I recall sitting in my ninth grade biology class and feeling awed at how perfectly our bodies are designed. It is infinitely complex at baseline - just keeping the status quo. True magic happens when badness ensues and the body begins to change it’s patterns to compensate. Must. Keep. Things. Going. It’s amazing to me. That’s the moment I knew I would go into the healthcare field.

To this day I remind myself that just because modern medicine offers the capability to tweak things, sometimes the best thing we can do is just stay out of the way. First, do no harm. It’s tough though, because when things are hitting the fan, the instinct is to look at a set of patient problems and try to optimize them. If you fail to recognize when an abnormal finding is actual a new normal in a chronically abnormal person you may jump to fix things, unintentionally worsening things. That’s a heavy use of the noun things, but you get what I’m putting down right?

COPD is a perfect example of this phenomenon so in this post I will discuss the normally abnormal derangement’s that can occur in a patient with COPD. Why they occur, how to interpret them, when to intervene, and when to leave them alone.

There are four commonly abnormal lab findings in a patient with chronic COPD.

Let me clarify one thing before we get to talking about the physiology behind these abnormals. Bicarb and Carbon dioxide are written the same way: C02. Probably because in medicine we love for things to be easy to understand.

PaCO2 is the partial pressure of carbon dioxide, this is the measure of C02 gas dissolved in the arterial blood. Controlled by the lungs.

CO2 on the CMP is total blood carbon dioxide which is comprised of Bicarbonate/HCO3- (95% of tCO2 is bicarb) + a very small amount of dissolved CO2 + Carbonic Acid (H2CO3). Therefore CO2 when read from the metabolic panel drawn from the serum is a reflection of our Bicarb level. Controlled by the kidney.

HCO3 aka bicarb on an ABG is a calculated number derived from the sample using the Henderson–Hasselbalch equation. The true bicarb level in the serum is slightly higher than this calculated number. Therefore, when assessing for metabolic acidosis/alkalosis you really must evaluate the serum bicarb (CO2 on CMP).

Here’s the pathway in COPD.

In a patient with COPD too much carbon dioxide is retained chronically. This results in raised PaCO2 on ABG. It does not equate to a drop in pH in normal situations and those without co-morbidities because of these compensatory actions:

1. Buffering occurs first. Bicarb (- charge) leaves the cells to enter ECF in the bloodstream to buffer the acid. Increases serum Bicarb.

2. Because the cells crave electrical neutrality a (- charge) must replace it in the ICF. This anion is Chloride. Thus low serum Cl levels.

3. The kidneys do the heavy lifting by telling the body to retain bicarb. Increases serum Bicarb.

4. The kidneys also tell the body to excrete carbon dioxide (in the form of carbonic acid).

The net effect is a chronic respiratory acidosis which is fully compensated (thank you buffering and renal systems) by an induced metabolic alkalosis.

That, my friends is a well orchestrated machine which need not receive any tweaking from us. Is it normal, nope, not for you or I. But for this patient it is their new normal. It is harming the patient? If the answer is no, do not fall victim to the temptation to make things fit your ideal of lab values that aren’t red, aka “normal.” A pt who is not in respiratory distress that has a compensated hypercarbia does not need intervention.

So when should you intervene?

1. If the pH drops below normal and the patient is symptomatic.

   • AMS, cardiac instability,

2. If there is a threat to the patient’s status quo pulmonary status. (2/2 risk of impending acidosis)

   • Any situation in which there is increased respiratory demand (sepsis, acidosis, pulmonary pathology, etc.)

   • Any situation in which the respiratory drive is altered (over-sedation, neuro injury, etc.)

   • Any situation in which the already compromised alveolar hypoventilation could be worsened (PE,

3. Be weary and overly cautious in patients with co-morbidites that pose a threat to chronic COPD:

   • Renal failure - main compensation is gone

   • Heart failure - also a prognostic indicator as advancing COPD leads to RHF then LHF

   • Anxiety - don’t underestimate this, these folks have poor pulmonary reserve. Tachypnea -> faster/shallower breaths -> dynamic hyperinflation/autoPEEP/retained airway volumes -> higher CO2 and lower O2 -> worsened dead space ventilation -> worse air hunger -> worse acidosis -> cardiac instability.

   • Those on sedatives, esp those with a direct respiratory depressant effect

4. If you worry that the metabolic alkalosis represents a contraction alkalosis rather than chronic resp acidosis compensation, check a urine chloride level. If it >20 it’s compensation, if it is <10 it could be contraction alkalosis (give them fluids back/stop diuretic).

Don’t forget to join us live on Thursday’s at 3pm EST via Youtube where a community of nurses, nurse practitioners, and np students discuss both professional and educational topics. This week we will talk about COPD labs.