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Venous obstruction and cerebral perfusion during experimental cardiopulmonary bypass
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Thoraxkirurgi.
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2010 (Engelska)Ingår i: Interactive Cardiovascular and Thoracic Surgery, ISSN 1569-9293, E-ISSN 1569-9285, Vol. 11, nr 5, s. 561-566Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

To investigate the effects on cerebral perfusion by experimental venous congestion of the superior vena cava (SVC) during bicaval cardiopulmonary bypass (CPB) at 34 °C, pigs were subjected to SVC obstruction at levels of 75%, 50%, 25% and 0% of baseline SVC flow at two arterial flow levels (low, LQ, high, HQ). The cerebral perfusion was examined with near-infrared spectroscopy (NIRS), cerebral microdialysis and blood gas analysis. SVC obstruction caused significant decreases in the NIRS tissue oxygenation index (TOI) and in SVC oxygen saturations (P<0.05, both groups), while the mixed venous saturation was decreased only in the LQ group. Sagittal sinus venous saturations were measured in the HQ group and found significantly reduced in response to venous congestion (P<0.05). No microdialysis changes were seen at the group level, however, individual ischemic patterns in terms of concomitant venous desaturation, decreased TOI and increased lactate/pyruvate occurred in both groups. The total venous drainage remained stabile throughout the experiment, indicating increased flow in the inferior vena cava cannula. The results indicate that SVC congestion may impair cerebral perfusion especially in the case of compromised arterial flow during CPB. Reduced SVC cannula flow may pass undetected during bicaval CPB, if SVC flow is not specifically monitored.

Ort, förlag, år, upplaga, sidor
2010. Vol. 11, nr 5, s. 561-566
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:uu:diva-140803DOI: 10.1510/icvts.2010.238535ISI: 000208483300014PubMedID: 20696750OAI: oai:DiVA.org:uu-140803DiVA, id: diva2:384413
Tillgänglig från: 2011-01-10 Skapad: 2011-01-10 Senast uppdaterad: 2017-12-11Bibliografiskt granskad
Ingår i avhandling
1. Cerebral Perfusion and Metabolism during Experimental Extracorporeal Circulation
Öppna denna publikation i ny flik eller fönster >>Cerebral Perfusion and Metabolism during Experimental Extracorporeal Circulation
2011 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Neurologic injuries are major causes of mortality and morbidity after cardiac surgery. This thesis aimed to investigate cerebral metabolism and perfusion abnormalities in pigs during hypothermic circulatory arrest, selective antegrade cerebral perfusion (SACP) and extracorporeal circulation following progressive venous stasis.

Hypothermic circulatory arrest induced a metabolic pattern consistent with overt ischaemia, which was absent following SACP. In contrast, metabolism during SACP was influenced by the perfusate temperature, where a colder perfusate (20 °C) preserved cellular metabolism and membrane integrity better than a warmer perfusate (28 °C).

The minimum SACP flow required to maintain metabolism during hypothermia at 20 °C was investigated with magnetic resonance imaging, protein S100β, near infrared spectroscopy and microdialysis. The findings suggested an ischaemic threshold close to 6 ml/kg/min in the present models. Furthermore, regional differences in perfusion with a hemispheric distribution were apparent at all flow levels and differed from earlier studies where the differences were uniform and followed a neuranatomical pattern.

Venus stasis following superior vena cava congestion produced measurable signs of impaired cerebral perfusion and patterns of cerebral ischaemia were evident in individual animals. As venous pressure increased, the mean arterial pressure stayed more or less unchanged, generating reduced cerebral perfusion pressure and consequently an increased risk of ischaemia, which may impair cerebral perfusion, especially in cases of compromised arterial flow during extracorporeal circulation.

In conclusion, cerebral metabolism and perfusion are influenced by temperature, SACP flow levels and venous congestion. In clinical practice, the regional differences in perfusion during SACP may be of pathogenic importance in focal cerebral ischaemia. Furthermore, the reduced superior vena cava cannula flow may pass undetected during bicaval cardiopulmonary bypass if the superior vena cava flow is not specifically monitored.

Ort, förlag, år, upplaga, sidor
Uppsala: Acta Universitatis Upsaliensis, 2011. s. 85
Serie
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 649
Nyckelord
cerebral perfusion
Nationell ämneskategori
Fysiologi
Forskningsämne
Thoraxkirurgi
Identifikatorer
urn:nbn:se:uu:diva-147486 (URN)978-91-554-8016-5 (ISBN)
Disputation
2011-04-08, Enghovssalen, Hus 50,, Thoraxkliniken, Akademiska Sjukuset, 17185, Uppsala, 13:15 (Svenska)
Opponent
Handledare
Forskningsfinansiär
Vetenskapsrådet
Tillgänglig från: 2011-03-17 Skapad: 2011-02-25 Senast uppdaterad: 2018-01-12Bibliografiskt granskad
2. Cerebral Perfusion during Cardiopulmonary Bypass
Öppna denna publikation i ny flik eller fönster >>Cerebral Perfusion during Cardiopulmonary Bypass
2013 (Engelska)Licentiatavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Impaired superior vena cava (SVC) cannula outflow during cardiopulmonary bypass (CPB) is a frequent issue, often manifested by only marginal changes in routine monitoring parameters. Nevertheless, significant impact on cerebral perfusion may result. When detected, remedial actions involve cannula repositioning, raising the operating table, increasing the mean arterial pressure (MAP) and adding vacuum-assisted venous drainage to the CPB system. Increased venous outflow enables increased arterial flow and thereby also increased MAP and cerebral perfusion pressure (CPP). Although representing a common clinical problem, controlled studies on SVC obstruction are few and the phenomenon has not been satisfactorily characterized. This licentiate thesis is based on two animal studies. The first (I) study describes the effects on cerebral perfusion and oxygen saturation by stepwise SVC cannula obstruction in increments of 25% until fully occluded. The second (II) study describes the effects on CPP and cerebral perfusion of two different strategies for dealing with restricted cerebral venous outflow. In Study I, ten pigs during 34 ºC CPB were examined. The animals were divided into two groups receiving either low CPB blood flow (LQ), or normal CPB blood flow (HQ). Cerebral perfusion and oxygen saturation were monitored by blood gases, near-infrared light spectroscopy (NIRS) of tissue oxygen saturation (TOI), and cerebral micro-dialysis. SVC obstruction caused increased CVP and deteriorated cerebral oxygen saturation parameters, but no metabolic effects were detectable at the group level by the micro-dialysis. However, four of ten animals showed a combined pattern of decreased TOI and SVC oxygen saturation along with increased lactate/pyruvate ratio. The phenomenon appeared in both groups and in connection with both obstruction and release of obstruction, indicating the presence of individual sensitivity to impaired cerebral perfusion. CPB tubing flow measurements revealed that the total venous drainage was preserved even with the SVC completely clamped, indicating that the drainage, but not the CVP elevation, could be fully compensated by the inferior vena cava. In Study II, intracranial pressure monitoring, NIRS, and cerebral laser-Doppler flow measurements were used for surveillance along with blood gases and analysis of the glial cellmarker S100ß in sagittal sinus blood. A SVC obstruction of 75% was applied in order to achieve a distinct CPP reduction in fourteen pigs subjected to 34 ºC CPB. Two randomly assigned strategies for restoration of the CPP were examined; vasopressor treatment (VP)and partial release of obstruction (PR) mimicking a successful repositioning of the SVC cannula. Both strategies successfully restored the CPP to baseline levels, without immediate signs of severe ischemia, although intracranial and central pressures remained elevated in the VP group throughout the experiments. The analysis of S100ß showed no signs of brain damage. In conclusion, SVC congestion may impair cerebral perfusion during CPB. Reduced SVC cannula flow may pass undetected during bi-caval CPB due to a compensatory increase in IVC flow. Experimental SVC obstruction during CPB may reduce the CPP, resulting in impaired cerebral perfusion. Both vasopressor therapy and improved venous drainage can in the short term individually restore the CPP during these circumstances.

Ort, förlag, år, upplaga, sidor
Uppsala: Uppsala University, Department of Surgical Sciences, 2013
Nationell ämneskategori
Anestesi och intensivvård
Identifikatorer
urn:nbn:se:uu:diva-204734 (URN)
Presentation
2013-08-27, Klassrummet, Inst f kir vet, Akademiska sjukhuset, ing 70, Uppsala, 14:00 (Svenska)
Handledare
Tillgänglig från: 2013-08-14 Skapad: 2013-08-09 Senast uppdaterad: 2014-07-24Bibliografiskt granskad
3. Cerebral perfusion during cardiopulmonary bypass with special reference to blood flow
Öppna denna publikation i ny flik eller fönster >>Cerebral perfusion during cardiopulmonary bypass with special reference to blood flow
2015 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Cardiopulmonary bypass (CPB) is an important method that enables open heart surgery. There is a risk of neurological complications, and efforts to minimize those include optimization of the cerebral perfusion during CPB. This thesis focuses on such optimization of flow conditions in case of obstructed venous drainage, carotid stenosis and during selective antegrade cerebral perfusion (SACP).

In a pig model of impaired venous drainage from the superior vena cava (SVC), stepwise obstruction increased the central venous pressure (CVP) and caused impaired oxygenation. Cerebral micro-dialysis revealed ischemic responses in some but not all of the pigs.

Further experiments, using the same model, aimed to restore cerebral perfusion pressure (CPP) reduced by 75% superior venous obstruction. Both vasopressor treatment and increased venous drainage were effective in normalizing the CPP and improving the cerebral oxygenation. The intracranial pressure was elevated in the vasopressor group, but no signs of brain damage were observed.

The arterial flow during CPB can be altered between pulsatile and non-pulsatile profiles. Switching between these modes was performed during CPB in 20 patients with or without carotid stenosis. The effects on cerebral oxygenation and mean arterial pressure (MAP) were examined. The MAP was significantly lowered by pulsatile flow, but the flow profile did not affect the cerebral oxygenation. No differences were seen between patients with or without carotid stenosis.

SACP is used to ensure the cerebral perfusion during deep hypothermic circulatory arrest (HCA). The cerebral blood flow (CBF) was examined using positron-emission tomography (PET) technique in 8 pigs divided into HCA and HCA+SACP groups. The CBF was downregulated by 70% to 0.10 ml/cm3/min by 20°C hypothermia. A pump flow of 6 ml/kg/min preserved the CBF level without signs of cerebral desaturation. The fluorodeoxyglucose (FDG) uptake after re-warming to 37°C was similar after SACP compared with HCA alone.

In conclusion, experimental SVC obstruction may impair the cerebral perfusion. Vasopressors can restore the CPP during SVC obstruction and improve cerebral oxygenation. In patients, pulsatile flow can lower the MAP in absence of effects on the cerebral oxygenation. During experimental HCA, SACP at 6 ml/kg/min can preserve the CBF at 0.10 ml/cm3/min.

Ort, förlag, år, upplaga, sidor
Uppsala: Acta Universitatis Upsaliensis, 2015. s. 61
Serie
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 1108
Nationell ämneskategori
Anestesi och intensivvård
Identifikatorer
urn:nbn:se:uu:diva-248686 (URN)978-91-554-9257-1 (ISBN)
Disputation
2015-06-11, Robergsalen, Ingång 40, 4 tr, Akademiska sjukhuset, Uppsala, 13:15 (Svenska)
Opponent
Handledare
Tillgänglig från: 2015-05-21 Skapad: 2015-04-07 Senast uppdaterad: 2015-07-07Bibliografiskt granskad

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