# Normal Range Oxygen Saturation readings in CHF Patients



## TYMEDIC (Feb 18, 2012)

Looking for a little insight here. I had a patient suffering from a prolonged pneumonia accompanied with CHF/pulmonary hypertension. Audible congestion noted, auscultated sounds of scattered rhonchi, rales, slight expiratory wheeze. Vitals assessed, initial spo2 reading of 89. high flow nrb=98%. ETc02-poor wave form, slight rep. alkalosis. rapid, shallow, respirations at 34. 12-lead revealed bifisicular block, LVH. 
18g IV established.
Now I wanted to splint the airways open with CPAP. Got into an argument with my Partner. He wanted to keep the NRB on and TX. There was clear signs of distress there, but he opted to treat as such due to normal saturation levles. There is a differance between hypoxia and hypoxemia. 
Has anyone ever seen such a patient? Was NRB better than CPAP? False readings in CHF Patient's?


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## usalsfyre (Feb 18, 2012)

The NRB will not particularly help the work of breathing. Have your partner look up shunt physiology and the types (and causes of respiratory failure).

There is a difference between hypoxia and hypoxemia, but unless you suspect a cytotoxic cause for the hypoxia it's a somewhat moot point to most medics.


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## TheGodfather (Feb 18, 2012)

TYMEDIC said:


> Looking for a little insight here. I had a patient suffering from a prolonged pneumonia accompanied with CHF/pulmonary hypertension. Audible congestion noted, auscultated sounds of scattered rhonchi, rales, slight expiratory wheeze. Vitals assessed, initial spo2 reading of 89. high flow nrb=98%. ETc02-poor wave form, slight rep. alkalosis. rapid, shallow, respirations at 34. 12-lead revealed bifisicular block, LVH.
> 18g IV established.
> Now I wanted to splint the airways open with CPAP. Got into an argument with my Partner. He wanted to keep the NRB on and TX. There was clear signs of distress there, but he opted to treat as such due to normal saturation levles. *There is a differance between hypoxia and hypoxemia. *
> Has anyone ever seen such a patient? Was NRB better than CPAP? False readings in CHF Patient's?



im confused with a few things:

1) this chronic pneumonia, CHF, pulmonary HTN... was that diagnosed, or was that predicted? 
2) *see bold text* what would you define the difference as? (i agree there is a difference, but i'm unsure what you're definition of the 2 would be)
3) if your spo2 pulse waveform was matching the patient's pulse + there was no evidence of shunting/hypothermia, the spo2 would be accurate.

the compensatory respiratory alkalosis may be perfusing adequately, but the patient could still be in distress. ask them if they are having trouble breathing; is this normal for them? if not, sure CPAP/BiPAP would be fine.

lots of variables though, we really don't have a big picture of the entire call, so it would be difficult to give a solid answer. if the patient remained stable during the transport, i'd say mission success and no reason to get bent out of shape about it. live and learn.


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## TYMEDIC (Feb 18, 2012)

I understand it. He wont. In other terms, is it basically hypoxaemia happening; shunting is occurring and blood leaving normal alveoli is already 100% saturated. Is that where the "false" satuaration readings coming from?


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## TheGodfather (Feb 18, 2012)

[source: ASTNA Patient Transport: Principles & Practice]


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## TYMEDIC (Feb 18, 2012)

with the patient's HX, the diagonsis I had for the patient, was a pneumonia that was being treated with anti-biotics and really an eserbation of CHF. assessed lung sounds provide evidence of the two diseases. No, this perticular "episode" for the patient was not normal. The patient was in repiratory distress and I believe the lungs shouldve been splinted via CPAP. What still is bugging me, is the damn saturation reading, per the patient's status and complaints, it should have been lower, and angers me even more with my partner treating the machine and not the patient.


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## TheGodfather (Feb 18, 2012)

and you would be getting correct low saturation readings with severe pulmonary shunting/atelactasis/fluid collection


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## TYMEDIC (Feb 18, 2012)

isnt shunting more geared towards COPD, Ashma, particularly bronchitis?


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## TheGodfather (Feb 18, 2012)

http://en.wikipedia.org/wiki/Pulmonary_shunt


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## TYMEDIC (Feb 18, 2012)

agreed....but still doesnt tell me why that pulse ox was reading 98 percent in a patient with severe respiratory issues. With the shunting, your gonna have that O2 trapped in the dead spaces and increased CO2 levels and low O2 levels,  hense low readings on the pulse ox. More or less, an activated hypoxic-drive. Why is the pulse ox 98 percent?


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## 8jimi8 (Feb 18, 2012)

A better question: why wouldn't you expect shunt in pneumonia?


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## TYMEDIC (Feb 18, 2012)

I mis spoke. I agree 100percent. 
pneumonia 
pulmonary oedema 
atelectasis 
pulmonary haemorrhage 
pulmonary contusion 
I understand it the logic, but with the S/S of that perticular patient and what i diagnosed, The treatment would favor CPAP that I wanted to do. With the shunting, you ultimatly would have low saturation level readings wouldnt you? Just doesnt make much sense to me that the gas exchange would be adequate enough to display a 98%.


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## JPINFV (Feb 18, 2012)

Why would you expect a patient in respiratory distress to automatically be hypoxic? If the problem is diffusion, then increasing the minute volume (respiratory rate X tidal volume) can compensate for the decreased diffusion by maintaining a higher PAO2. This increased tidal volume is also what is going to cause the respiratory alkalosis. As such, this is why an oxygen saturation has to be incorporated into the rest of the assessment (including work of breathing) instead of just using it alone to make treatment decisions. 

Something else to remember is that perfusion in the lungs is controlled completely opposite to perfusion in the tissue. In the tissue, areas of low oxygen partial pressure gets preferentially perfused. In the lungs, alveolar with high oxygen partial pressure gets preferentially perfused. So the areas with better ventilation and diffusion are going to get more blood, thus bypassing the areas with low ventilation and diffusion.


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## TYMEDIC (Feb 18, 2012)

well put


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## usalsfyre (Feb 18, 2012)

Another factor your not taking into account is the alveolar to arterial oxygen ratio. Even a 98% SpO2 on a patient on 15L via NRB become suspect. This patient should be at 100% and have a PaO2 (if you could measure it) north of 300 (assuming I'm remembering the figures correctly). If it takes 15L of O2 and tachypnea to maintain otherwise "normal" numbers there's a serious derangement somewhere. 

A NRB does nothing to ease this patient's work of breathing. CPAP does. That alone should be enough to sway the decision. Not treating the work of breathing will lead to respiratory fatigue, failure and intubation. 

I won't say CPAP is benign, but it's a lot safer than the alternative.


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## TYMEDIC (Feb 18, 2012)

Thats what I was thinking. Thanks for the input.


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## systemet (Feb 19, 2012)

TYMEDIC said:


> agreed....but still doesnt tell me why that pulse ox was reading 98 percent in a patient with severe respiratory issues.With the shunting, your gonna have that O2 trapped in the dead spaces and increased CO2 levels and low O2 levels,  hense low readings on the pulse ox. More or less, an activated hypoxic-drive. Why is the pulse ox 98 percent?



Because you've just increased the alveolar PAO2 by using a high Fi02.  Even though there's a limited area of lung surface that's being ventilated, and not all of this may be perfused due to interstitial edema, and there may be a diffusion problem as well -- the amount and concentration of oxygen inspired has been dramatically increased.

At this point, the patient may be able to maintain a normal arterial pO2.  They may even be saturated above normal.  But as someone said, hypoxemia =/= hypoxia.  You can still have regions of tissue that aren't being adequately perfused, and therefore aren't getting adequate oxygen delivery (aka "stagnant hypoxia").

The issue here is how long the patient can compensate, and whether critical cardiac ischemia (or ischemia to other organs) is occurring.  Right now they may be able to work hard enough to ventilate themselves, and maintain a normal pO2 -- but for how long?  Once they tire, things may deteriorate rapidly.  This is also true of many asthmatics --- some really sick patients maintain SpO2's in the high 90's before they suddenly crap out and may need aggressive therapy during this time.

If you've got high cardiac filling pressures (aka high wall tension), fast heart, and an overloaded LV, cardiac oxygen demand (mVO2) is going to be high.  Oxygen supply may not meet this demand --> ischemia, worsening cardiac output, worsening pulmonary perfusion, more failure, more demand, less supply, etc.  This can result in infarction despite a normal pO2.  

So you're assumption here that because they are dyspneic, and have laboured respirations, accessory muscle use, etc., that the SpO2 must be low, is incorrect.

Another issue is what's happening to their CO2 during this period.  They may be maintaining a normal pO2, but becoming hypercarbic.  Combined with a degree of stagnant hypoxia and lactic acidosis, they may be acidotic.  These are also issues that the SpO2 probe won't detect.  Capnography may be less helpful than normal here as the A-a gradient increases.


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## TYMEDIC (Feb 19, 2012)

Well put Chief, understood. Now to go more in depth with the outcome here. Due to heavy scrutany by me and my capt with his poor ALS intervention treatment with this patient. Now he got in touch with the acccepting rn in the er for this patient and per my partner, she stated that he was admitted in the ICU for a metabolic issue, Hyperkelemia. Now what I saw with this patient, assessments, presentation, and understandings. That just doesnt make sense to me. With the increased, rapid, shallow, slightly irregular respirations would prodominently cause respiratory alkalosis, not acidosis-that really needs to occur to cause a severe enough hyperkelemia. I dont doubt that the patient had some metabolic issues secondary to the impending respiratory failure; prolonged pheumonia and CHF. But what I got on my assessment with 12-lead, ETCO2, D-stick, and just pure patient presentation alone, I would lean towards a respiratory alkalosis, poss. HYPOKELEMIA. Im dont doubting that there is a sig. diffusion issue going on. But, im calling BS on that. If you have a PRIMARY metabolic issue such as hyperkelemia that is severe enough to over take the resp. failure issue, I would lead to believe that the patient would be pretty close to a polymorphic v-tach with some a influx in the interface and electrolyte levels; especially with the increased minute volume and collected increased oxygen demand. Yes, hes old, yes hes severly sick, but that clinical dianoses is crap. And not to treat the underlined issue (respiratory) first with ALS intervention and I dont mean quick intubation, more or less a positive pressure splint of the airways, is foolish. Now, how could a patient be severly hyperkelemia in presence of respiratory alkalosis. Furthermore, it didnt look like there was a sig. build of of bi-carb and the body was compensating with the increased respiratory drive to aid in blow-off, such as kuasmalls. It presented in clear cut, good ole, pulmonary edema-impending resp. failure.


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## JPINFV (Feb 19, 2012)

Without an arterial blood gas, acid-base status is really just a shot in the dark as multiple acid-base conditions can occur at the same time. Just because the patient had a respiratory alkalosis going on doesn't mean it there couldn't be a metabolic acidosis (anion-gap, non-anion gap, or both) going on at the same time. This also ignores the fact that there could be another disease or medication causing hyperkalemia.


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## systemet (Feb 20, 2012)

TYMEDIC said:


> Now he got in touch with the acccepting rn in the er for this patient and per my partner, she stated that he was admitted in the ICU for a metabolic issue, Hyperkelemia.



I went to the medical examiner's office as a paramedic student once, and he made what seemed at the time to be a very controversial statement, "Nobody dies from aspiration".  As a group of students we fundamentally failed to grasp his meaning, and got in a long and pointless argument that inevitably ended when the pathologist-medical examiner lost their interest.  Both sides left thinking that they had won, but only one was right.

Hyperkalemia may be the admitting diagnosis, but hyperkalemia doesn't just appear by itself.  It's caused by something else.

JPINFV has pointed out a number of potential causes.  One I'd consider here is that the patient has developed renal insufficiency / acute renal failure, resulting in fluid retention, volume overload, and an inability to excrete potassium.  This could cause a CHF exacerbation and some degree of shock and lactic acidosis.



> Now what I saw with this patient, assessments, presentation, and understandings. That just doesnt make sense to me. With the increased, rapid, shallow, slightly irregular respirations would prodominently cause respiratory alkalosis, not acidosis-that really needs to occur to cause a severe enough hyperkelemia.



They're only going to get hypocapnic if they have enough perfused lung surface, and enough ventilation to that perfused region to have a net increased excretion of CO2 over time.  

They can be as dyspneic and tachypneic as they want, but if there's minimal gas exchange occurring they're not going to blow off CO2.

If the CO2 is low, i.e. there is some degree of respiratory alkalosis, this may be compensating (partially or completely) for an underlying metabolic acidosis.  It doesn't have to be the primary disturbance.

You don't need to have respiratory acidosis to have hyperkalemia.  A metabolic acidosis will also cause a K+ shift.  



> I dont doubt that the patient had some metabolic issues secondary to the impending respiratory failure; prolonged pheumonia and CHF. But what I got on my assessment with 12-lead, ETCO2, D-stick, and just pure patient presentation alone, I would lean towards a respiratory alkalosis, poss. HYPOKELEMIA.



We really don't have the tools to assess this on the ambulance.  There are 12-lead changes that point to hyperkalemia, e.g. 






But even ED physicians are batting at around a 40% sensitivity for detecting hyperkalemia (>5.0 mmmol/L) on ECG changes, and only 60% or so at detecting critical hyperkalemia (>6.5 mmol/L).  (Wrenn et al.)  [Granted this study is just two docs looking at ECGs, but it gives us an idea of rough figures].  So the ECG's useful, but it isn't always going to tell us the story.

In this study, specificity was around 85%, so there were quite a few patients who weren't hyperkalemic who were labelled as such by the physicians.

Wrenn KD, Slovis CM, Slovis BS.  The ability of physicians to predict hyperkalemia from the ECG. Annals of Emergency Medicine 20(11):1229–1232




> Im dont doubting that there is a sig. diffusion issue going on. But, im calling BS on that.



BS on what?  That your partner's lying / misinformed, that the RN is lying/misinformed, or that the physician or laboratory are lying / misinformed and have incorrectly measured the sample's K+?



> If you have a PRIMARY metabolic issue such as hyperkelemia that is severe enough to over take the resp. failure issue, I would lead to believe that the patient would be pretty close to a polymorphic v-tach with some a influx in the interface and electrolyte levels; especially with the increased minute volume and collected increased oxygen demand.



See the ECG changes above, and take a look at some case reports.  People can survive with high K+ for quite a while.  How do you know that the patient is close to a polymorphic VT before it happens, especially in the field?  This patient may have been.  The classic electrolyte disturbance associated with this is hypomagnesemia.  




> Yes, hes old, yes hes severly sick, but that clinical dianoses is crap. And not to treat the underlined issue (respiratory) first with ALS intervention and I dont mean quick intubation, more or less a positive pressure splint of the airways, is foolish.



It's hard to know from a distance based on an internet vignette, but it sounds like CPAP would have been a good idea here.




> Now, how could a patient be severly hyperkelemia in presence of respiratory alkalosis.



Because they're acidotic?  Because the kidney's are nuked and they're retaining K+ at a greater rate than alkalosis is shifting the K+ intracellualrly?  Because they've taken too much K-dur?  Ischemic gut? Too much spirinolactone?  Not so-benign-anymore prostatic hypertrophy? Renal failure?  Overusing their beta-agonist due to the pneumonia / being stupid?



> Furthermore, it didnt look like there was a sig. build of of bi-carb and the body was compensating with the increased respiratory drive to aid in blow-off, such as kuasmalls.



Don't take this the wrong way, but think about this a little bit.  



> It presented in clear cut, good ole, pulmonary edema-impending resp. failure.



But pulmonary edema also isn't a disease in and of itself.  It's a sign of a disease.  It can be due to volume overload, it can be due to a loss of plasma protein, failure of the LV, mitral valve issues, diffuse injury to the alveolocapillary membrane, lymphatic obstruction, emboli in the pulmonary vasculature, hypertension, inhalation injury, etc.

Like many of our patients, this one had a complex condition / history that was better revealed upon further evaluation by more skilled practitioners in the hospital with the aid of better diagnostic equipment.  This is ok -- not every piece of information is available to us in the field, and not all of these problems need fixing right away, or can be fixed in the ambulance.

I do agree that the CPAP sounded like a good idea.


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## TYMEDIC (Feb 20, 2012)

Thanks Systemnt, Well put. Ultimatly what I took out of that is that every problem does'nt need and or can be fixed in the field. I guess im kind of high strung in that regard. Thanks for the input all.


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## systemet (Feb 20, 2012)

TYMEDIC said:


> Thanks Systemnt, Well put. Ultimatly what I took out of that is that every problem does'nt need and or can be fixed in the field. I guess im kind of high strung in that regard. Thanks for the input all.



Cool.  Glad it was useful.  Hope I didn't come across as being too aggressive.  I wasn't try to be.


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## MSDeltaFlt (Feb 20, 2012)

TYMEDIC said:


> Looking for a little insight here. I had a patient suffering from a prolonged pneumonia accompanied with CHF/pulmonary hypertension. Audible congestion noted, auscultated sounds of scattered rhonchi, rales, slight expiratory wheeze. Vitals assessed, initial spo2 reading of 89. high flow nrb=98%. ETc02-poor wave form, slight rep. alkalosis. rapid, shallow, respirations at 34. 12-lead revealed bifisicular block, LVH.
> 18g IV established.
> Now I wanted to splint the airways open with CPAP. Got into an argument with my Partner. He wanted to keep the NRB on and TX. There was clear signs of distress there, but he opted to treat as such due to normal saturation levles. There is a differance between hypoxia and hypoxemia.
> Has anyone ever seen such a patient? Was NRB better than CPAP? False readings in CHF Patient's?



I've been reading this thread for a while and it seems that there is something that has been needing mentioning but has either been forgotten, overlooked, or never learned/realized in the first place.

Oxygenation and ventilation are two completely different things.  You can be in respiratory failure and still have a SpO2 of 99%.  That would be because your PACO2 is probably over 65 and I'm betting 80's - 100's. 

And then there's the psychological component of fear.  When your lungs are full, you're going to be air hungry.  If if you are breathing adequately, you won't feel like you are.

You guys have covered hypoxia and hypoxemia very well.  But you have not quite covered ventilation.

NRB won't work nearly as well as CPAP.  First off a tachypneic adult pt can have inspiratory flow rates/demands (the speed in which they can suck air into their lungs) of 300 L/min.  A 15 L/min NRB will as useful as mammory glands on male swine.  What the pt really needs here with supplemental oxygen is pressure and flow.  Some EMS flow systems can deliver flow rates of up to 140 L/min.  Not the best, but better than a NRB.

Along with that, the pt needs diuresis if CHF, and hydration, abx, and pulmonary toilet if pneumonia.


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## TYMEDIC (Feb 20, 2012)

with the usual suspect CHF, that was diagnosed with Hyperkelemia. Wouldnt the normal use of diuretics be detrimental to the patient? I agree with the ventilation input, def. agree with the use of positive pressure with flow. With the kidneys already working overtime with the compansation of of the increased pH by retaining H+, ultimatly excreting a ton of HCO3. I feel that the lasix would cause even more of an influx in the acid-base. With what I was observing, the patient was compensating for the respiratory issue further creating a huge issue with the kidneys. I understand it is a long drawn out compenstation measure with the kidneys and resp. but who knows if this is acute or chronic.


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## MSDeltaFlt (Feb 20, 2012)

TYMEDIC said:


> with the usual suspect CHF, that was diagnosed with Hyperkelemia. Wouldnt the normal use of diuretics be detrimental to the patient? I agree with the ventilation input, def. agree with the use of positive pressure with flow. With the kidneys already working overtime with the compansation of of the increased pH by retaining H+, ultimatly excreting a ton of HCO3. I feel that the lasix would cause even more of an influx in the acid-base. With what I was observing, the patient was compensating for the respiratory issue further creating a huge issue with the kidneys. I understand it is a long drawn out compenstation measure with the kidneys and resp. but who knows if this is acute or chronic.



Unless you have actual lab results, the only prehospital sign I can think of to indicate the possibility of hyperkalemia would be the observance of peaked T waves.  With the absence of either of those you have to look at history with regarding meds.  Question.  Should withhold Lasix in a CHF pt without the signs/symtpoms of pulmonary infection, could you back up Your decision?

If you can't back it up in black and white, do it.


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## TYMEDIC (Feb 20, 2012)

The patient did indeed have an infection which I believe was inconjunction with an esacerbation of the CHF. 100% agree with you. It all is black and white in prehospital. more or less I think, which is gonna kill this patient faster. The resp failure, or hyperkelemia? I agree, id give the furosmide along with CPAP, even with the both. The infection was being treated with antibotics.  I couldnt do any of it because i wasnt running lead and had to watch a NRB ride the patient all the way into the er. I thank you for the insight on the ventilation vs. oxygenation.


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## MSDeltaFlt (Feb 20, 2012)

TYMEDIC said:


> The patient did indeed have an infection which I believe was inconjunction with an esacerbation of the CHF. 100% agree with you. It all is black and white in prehospital. more or less I think, which is gonna kill this patient faster. The resp failure, or hyperkelemia? I agree, id give the furosmide along with CPAP, even with the both. The infection was being treated with antibotics.  I couldnt do any of it because i wasnt running lead and had to watch a NRB ride the patient all the way into the er. I thank you for the insight on the ventilation vs. oxygenation.



Also, if the pt was showing signs/symptoms of infection with auscultated rales, you probably shouldn't give lasix.  As the pt diureses the fluid being pulled from the lungs will dry the infiltrates making them harder to remove thus increasing the pt's hospital stay.  Best thing to do is CPAP, and NTG if the pt is hypertensive.


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## TYMEDIC (Feb 20, 2012)

agreed. Scattered rales, with rhonchi. Profound congestion. audible.


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## TYMEDIC (Feb 20, 2012)

Mike, the main issue with the disgussion, was that my partner that is a blundering fool. We had a critical patient, prolonged pneumonia accompaning CHF. the patient was tachnepic, tachycardic, high congestion, rales, slight exp. wheeze. He said no to the CPAP. along with others. This has been escalated. He then contacted the er and pretty much told me and my mentor that he was admitted for hyperkelemia. A metabolic issue he stated. He has no idea about anything, makes me upset. on top of that, he didnt use CPAP per his statement, "he wasnt belly breathing and o2sp was within normal parameters." haha


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## MSDeltaFlt (Feb 20, 2012)

Understood.  Just attempting to clarify from all of the imperical data that was accurate, but not quite on target regarding oxygenation versus ventilation.


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## DitchDoctor44289 (Mar 24, 2012)

C pap.


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## 18G (Mar 25, 2012)

What led to the suspicion of CHF? I've had patients whose lungs were full of fluid with really bad bilateral pneumonia. 

If pt. still had increased work of breathing after the NRB I would have went to CPAP. Take the work off the patient, decrease pt's. energy expenditure, recruit collapsed alveoli, increase surface area for diffusion, and if it is CHF, the CPAP will help reduce afterload as well. 

CPAP is pretty harmless overall.


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