• J P Ornato, A R Garnett, and F L Glauser.
• Department of Internal Medicine, Medical College of Virginia, Richmond 23298.
• Ann Emerg Med. 1990 Oct 1;19(10):1104-6.

Study ObjectiveTo further define the relationship between cardiac output (CO) and end-tidal carbon dioxide tension (ETCO2) at various levels of systemic flow.DesignProspective, controlled laboratory investigation.SettingAnimal laboratory.Type Of ParticipantsFourteen anesthetized, intubated sheep weighing 23 to 47 kg.InterventionsOne hundred seventy-two simultaneous measurements of thermodilution CO and ETCO2 were made during controlled arterial hemorrhage. After a 30-minute baseline control period, CO was sampled from approximately 0.6 to more than 8.0 L/min during a 60- to 90-minute period of controlled hemorrhage.MeasurementsThermodilution CO; arterial pressure using fluid-filled plastic 14-gauge catheters; ETCO2 using an infrared analyzer.Main ResultsA plot of CO versus ETCO2 suggested that the relationship was logarithmic rather than linear. Linear regression showed that ETCO2 was significantly related (r = .91; P less than .001) to a logarithmic transformation of the CO.ConclusionsThe relationship between CO and ETCO2 is logarithmic. Decreased presentation of CO2 to the lungs is the major, rate-limiting determinant of the ETCO2 during low flow. As the CO increases during resuscitation from shock or cardiac arrest, respiration becomes the rate-limiting controller of the ETCO2 (after the tissue washout of CO2 has occurred). Under such conditions, the ETCO2 provides useful information about the adequacy of ventilation provided that there is little ventilation/perfusion mismatch.

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