us to determine PaO2, PaCO2, ect. So how does that effect our treatment. And yes a patient in DKA can have ETCO2 in the single digits due to tachypnea, but lets say the proverbial paramedic not thinking tries to get the patient to slow respirations. If he is successful in doing so then ETCO2 would significantly rise. Again I go back to patient assessment prior to treatment. If you have access to recent lab work...awesome. This is often not the case. So me personally I would see how the patient presents (i.e anxiety, DKA, sepsis) and go from there. That is where we definitely agree.

[VentMedic]

With a patient with a PE, wouldn't the SpO2 be low?? Case and point I'm going to make is I had a patient who was later confirmed to have 4 PE's have a SpO2 of 64 and ETCO2 56.

If you are going by SpO2 you can be fooled. Look at my comment concerning this in my previous post or review the factors that influence SpO2.

You might also review the oxyhemoglobin dissociation curve.

As far as the other stuff there is nothing for us to determine PaO2, PaCO2, ect. So how does that effect our treatment.

This is exactly why a true diagnosis of hyperventilation is not possible. Tachypnea can be caused by rising PaCO2 as in impending respiratory failure. Too many confuse all tachypnea as "hyperventilating".

And yes a patient in DKA can have ETCO2 in the single digits due to tachypnea, but lets say the proverbial paramedic not thinking tries to get the patient to slow respirations. If he is successful in doing so then ETCO2 would significantly rise. Again I go back to patient assessment prior to treatment. If you have access to recent lab work...awesome. This is often not the case. So me personally I would see how the patient presents (i.e anxiety, DKA, sepsis) and go from there. That is where we definitely agree.

I have no problem with the statement about not telling a patient to slow down. I stated:

DKA and some sepsis (or whatever metabolic acidosis) patients can get their PaCO2 into the single digits and still be very acidotic.

in response to your statement:

and their ETCO2 will be 19 or lower.Thus making the patient alkalotic, not acidotic.

Edited April 15, 2009 by VentMedic

[tniuqs]

Well once again quite clearly we see many in EMS that do not understand that Ventilation C02 and PH, vs Oxygenation these are clearly separate issues ... and just because bedside your pulse ox is reading 100% does not mean that one is not hypoxic ... ie histotoxic and anemic hypoxia just for starters.

A hint .... just listen to Vent, has a much better understanding (and explanation) than most, I agree with every word.

Paco Peco Paco to you ! LOL>

and their ETCO2 will be 19 or lower.Thus making the patient alkalotic, not acidotic.

In the vast majority of cases and agreed ... Vent but should we introduce a large (rare) metabolic alkalosis component just for fun ... nah, when the relationship of PaCo2 and PH without any complications is misunderstood (hoping just a typo) we have serious problems from the get go.

This entire question should be removed from your exam bank, IMHO it perpetuates "generalities" and "myth" (s) as 30 years ago asthma was considered a phycological problem ONLY.

Hyperventilation is defined by Shapiro as PaCO2 > 30 mmHg so one needs a ABG to diagnose, ETCO2 will not help, in fact without a solid background in pulmonary pathophysiology it could be misleading.

Tachypnea is NOT = to Hyperventilation, nor is increased MV ... I will not even bother to state the definition of cyanosis by Shapiro as this would cause a **** storm of contraversy as well.

Just as is the general misunderstanding of Hypoxic Drive in EMS, hit the books to Mr/Ms Instuctor would be my suggestion.

cheers

reason for <edit> can't say shit here.

Edited April 15, 2009 by tniuqs

[tniuqs]

With a patient with a PE, wouldn't the SpO2 be low??

Dependant on the size of the PE, Aa Gradient is a better way to dx ... again ABG use the applied step on the gas methodology for treatment, either clot busters or embolectomy (loosing favour) Angio suite notification an idea too.

Case and point I'm going to make is I had a patient who was later confirmed to have 4 PE's have a SpO2 of 64 and ETCO2 56.

Got CPAP or BiLevel Support (far better) on your Truck ?... PEEP/ EPAP em up ... but slowly treat these as in titrating a trop.

As far as the other stuff there is nothing for us to determine PaO2, PaCO2, ect. So how does that effect our treatment.

Patient history, current meds and the golden question ... When this happened last time what helped you ?

And yes a patient in DKA can have ETCO2 in the single digits due to tachypnea, but lets say the proverbial paramedic not thinking tries to get the patient to slow respirations.

First Hit that Paramedic with a stick about the head send him back to school .... Maybe do a BGL ? Then fluids (dependant on BP)and ask when they last had their last insulin, get a baseline, the definitive answer is treatment is in ER, unless you give insulin on sliding scale.

If he is successful in doing so then ETCO2 would significantly rise.

In a true DKA not a hope ... so good luck with that, the patients brain is dictating things on a lizard level, just saying, your wasting your breath.

Again I go back to patient assessment prior to treatment. If you have access to recent lab work...awesome. This is often not the case. So me personally I would see how the patient presents (i.e anxiety, DKA, sepsis) and go from there. That is where we definitely agree.

A Temp maybe a good idea too, as one could have both Sepsis and DKA ... treat the life threat first.

cheers

[VentMedic]

I hate to disagree with you there bud, but you actually blow off all your CO2 and have an over abundance of O2 when a person hyperventilates. That is why you will see when you place the person on SpO2 and ETCO2 monitors that the person's SpO2 will be 100% and their ETCO2 will be 19 or lower.Thus making the patient alkalotic, not acidotic. Its again important to evaluate the patient, because if they are hyperventilating secondary acidosis( Example DKA ), we do not want to coach the patient into slowing their respiration.

Let me give some examples of how pH can affect the PaO2 and SpO2. You can also work the numbers for yourself on an interactive oxyhemoglobin dissociation curve website.

http://www.health.adelaide.edu.au/paed-ana...gen/oxygen.html

I will also be using SaO2 and not SpO2 for the examples. Using SpO2 may still not be an adequate reflection of PaO2. Quoted textbook values for SaO2 and PaO2 are usually at a pH of 7.4.

SaO2 97%

PaO2 at a pH of:

7.4 is 92 mmHg

7.3 is 101 mmHg

7.5 is 84 mmHg

SaO2 91%

PaO2 at a pH of:

7.4 is 60 mmHg

7.3 is 64 mmHg

7.5 is 51 mmHg

A person with an acidosis may have a higher PaO2 for the same saturation but O2 delivery at the tissue level may be an issue.

A person can have an alkalotic pH such as what you might get with some that hyperventilate but will lower their PaO2.

A person can also increase their MV by breathing faster to raise their PaO2 but not enough to dramatically shift the curve. Deadspace ventilation can play a role in this.

Here is a good site to explain tachypnea and deadspace ventilation.

http://www.ccmtutorials.com/rs/mv/strategy/page16.htm

I am willing to bet Dustdevil and Tniugs remember when we used to add deadspace to the older ventilator circuits to change ABG values before the newer technology appeared.

Also as Tnuigs mentioned, the A-a gradient will also determine how sick a patient is. If the patient is on an FiO2 of 1.0 and has a PaO2 of 65, even with a decent SpO2 or SaO2, I would say that person has a problem.

Here's another link about acid/base and ABG interpretation.

http://www.rcsw.org/Download/2006_RCSW_con...%20Analysis.ppt