Cardiopulmonary bypass (CPB) is used during cardiac-surgery and provides oxygenated blood to the tissues. Ensuring adequate oxygenation is essential for the preservation of organ function during CPB. Both hypoxia and hyperoxia result in undesired outcomes and a narrow window for optimal oxygenation exists. Current perioperative monitoring techniques are not always sufficient to monitor adequate oxygenation, especially in high-risk patients. Near-infrared spectroscopy (NIRS) tissue oxygen measurement (StO2) is widely used to monitor tissue oxygenation but responds slowly to change. However, the novel non-invasive COMET-monitor measures the mitochondrial oxygen tension (mitoPO2) in the epidermis using the enhanced mitochondrial Protoporphyrin IX Triplet State Lifetime Technique (PpIX-TSLT). The mitoPO2 reflects the local balance between oxygen supply and consumption and provides an insight into the microcirculatory system . This pilot study investigates the correlation between mitoPO2 versus StO2 and varying hemodynamic conditions during CPB and the development of acute kidney injury (AKI).
This single center observational study examined 41 cardiac-surgery patients requiring CPB. Six-hours pre-operatively, patients received a 5-aminolevulinc acid plaster on the upper arm to facilitate the mitoPO2 measurements. After induction of anesthesia, both the COMET and INVOS measurements were executed in 5-minute intervals throughout the procedure. To compare mitoPO2 with StO2, NIRS probes were placed near the COMET probe. Post-operatively, both measurements were stopped simultaneously, and the patients were observed until discharge for the development of AKI.
NIRS data was available for 31 of the 41 patients. The median mitoPO2 at the start of surgery was 63.5 [40.0 – 74.8] mmHg and significantly decreased (p<0.01) to 36.4 [18.4 – 56.0] mmHg by the end of the surgery. The average mitoPO2 was 44.1 [30.6 – 53.3] mmHg. The median StO2 was 80.5 [76.8 – 84.3] mmHg and did not change significantly. Clamping of the aorta and the switch to non-pulsatile flow resulted in a median mitoPO2 decrease of 7 mmHg (p<0.01). The cessation of the clamping period and return to pulsatile flow resulted in an increase of 4 mmHg (p<0.01). Lastly, 4 patients developed AKI according to the KDIGO criteria, this group spent 32% of the operation time with a mitoPO2 value under 20 mmHg as compared to 8% in the non-AKI group.
In contrast to StO2, the mitoPO2 decreased significantly during CPB time. A hemodilution study in pigs also demonstrated that mitoPO¬2 is more likely to change than StO2, which reacted slowly to change. The mitoPO2 also significantly decreased during non-pulsatile flow and increased once pulsatile flow returned, whilst the StO2 did not. This highlights the sensitivity of mitoPO2 to detect circulatory and microvascular changes early through the analysis of oxygen delivery on a cellular level. Lastly, the association found between the AKI and the non-AKI group in time spent below a mitoPO2 of 20 mmHg must be further examined in a well powered study. However, it highlights the potential of this technique to be an early predictor of ischemia.
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