Questioning Routine oxygen on PCA patients

#CageRattler
Should patients on Patient Controlled Analgesia (PCAs) be given oxygen routinely?

In this first of our dogma busting #dogmalysis posts, I wanted to review the evidence supporting the use of supplemental oxygen when a patient is attached to an intravenous PCA.   But couldn't find any.

Let's review the typical scenario.   Mavis has just undergone a total knee replacement surgery and returns from PACU (recovery) with a Patient Controlled Analgesia infusion.  She is receiving supplemental oxygen at 2lpm via nasal prongs.  It is estimated that she is getting 24-28% oxygen.

She is easily roused from dozing comfortably with a respiration rate of 14. A heart rate of 72 and is normotensive at 115/70.  she has good pink colour, her oximetry sats are 99% with a good reliable pleth wave.

Two questions come to light from this.

1.  Why is she getting oxygen?
2.  Does she need it?

The first question typically is answered : "because  policy states all patients on PCA must receive supplemental oxygen"
The second question's answer is No.

There is no evidence for supplemental oxygen in patients on PCA.  Oxygen use historically came from its use in patients in respiratory failure, where the treatment of desaturation was oxygen delivery.  It still is the cornerstone of managing respiratory failure.  Different jurisdictions have different thresholds for application of oxygen, but it is widely accepted by the AHA and Australian Resuscitation Council that oxygen should be used when sats drop below 94% (lower in COPD patients).

Here we have a well saturated post operative patient on a narcotic infusion.  She does not meet criteria for oxygen delivery until an assessment of her saturations on room air (21%) has taken place.

So why is she on oxygen (other than an outdated policy), what clinical indication is there for supplemental oxygen?   Respiratory depression risk?? Nope- let's look at this.

Narcotics (mostly) bind at the Mu , Kappa, and Delta receptors in the central nervous system.  All three receptors are like switches that, when flicked on, interpretation of pain is dulled.
The Mu receptor, when stimulated, also causes euphoria in low doses, and sedation in large doses; pinpoint pupils, slowed gastric motility and large (bigger than sedative doses, depresses the respiratory drive.

It's this respiratory depression that we fear, and rightfully so, because respiratory depression causes CO2 retention, and subsequently, as CO2 accumulates, respiratory acidosis.   We breathe (in part) to regulate our acidity of blood. This is where the post might get a bit sciencey.

Blood pH is kept in a tight range of 7.35-7.45.  A drop in pH below 7.35 is termed acidosis and the deeper the acidosis is, the less capable is the red blood cell's ability to carry oxygen.  In early acidosis, no desaturation occurs, but once a threshold is met, and acidosis reaches a critical stage, haemoglobin dumps oxygen, causing a desaturation event.   Slow shallow breathing reduces the "blowing off" of acidic CO2 gas which, when built up, drops pH into acidosis.   Because this is regulated by breathing rate and depth, this form of acidosis is called Respiratory Acidosis.

So your post op patient develops respiratory depression.  Her respiratory rate drops to 6. She is difficult to rouse, but isn't turning blue because she has been receiving supplemental oxygen via nasal prongs, yet her CO2 (if you'd measured it is sky high, and she has acidosis).  But sats are looking ok, because desaturation is a late sign of respiratory depression and it is delayed by unnecessary over oxygenation.

Now what?    Her acidosis worsens to the extent that her blood now can't carry oxygen. This sudden desaturation point has been met, and your patient decompensated into respiratory failure.

Now what do you do?  You hit the blue button on the wall!
In the crisis you see her sats hit 80% so it seems reasonable that you'd put high flow oxygen on, but the cause of this patients desaturation is not a lung disease (COPD, pneumonia, OE) it is acidosis, and acidotic blood won't carry oxygen.

Mavis needs stimulation, narcotic reversal (Naloxone), and to be bagged up to blows off CO2.   Her acidosis is what is killing her, and you must correct her acidotic blood before oxygen will have any effect.

Oxygen has no evidence based rationale as a supplement in post op patients on PCA.  You want to review sedation scores and respiratory rates, but saturation monitoring is of little use because by the time you see saturations that sink, your patient is too sick for its use to be of value without correcting acidosis first.

By all means have oxygen handy, but know this.  Oxygen does not prevent respiratory depression in PCA patients.

Look into your policies, see what they say. Challenge the dogma, generate a culture of practice from evidence.

If you find research that supports use, please let me know. I can't

#cagerattler