Ventilatory failure
Consider, how is it possible to have ventilatory respiratory failure without a high CO2
Increased carbon dioxide production. An example would be someone that's in DKA and thus is in a profound metabolic acidosis. They are unable to compensate for this metabolic acidosis by increasing their minute ventilation to a sufficient degree, and this may be unable to maintain their ventilatory requirement despite a Low CO2
Think of this as a in versus out problem.
Other scenarios that meet this description are thyroid storm malignant hyperthermia cyanide salicylate poisoning trauma or burn injuries
Workup
A RN calls you with a critical result on a patient who has a pCO2 that is 80 mmHg. What 2 (+1) pieces of information do you want?
- RR => determine won't breath (opiates, give narcan. Obesity/a on c respiratory failure) vs can't breath
- pH (or by Henderson Hasselbach - bicarbonate) => determines the chronicity of the abnormality by the presence or absence of metabolic compensation.
- The +1 is mental status, because that will influence how you can treat the situation of "Acute Can't Breath"
If you have a patient in respiratory distress - you can skip the first step and move to the assumption of Acute Can't Breath
Importantly: hypoxemia is a weak driver of dyspnea (though it can amplify the effect of acidosis and CO2 on the respiratory center, particularly under PaO2 60) - https://derangedphysiology.com/main/cicm-primary-exam/required-reading/respiratory-system/Chapter%200201/relationship-arterial-carbon-dioxide-and-alveolar-ventilation
Think of this as a: What is your ventilation requirement, and is it increased? Vs What is the maximal sustainable ventilation, and is it decreased? (Kapitan KS. Ventilatory failure. Can you sustain what you need? Ann Am Thorac Soc. 2013;10(4):396-399.)
Reasons for an increased Minute Ventilation Requirement
The relationship between Minute ventilation (VE), CO2 production (VPCO2), Deadspace fraction (VD/VT), and PaCO2 is given by:
VE = k * VPCO2 / [ ( 1 – VD/VT) * PaCO2
Thus, increased requirement occurs with:
- Increased VPCO2
- Increased VD/VT
- Decreased PaCO2
Reasons for a decreased Maximal Sustainable Minute Ventilation
-
Inertial loads (e.g. heavy lungs, heavy chest)
-
Elastic Loads (e.g. stiff lungs from fibrosis
-
Resistive Loads (e.g. airflow limitation)
-
Mechanical disadvantage (e.g. weakness, injury, hyperinflation)
Work of breathing
Respiratory Drive
https://www.atsjournals.org/doi/abs/10.1513/AnnalsATS.202007-814CC
Increased as a result of hypercapnia, acidosis, and the effect of those two is potentiated after PaO2 <60 mmHg (https://pubmed.ncbi.nlm.nih.gov/32016537/).
Also increased when altered respiratory mechanics dissociate drive from mechanical results. And inflammation (J-fibers?)
Can be monitored by P0.1 (occlusion for the first 0.1 s of an inhalation breath) or Pocc (1 s, less reliable)
Also: overdrive ventilation and bicarbonate study https://twitter.com/phlegmfighter/status/1346971355799904262?s=20