Changes in cerebral oxygen saturation during transcatheter aortic valve replacement

Abstract

Cerebral oxygen saturation (rSO2) is a non-invasive monitor used to monitor cerebral oxygen balance and perfusion. Decreases in rSO2 >20 % from baseline have been associated with cerebral ischemia and increased perioperative morbidity. During transcatheter aortic valve replacement (TAVR), hemodynamic manipulation with ventricular pacing up to 180 beats per minute is necessary for valve deployment. The magnitude and duration of rSO2 change during this manipulation is unclear. In this small case series, changes in rSO2 in patients undergoing TAVR are investigated. Ten ASA IV patients undergoing TAVR with general anesthesia at a university hospital were prospectively observed. Cerebral oximetry values were analyzed at four points: pre-procedure (baseline), after tracheal intubation, during valve deployment, and at procedure end. Baseline rSO2 values were 54.5 ± 6.9 %. After induction of general anesthesia, rSO2 increased to a mean of 66.0 ± 6.7 %. During valve deployment, the mean rSO2 decreased <20 % below baseline to 48.5 ± 13.4 %. In two patients, rSO2 decreased >20 % of baseline. Cerebral oxygenation returned to post-induction values in all patients 13 ± 10 min after valve deployment. At procedure end, the mean rSO2 was 67.6 ± 8.1 %. As expected, rapid ventricular pacing resulting in the desired decrease in cardiac output during valve deployment was associated with a significant decrease in rSO2 compared to post-induction values. However, despite increased post-induction values in all patients, whether related to increased inspired oxygen fraction or reduced cerebral oxygen consumption under anesthesia, two patients experienced a significant decrease in rSO2 compared to baseline. Recovery to baseline was not immediate, and took up to 20 min in three patients. Furthermore, baseline rSO2 in this population was at the lower limit of the published normal range. Significant cerebral desaturation during valve deployment may potentially be limited by maximizing rSO2 after anesthetic induction. Future studies should attempt to correlate recovery in rSO2 with recovery of hemodynamics and cardiac function, provide detailed neurological assessments pre and post procedure, determine the most effective method of maximizing rSO2 prior to hemodynamic manipulation, and provide the most rapid method of recovery of rSO2 following valve deployment.

The silent and apparent neurological injury in transcatheter aortic valve implantation study (SANITY): concept, design and rationale

“…Accepted thresholds for cerebral ischemia are a rSO 2 of <50% or a decline of >20% [30]. This will be applied during the intra-operative period of the SANITY study with use of INVOS™ (Covidien, Boulder, CO) specifically to monitor the cerebral oxygen delivery compromise associated with the procedure, and in particular with rapid ventricular pacing [31,32]. …”

Effect of Transcatheter Aortic Valve Replacement on Retinal Layer Thickness Measured by Optical Coherence Tomography

“…Autoregulation allows the retina to adapt its vessel diameters and blood flow to changes in demand for local metabolic supply, thus naturally affecting the correlation between retinal oxygen extraction and cardiac output. 14,15 Autoregulation can elucidate the transient localized GCC defects and increased left central macular thickness on the first day postoperatively. We did not detect a significant difference between preoperative and postoperative first month RNFL, GCC, and macula thicknesses.…”

Effect of gelatin-polysuccinat on cerebral oxygenation and microcirculation in a porcine haemorrhagic shock model

“…We observed persisting crSO 2 deterioration with an approximate 20% decrease from the individual baseline value. In clinical scenarios, drops of 20–25% describe a red line that may require urgent intervention to minimize cerebral ischaemia [ 34 – 36 ]. In perioperative settings, these kinds of deoxygenation events are associated with neurocognitive dysfunction, cerebral ischaemia and morbidity [ 34 – 36 ].…”

“…Therefore, we can only speculate on potential risk for hypoxaemic brain damage in the long run. The correlation between crSO 2 impairment and adverse patient outcome, however, is well examined [ 34 – 36 ]. For experimental reasons, we choose a scenario without any vasopressor support to address the mere effects of fluid resuscitation.…”