CO2 Monitoring Review

Myron Yaster MD

Original article

Susan Humphreys, Andreas Schibler, Britta S von Ungern-Sternberg. Carbon dioxide monitoring in children-A narrative review of physiology, value, and pitfalls in clinical practice. Paediatr Anaesth. 2021 Aug;31(8):839-845. PMID: 3400890

When I was a new anesthesia resident at the University of Pennsylvania in the late 1970s, anesthesia monitoring was really primitive, I mean really primitive.  Finger on the pulse, ECG (sometimes), precordial stethoscope, and a manual BP cuff. That was it…there was neither pulse oximetry nor capnography nor automated non-invasive blood pressure monitoring.  The importance of arterial CO2 and O2 (measured by arterial blood gas) was well understood, particularly their effects on the control of ventilation in both the awake and anesthetized state.  John West’s seminal text book “Pulmonary gas exchange: ventilation blood flow and diffusion”, which is still in print, was required reading and “woe on you” as a resident if you hadn’t read it or understood V/Q mismatch when asked about it in the OR or ICU. Indeed, I basically learned that whenever an attending asked me any pulmonary physiology question, if I answered “V/Q mismatch” I would invariably get the answer right! 

The anesthesia machines were really different too.  CO2 E cylinders where staples on many anesthesia machines and there was a button that when unscrewed could remove the CO2 absorber from the circuit to allow CO2 rebreathing and thereby hasten “wake up”.  One of my attendings, during an adult ortho procedure at the Philadelphia VA, surreptitiously unscrewed this button while talking to me to see how I would react and then left the room.  Over the next 15 minutes, the patient became diaphoretic, hypertensive, and tachycardic.  I sent off a stat blood gas which revealed a PaCO2 over 100!  I called a code thinking I was dealing with malignant hyperthermia.  The world, including my attending, came running into my room. As they were bringing in ice, mixing dantrolene, and inflating a rubber raft, my attending sheepishly realized that he had removed the CO2 absorber from the circuit and forgotten that he did it.  He rescrewed in the button, returning the CO2 absorber cannister into the circuit, and within minutes, voila! all was well with the world again.  Many lessons learned!

Jump to the modern era where capnography and pulse oximetry are ubiquitous (and the ability to easily remove the CO2 cannister from the circuit is not).  Anesthesia ventilators increasingly resemble ICU ventilators and when guided by capnography the control of ventilation can be accomplished with exquisite efficiency and accuracy. The key is CO2 and its measurement.  This review paper by Humphreys et al. is a must read for all trainees and for those who teach them (and perhaps for all of the rest of us, like me, who may need a review). This paper answers the following questions:  How is CO2 produced and excreted, how does capnography (and transcutaneous monitoring) work, what is the connection between PaCO2 and End Tidal CO2, what do the capnography screen images mean and how can we interpret capnography abnormalities?  It also provides an understanding of the limitations of capnography, the effects of additional dead space attributable to apparatus and anesthesia, and ventilation/perfusion mismatch in interpreting capnography.  Finally, from a pediatric perspective, it also discusses the effects of age, weight, and respiratory rate as well as cardiopulmonary comorbidities on capnography and its interpretation.

Myron Yaster MD

PS:  I am a firm believer that in the OR “CO2 is good for you”!(1) In virtually every OR in the U.S., patients are routinely hyperventilated to ETCO2s in the low 30s or even high 20s.  With the exception of patients with pulmonary artery hypertension or with “tight” brains, my own practice is to routinely hypoventilate patients to the mid 50s which is what would happen in spontaneously breathing anesthetized patients.  Hypoventilation and mild acidosis produce many salutary effects, including increased cardiac output, blood pressure, and heart rate, as well as increased blood flow to organs that are vulnerable to ischemia, such as the brain, heart, and kidneys. Perhaps most importantly to the anesthesiologist, acidosis causes a rightward shift in the oxygen dissociation curve, which improves oxygen unloading to all of the tissues in the body. Finally, because hydrogen ion is the primary driver of ventilation at the chemoreceptor in the brainstem, it is the primary driver of ventilation. With elevated CO2, patients will simply just start breathing spontaneously when they are removed from the ventilator, and as they do, they will hasten the removal of residual anesthetic gasses and hasten wakeup. Indeed, this is why the old anesthesia machines had CO2 E cylinders and the button that could remove the CO2 absorber from the circuit.

References

1.           Yaster M, Gross JB: CO2 is Good for You! Anesth Analg 2021; 132: e13