| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Ann Thorac Surg 2001;72:S2233-S2234
© 2001 The Society of Thoracic Surgeons
a Surgical Service, VA Boston Healthcare System, 1400 VFW Parkway, West Roxbury, MA 02132, USA
e-mail: shukri.khuri{at}med.va.gov
I would like to supplement Dr Khabbaz’s presentation with a discussion related to a very frequently asked question, which Dr Khabbaz did not address in his excellent talk. In fact, the most frequently asked questions about myocardial pH monitoring are the following: When you observe, in the course of a cardiac surgical operation, that the pH in the anterior or posterior wall of the left ventricle is falling to low levels, can you do anything about it? How can you intervene to reverse myocardial acidosis, or even eliminate it all together, in both the anterior and posterior walls of the left ventricle? In the next five minutes, I will try to address both of these questions.
Our group has been measuring myocardial pH in humans since 1982. Since then, we have acquired an experience in intraoperative myocardial pH monitoring based on more than 700 mostly complex, cardiac surgical patients in whom we measured pH continuously, simultaneously in both the anterior and posterior left ventricular walls. In the initial tercile of these patients, we were learning what these measurements meant by simply recording the pH values and correlating them later with clinical events. In this group of patients, we observed frequently progressive acidosis that led to very low levels of myocardial pH during both the period of aortic clamping and the period of reperfusion after aortic clamp release. We did very little then to change these pH levels, since the initial intention had been to characterize the clinical correlates and gain a better understanding of the clinical significance of the pH changes observed.
When it became obvious to us, through a variety of clinical observations and experimental studies, that myocardial acidosis resulted in adverse outcomes, we went through a period of clinical experimentation to explore and devise effective maneuvers that would reverse and prevent the onset of myocardial tissue acidosis intraoperatively. For example, in a patient undergoing an aortic valve replacement and a single saphenous vein CABG to the LAD, a balloon-tipped catheter was inserted into the coronary sinus for cardioplegia delivery. When the aorta was clamped, a bolus of cold blood cardioplegia was given through the aortic root that elicited a rise in myocardial pH in both the anterior and posterior walls. Then the pH in both walls progressively fell as the saphenous vein was being sutured to the LAD. After completing the distal anastomosis, continuous blood cardioplegia was given through the proximal end of the graft, the aortic root was opened, and the aortic valve was excised. The pH in the anterior wall rose to normal levels soon after cardioplegia was administered through the graft to the LAD. However, the pH in the posterior wall continued to fall despite the continuous antegrade and retrograde administration (through the graft to the LAD and through the coronary sinus) of blood cardioplegia at the rate of 200 to 300 mL/min. As the valve was being excised, the pH in the posterior wall fell to an alarming level of 6.0, but in the anterior wall it remained at 7.1. This suggested that the cardioplegic solution was reaching only the anterior wall, and we suspected a steal phenomenon. A Spencer cannula was used to occlude the orifice of the left main coronary artery; and although no cardioplegic solution was administered through it, it affected a marked rise in the posterior pH from 6.0 to 7.0 within 10 minutes from its insertion. This confirmed that before the insertion of the Spencer cannula, the cardioplegic solution that had been administered through the graft to the LAD had been going preferentially proximally to the aortic root, where the resistance was lower than that of the distal vascular bed. Blocking the orifice of the left main forced the cardioplegic solution toward the distal vascular bed and through collaterals to the posterior wall. Our experience has shown that retrograde cardioplegia is more likely to protect the anterior than the posterior wall, although the situation from patient to patient can be very variable. In this particular case, once the orifice of the left main was blocked, the administration of blood cardioplegia continuously through the graft to the LAD alone resulted in normal myocardial pH levels in both the anterior and the posterior walls. Thus, in this particular patient, myocardial protection during the last hour of aortic clamping was achieved by the continuous administration of cold blood cardioplegia at 75 to 100 mL/min, only through the graft to the LAD. The patient defibrillated spontaneously and weaned from cardiopulmonary bypass without inotropic support. Had we not monitored the pH in the posterior wall, and had we not done anything about it, the posterior wall would have been subjected to more than 1 hour of severe acidosis (pH < 6.0) and we probably would have wondered why the patient was not easily weaned from CPB, or why he was having arrhythmias and evidence of ischemia following the release of the aortic clamp. Recent studies, which we will be publishing soon, have clearly shown improved 30-day and long-term postoperative outcomes when the integrated mean pH during the period of aortic clamping is kept at or above pH 6.8. They have also shown that myocardial pH, when measured simultaneously in the anterior and posterior walls of the left ventricle, provides a good presentation of the global acid–base balance in the left ventricular myocardium.
The case I described above illustrates one of a series of maneuvers that we have learned over the years, and that the surgeon can apply to maintain a normal acid–base state in the myocardium in the course of cardiac surgery. Collectively, we refer to these maneuvers as "pH-guided myocardial management," the assumption being that there is no specific myocardial protection technique that consistently and predictably prevents the onset of myocardial acidosis in all patients. Each patient responds differently to the various modalities of cardioplegia administration, in regard to the onset of myocardial acidosis. Yes, we can prevent and reverse the onset of myocardial acidosis during cardiac surgery, but only if we monitor continuously the regional myocardial pH changes and devise our cardioplegia administration (or other protective modalities) accordingly, in real time.
Early in our experience, when we were only monitoring myocardial pH without intervening to change it, we observed that in 50% of the patients, the mean pH during the period of aortic clamping was less than 6.3 in either the anterior or the posterior wall. In contrast, in the latter part of our experience, as we applied and learned more about pH-guided myocardial management, more than 60% of our patients have a mean pH during the period of aortic clamping of 6.8 or greater. We estimate that this percentage will improve further as we learn more about pH-guided myocardial management.
Footnotes
Doctor Khuri discloses that he has a financial relationship with Terumo Cardiovascular Systems, Inc.
This article has been cited by other articles:
|
|
 |
|
  S. F. Khuri, N. A. Healey, M. Hossain, V. Birjiniuk, M. D. Crittenden, M. Josa, P. R. Treanor, S. F. Najjar, D. J. Kumbhani, and W. G. Henderson Intraoperative regional myocardial acidosis and reduction in long-term survival after cardiac surgery J. Thorac. Cardiovasc. Surg., February 1, 2005; 129(2): 372 - 381. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |
