PubMed · 2720884
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R Segstro. 1989. Nasal sensor attachment.. https://pubmed.ncbi.nlm.nih.gov/2720884/
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With improvement in supportive care patients rarely die from their presenting illness but rather from its sequela, namely sequential multi-organ failure. Tissue hypoxia is believed to be the causation of multi-organ dysfunction syndrome (MODS). The expedient detection and correction of tissue hypoxia may therefore limit the development of MODS. The standard oxygenation and hemodynamic variables (blood pressure, arterial oxygenation, cardiac output) which are monitored in critically ill patients are 'upstream' markers and provide little information as to the adequacy of tissue oxygenation. Global 'downstream' markers such as mixed venous oxygen saturation and blood lactate are insensitive indicators of tissue hypoxia. Sublingual PCO(2) is a regional marker of microvascular perfusion and tissue hypoxia that holds great promise for the risk stratification and end-point of goal directed resuscitation in critically ill patients. This paper reviews the technology and application of sublingual PCO(2) monitoring.
The aim of the present study was to assess the feasibility of measuring combined arterial oxygen saturation measured by pulse oximetry (Sp,O2) and cutaneous carbon dioxide tension (Pc,CO2) to monitor ventilation and quantify change in Pc,CO2 during bronchoscopy. Combined Sp,O2 and Pc,CO2 were measured at the ear lobe in 114 patients. In four patients, the ear-clip slipped and they were excluded. In total, 11 patients had artefacts with Sp,O2 recordings, thus, Sp,O2 was analysed in 99 patients. Spirometry data were available in 77 patients. Multivariate analysis of covariance and logistic regression were used for statistical analyses. Mean baseline Pc,CO2 was 4.78+/-1.06 kPa (36+/-8 mmHg) and mean rise in the Pc,CO2 during bronchoscopy was 1.26+/-0.70 kPa (9.5+/-5.3 mmHg), while mean Pc,CO2 at the end of bronchoscopy was 5.85+/-1.19 kPa (44+/-9 mmHg) . Baseline Pc,CO2 and the lowest Sp,O2 were significantly associated with peak Pc,CO2 and the change in Pc,CO2 during bronchoscopy. Risk of significant hypoxaemia (Sp,O2<or=90%) was lower for a higher baseline Sp,O2. Peak Pc,CO2 was directly associated with significant hypoxaemia. There was no significant association in the baseline Pc,CO2, peak Pc,CO2, baseline Sp,O2 or the lowest Sp,O2 comparing patients with and without chronic obstructive pulmonary disease. In conclusion, it is feasible to measure combined pulse oximetry and cutaneous carbon dioxide tension effectively to monitor ventilation during flexible bronchoscopy.
Technologies now exist that measure carbon dioxide levels transcutaneously. Rapid assessment of patients who have depressed ventilation or suspected sepsis can improve treatment decisions including the need for admission to the ICU and pulmonary artery catheterization.