Changes in cerebral oxygen saturation during transcatheter aortic valve replacement

Jessica Brodt, Greta Vladinov, Catalina Castillo-Pedraza, Raymond Cooper, Edward Maratea

Research output: Contribution to journalArticle

7 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)649-653
Number of pages5
JournalJournal of Clinical Monitoring and Computing
Volume30
Issue number5
DOIs
StatePublished - Oct 1 2016

Fingerprint

Oxygen
Hemodynamics
General Anesthesia
Oximetry
Brain Ischemia
Intubation
Oxygen Consumption
Cardiac Output
Anesthetics
Transcatheter Aortic Valve Replacement
Reference Values
Anesthesia
Perfusion
Morbidity
Population

All Science Journal Classification (ASJC) codes

  • Health Informatics
  • Critical Care and Intensive Care Medicine
  • Anesthesiology and Pain Medicine

Cite this

Changes in cerebral oxygen saturation during transcatheter aortic valve replacement. / Brodt, Jessica; Vladinov, Greta; Castillo-Pedraza, Catalina; Cooper, Raymond; Maratea, Edward.

In: Journal of Clinical Monitoring and Computing, Vol. 30, No. 5, 01.10.2016, p. 649-653.

Research output: Contribution to journalArticle

Brodt, Jessica ; Vladinov, Greta ; Castillo-Pedraza, Catalina ; Cooper, Raymond ; Maratea, Edward. / Changes in cerebral oxygen saturation during transcatheter aortic valve replacement. In: Journal of Clinical Monitoring and Computing. 2016 ; Vol. 30, No. 5. pp. 649-653.
@article{852e746a8ec044c4948f9a57bebc073e,
title = "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.",
author = "Jessica Brodt and Greta Vladinov and Catalina Castillo-Pedraza and Raymond Cooper and Edward Maratea",
year = "2016",
month = "10",
day = "1",
doi = "10.1007/s10877-015-9758-8",
language = "English (US)",
volume = "30",
pages = "649--653",
journal = "Journal of Clinical Monitoring and Computing",
issn = "1387-1307",
publisher = "Springer Netherlands",
number = "5",

}

TY - JOUR

T1 - Changes in cerebral oxygen saturation during transcatheter aortic valve replacement

AU - Brodt, Jessica

AU - Vladinov, Greta

AU - Castillo-Pedraza, Catalina

AU - Cooper, Raymond

AU - Maratea, Edward

PY - 2016/10/1

Y1 - 2016/10/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84960338518&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84960338518&partnerID=8YFLogxK

U2 - 10.1007/s10877-015-9758-8

DO - 10.1007/s10877-015-9758-8

M3 - Article

VL - 30

SP - 649

EP - 653

JO - Journal of Clinical Monitoring and Computing

JF - Journal of Clinical Monitoring and Computing

SN - 1387-1307

IS - 5

ER -