Can hypocapnia reduce cerebral embolization during cardiopulmonary bypass?
Background. Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in arterial carbon dioxide tension (PaCO 2) can reduce cerebral embolization during cardiopulmonary bypass. This study examined the effects...
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| Published in: | The Annals of thoracic surgery Vol. 72; no. 3; pp. 845 - 849 |
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| Main Authors: | , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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01-09-2001
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| Abstract | Background. Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in arterial carbon dioxide tension (PaCO
2) can reduce cerebral embolization during cardiopulmonary bypass. This study examined the effects of brief PaCO
2 manipulations on cerebral embolization in patients undergoing cardiac valve procedures.
Methods. Patients were prospectively randomized to either hypocapnia (PaCO
2 = 30 to 32 mm Hg, n = 30) or normocapnia (PaCO
2 = 40 to 42 mm Hg, n = 31) before aortic cross-clamp removal. With removal of the aortic cross-clamp embolic signals were recorded by transcranial Doppler ultrasonography for the next 15 minutes.
Results. Despite significant differences in PaCO
2, groups did not differ statistically in total cerebral emboli counts. The mean number of embolic events was 107 ± 100 (median, 80) in the hypocapnic group and 135 ± 115 (median, 96) in the normocapnic group, respectively (
p = 0.315).
Conclusions. Due to the high between-patient variability in embolization, reductions in PaCO
2 did not result in a statistically significant decrease in cerebral emboli. In contrast to experimental studies, the beneficial effect of hypocapnia on cerebral embolization could not be demonstrated in humans. |
|---|---|
| AbstractList | Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in arterial carbon dioxide tension (PaCO2) can reduce cerebral embolization during cardiopulmonary bypass. This study examined the effects of brief PaCO2 manipulations on cerebral embolization in patients undergoing cardiac valve procedures.
Patients were prospectively randomized to either hypocapnia (PaCO2 = 30 to 32 mm Hg, n = 30) or normocapnia (PaCO2 = 40 to 42 mm Hg, n = 31) before aortic cross-clamp removal. With removal of the aortic cross-clamp embolic signals were recorded by transcranial Doppler ultrasonography for the next 15 minutes.
Despite significant differences in PaCO2, groups did not differ statistically in total cerebral emboli counts. The mean number of embolic events was 107 +/- 100 (median, 80) in the hypocapnic group and 135 +/- 115 (median, 96) in the normocapnic group, respectively (p = 0.315).
Due to the high between-patient variability in embolization, reductions in PaCO2 did not result in a statistically significant decrease in cerebral emboli. In contrast to experimental studies, the beneficial effect of hypocapnia on cerebral embolization could not be demonstrated in humans. BACKGROUNDCerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in arterial carbon dioxide tension (PaCO2) can reduce cerebral embolization during cardiopulmonary bypass. This study examined the effects of brief PaCO2 manipulations on cerebral embolization in patients undergoing cardiac valve procedures.METHODSPatients were prospectively randomized to either hypocapnia (PaCO2 = 30 to 32 mm Hg, n = 30) or normocapnia (PaCO2 = 40 to 42 mm Hg, n = 31) before aortic cross-clamp removal. With removal of the aortic cross-clamp embolic signals were recorded by transcranial Doppler ultrasonography for the next 15 minutes.RESULTSDespite significant differences in PaCO2, groups did not differ statistically in total cerebral emboli counts. The mean number of embolic events was 107 +/- 100 (median, 80) in the hypocapnic group and 135 +/- 115 (median, 96) in the normocapnic group, respectively (p = 0.315).CONCLUSIONSDue to the high between-patient variability in embolization, reductions in PaCO2 did not result in a statistically significant decrease in cerebral emboli. In contrast to experimental studies, the beneficial effect of hypocapnia on cerebral embolization could not be demonstrated in humans. Background. Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in arterial carbon dioxide tension (PaCO 2) can reduce cerebral embolization during cardiopulmonary bypass. This study examined the effects of brief PaCO 2 manipulations on cerebral embolization in patients undergoing cardiac valve procedures. Methods. Patients were prospectively randomized to either hypocapnia (PaCO 2 = 30 to 32 mm Hg, n = 30) or normocapnia (PaCO 2 = 40 to 42 mm Hg, n = 31) before aortic cross-clamp removal. With removal of the aortic cross-clamp embolic signals were recorded by transcranial Doppler ultrasonography for the next 15 minutes. Results. Despite significant differences in PaCO 2, groups did not differ statistically in total cerebral emboli counts. The mean number of embolic events was 107 ± 100 (median, 80) in the hypocapnic group and 135 ± 115 (median, 96) in the normocapnic group, respectively ( p = 0.315). Conclusions. Due to the high between-patient variability in embolization, reductions in PaCO 2 did not result in a statistically significant decrease in cerebral emboli. In contrast to experimental studies, the beneficial effect of hypocapnia on cerebral embolization could not be demonstrated in humans. |
| Author | Ipsiroglu, Osman Cook, David J Schima, Heinz Pezawas, Thomas Plöchl, Walter Krenn, Claus G Gollob, Eva Grubhofer, Georg Wollenek, Gregor |
| Author_xml | – sequence: 1 givenname: Walter surname: Plöchl fullname: Plöchl, Walter email: walter.ploechl@univie.ac.at organization: Department of Cardiothoracic and Vascular Anesthesiology and Intensive Care, University of Vienna, Vienna, Austria – sequence: 2 givenname: Claus G surname: Krenn fullname: Krenn, Claus G organization: Department of Cardiothoracic and Vascular Anesthesiology and Intensive Care, University of Vienna, Vienna, Austria – sequence: 3 givenname: David J surname: Cook fullname: Cook, David J organization: Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota, USA – sequence: 4 givenname: Eva surname: Gollob fullname: Gollob, Eva organization: Department of Cardiothoracic Surgery and Ludwig-Boltzmann-Institut For Cardiosurgical Research, University of Vienna, Vienna, Austria – sequence: 5 givenname: Thomas surname: Pezawas fullname: Pezawas, Thomas organization: Department of Cardiothoracic and Vascular Anesthesiology and Intensive Care, University of Vienna, Vienna, Austria – sequence: 6 givenname: Heinz surname: Schima fullname: Schima, Heinz organization: Department of Cardiothoracic Surgery and Ludwig-Boltzmann-Institut For Cardiosurgical Research, University of Vienna, Vienna, Austria – sequence: 7 givenname: Osman surname: Ipsiroglu fullname: Ipsiroglu, Osman organization: Department of Pediatrics, University of Vienna, Vienna, Austria – sequence: 8 givenname: Gregor surname: Wollenek fullname: Wollenek, Gregor organization: Department of Cardiothoracic Surgery and Ludwig-Boltzmann-Institut For Cardiosurgical Research, University of Vienna, Vienna, Austria – sequence: 9 givenname: Georg surname: Grubhofer fullname: Grubhofer, Georg organization: Department of Cardiothoracic and Vascular Anesthesiology and Intensive Care, University of Vienna, Vienna, Austria |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11565668$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1016/S0022-5223(19)35735-6 10.1016/0003-4975(95)00096-4 10.1016/S0003-4975(97)80352-9 10.1016/0003-4975(91)90793-P 10.1016/S0003-4975(99)01327-2 10.1016/0003-4975(89)90668-1 10.1161/01.STR.28.4.692 10.1016/S0003-4975(10)64768-6 10.1016/S0022-5223(19)35633-8 10.1056/NEJM199612193352501 10.1161/01.STR.31.3.707 10.1161/01.STR.28.10.1988 10.1152/ajplegacy.1964.206.1.25 10.1161/01.STR.27.1.87 10.1016/0003-4975(95)00236-E 10.1016/S0022-5223(96)70230-1 10.1136/bmj.291.6506.1384 10.1016/S0022-5223(95)70386-1 10.1097/00000542-199711000-00009 10.1016/S0003-4975(10)62077-2 10.1161/01.STR.25.7.1393 10.1097/00000542-199901000-00024 |
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| Snippet | Background. Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that... Cerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions in... BACKGROUNDCerebral embolization is a major cause of central nervous dysfunction after cardiopulmonary bypass. Experimental studies demonstrate that reductions... |
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| SubjectTerms | Carbon Dioxide - blood Cardiopulmonary Bypass - adverse effects Cerebrovascular Circulation Echocardiography, Transesophageal Female Humans Hypocapnia Intracranial Embolism - blood Intracranial Embolism - diagnostic imaging Intracranial Embolism - etiology Intracranial Embolism - prevention & control Male Middle Aged Monitoring, Intraoperative Ultrasonography, Doppler, Transcranial |
| Title | Can hypocapnia reduce cerebral embolization during cardiopulmonary bypass? |
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