While quantitative waveform capnography and pulse oximetry are both infrared technologies and may seem like similar measurements, they assess very different things. Capnography is a direct measurement of ventilation and, indirectly, circulatory and metabolic status. Pulse oximetry measures the color of the hemoglobin (Hgb) molecule and then uses mathematic algorithms to estimate the percent of Hgb saturation.
Hemoglobin is a helix-type molecule that coils tighter and appears redder as it becomes saturated and uncoils and appears bluer as it desaturates. The more red/blue the Hgb the higher/lower the saturation percentage estimated by pulse oximetry. An important technological limitation to know regarding pulse oximetry is that it cannot decipher what is bound to the Hgb molecule. This becomes crucial to understand in the context of carbon monoxide poisoning.
Carbon monoxide is 200 times more attracted to hemoglobin than oxygen. Therefore, a patient with carbon monoxide poisoning will read 100% on their pulse oximetry as carbon monoxide’s higher affinity causes the Hbg molecule to coil tightly and appear very red (hence the textbook “cherry red” appearance of postmortem carbon monoxide patients). However, a patient with carbon monoxide poisoning is obviously NOT oxygenated.
Additional problems with pulse oximetry are related to intermittent readings, usually secondary to artifact caused by low perfusion, cold fingers, long finger nails and/or nail polish, patient movement, your partner hitting a curb at 90 mph, etc. Also, there are significant delays in measuring pulse oximetry in the finger from what is going on centrally in the core. This is the biggest reason for central pulse oximetry monitoring on critical patients, particularly pediatric patients. Nonetheless, pulse oximetry still has value as long as the provider understands the technological limitations and uses it in conjunction with capnography to complete the clinical picture.
End tidal carbon dioxide (ETCO2) is the technical term for the amount of CO2 measured in exhaled air. The actual unit of ETCO2 is a measurement of pressure (NOT parts!) reported in millimeters of mercury (mmHg). ETCO2 is normally 35-45 mmHg in a healthy individual. Several factors can change a person’s ETCO2, such as ventilatory factors and circulatory/metabolic status (circulator/metabolic capnography changes are discussed in other articles).
As respiratory distress worsens, ventilations become less effective leading to decreased gas exchange, hypercapnia and a rise in ETCO2. While a rise in ETCO2 does not directly cause ventilatory failure, it is an indicator to the severity of the respiratory issue. There is no absolute ETCO2 value that indicates when respiratory distress has become severe enough to cause ventilatory failure, as it depends on the patient’s baseline ETCO2 levels and the respiratory pathology involved. However, one study suggests that in patients with normal ETCO2 values for their baseline, an ETCO2 of approximately 70-80 mmHg1 is an indicator that their respiratory distress is severe enough for ventilatory failure to be eminent.
Partial pressure of arterial carbon dioxide (PaCO2) is the measurement of CO2 pressure in arterial blood that is obtained through lab values. In healthy patients, ETCO2 and PaCO2 values can be used virtually interchangeably as there are only a few pressure points of difference. ETCO2 can never be higher than PaCO2, but the reverse can be true. During disease the difference between PaCO2 and ETCO2, called the “PaCO2 – ETCO2 gradient”, can grow and be a quantitative indicator of the severity of the pathology. For simplicity, I use the term “CO2 gap” to reference the difference between the pressure of carbon dioxide in the body (PaCO2) vs. the pressure of carbon dioxide being measured at the lips (ETCO2); the bigger the CO2 gap, the worse the respiratory pathology and/or ventilation issue. During ventilatory failure, tidal volume falls and the end TIDAL carbon dioxide pressure falls as well even though the PaCO2 pressure in the system continues to build. ETCO2 should be greater than 50 in respiratory distress, not low or normal. Ventilatory failure is defined via ETCO2 as a low or “normal” number in the clinical picture of severe respiratory distress. If you support a patient’s tidal volume in ventilatory failure via mechanical assistance, CPAP, BiPAP or coaching them to breathe deeper and the intervention is effective, ETCO2 numbers should rise to where you would expect them to be in respiratory distress. For more on this counterintuitive phenomenon, check out the article on ETCO2 and low tidal volume that uses a CPAP case study as a guide for explanation.
In summary, pulse oximetry is an infrared technology that measures the color of hemoglobin and estimates percent saturation. Pulse oximetry cannot determine what is bound to the hemoglobin and can be fooled by carbon monoxide. Peripheral oximetry readings will be significantly delayed when a patient becomes apneic or begins to decline in respiratory distress. ETCO2 is the pressure of carbon dioxide detected in exhaled air at the lips and will change quickly when a patient becomes apneic or enters into respiratory distress. PaCO2 is the pressure of carbon dioxide in the body, technically the arterial side. In healthy individuals, there is little difference between PaCO2 and ETCO2. However, in the respiratory patient, or the patient with a significant pulmonary embolism, the CO2 gap grows; the bigger the gap the worse the problem. The difference between ETCO2 and PaCO2 will be the largest in ventilatory failure patients where the tidal volume is so low, they cannot deliver a breath to the sensor on the lips in normal amounts so pressures fall at the lips, even though PaCO2 is increasing.
1. Krauss, B and Hess, D. Capnography for Procedural Sedation and Analgesia in the Emergency Department. Annals of Emergency Medicine, 2007, 50: 172-181.