ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Yoshifumi Naka
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by O’Malley, C. M. N.
Right arrow Articles by Bennett-Guerrero, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by O’Malley, C. M. N.
Right arrow Articles by Bennett-Guerrero, E.

Ann Thorac Surg 2003;75:1886-1891
© 2003 The Society of Thoracic Surgeons


Original article: cardiovascular

Abnormal gastric tonometric variables and vasoconstrictor use after left ventricular assist device insertion

Catherine M. N. O’Malley, FFARCSIa*, Robert J. Frumento, MS, MPHa, Berend Mets, MD, PhDa, Yoshifumi Naka, MD, PhDb, Elliott Bennett-Guerrero, MDa

a Department of Anesthesiology, New York, New York, USA
b Department ofSurgery, Columbia University College of Physicians and Surgeons, New York, New York, USA

Accepted for publication January 10, 2003.

* Address reprint requests to Dr O’Malley, Department of Anesthesiology, Columbia University College of Physicians and Surgeons, 630 West 168th Street, PH5-505, New York, NY 10032, USA.
e-mail: co2001{at}columbia.edu


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Abnormal gastric tonometric variables, a surrogate for splanchnic ischemia, occur in approximately 50% of patients at the end of routine cardiac operations and are associated with postoperative morbidity. We sought to determine whether gastric tonometric variables deteriorate after left ventricular assist device insertion and to explore the association between abnormal gastric tonometric variables and vasoconstrictor use.

METHODS: Nineteen patients who had insertion of a left ventricular assist device were enrolled in a prospective, observational study. Automated air tonometry was used to determine the difference between gastric and arterial partial pressure of carbon dioxide (CO2 gap) at five time points perioperatively.

RESULTS: Compared with baseline, systemic blood flow was significantly increased at the end of operation (1.9 ± 0.6 versus 2.9 ± 0.7 L · min-1 · m-2, p < 0.0001). Tonometric variables, which were normal at baseline, became abnormal in 90% of patients (baseline CO2 gap 4 ± 2 mm Hg versus end of operation CO2 gap 24 ± 15 mm Hg, p < 0.0001). Elevated CO2 gaps correlated with larger doses of norepinephrine (r = 0.69, p = 0.001) and vasopressin (r = 0.88, p < 0.0001). Abnormal gastric tonometric variables at the end of operation correlated with postoperative intensive care unit length of stay (r = 0.70, p = 0.0009) and multiple organ dysfunction score (r = 0.64, p = 0.0033).

CONCLUSIONS: Despite a significant increase in systemic blood flow after left ventricular assist device implantation, abnormal gastric tonometric variables developed and were associated with larger vasoconstrictor dose. These data provide evidence that gastric ischemia can develop independently of changes in systemic blood flow and support the potential role of vasoconstrictors as a cause of splanchnic ischemia.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Cardiac transplantation as a treatment for intractable heart failure has been remarkably successful, but donor organ supply is limited. Consequently, the left ventricular assist device (LVAD) has been developed to provide circulatory support for patients awaiting heart transplantation. However, LVAD insertion is often associated with significant morbidity and mortality. Postoperatively, patients have high incidences of renal failure (53%), hepatic dysfunction (23%), hematologic abnormalities (58%), and right heart failure (12%) [1, 2]. Three-month event-free survival in LVAD recipients is estimated to be approximately 33% [2].

Gastric tonometry involves the measurement of gastric partial pressure of carbon dioxide, which when elevated appears to be a reasonable surrogate for gastric mucosal ischemia [37]. Numerous studies have shown an association between abnormal gastrointestinal tonometric variables and adverse outcome after major operations [815]. In these studies the incidence of abnormal gastric tonometric variables ranged from 25% to 62% [810, 1215]. To date, no published studies have reported gastric tonometric variables in LVAD recipients. This patient population is of particular interest because they have a high incidence of morbidity despite the fact that systemic blood flow rates are usually normal or above normal at the end of operation.

Vasoactive medications have variable effects on splanchnic blood flow as determined by direct blood flow measurement as well as by indirect techniques such as gastric tonometry [16]. The relative influences of low systemic blood flow, blood volume, and vasoconstrictors on gastric tonometric variables are poorly understood. Insertion of an LVAD represents a unique model of normal or supernormal systemic blood flow in patients likely to be receiving vasoconstrictors. Therefore, we hypothesized that despite an increase in systemic blood flow after LVAD insertion, abnormal gastric tonometric values occur and that factors other than systemic blood flow play an important role in the development of gastric mucosal ischemia in patients who undergo LVAD implantation.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Patient selection
The study was approved by the institutional review board, and written, informed consent was obtained from all patients. Nineteen patients who had insertion of a HeartMate left ventricular assist device (Thoratec Corporation, Pleasanton, CA) at Columbia Presbyterian Medical Center (New York, NY) were enrolled in a prospective, observational study. Other unrelated data have been collected on this same group of patients and will be reported elsewhere. Exclusion criteria included age less than 18 years, contraindication to the insertion of an orogastric tube, preoperative cardiac arrest, and preoperative multiple organ failure.

Patient care and monitoring
General anesthesia was induced with midazolam hydrochloride, fentanyl citrate, and etomidate and was maintained with a balanced technique of midazolam hydrochloride, fentanyl citrate, and isoflurane. Standard monitoring was used according to the recommendations of the American Society of Anesthesiology. In addition, an intraarterial catheter, a pulmonary artery catheter, and transesophageal echocardiography were utilized. All operations were performed by the same attending staff, and the same technique of LVAD implantation was used in all study patients. The LVAD was implanted in a preperitoneal pocket created in the abdominal upper left quadrant through an extended midline sternotomy incision. All patients underwent standard, nonpulsatile, moderate hypothermic (32°C) cardiopulmonary bypass with flow rates of 1.8 to 2.4 Lmin-1m.

Gastrointestinal tonometry
After endotracheal intubation, a gastric tonometry catheter (TRIP NGS catheter, Datex-Ohmeda, Tewksbury, MA) was passed through the mouth into the stomach. Catheter position was confirmed by aspiration of gastric contents or auscultation and catheter placement was secured by taping the apparatus to the patient.

The tonometry catheter is a modified nasogastric tube with a semipermeable balloon at the distal end. After insertion into the stomach, air is automatically instilled into the balloon by the Tonocap device (Datex-Ohmeda, Tewksbury, MA). After an equilibration period of at least 10 minutes, the balloon’s contents are automatically withdrawn by the Tonocap, and its infrared analyzer measures the gastric partial pressure of carbon dioxide (PgCO2).

Tonometric measurements were made, and blood was simultaneously sampled for arterial blood gas analysis at the following time points: (1) after induction of general anesthesia and placement of the tonometry catheter (baseline), (2) before initiation of cardiopulmonary bypass (pre-CPB), (3) immediately after the administration of protamine (protamine), (4) 10 minutes after chest closure (chest closure) and (5) after the application of the surgical dressing or on intensive care unit (ICU) admission (end of operation). All arterial partial pressure of carbon dioxide (PaCO2) measurements were corrected for esophageal temperature using an established equation as described by Andritsch and associates [17]. Because PgCO2 is measured from a gaseous medium, it does not require correction for temperature.

The equation PgCO2 - PaCO2 (temperature corrected) was used to calculate the CO2 gap. In contrast to the CO2 gap, the calculated gastric intramucosal pH (pHi) is not specific for the gastrointestinal system and is presented merely for comparison with previously published studies [4, 5, 7]. The pHi was calculated according to the manufacturer’s guidelines (by inserting PgCO2 and the arterial bicarbonate levels into a modified Henderson-Hasselbalch equation). A CO2 gap more than 8 mm Hg [7] and a pHi less than 7.32 [10, 15] are considered to represent abnormal values for these tonometric variables.

Other patient data
Preoperative demographic and hemodynamic data were collected, and the doses of vasoconstrictors administered were recorded. Intraoperative hemodynamic variables were recorded at the same time points as the tonometric variables. Organ function was assessed on postoperative day 3 by using the established multiple organ dysfunction (MOD) score (Table 1). [18] All subjects were followed up postoperatively until heart transplantation, hospital discharge, or death.


View this table:
[in this window]
[in a new window]
 
Table 1. Multi-Organ Dysfunction Scorea

 
Statistics
Data are presented as mean ± standard deviation (median). The primary outcome variable was the CO2 gap at the end of operation. Secondary outcome measures for this study were ICU length of stay and the MOD score. The associations between the primary and secondary outcomes, and between the primary outcome and other end of operation variables, were tested using Pearson’s test of correlation. Multivariate analysis was performed in which systemic blood flow and vasoconstrictor dose were entered as possible predictors and the CO2 gap at the end of operation was considered the primary outcome variable. In addition, perioperative measurements of gastric tonometric and hemodynamic data were compared with baseline values using a paired t test or Mann-Whitney test where appropriate. For the use of vasoactive therapy, proportions were compared using Fischer’s exact test. A p value of less than 0.05 (two tailed) was considered to be statistically significant.


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Nineteen patients were enrolled in this prospective, observational study. Three patients (16%) had undergone a previous cardiac operation. Preoperative characteristics are shown in Table 2. Baseline cardiac index was 1.9 ± 0.6 L · min-1 · m-2. All patients had tonometric values within normal limits at baseline (CO2 gap 4 ± 2 mm Hg, pHi 7.37 ± 0.04).


View this table:
[in this window]
[in a new window]
 
Table 2. Patient Characteristics and Preoperative Data (n = 19)

 
Compared with baseline, systemic blood flow was significantly increased at all study time points after LVAD insertion (Table 3). Despite this increase in systemic blood flow, CO2 gap was increased significantly at all study time points after cardiopulmonary bypass (Table 3). Ninety percent (n = 17) of patients had an increased CO2 gap at the end of operation (24 ± 15 mm Hg; p < 0.0001). Compared with baseline, pHi was significantly decreased at all subsequent time points (Table 3).


View this table:
[in this window]
[in a new window]
 
Table 3. Tonometric Variables and Systemic Blood Flow (n = 19)

 
Mean arterial pressure, heart rate, and pulmonary arterial diastolic pressure did not differ significantly from baseline; however, central venous pressure was elevated at the end of operation (17 ± 5 mm Hg, p = 0.0007) compared with baseline (12 ± 5 mm Hg) (Table 4). The types of vasoactive agents that were administered intravenously to patients preoperatively and at the end of operation are shown in Table 4. Univariate analysis of the association between the end of operation variables and the CO2 gap at the end of operation showed that norepinephrine dose (r = 0.69, p = 0.001) and vasopressin dose (r = 0.88, p < 0.0001) were associated with an elevated CO2 gap (Table 5). Of note, one patient received no vasoconstrictor therapy at the end of operation, and one patient received vasopressin only; all other patients received a norepinephrine infusion with or without a vasopressin infusion. Multivariate analysis confirmed that larger doses of norepinephrine (p = 0.001) or vasopressin (p < 0.0001) were associated with an elevated CO2 gap at the end of operation independent of systemic blood flow.


View this table:
[in this window]
[in a new window]
 
Table 4. Baseline and End of Surgery Hemodynamic Variables and Vasoactive Therapy (n = 19)

 

View this table:
[in this window]
[in a new window]
 
Table 5. Correlation of End of Surgery Variables with CO2 Gap (n = 19)

 
Intensive care unit length of stay was 14 ± 10 (median 10) days. The MOD score on postoperative day 3 was 10 ± 5 (median 10). The CO2 gap at the end of operation was associated with prolonged ICU length of stay (r = 0.70, p = 0.0009) and with a higher MOD score (r = 0.64, p = 0.0033).

Twelve patients were discharged home with a LVAD in place, and 4 patients had successful heart transplantation on the same hospital stay. Three patients died in the ICU within 14 days of operation. In comparison to those patients who survived, patients who died had a greater CO2 gap (45 ± 13 mm Hg versus 20 ± 12 mm Hg, p = 0.0044) and a lower pHi (7.12 ± 0.02 versus 7.19 ± 0.08 mm Hg, p < 0.0001).


    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Splanchnic ischemia is associated with the development of systemic inflammatory response syndrome, multiple organ dysfunction syndrome, and multiple organ failure [6, 19]. Possible mechanisms for the role of gut hypoperfusion in the pathogenesis of these complications include leakage of bacterial endotoxin across the gut wall into the systemic circulation and ischemia-reperfusion injury [6, 9]. The only Food and Drug Administration–approved monitor of the gastrointestinal tract is gastric tonometry, which provides a surrogate for the adequacy of splanchnic perfusion. An elevated CO2 gap is considered indicative of an imbalance between gastric perfusion, metabolism, and alveolar ventilation [7] and is believed to be the most accurate reflection of splanchnic ischemia [4, 5, 7], with a gap of more than 8 mm Hg considered abnormal [7, 11, 14]. Consistent with other studies, we focused on the end of operation time period for the assessment of gastric tonometric data [8, 11, 15].

It has been previously shown that abnormal gastric tonometric variables occur in approximately 50% of patients who had routine cardiac operations [810]. We found that despite a marked improvement in systemic blood flow, gastric tonometric variables worsened after insertion of the LVAD in 90% of patients. The PgCO2 and CO2 gap values were increased at all time points after LVAD implantation despite the maintenance of normal or supernormal systemic blood flow.

It might be expected that splanchnic ischemia would be more common in individuals who had LVAD insertion, as this procedure is considered to carry higher risk than routine cardiac surgery. However, all of the patients in this study had a normal CO2 gap before commencement of the operation. This finding is compatible with the results of other studies [20] and with data from elective cardiac surgical patients at our institution. In 42 patients who had routine coronary artery bypass grafting with or without valve operation using cardiopulmonary bypass at this institution, baseline CO2 gap was 4.3 ± 6.8 mm Hg in association with a cardiac index of 2.2 ± 0.6 L · min-1 · m-2. In particular, patients who had an uncomplicated postoperative course had a baseline CO2 gap of 4.0 ± 7.8 mm Hg in association with a cardiac index of 2.1 ± 0.6 L · min-1 · m-2 (versus 1.9 L · min-1 · m-2 in LVAD recipients). These findings indicate that gastric tonometric variables may be normal despite a relatively low cardiac output and, in the case of LVAD recipients, poor overall preoperative clinical status.

In addition, the mean ± standard deviation CO2 gap at the end of operation was 7.5 ± 9.2 mm Hg in patients who had elective operations versus 24 ± 15 mm Hg in LVAD recipients. This occurred even though cardiac output at the end of operation was lower in the routine cardiac surgical patients than in the LVAD recipients (2.4 ± 0.6 L · min-1 · m-2 versus 2.9 ± 0.7 L · min-1 · m-2). These results are consistent with the observation in experimental models and other clinical studies that the splanchnic circulation is more susceptible to the effects of hypovolemia and catecholamines or vasoconstrictors than to isolated low cardiac output.

Several potential mechanisms for the development of gastrointestinal ischemia or elevated CO2 gap during LVAD operation warrant comment. First, hypovolemia may cause a reduction in gastrointestinal blood volume or perfusion or both secondary to reflex splanchnic vasoconstriction [11, 21]. In this study, central venous pressure was higher at the end of operation, which in another patient population might rule out the presence of hypovolemia. In this setting, however, a normal or elevated central venous pressure is not a reliable marker for euvolemia given the presence of right ventricular dysfunction, which is common after LVAD insertion.

Another potential cause of abnormal tonometric variables is poor blood flow to the gastrointestinal tract as a consequence of low cardiac output. Low-flow states may be associated with poor washout of mucosal CO2 leading to an increase in PgCO2. Although there appear to be no studies of the distribution of cardiac output after LVAD insertion in humans, it has been shown in animal models that in circumstances of low systemic flow rates after LVAD insertion, gastrointestinal blood flow is compromised [22, 23]. In our study, the abnormal changes in CO2 gap occurred despite the marked increase in systemic blood flow that occurred after LVAD insertion. This finding suggests that the etiology of abnormal gastric tonometric variables may be independent of global systemic flow in LVAD recipients.

Indeed, our data suggest that redistribution of blood flow away from the gastrointestinal tract or maldistribution of flow at the microcirculatory level may result from the administration of vasoactive drugs commonly used perioperatively. Different drugs have variable effects on splanchnic blood volume or blood flow as reflected by changes in tonometric variables and by measurements of gut perfusion [16, 19]. In this study 90% of patients who had LVAD insertion developed abnormal gastric tonometric variables at the end of operation, and there was a strong association between vasopressor dose and CO2 gap. High doses of vasoconstrictor medications are not generally required after routine cardiac operation but are common in LVAD recipients [24]. Therefore, the administration of high doses of norepinephrine and vasopressin might explain, at least in part, the finding of abnormal gastric tonometric variables in our study patients that are not seen in elective cardiac surgical patients. It is important to note that this observational study cannot definitively prove a causal relationship. Furthermore, we cannot rule out other contributing factors. For example, it is possible that the systemic vasodilator response observed after LVAD implantation, which necessitates the administration of vasoconstrictors, may itself contribute to the development of abnormal gastric tonometric variables. Only a prospective, randomized, clinical trial can demonstrate the cause of abnormal gastric tonometric variables (and presumably splanchnic ischemia) in LVAD recipients.

One might question the clinical relevance of abnormal gastric tonometric variables, particularly the CO2 gap. However, numerous studies in cardiac [811], vascular [12], and general surgical patients [1315] have demonstrated that abnormal gastrointestinal tonometric variables are strong predictors of postoperative complications and prolonged hospital stay. Furthermore, interventions that improve gastric tonometric variables may improve outcome after cardiac operation [11]. Another novel finding of our study is that gastric hypercarbia and an elevated CO2 gap at the end of operation were associated with a prolonged ICU length of stay and a high MOD score in patients who had LVAD insertion. The ICU length of stay has been used as an outcome measure in other studies of gastric tonometry and outcome in surgical patients [1114] and is an important determinant of resource utilization. The MOD score, although not specifically validated in LVAD recipients, is a direct measure of organ dysfunction and morbidity and is associated with long-term clinical outcome [18]. The association between abnormal gastric tonometric variables and morbidity in LVAD recipients, demonstrated by our findings, has not been previously reported.

This study is subject to some potential limitations. This investigation was designed as a prospective, observational study and as such is limited by the lack of a control group. However, we have presented data from other cardiac surgical patients at our institution. Although these data are not eligible for statistical analysis, they are useful for comparison. It is reassuring that baseline gastric tonometric variables and cardiac output were comparable between our study patients and elective cardiac surgical patients. Furthermore, the difference in gastric tonometric variables between LVAD recipients and patients who had routine cardiac operation at the end of operation supports the view that the splanchnic circulation is more susceptible to the effects of hypovolemia and catecholamines or vasoconstrictors than to isolated low cardiac output.

Another potential limitation is that this was a single-center study; therefore these findings cannot be strictly generalized to other cardiac surgical centers. However, outcome data after LVAD insertion at our institution compare favorably with the results from other centers [25]. A further theoretical source of error is the fact that the research coordinator responsible for the collection of perioperative data was not blinded to the tonometric measurements. This is unlikely to account for the highly significant associations observed between tonometric variables and other outcomes and is an unlikely source of bias for several reasons. We used an automated technique of tonometry leaving little room for observer bias. Additionally, perioperative care could not have been affected by measurements of tonometric variables because all clinicians were blinded to the tonometric data.

Our findings in patients who had LVAD implantation demonstrate that abnormal gastric tonometric variables (and presumably splanchnic ischemia) may develop despite adequate cardiac output and systemic blood flow and are associated with higher doses of vasoconstrictors. The development of an elevated CO2 gap at the end of operation predicts prolonged ICU length of stay and a high postoperative MOD score in these patients, which supports a role for the gut in the pathogenesis of postoperative organ dysfunction.


    Acknowledgments
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Financial support for this study was provided from departmental sources.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Bank A.J., Mir S.H., Nguyen D.Q., et al. Effects of left ventricular assist devices on outcomes in patients undergoing heart transplantation. Ann Thorac Surg 2000;69:1369-1374.[Abstract/Free Full Text]
  2. Oz M.C., Argenziano M., Catanese K.A., et al. Bridge experience with long-term implantable left ventricular assist devices. Are they an alternative to transplantation?. Circulation 1997;95:1844-1852.[Abstract/Free Full Text]
  3. Mythen M.G., Webb A.R. The role of gut mucosal hypoperfusion in the pathogenesis of post-operative organ dysfunction. Intensive Care Med 1994;20:203-209.[Medline]
  4. Schlichtig R., Mehta N., Gayowski T.J. Tissue-arterial PCO2 difference is a better marker of ischemia than intramural pH (pHi) or arterial pH-pHi difference. J Crit Care 1996;11:51-56.[Medline]
  5. Vincent J.L., Creteur J. Gastric mucosal pH is definitely obsolete–please tell us more about gastric mucosal PCO2. Crit Care Med 1998;26:1479-1481.[Medline]
  6. Bennett-Guerrero E. Systemic inflammation. In: Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac anesthesia. Philadelphia: W.B. Saunders, 1998:297–318
  7. Chapman M.V., Mythen M.G., Webb A.R., Vincent J.L. Report from the meeting: Gastrointestinal Tonometry: State of the Art. 22-23 May 1998, London, UK. Intensive Care Med 2000;26:613-622.[Medline]
  8. Bennett-Guerrero E., Panah M.H., Bodian C.A., et al. Automated detection of gastric luminal partial pressure of carbon dioxide during cardiovascular surgery using the Tonocap. Anesthesiology 2000;92:38-45.[Medline]
  9. Hamilton-Davies C., Barclay G.R., Cardigan R.A., et al. Relationship between preoperative endotoxin immune status, gut perfusion, and outcome from cardiac valve replacement surgery. Chest 1997;112:1189-1196.[Abstract/Free Full Text]
  10. Fiddian-Green R.G., Baker S. Predictive value of the stomach wall pH for complications after cardiac operations: comparison with other monitoring. Crit Care Med 1987;15:153-156.[Medline]
  11. Mythen M.G., Webb A.R. Perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 1995;130:423-429.[Abstract/Free Full Text]
  12. Pargger H., Hampl K.F., Christen P., Staender S., Scheidegger D. Gastric intramucosal pH-guided therapy in patients after elective repair of infrarenal abdominal aneurysms: is it beneficial?. Intensive Care Med 1998;24:769-776.[Medline]
  13. Theodoropoulos G., Lloyd L.R., Cousins G., Pieper D. Intraoperative and early postoperative gastric intramucosal pH predicts morbidity and mortality after major abdominal surgery. Am Surg 2001;67:303-308.[Medline]
  14. Mythen M.G., Webb A.R. Intra-operative gut mucosal hypoperfusion is associated with increased post-operative complications and cost. Intensive Care Med 1994;20:99-104.[Medline]
  15. Mythen M.G., Purdy G., Mackie I.J., McNally T., Webb A.R., Machin S.J. Postoperative multiple organ dysfunction syndrome associated with gut mucosal hypoperfusion, increased neutrophil degranulation and C1- esterase inhibitor depletion. Br J Anaesth 1993;71:858-863.[Abstract/Free Full Text]
  16. Silva E., DeBacker D., Creteur J., Vincent J.L. Effects of vasoactive drugs on gastric intramucosal pH. Crit Care Med 1998;26:1749-1758.[Medline]
  17. Andritsch R.F., Muravchick S., Gold M.I. Temperature correction of arterial blood-gas parameters: a comparative review of methodology. Anesthesiology 1981;55:311-316.[Medline]
  18. Marshall J.C., Cook D.J., Christou N.V., Bernard G.R., Sprung C.L., Sibbald W.J. Multiple organ dysfunction score: a reliable descriptor of a complex clinical outcome. Crit Care Med 1995;23:1638-1652.[Medline]
  19. Ackland G., Grocott M.P., Mythen M.G. Understanding gastrointestinal perfusion in critical care: so near, and yet so far. Crit Care 2000;4:269-281.[Medline]
  20. Boldt J., Brosch C., Suttner S., Piper S.N., Lehmann A., Werling C. Prophylactic use of the phospodiesterase III inhibitor enoximone in elderly cardiac surgery patients: effect on hemodynamics, inflammation, and markers of organ function. Intensive Care Med 2002;28:1462-1469.[Medline]
  21. Hamilton-Davies C., Mythen M.G., Salmon J.B., Jacobson D., Shukla A., Webb A.R. Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Med 1997;23:276-281.[Medline]
  22. Miyama M., Dihmis W.C., Deleuze P.H., et al. The gastrointestinal tract: an underestimated organ as demonstrated in an experimental LVAD pig model. Ann Thorac Surg 1996;61:817-822.[Abstract/Free Full Text]
  23. Uozaki Y., Dihmis W.C., Yamauchi H., et al. Intestinal tissue oxygenation and tumor necrosis factor-alpha release during systemic blood flow changes in pigs with left ventricular assist devices. Artif Organs 2001;25:53-57.[Medline]
  24. Mets B. Anesthesia for left ventricular assist device placement. J Cardiothorac Vasc Anesth 2000;14:316-326.[Medline]
  25. DeRose J.J., Jr, Umana J.P., Argenziano M., et al. Implantable left ventricular assist devices provide an excellent outpatient bridge to transplantation and recovery. J Am Coll Cardiol 1997;30:1773-1777.[Abstract]



This article has been cited by other articles:


Home page
Anesth. Analg.Home page
J. A. DiNardo
Phenoxybenzamine Is Indicated in Treatment of Hypoplastic Left Heart Syndrome: Con
Anesth. Analg., August 1, 2007; 105(2): 310 - 311.
[Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Yoshifumi Naka
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by O’Malley, C. M. N.
Right arrow Articles by Bennett-Guerrero, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by O’Malley, C. M. N.
Right arrow Articles by Bennett-Guerrero, E.


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