The EACTAIC Education Committee has organised the seminar episode in collaboration with the University of Bern, Bern, Switzerland.
The University of Bern, Bern, Switzerland, supported this seminar episode.
What’s in it for me?
After participating in this seminar episode, you will better understand:
The evidence supports the preferred intraoperative Fraction of inspired oxygen during cardiac surgery.
The changes in cerebral flow during antegrade cerebral perfusion.
Red blood cells (RBCs) transfusion threshold for cardiac surgery.
The values of intraoperative TEE reassessment of preoperative echocardiographic findings to guide the right surgical decision for cardiac surgery.
Take Home Message:
Moderation:
A. Kauert-Willms / G. Erdoes, MD, PhD
Programme:
Time
Topic
Speaker
18.00 – 18.15
How much is just fine with fraction of inspired oxygen?
D. Günsch
18.15 – 18.30
How much is just fine with cerebral flow during antegrade cerebral perfusion?
A. Levis
18.30 – 18.45
How much is just fine with RBC transfusion?
D. Gerber
18.45 – 19.00
How much is just fine with Intraoperative reassessment of preoperative echocardiography findings?
T. Hirschi
19.00 – 19.30
Open Discussion
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In contrast to O2, CO2 is a coronary vasodilator like in the cerebrovascular system. We only studied short time effects, and COPD GOLD III and higher was among the exclusion criteria for this study. However, there is little data if the relationship of coronary blood flow and chronic paO2 and paCO2 deflections re-equilibrates if chronic. Importantly, it is known that hypoxemia and hypercapnia have synergistic effects, one could think that hyperoxia and hypercapnia have competeing effects. Importantly, there is a paper of our group that has just been accepted for publication, that you will be able to read soon in Frontiers in Anaesthsiology by Fischer et al. The data presented in this manuscript demonstrate that hyperoxia does not only cause vasoconstriction, but also blunts the vasodilatory reflex to a paCO2 increase. This however is an animal model but we onyl have little data in a patient setting so far.
TAPSE was obtained by anatomic M-Mode from the RV-cenetered ME 4CH-view.
No, these were TEE images. However, in some of the tools in TOMTEC arena, the images need to be flipped to allow for analysis of TEE images. Maybe this may have caused confusion.
All the steady measurements occurred bevore CPB. There are many factors that lead to diastolic dysfunction, with ischemia being an important one. But alone cardioplegia, transcient edema and cooling can be important contributors to diastolic dysfunction post CPB. In my experience some ventricles seems quite "stiffer" already visually, but usually that alleviates with prolonged reperfusion time. So in my oppinion, attributing diastolic dysfunction post CPB solely to ischemia would be too limited. When assessing ischemia post-CPB I would at the moment refrain to systolic measures. Systolic strain may be a very sensitive marker. But we definitely need more data in this field with newer measurements.
There are plenty of studies that demonatrate that hyperoxia in the setting of ischemia-/reperfussion injury leads to increased ROS and therefore more cellular injury and damage (apoptosis and necrosis) and immune responses triggering capillary leak and interstitial and cellular edema. It has been shown in quite a few studies that reduction of oxygen partial pressure attenuates the I/R injury. But I don't think these principles are widely applied in clinical practice. But importantly, our study focussed on outcome parameters before incision and CPB/cardioplegia.
TEE assessment were taken before incision to avoid sympathetic responses to surgerical stimuli and altered hemodynamics with an open chest as a confounder. Importantly, we wanted this study to also be applicable for patients with CAD undergoing non-cardiac surgery. The study intervention an observation was completed when the final image was obtained before incision. But of course this is an important question and should prompt studies to look at the role of intra-OP FiO2 and outcome through the intire surgery and post-OP period.
No, this can also be seen in studies where paO2 was lowered to 70-80mmHg. There is indirect evidence in an early study by us from 2013 and there will be data coming out that has direct coronary flow measurements showing this effect soon in Frontiers in Anaesthesiology by Fischer et al (article accepted for publication)
Yes. With cannulation of right subclavian artery we use approx. 1L/m after clamping of the Truncus for ACP. If ICA left and left subclavian artery are additionaly cannulated, we use another 600-800ml/min over for both togheter. To my knowledge, there are no data on what specific flow rate should be aimed for for every of those cannulation strategies.
We start with 100% FiO2 and titrate it down, with the goal of PaO2 not exceeding 150-200mmHg (in order to prevent formation of free oxygen species). The FiO2 can often be reduced to 30%. It is important not to forget increase it to 100% before the end of circulatory arrest in order to sufficiently oxygenize the ischemic blood coming from the lower body.
We primarily aim for a certain flow rate when ACP is started and closely watch the NIRS. In our experience, if there is a short interruption of cerebral blood flow, the NIRS drops significantly even in the short period before ACP is installed (for example when the aorta is cannulated directly and ACP is imitated through ICA when already in HCA; in case of subclavian cannulation with clamping of the Truncus brachiocephalicus it might not fall at all). After ACP is installed NIRS should raise again and reach pre-HCA values within minutes. If this is not the case we would start to identify possible causes and solutions, including a higher flowrate. In our experience, increasing flow rate to significantly higher levels is often limited by the pressure limit we agreed upon for safety reasons, and repositioning of a cannula in case there is increased resistance is of more help, as well as avoiding hyperventilation, anemia etc.
For acute aortic dissection and elective cases involving total arch we aim for 26° C body temp (usually bladder) and use 20° perfusate for ACP. For elective hemiarch procedures we aim at 28°C. Newer techniques with higher core temperatures and beating heart are an interesting evolution, but not yet routinely used at our center.
Our goal of 8-10ml is the standard for moderate hypothermia at 26-28°C, and most literature with comparable flow rates includes deep to moderature temperature management (20-28°C). In general, a 10 degree drop in temperature would reduce metabolic activity 50%.
A very interesting option. In literature, the trend in MCAFV is a valuable monitor tool (rather than absolute values), but has been abandoned by many centers in the past years due to failing to obtain a window (up to 20% of patients) and challenges in handling (experience of personel, dislocation during procedure etc). We don’t use it routinely to guide ACP but in the context of studies including embolic load. In the future, investigation of cerebral autoregulation during cardiopulmonary bypass and ACP, including, TCD, is an interest of ours.
For PaO2 and TCD see question above. ACP is taken from the CPB with the same transfusion limits as for the whole case.
To my knowledge, evidence on this issue is weak. Aiming for a higher haematocrit for patients at risk of injuries makes intuitive sense and has been propagated by many clinicians. As shown in the webinar, at least for myocardial infarction with already evident malperfusion of the myocardium, this approach could not be confirmed in randomized controlled studies. Until better studies are published, we have to balance longstanding expert opinions here against a robust trend in the data, showing that restrictive transfusions are usually safe. The target of 34% seems very high and it seems very probable, that a target of 28% would be already high enough.
When looking retrospectively at data, transfusions are a quality marker, for sure. But for those dealing with bleeding, instable patients, the "restrictive versus liberal"-question is relevant, as it provides some evidence on when a transfusion is appropriate. But this is exactly why I propose benchmarking and monitoring here, because the transfusion incidence (albeit with many complex interactions) can serve as a quality marker.
Yes, I would suggest taking DO2 in account whenever deciding on transfusions, and not to rely solely on haemoglobin levels. It's use has not been validated and due to the low specificity, the combination with other factors seems reasonable for decisions when to transfuse or whether one can tolerate even lower haemoglobin levels than 7g/dl. The influence of transfusions on DO2 has been questioned, as there are there are concerns that the higher viscosity might hamper cardiac output or efficient oxygen delivery to tissues. And one last note: in the TRICS III study, incidence of low cardiac output state was not different between liberal and restrictive groups.
We have not implemented this in a fixed manner. But for patients in the range between 7 g/dl and 9g/dl we usually take in account multiple parameters (hemodynamic stability, do you anticipate retransfusions, balance between oxygen delivery and consumption) and often include the age as one factor here.
This is a complex question. For long, different thresholds where recommended for cyanotic versus non-cyanotic lesions, but the evidence is sparse. One good article to read is "Patient Blood Management in Pediatric Cardiac Surgery: A Review" by Cholette Jill in Anesthesia & Analgesia, 2018. Even more than in the adult population, transfusion strategies in paediatric cardiac patients cannot be viewed at isolated from e.g. perfusion management or the management on the ICU. When ensuring adequate oxygen delivery, haematocrit values of 25% on CPB are often reported.
In our center the CV-anaesthesist performs the echo imaging during the cardiac procedures in the OR. This guarantees the surgeon a 24/7 availability of TOE for all cardiac operations and interventions, even for urgent cases. For doubtful decisions we can always ask our echo-specialists from the Cardiology Departement if available and decisions can be made in team.
Talk: How much is just fine with fraction of inspired oxygen? Speaker: Dominik Günsch (Bern, Switzerland) https://youtu.be/f1BSJNIz3pQ
Talk: How much is just fine with cerebral flow during antegrade cerebral perfusion? Speaker: Anja Levis (Bern, Switzerland) https://youtu.be/qD50tP9oj-8
Talk: How much is just fine with RBC transfusion? Speaker: Daniel Gerber (Bern, Switzerland) https://youtu.be/nsnBrX6Tsyw
Talk: How much is just fine with Intraoperative reassessment of preoperative echocardiography findings? Speaker: Trevor Hirschi (Bern, Switzerland) https://youtu.be/tqP6u-O6oxI
