Nutritional manipulation of carbon dioxide production

Again, the available enteral supplements

It has been held as gospel truth that high-fat, low-carb supplements decrease CO₂ production in the CO₂-retaining population of respiratory failure patients. This practice is supported by heterogenous studies with small effect sizes. The one specific study which is frequently referred to is the al Saady paper from 1989, which in a cohort of 40 randomised patients found that the high-fat low-carb diet caused a reduction in ventilator days (by 62 hours) and an average decrease in PaCO₂ (by 16%). There is also evidence to suggest suggest that there is an increase in CO₂ production for patients who are overfed, irrespective of what form the nutrition takes. The Canadians suggest that there is insufficient evidence to make a firm recommendation about this practice. The prevailing opinion is that the use of high-fat diets should be targetted at the population of acute COPD patients who are spontaneously ventilated.

Is there any scientific foundation to the assertion that high fat diets result in decreased CO2 production?

Yes, there is sound theory underpinning this. The respiratory quotient for pure carbohydrate oxidation is 1.0 (that is, the ratio of CO₂ production to O₂ consumption). During the complete oxidation of a 6-carbon glucose molecule (C₆H₁₂O₁₂), 6 molecules of CO₂ and 6 molecules of H₂O are produced. For fat, the respiratory quotient is about 0.7. A fatty acid contains less oxygen than glucose, and thus consumes more exogenous oxygen in the course of its metabolism. Thus, during the complete metabolism of the 16-carbon palmitic acid (C₁₆H₃₂O₂) one ends up needing 23 molecules of oxygen, giving a respiratory quotient of 0.696 (16 divided by 23). Notice how the amount of CO2 produced is the same. It doesn't matter what is burned- there is one CO₂ molecule produced per every carbon atom metabolised.

Thus, if one were to feed their patient fewer carbon atoms, one would expect less CO2 production.

Now, we know the fatty acid would produce 7 ATP per carbon atom, and glucose produces only 5 ATP per carbon. Thus one needs to give their patient less fat than glucose to achieve the same caloric goal. Therein lies the lure of fat. Pulmocare which is 55% fat should be metabolised into fewer CO2 atoms while still supplying adequate nutrition.

But, does this actually happen?

Is there experimental evidence to support the theory that high fat diets result in decreased CO2 production?

In 1992, a group from the Osler Chest Unit in Oxford published their findings in Thorax. They tortured ten COPD patients with Pulmocare, Ensure Plus and artificially sweetened water. This group achieved a small change in blood gases (PaCO₂ increased by 1.3%, with a peak at 30 minutes post ingestion), but they also discovered that exercise tolerance was significantly impaired after a high-carbohydrate meal. The magnitude of the rise in PaCO₂ was attributed to the increased respiratory rate.

Similarly, a study from Beijing examined the effects of high-fat and high-carb diets on 60 malnourished COPD patients, and reached an improvement in various pulmonary endpoints in the fatty-diet group (after 3 weeks of such a diet).

Indeed, such is the experimental evidence that the Chest systematic review of nutrition in stable COPD was forced to conclude that "those with marginal ventilatory reserve might benefit from a dietary regimen in which a high percentage of calories are supplied by fat."

But of course, these were all studies and guidelines to direct treatment of ambulant stable COPD patients. What happens in the ICU?

Does the use of Pulmocare actually improve outcomes for a ventilated COPD patient in the ICU?

The already-mentioned al Saady paper is one of two papers specifically dealing with high-fat, low-carb ICU diets. Their outcome was positive.

The other one was the van den Berg trial, which measured PaCo2 and respiratory quotient. They found that the RQ is indeed more favorable among the high-fat group, but there was no change in the PaCO2 during weaning from the ventilator.

The Canadians observed that both papers were inadequately powered, and were forced not to make any firm recommendation. They did however reach an ambiguous and spongy conclusion that "A high fat, low CHO enteral formula may be associated with a reduction in ventilated days in medical ICU patients with respiratory failure".

We refer to our founding fathers. What does The Manual say? Naughton and Tuxen's chapter on acute respiratory failure in COPD (Ch 26, pp. 343-354) notes briefly that in spontaneously ventilated patients with COPD, a high-fat low-carb diet is preferred; however their emphasis was on correcting malnutrition.

Their recommendation does not have a reference, and so a cornered exam candidate cannot refer to any specific paper as the source of this wisdom.