| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 2000;70:1521
© 2000 The Society of Thoracic Surgeons
Discussion
DR KIRK R. KANTER (Atlanta, GA): How long would you leave these 4-French catheters in the superior vena cava? Were you not concerned about clotting of the SVC for the subsequent Glenn? Because your experience is now over several years and some of these have come back, have you seen difficulties with clotting of the SVC?
DR HOFFMAN: Almost everyone who hears this sort of presentation asks that. We have not had significant thrombotic complications from these catheters. We avoid neck lines in these patients. We often will have a right atrial catheter also, but we treat these catheters well. We use a heparin flush and do not put a lot of other stuff through them. They are typically in until the chest is closed, which is anywhere from postoperative day 2 to 4.
DR TOM R. KARL (Melbourne, Australia): I would like to thank Dr Hoffman, Dr Tweddell, and colleagues for this interesting study, which I might add was very elegantly presented. I would like also to call attention to some of the previous contributions from this group that have helped us in our understanding of this peculiar physiology in the post-Norwood patients.
To me, the study has followed a protocol that requires active intervention for hemoglobin saturation below 50% in the superior vena cava, even in the presence of otherwise satisfactory physiology. I had an opportunity to review the manuscript in which the authors cite evidence from their own work, and the work of others, that this strategy can improve the outcome of the Norwood operation. And of course, their excellent clinical results would support the routine use of this technology. There may be other factors operative however.
In Melbourne, we looked at a number of clinical and biochemical parameters that might have had predictive value for the appearance of major adverse events in the postoperative period. This study (conducted by Trevor Duke) included, but was not limited to, patients undergoing the Norwood operation. Of eight hemodynamic and biochemical parameters that we examined, including SVC or pulmonary artery hemoglobin saturation, only the mean arterial pressure index and the serum lactate level at various postoperative time points had any predictive value. In fact, in our study, a serum lactate level of 7 mmol/L suggested that there was a 50% probability of a major adverse event in the absence of specific intervention.
So my questions are as follows. (1) Do you think that serum lactate could be useful in this regard as the low cost and technical simplicity and independence of arterial PO2 would make this type of monitoring available to nearly every cardiac unit? (2) Have you looked at elevations in serum lactate level in terms of a correlation with superior vena caval hemoglobin saturation, which might possibly be another indicator that the patient has crossed the threshold of anaerobic metabolism?
Thanks again for a great study and presentation.
DR HOFFMAN: We did not routinely measure lactate. Sometimes when we wanted confirmatory evidence and we thought that things were bad, we would send it. I do not have that data available to present.
You have to suspect a clinical deterioration in order to send the lactate. And we have some pretty good data that the fall in base excess is not exactly time consonant with the fall in venous saturation. As a matter of fact, sometimes it lags by a couple hours.
My reading of the literature suggests that the appearance of lactate in the circulation may reflect more reperfusion than perfusion, and that it is certainly a balance between production of lactate and clearance in the hepatic circulation. So I am not surprised that a high lactate predicts poor outcome. We have tried to intervene before we would get to that point. We are not anticipating routinely measuring lactates in the future.
DR ERLE H. AUSTIN (Louisville, KY): I would like to compliment you on your elegant study and your superb results. I think we all know that the postoperative management of these children is often what makes the difference and has probably been the most important factor in improving survival rates in these patients over the past several years. Our group has also been using mixed venous saturation to monitor these patients and, like you, has found it useful. I was going to ask what Dr Karl asked about whether you had used lactate measurements. We have found serum lactates useful in following these children.
Would you tell us how you use this information (major decreases in mixed venous O2) in your management. You briefly mentioned something about altering (what you called) inodilator therapy, but I wonder if you could tell us a little bit more. There are a lot of different things that we have learned to try in patients whose mixed venous saturations drop. What do you use first? And tell us something about your experience with that. Thank you.
DR HOFFMAN: I do not think we have any secrets that other people do not have. One of the things that is not evident from the data as presented is how fast the venous saturation can change, if you have a real-time monitor, in response to your interventions. So in a patient who has a high pulmonary-to-systemic blood flow ratio and low venous saturation, we would tend to use something to induce more reduction in systemic vascular resistance. We have a fair amount of experience in nitroprusside, which we have found is not as helpful as phenoxybenzamine, so we will sometimes start a phenoxybenzamine infusion postoperatively.
We have a little bit of experience modulating blood gases. I would add that hypercapnia also is a systemic vasodilator. So although theoretically induction of hypercapnia raises the pulmonary vascular resistance, it may also be effective by reducing the systemic vascular resistance.
If the venous saturation is low and you have got balanced pulmonary and systemic flow ratios, then you need more inotropic support. Depending on what the other mix is, we use epinephrine or norepinephrine.
The key in our experience, I think, has been an online monitor, which can show tremendously significant changes in what appears to be otherwise stable circulatory status within minutes. Even if you are sending blood gases every 30 minutes, the lactate is not going to change that much. And the arterial blood pressure is relatively constant in our experience until things are really bad.
| ||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
