HELP with ABGs and Correction by Ventilatory Settings

core0 · Oct 28, 2013

In a patient with a history of COPD who comes into the hospital and is diagnosed with Acute Respiratory Failure and pneumonia...
ABG 1: CO2 54, HCO3 30, O2 52, pH 7.25. Pt is given 28% with a venturi mask.
ABG 2 30 minutes later: CO2 48, HCO3 30, O2 58, pH 7.42
Based on these results, the patient is intubated.
2 hours after intubation, mode SIMV at 14, 50% FIO2, TV 750, and 5 PEEP:
pH 7.30
PO2 60
PCO2 64
HCO3 30
I realize these results are not what is expected after 2 hours on the vent. The pH is still acidic, the O2 is low, the PCO2 is high and acidic, and the HCO3 is increased and trying to compensate.
My question is....What ACTIONS would you take to correct this ABG? Would you increase the RR? Increase the FIO2? Increase the PEEP? I would imagine you wouldn't increase the tidal volume? What else? THANKS!

Think about ventilation and oxygenation separately. While this is an over simplification, ventilation (CO2 exchange) is a function of minute ventilation which is made up of tidal volume and rate (rate x tv = minute ventilation). Oxygenation is controlled by PEEP and FiO2 (%oxygen). So if you want to increase oxygenation you increase FiO2 or PEEP. If you want to increase ventilation you increase rate or tidal volume.

http://www.nursingcenter.com/lnc/static?pageid=1030183

Unfortunately its more complicated. What is your plateau pressures, does the patient have ARDS?

Presuming the patient has ARDS (PF ratio

http://www.ardsnet.org/system/files/Ventilator%20Protocol%20Card.pdf

mortalol · Oct 28, 2013

hmmm i wonder what his O2 were before...

i don't know, FiO2 50% for a patient with pneumonia seems low to me.

TraumaSurfer · Oct 28, 2013

Let's look at the whole picture here rather than just the knobology.

In a patient with a history of COPD who comes into the hospital and is diagnosed with Acute Respiratory Failure and pneumonia...

This tells you there is probably a V/Q mismatch.

ABG 1: CO2 54, HCO3 30, O2 52, pH 7.25. Pt is given 28% with a venturi mask.

Based on the clinical information of ARF and PNA, why is this person only on a 28% VM? Is the old "only give 2 LPM regardless of distress" in play here? If a person is in distress, give oxygen to relieve their discomfort. The next ABG sums up my statement.

ABG 2 30 minutes later: CO2 48, HCO3 30, O2 58, pH 7.42

You have a PaO2 appropriate for oxygen of 1 - 2 L in a COPD patient but he is obviously struggling since there is a pH of 7.42. True COPD patients who are retainers rarely if ever raise their pH above 7.42 unless they are "hyperventilating" from a PE or having the needle poking the radial artery or bone during the arterial stick, some metabolic disorder or THEY ARE IN PROFOUND distress. In this situation it would be the withholding of oxygen on a hypoxic patient with a known PNA and Acute Respiratory failure.

Based on these results, the patient is intubated.

The second set of ABGs were great especially if he want only on 28% O2. What probably bought him the tube was his clinical presentation of "I am about to die because I can not get enough oxygen". Hence the V/Q mismatch and 28% VM.

Not getting enough oxygen leads to pulmonary vasoconstriction and pulmonary hypertension. COPD patients may also have Cor Pulmonale. This brings us to the ventilator.

2 hours after intubation, mode SIMV at 14, 50% FIO2, TV 750, and 5 PEEP:
pH 7.30
PO2 60
PCO2 64
HCO3 30

First, SIMV in Acute Respiratory Failure? What was the Pressure Support? Was it really adequate for someone in Acute Respiratory Failure? You would probably have to nearly match his VT given by the ventilator which with a new PNA, that would have to have been a PS of about 30 cmH2O. What was his plateaus which might have been difficult at best to get.

I realize these results are not what is expected after 2 hours on the vent. The pH is still acidic, the O2 is low, the PCO2 is high and acidic, and the HCO3 is increased and trying to compensate.

Why do you think the HCO3 is trying to compensate? What was the anion gap and the CO2 on the CMP or Chem Panel? If the lungs are in a severe chronic state, this person might very well be a CO2 retainer which means he lives with an HCO2 of 30.

Another reason for the increase in PaCO2, other than a poor ventilator mode choice, is the deadspace from the pulmonary vasoconstriction from a prolonged hypoxic state. This is what is not used to explain a sudden increase in PaCO2 rather than the old "knocked out his hypoxic drive".

What are some of the other reasons he could be acidotic? Lactate? Anion Gap? Infection? Dehydration?

My question is....What ACTIONS would you take to correct this ABG? Would you increase the RR? Increase the FIO2? Increase the PEEP? I would imagine you wouldn't increase the tidal volume? What else? THANKS!

Again you will need to look at the whole picture including the CXR.

How tall is this person? You will need that to determine the appropriate weight to calculate the tidal volume.

What else has been done? What are his vital signs? Is he hyper or hypotensive? What is his lactate? Urinary output? These all should play a huge part in determining your ventilator course. Does the CXR show unilateral or bilateral disease process? Air follows the path of least resistance. Any blebs or signs of hyperinflation? How do his labs look? Is he dehydrated? How old is he? Any other disease processes? What about sedation? Ventilator synchrony? Has a central line been place and is there CVP monitoring?

Ventilator management is much more than turning a couple of knobs. You have to management the patient.

TraumaSurfer · Oct 28, 2013

http://www.nursingcenter.com/lnc/static?pageid=1030183
Unfortunately its more complicated. What is your plateau pressures, does the patient have ARDS?
Presuming the patient has ARDS (PF ratio

http://www.ardsnet.org/system/files/Ventilator Protocol Card.pdf

The patient has a history of COPD. We do not know his age or his CXR. If the person can not get their PaO2 above 100 mmHg on a good day and a NRB mask, what makes you think this ratio would apply to them?

Plateau pressures on a COPD patient in SIMV may also be misleading.

As far as PEEP, again, gotta know the CXR and many other factors which I mentioned in my other post. Bilateral infiltrates do not always mean ARDS and may be more of a sepsis pathway. Don't go cranking on the knobs until you considered the data, options and corrected or in a place to start correcting. Crank the PEEP and you tank the BP along with blowing a bleb or two will get you nowhere fast.

Consider the whole patient and all the disease processes you will be treating.

ktliz · Oct 28, 2013

Yeah, I don't get the venturi mask. Wouldn't this patient immediately buy themselves CPAP? And hopefully not need to be intubated?

(I'm a fairly new critical care nurse who relies heavily on my respiratory therapists!)

Do-over, ASN, RN · Oct 29, 2013

Why not bipap first, instead of the venturi or the vent. Were the gases really that bad for a history of COPD?

ktliz · Oct 29, 2013

Wouldn't this patient immediately buy themselves CPAP?

Whoops, meant BiPap.

core0 · Oct 29, 2013

The patient has a history of COPD. We do not know his age or his CXR. If the person can not get their PaO2 above 100 mmHg on a good day and a NRB mask, what makes you think this ratio would apply to them?

Umm if you can't get the PaO2 above 100 on an NRB then yes the P:F ratio would apply to them.

Plateau pressures on a COPD patient in SIMV may also be misleading.

Can you explain this. We don't use much SIMV but the principle is similar to (S)CMV. You do an inspiratory hold at the designated TV and PEEP and you get a plateau pressure. Not sure how this would be misleading.

As far as PEEP, again, gotta know the CXR and many other factors which I mentioned in my other post. Bilateral infiltrates do not always mean ARDS and may be more of a sepsis pathway. Don't go cranking on the knobs until you considered the data, options and corrected or in a place to start correcting. Crank the PEEP and you tank the BP along with blowing a bleb or two will get you nowhere fast.

Actually one of my points was that you don't have enough information to make a judgement about how to manipulate the vent. As an exercise to demonstrate the relationship between PEEP and FiO2 and PaO2 it might work but its much more complex than given in the example. To use your example you are assuming all people with COPD have blebs. COPD is a continuum. Some patients have relatively mild COPD and relatively normal physiology. Some have horrible obstructive physiology and are a nightmare to ventilate. As for ARDS, ARDS and sepsis go hand in hand, or more appropriately ARDS and SIRS go hand in hand.

Consider the whole patient and all the disease processes you will be treating.

Good point. But again its unclear for the original statement what is going on. A lot of missing information.

core0 · Oct 29, 2013

Why not bipap first, instead of the venturi or the vent. Were the gases really that bad for a history of COPD?

It depends on the disease process. The OP stated the patient has PNA and acute respiratory failure with a history of COPD. I would agree that the gas wasn't that bad but if the patient was struggling and you weren't making headway the early intubation is probably the way to go. Generally BIPAP is a bridge therapy. For COPD the evidence is fairly compelling that you can bridge someone on BIPAP while aggressively treating their COPD. For other etiologies such as CHF the picture is more mixed. There are studies that show you can avoid intubation while you aggressively diurese. However, at least one study showed an increased incidence of MI in the BIPAP group vs intubation.

In the OPs case since the stated diagnosis is PNA presumably its going to take more than 24 hours to turn around. While I agree that I wouldn't have necessarily intubated just based on the gas that was shown, if I thought the patient was going to decompensate further I would intubate early. A common mistake with BIPAP is that you continue as the patient worsens and you end up intubating on 100% with a sat of 90% which means you have no reserve if things don't go smoothly.

On the other hand the Europeans are much more likely to use Bipap for longer periods of time as a rescue opposed to a bridge therapy.

TraumaSurfer · Oct 29, 2013

Umm if you can't get the PaO2 above 100 on an NRB then yes the P:F ratio would apply to them.

PF ratio is normally calculated while on a ventilator. But, to show my point, some COPD patients and others with long term pulmonary disease do not oxygenate well. It would probably take a ventilator and a high FiO2 to get some to 100 mmHg on a good "normal" day. That does not mean they have ARDS or need ECMO. You also have to take into consideration other factors which can lower the PaO2.

This is also why hyperoxic and shunt studies are done in PFT labs on high risk patients prior to major surgeries. The patient is placed on 100% O2 via closed system for 20 - 30 minutes. Baseline and end time ABGs are drawn. BTW: They did not go apneic during this time. :woot:

Can you explain this. We don't use much SIMV but the principle is similar to (S)CMV. You do an inspiratory hold at the designated TV and PEEP and you get a plateau pressure. Not sure how this would be misleading.

SIMV consider of a mandatory VT breath and a PS breath setting. If the patient is breathing spontaneously the PS breath is utilized. Some really don't understand this breath setting and may set it as low as 5 cmH2O or what some used to call "compensating for the tube" which leaves no or little support for the rest of the breath. This is great for a SBT to have 5/5 in a pure PSV mode for 20 minutes for extubation criteria but not for acute lung injury. Others will pull out some number like 10 without knowing why other than just because that is what we always use. You see this on CCT/Flight teams a lot. Often this gives a VT of about 100 or less and only increases the work of breathing. However, if you are doing a Plateau Pressure and catch the PS breaths, you will get a Plateau of 10 or 15 or somewhere inbetween depending on flow termination. This is why when you look at the vent documentation on computer charting you will see Plateau Pressures all over the map, especially if nurses are also doing them, because they weren't paying attention to the graphics and the breath delivered. This mode also causes asynchrony due to variations of flow patterns and how much PS is given which makes the reading erratic. I don't know of many still using this mode except in NICU (neonatal) but then that is a whole different set of reasons as to why it is used there.

Actually one of my points was that you don't have enough information to make a judgement about how to manipulate the vent. As an exercise to demonstrate the relationship between PEEP and FiO2 and PaO2 it might work but its much more complex than given in the example. To use your example you are assuming all people with COPD have blebs. COPD is a continuum. Some patients have relatively mild COPD and relatively normal physiology. Some have horrible obstructive physiology and are a nightmare to ventilate. As for ARDS, ARDS and sepsis go hand in hand, or more appropriately ARDS and SIRS go hand in hand.

You should NOT have to assume about the blebs. That is what CXRs are for. Chances are this pt may also have had a CT Scan in their records.

What you are referring to for PEEP and FiO2 is finding optimal PEEP which can be done utilizing the graphics before just pulling a lot of unnecessary ABGs.

Mild, Moderate and Severe are degrees determined by PFT studies with the percentages noted such as FEV1 and FVC. It does not always determine oxygenation. There are many COPD patients who are determined by testing to be Severe by ATS or GOLD but are not requiring home oxygen. People with severe COPD are not always CO2 retainers either.

Those with severe obstructive disease is why there are different ventilator modes, mucolytics/airway clearance devices and even heliox. For oxygenation there is nitric oxide and other vasodilating drugs. It is not always just the lungs creating these issues.

Before jumping fully into a full ARDSnet assumption, deal with some of the factors associated with Sepsis such as raising the MAP of the BP. Improve the circulation and cardiac output along with oxygen utilization (ScO2, SvO2). Get the lactate trending lower. Perfuse the kidneys. Once these things turn around, the pulmonary status will also. You can still use basic lung sparing principles but there may not be a need to do a full ARDSnet press.

ARDS is also one of the more misunderstood diagnoses. It is either way over diagnosed unnecessarily before pertinent clinical data is in or under diagnosed and under treated by some conservatives. I think there was another thread recently which was a good illustration of that.

However, the bottom line is still don't over treat the ventilator until you have treated the patient.

TraumaSurfer · Oct 29, 2013

On the other hand the Europeans are much more likely to use Bipap for longer periods of time as a rescue opposed to a bridge therapy.

Actually the US has been utilizing CPAP and BIPAP for several decades for longer periods of time.

Either CPAP or BIPAP would have been better than just a 28% VM in this situation.

Some will start with CPAP if the patient is breathing rapidly to allow the pt to synch with the flow while the airways are being supported with some positive pressure. The may then ease the patient into BIPAP or some other mode depending on the technology being used. "BIPAP" is no longer your grandma's machine. The new machines are quite sophisticated and can do may things for patient comfort and avoid intubation.