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Ann Thorac Surg 1996;62:231-232
© 1996 The Society of Thoracic Surgeons
DR JOSEPH I. MILLER, JR (Atlanta, GA): First I would like to thank Dr Reed for the excellent presentation and the opportunity of reviewing the manuscript.
Doctor Reed has postulated that right ventricular pump dysfunction defined by a decreased right ventricular ejection fraction occurs after pulmonary resection. I would raise three issues. Clinically what are the implications of the study? I think they can be looked at threefold. In lobectomy, with appropriate physiologic criteria, the effect on right ventricular function of resection probably has little value; I realize that in your manuscript you said that there were only a few of the patients who had undergone pneumonectomy, and I think that is where the real clinical importance of your study probably is. The publication of Kirklin's classic paper on the effect of preload on postpneumonectomy pulmonary edema in 1981 essentially eliminated postpneumonectomy pulmonary edema by fluid restriction in the majority of pneumonectomy patients.
I would like to ask you, what do you think the value of measurement of right ventricular ejection fraction may play in evaluation of the pneumonectomy patient? Also equally important in your study may be the effect of this new and evolving field of lung volume reduction surgery. In this group of patients with advanced generalized emphysema, the majority of surgeons do use certain criteria for pulmonary exclusion based on pulmonary hypertension. It is now known that there are 7 patients who have died of pulmonary hypertension after lung volume reduction despite normal preoperative pressures. I would like to ask you if you have any feeling of where a measurement of the ejection fraction might be of help in determining which patients would be suitable for operability either in pneumonectomy or in this lung volume reduction group.
DR REED: Thank you, Dr Miller. I agree with you that I think that a key future area of interest will be looking at the pneumonectomy group. As you noted, we did not have very many patients who underwent pneumonectomy in our past series. We obviously did not believe that we could preload-augment pneumonectomy patients on postoperative day 2. However, with in some cases up to half of the vascular bed being reduced, I suspect that if we studied this group, we would indeed see that right ventricular afterload plays a role.
In regard to that, I think that in patients who have pulmonary hypertension preoperatively, we at least have clearly shown that we can safely administer PGE1 at a low dose. That optimal dose, by the way, is 0.025 µg•kg-1•min-1. What will be more useful, I think, is future drugs that are coming on line, particularly the endothelin receptor antagonists. It looks like we are going to have an oral antagonist, which will be useful because we need to study these groups not only in the intensive care unit setting but in more prolonged settings, and an oral drug will allow us to do this.
So I think a lot more work needs to be done in this area, particularly in the pneumonectomy group, and also looking at whether we can correlate even after lobectomy those patients with particularly severe right ventricular dilatation and the development of postoperative arrhythmias.
DR THOMAS M. EGAN (Chapel Hill, NC): I enjoyed your study because it reminds us that we can always continue to learn things every day from patients whom we operate on.
Do you think it is possible that your changes in right ventricular function are really a reflection of left ventricular dysfunction and septal wall motion abnormalities? Did you look at any of these patients with echocardiography to look at left ventricular function?
DR REED: Many of these patients in the early studies and subsequent studies were screened with echocardiography. We always eliminated any patient from our study who had any hint of left ventricular dysfunction.
DR EGAN: But did you do echocardiography on postoperative day 2 to see what happens to the left ventricle when your right ventricular dysfunction is being documented?
DR REED: No, we did not, and that is a very good suggestion.
DR JOSEPH LoCICERO III (Boston, MA): Doctor Reed, this was an excellent presentation and really a very difficult study to do. Studying these patients on postoperative day 2 is fraught with all kinds of problems, of course.
I would just like to make a couple of observations. Ventricular stroke work index is a rate-dependent variable, and we know that the things you listed in addition to that rate are important determinants of right or left ventricular function. Maybe it would be interesting, if possible, for you to get from your laboratory a single-beat determinant of work. There are ways to do this. It is not necessarily easy to do. In conjunction with that, were any of your patients receiving calcium-channel blockers or other agents that might have affected their heart rate? We have found from our laboratory that PGE1, even under constant infusion, is affected by calcium flux in the pulmonary artery. Finally, concerning rate, did any of your patients go into supraventricular tachycardia, whether during this study or postoperatively after your study?
DR REED: First of all, none of these patients were receiving calcium-channel blockers. None of them required any afterload support in the postoperative period.
DR LoCICERO: Did any go into supraventricular tachycardia even at postoperative day 2 or later?
DR REED: In our previous studies we have correlated dysfunction with tachyarrhythmias, particularly atrial fibrillation. There is a trend. Those patients who have more severe dysfunction postoperatively are those patients who are most likely to have an arrhythmia.
Related Article
Ann. Thorac. Surg. 1996 62: 225-231.
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