Please see Bibliography of References for a list of abstracts, manuscripts and posters.
Miner JR, Petersen G, Byrd C, Clinton J, Smith S. Ann Emerg Med. 2008;52(4, Supplement):S57-S58. Abstract 51.
Study Objectives: Near infrared tissue hemoglobin O2 saturation (StO2) has been shown to correlate with tissue perfusion and adequacy of ongoing resuscitation. Capnography has been shown to measure similar physiologic changes as the StO2 in patients with in hypoperfusion states. The objective of this study was to determine whether changes in StO2 correlate with capnographic changes in end tidal CO2 (EtCO2) in emergency department patients (intubated and non-intubated) undergoing resuscitation for hypotension and shock, and to determine if this relationship correlates with shock etiology or with cardiac function.
Methods: This was a prospective, observational study in an urban Level 1 Trauma Center. Subjects were selected from a convenience sample of adult patients with a shock index (SI) of > 0.9 (SI=heart rate/systolic blood pressure). EtCO2, heart rate, blood pressure, respiratory rate, and pulse oximetry were recorded at oneminute intervals by trained research associates. EtCO2 was measured by nasal cannula in non-intubated subjects and by in-line EtCO2 monitors in intubated subjects. StO2 values were recorded continuously. All patients underwent cardiac ultrasound by a trained emergency physician (EP) who determined left ventricular function as either 1) normal, 2) hyperdynamic, or 3) moderate/severe dysfunction. The EP determined each patient’s shock etiology as hypovolemic-hemorrhagic, septic, neurogenic, cardiogenic, or respiratory. The StO2 values were compared with EtCO2 values using linear regression. Correlation between intubation status, cardiac function and shock etiology groups was compared using multivariate regression.
Results: 80 patients were enrolled (age 56.0 +17.8, range 19 to 93, 52.5% male) of which 29 (36%) were intubated. Shock etiologies included 18 cardiogenic, 24 hypovolemic-hemorrhagic, 7 neurogenic, 19 sepsis, and 12 respiratory. Cardiac ultrasound revealed 39 with normal LV function, 24 with moderate/severe dysfunction, and 19 with hyperdynamic function. The initial StO2 was 62.9 + 17.2, range 30 to 91. The initial EtCO2 was 17.8 +9.6, range 4 to 64. The correlation coefficient between StO2 and EtCO2 was 0.13 (95% CI -0.31 to 0.58, p=0.56). Among intubated patients it was 0.61 (p=0.02) and among non-intubated patients it was -0.51 (p=0.10). The correlation between initial EtCO2 and initial StO2 was 0.17 (p=0.57) for moderate/severe cardiac dysfunction, 0.03 (p=0.83) for normal cardiac function, and -0.65 (p=0.03) for patients with hyperdynamic cardiac function. There was no difference in the correlation between initial EtCO2 and initial StO2 based on shock etiology.
Conclusion: StO2 and EtCO2 values do not correlate when compared among all patients. EtCO2 is only directly correlated to StO2 values in intubated patients. The nature of the correlation is different between intubated and non intubated patients. The relationship is stronger among patients with hyperdynamic cardiac function than in patients with normal or decreased function. The etiology of the shock did not change this relationship.