ANESTHESIOLOGY AND PAIN MANAGEMENT 1. Kelley SD, Ramsay MA. Respiratory rate monitoring: characterizing performance for emerging technologies. Anesth Analg 2014;119(6): 1246–1248. 2. Kudenchuk PJ, Brown SP, Daya M, Morrison LJ, Grunau BE, Rea T, Aufderheide T, Powell J, Leroux B, Vaillancourt C, Larsen J, Wittwer L, Colella MR, Stephens SW, Gamber M, Egan D, Dorian P; Resuscitation Outcomes Consortium Investigators. Resuscitation Outcomes Consortium-Amiodarone, Lidocaine or Placebo Study (ROC-ALPS): Rationale and methodology behind an out-of-hospital cardiac arrest antiarrhythmic drug trial. Am Heart J 2014;167(5):653–659.e4. 3. Ramsay M. Breathing is good. J Clin Monit Comput 2014 Jul 26 [Epub ahead of print]. 4. Ramsay M. Listening to breathing again! J Clin Monit Comput 2014; 28(6):559–560. 5. Ramsay M. Th e biological cost of the depression of consciousness. Revista Colombiana de Anestesiologia 2014 Dec 13 [Epub ahead of print]. 6. Ramsay MAE, Newman KB, Jacobson RM, Richardson CT, Rogers L, Brown BJ, Hein HAT, De Vol EB, Daoud YA. Sedation levels during propofol administration for outpatient colonoscopies. Proc (Bayl Univ Med Cent) 2014;27(1):12–15. 7. Ramsay MAE, Newman KB, Leeper B, Hamman BL, Hebeler RF Jr., Henry AC, Kourlis H Jr., Wood RE, Stecher JA, Hein HAT. Dexmedetomidine infusion for analgesia up to 48 hours after lung surgery performed by lateral thoracotomy. Proc (Bayl Univ Med Cent) 2014;27(1):3–10. 8. Stiell IG, Brown SP, Nichol G, Cheskes S, Vaillancourt C, Callaway CW, Morrison LJ, Christenson J, Aufderheide TP, Davis DP, Free C, Hostler D, Stouff er JA, Idris AH; Resuscitation Outcomes Consortium Investigators. What is the optimal chest compression depth during outof-hospital cardiac arrest resuscitation of adult patients? Circulation 2014;130(22):1962–1970.

Study Objective: The objective of this study was to examine the utility of the transesophageal echo-Doppler device in evaluating hemodynamic changes during laparoscopic cholecystectomy.Design: This was a prospective, controlled, observational open study.Setting: The study took place in a university hospital.Patients: Twenty patients with ASA physical statuses II and III undergoing laparoscopic cholecystectomy were enrolled into the study.Interventions and Measurements: A standardized general anesthetic and surgical technique was used for all patients. Similar depth of hypnosis (using bispectral index monitoring) was maintained in all patients. Hemodynamic parameters including mean arterial pressure (MAP), cardiac index (CI), left ventricular (LV) ejection time interval indexed to the heart rate, maximum acceleration, peak velocity, and systemic vascular resistance (SVR) were recorded at predetermined intervals: before incision, after peritoneal CO2 insufflation and head-up tilt, every 10 minutes thereafter, and after deflation of the abdomen and return to supine position.Main Results: The transesophageal echo-Doppler probe placement was achieved in 3 to 5 minutes in all patients, and the probe position was maintained after creation of pneumoperitoneum and change in positioning. Induction of pneumoperitoneum and head-up tilt resulted in a significant increase in MAP and SVR (P <.05) that remained higher until deflation. The CI, LV ejection time interval indexed to the heart rate (a measure of LV filling), and maximum acceleration (a measure of contractility and global ventricular function) remained stable.Conclusions: The transesophageal echo-Doppler device can be used during laparoscopic cholecystectomy. The LV function, as determined by measurement of CI and maximum acceleration, was preserved during laparoscopic cholecystectomy despite significant increases in afterload (ie, MAP and SVR). (c) 2005 Elsevier Inc. All rights reserved.

Medical College of Wisconsin and Zablocki VA Medical Center, Milwaukee, Wisconsin. tjebert@mcw.eduI believe Dr. Mychaskiw and Dr. Badr indicate four areas of concern in their Letter to the Editor. The first relates to the clinical choice of using extremely high doses of dexmedetomidine, the second refers to case management and oxygen therapy, the third is the perception that the Journal endorses the technique of “off-label” use of dexmedetomidine, and the fourth has to do with my conflict of interest disclosure. I believe the first two concerns are questions about the editorial review process. Clearly, expert reviewers provided sufficient enthusiasm to have the case reports published. I was not involved in the review and cannot comment except on one area of concern; my personal belief is oxygen is generally good for patients, even during spontaneous ventilation.I do wish to comment on the third issue of the Journal’ s perceived “endorsement” of the “off-label” use of dexmedetomidine in the clinical care of several difficult cases. Case reports are meant to “draw attention to important and novel clinical situations, treatments, and complications.” I commend the Journal for asking for expert commentary on the described use of dexmedetomidine with a focus on further education and safety. Without the editorial by Dr. Maze and myself,1the clinician might not have been aware of the “caveats” and “potential side effects of large concentrations of dexmedetomidine” described in detail in our editorial. The concerns we expressed were: 1) reports of apnea from bolus administration of dexmedetomidine in patients with a history of sleep apnea; 2) hypertension, both pulmonary and systemic; and 3) bradycardia. Clearly an endorsement of “off-label” use of dexmedetomidine was not intended or given. However, the off-label use of anesthesia-related drugs is extensive. Consider a careful read of the Food and Drug Administration labeling of drugs such as the use of the antiepileptic drug gabapentin for pain syndromes, dexamethasone for postoperative nausea and vomiting, intrathecal use of fentanyl, meperidine for shivering, and many drugs used in the pediatric population. The list of accepted drug usages that are not supported by Food and Drug Administration labeling is lengthy. With each unapproved use came case reports followed by controversy (e.g. , letters to editors), followed by controlled studies and ultimately accepted practice when the risk:benefit ratio was proven despite package labeling. Finally, Drs. Mychaskiw and Badr express concern with my attestation that I maintain no financial interest or commercial activity in the topic of our editorial and further perceive that I have received “substantial financial support and honoraria” from Abbott Laboratories (Abbott Park, IL). Perhaps a careful review of my income statements would have eliminated their adjective “substantial.” Importantly, Hospira Inc. (Lake Forest, IL) owns and markets dexmedetomidine, and they claim no financial relationship to Abbott Laboratories and are listed as a separate company on the New York Stock Exchange. I have not received research funding from Hospira Inc. and do not speak on their behalf. Previously, Abbott Laboratories had marketed dexmedetomidine; my last support from them for a dexmedetomidine study was in 1999. The volunteer studies I refer to in our editorial were funded in the early 1990s. Based on the lack of support for studies with dexmedetomidine for 5 yr and the absence of speaking on this topic on behalf of Hospira Inc, I stand by the strict interpretation of my attestation at the time of the publication of our editorial.Medical College of Wisconsin and Zablocki VA Medical Center, Milwaukee, Wisconsin. tjebert@mcw.edu

DEXMEDETOMIDINE is a highly selective α 2 adrenoceptor agonist that has sedative and analgesic properties with associated reduction in opioid and anesthetic requirements. 1-11 One significant advantage of dexmedetomidine is that in the clinical dose range there is no respiratory depression. 12-14 The agonistic action on the α 2 adrenoceptors in the sympathetic ganglia modulates the release of catecholamines, resulting in a sympatholytic effect and reports of bradycardia and hypotension. 15-19 As the dose of dexmedetomidine is increased, there is a direct action on the blood vessels causing vasoconstriction and a possible increase in blood pressure. 3,18 This report describes three patients who presented for surgery with potential airway management challenges. Dexmedetomidine was administered to these patients in increasing doses until general anesthesia was attained. The effects of these high doses of dexmedetomidine on respiratory function and hemodynamics are described. The rate of dexmedetomidine infusion was administered based on actual patient body weights.

This case report describes a patient who underwent orthotopic liver transplantation and developed extensive hyperacute venous and arterial intravascular thromboses and thromboemboli intraoperatively. The patient was receiving antifibrinolytic therapy with aprotinin. The safety of routine aprotinin therapy in liver transplantation is examined. The value of the thrombelastograph (TEG) as a qualitative assessment of the coagulation system is emphasized.

Objective We undertook this study to understand the factors at our transplant center that contribute to patients' return to the ICU after their liver transplant and their initial discharge from that unit. Patients who, after liver transplantation, fail discharge from the Intensive Care Unit (ICU) and must be readmitted to that unit may well utilize many more resources than those patients who are well enough to stay out of the ICU. Design A retrospective review of a prospectively maintained liver transplant research database followed by a retrospective review of (a subgroup) patient charts and contemporaneous controls. Setting A large metropolitan tertiary care center and adult liver transplant center. Patients A total of 1,197 consecutive adult patients who underwent their initial liver transplantation from 1984 to 1996. Intervention Readmission to the intensive care unit after adult liver transplantation and discharge from that unit. Main Results Only recipient age, pretransplant synthetic function labs (protime and albumin), bilirubin levels, and intraoperative blood product requirements could be statistically linked to the group requiring ICU readmission. The primary etiology for ICU readmission was cardiopulmonary deterioration. Readmission was associated with significantly lower patient and graft survivals. A detailed review of 23 patients transplanted from October 1994 to June 1996 was made, with special emphasis on cardiopulmonary status (hemodynamics, respiratory variables, and chest radiograph findings). This subgroup was compared with 30 temporally matched controls who were not readmitted to the ICU. Intravascular fluid overload and lower inspiratory capacity were significant factors related to ICU readmission. Readmitted patients had a longer hospitalization with higher hospital charges than the control group. Conclusions We conclude that the most important means of preventing ICU readmission in liver transplantation patients is to optimize cardiopulmonary function and status. Close monitoring of fluid balance to avoid hypervolemia is essential. Readmitted patients have a greater resource utilization and have lower survival rates.

S418 INTRODUCTION: There is evidence that patients with hepatic cirrhosis have elevated levels of exhaled nitric oxide (NO). [1] This study was designed to examine the effect of orthotopic liver transplantation (OLT) on the perioperative concentrations of exhaled NO in patients with end-stage liver disease. METHODS: After IRB approval and informed consent, 4 patients undergoing orthotopic liver transplantation were studied. Exhaled NO concentrations were measured using a rapid response chemiluminescence analyzer (Sievers Instruments Inc. Boulder, Co). A restricted exhaled breath technique was utilized. Contamination by nasopharyngeal NO was excluded by using a constant exhalation pressure of 20 torr and 46 ml/s exhalation flow rate. Initial measurements were taken just prior to induction of anesthesia. Post-transplant measurements were taken daily after completion of surgery with the patient extubated. Laboratory data (PT, AST, ALT) were also obtained to determine if signs of graft dysfunction affected levels of exhaled NO. RESULTS: All patients maintained elevated levels of exhaled NO post-operatively, however, patients 1 and 3 displayed signs of acute cellular rejection. In both of these patients the exhaled NO concentrations peaked at a level above that measured in the preoperative period. Patient 1 increased from 38.4ppb to 49ppb and patient 3 increased from 35.3ppb to 42.3ppb, respectively. See Table 1.Table 1: Exhaled NO Concentrations in extubated OLT patients. (Normal exhaled NO value for a healthy individual [similar]10ppb.)DISCUSSION: Nitric oxide is hypothesized as being the mediator of peripheral vasodilation in patients with cirrhosis. Hepatocytes and Kuppfer cells have been shown to produce excessive amounts of NO in cirrhotic livers [2]. Because NO is thought to be rapidly inactivated by the circulating hemoglobin, it is likely that most of the exhaled NO is the result of excessive local production of NO by the lung, rather than the liver. Vascular and bronchial endothelial cells probably produce this NO and that would account for the maintained increased levels of exhaled NO after implantation of a new liver graft. Recent studies, however, have shown that some NO may not be deactivated by hemoglobin but is instead transported as s-nitrosyl hemoglobin [3-4]. This may then be circulated directly to the lungs where it is released as exhaled NO. If this is true, then the liver hepatocyte function could be a component of exhaled NO concentrations. This preliminary data does show some trends of an increase in exhaled NO with early signs of graft dysfunction. Further studies should be able to demonstrate if concentrations of exhaled NO are a reliable marker of graft dysfunction.

(M. A. E. Ramsay) Chief of Anesthesiology, Departments of Anesthesiology and Pain Management, Baylor University Medical Center, and Clinical Professor, University of Texas Southwestern Medical Center.(Spikes) Transplant Anesthesia Fellow, Departments of Anesthesiology and Pain Management, Baylor University Medical Center and the University of Texas Southwestern Medical Center.(East) Attending Staff Cardiologist, Department of Cardiology, Baylor University Medical Center.(Lynch) Respiratory Therapist, Department of Respiratory Medicine, Baylor University Medical Center.(Hein) Attending Staff Anesthesiologist, Departments of Anesthesiology and Pain Management, Baylor University Medical Center, and Clinical Professor, University of Texas Southwestern Medical Center.(K. J. Ramsay) Anesthesia Research Assistant, Department of Anesthesiology and Pain Management, Baylor University Medical Center.(Klintmalm) Director of Transplantation Services, Baylor Institute of Transplantation Services, Baylor University Medical Center.END-STAGE liver disease is associated with a hyperdynamic circulatory state. The pathophysiologic changes include a decreased systemic vascular resistance, an increased cardiac index, and portal hypertension together with the formation of vascular shunts. [1]These changes may be the result of an increased production of NO synthase and the resulting increase in endogenous nitric oxide (NO) causing profound vasodilation. [2]This hypothesis is further supported by the demonstration of an increased concentration of NO in the exhaled breath of patients with severe liver cirrhosis. [3,4]The pathophysiologic changes in the lung may include vascular dilatations, arteriolar wall thickening, and vascular lumen occlusion from thromboembolism. If vascular dilatations predominate in the lung, then hepatopulmonary syndrome (hypoxemia associated with hepatic dysfunction and intrapulmonary vascular shunts) may result. [5]If vascular wall thickening or occlusion predominates, then pulmonary hypertension may develop as a result of increased resistance to blood flow. All three pathologic states have been shown to exist simultaneously. [6]Pulmonary hypertension associated with end-stage liver disease may be found in up to 8.5% of patients presenting for liver transplantation. [7]It may be defined as a mean pulmonary artery pressure (PAP) of greater than 25 mmHg with a normal pulmonary artery occlusion pressure (PAOP) and pulmonary vascular resistance (PVR) of greater than 120 dynes [middle dot] s (-1)[middle dot]-5. [8]Pulmonary hypertension may further be divided into severe (mean PAP > 45 mmHg), moderate (mean PAP > 35 mmHg), or mild (mean PAP > 25 mmHg). [7]Patients with moderate and severe pulmonary hypertension have a reduced 3-year survival after liver transplantation compared to patients presenting with normal or mild pulmonary hypertension. [7]Therefore, we endeavor to reverse pulmonary hypertension before submitting a patient to liver transplantation in an attempt to improve outcome.Our previous experience and other reports have shown that inhaled NO does not reverse pulmonary hypertension associated with liver disease. [9,10]This is not entirely unexpected, because patients with severe cirrhosis have been reported to have increased levels of endogenously produced NO. [3,4]We now describe a patient with produced NO. [3,4]We now describe a patient with end-stage liver disease who responded to inhaled NO on several occasions.This case report describes a patient in whom the combination of inhaled NO and an infusion of epoprostenol were used together to successfully control pulmonary hypertension perioperatively in a patient undergoing liver transplantation.The patient was a 62-yr-old, 60-kg woman with end-stage liver disease as a result of hepatitis C, the Child-Turcotte Pugh Score was 10. A liver biopsy revealed severe cirrhosis, and she had a clinical course or progressive fatigue, muscle wasting, encephalopathy, and asymptomatic esophageal varices. Prothrombin time was 13.2 s, total bilirubin concentration was 1.6 mg/dl, serum aspartate aminotransferase and serum alanine aminotransferase concentrations were 71 IU/l and 55 IU/l, respectively (normal values 5-50 IU/l and 5-40 IU/l). A chest radiograph showed a prominent pulmonary artery and the electrocardiogram (ECG) showed a right-side heart strain pattern. Therefore, echocardiography was performed and revealed evidence of pulmonary hypertension. A right-side heart catheter was placed and a PAP of 63/18 mmHg (mean 38 mmHg), a pulmonary vascular resistance of 527 dynes [middle dot] s-1[middle dot] cm-5, a PAOP of 5 mmHg, and a cardiac output of 4.5 l/min were recorded. After Institutional Review Board approval and informed patient consent, inhaled NO was administered via a face-mask and nonrebreathing circuit from an I-NOvent (Ohmeda, Liberty Corner, NJ) system. Nitric oxide was increased by increments of 10 ppm and at a concentration of 40 ppm inhaled NO, PAPs decreased to 47/13 mmHg (mean 28 mmHg), and the PVR decreased to 383 dynes [middle dot] s (-1)[middle dot] cm-5. The PAOP remained at 5 mmHg, and cardiac output was 4.8 l [middle dot] min-1. At cessation of the trial of NO, PAPs reverted to baseline levels during the next 30 min. The inhaled NO trial was repeated the next day with similar results (see Table 1).An infusion of epoprostenol was then started at 2 ng [middle dot] kg-1[middle dot] min-1and increased to 7 ng [middle dot] kg-1[middle dot] min-1, the highest dose tolerated by the patient because of headaches. Mean PAPs were maintained between 32-35 mmHg before removing the pulmonary artery catheter. The patient received a continuous infusion of epoprostenol for 3 weeks before a donor liver became available. At arrival in the operating room for liver transplantation, PAPs of 46/13 mmHg (mean 29 mmHg), a PVR of 193 dynes [middle dot] s-1[middle dot] cm-5, and a PAOP of 16 mmHg were noted. Inhaled NO was again instituted via a facemask and PAPs further decreased to 40/13 mmHg (mean 24 mmHg), PVR decreased to 176 dynes [middle dot] s-1[middle dot] cm-5, and PAOP decreased to 13 mmHg. Nitric oxide was discontinued and the PAPs returned to baseline levels, but the epoprostenol infusion was continued.At reperfusion of the liver graft, PAPs increased to 46/23 mmHg (mean 34 mmHg), PVR increased to 320 dynes [middle dot] s-1[middle dot] cm-5, and PAOP decreased to 10 mmHg. At the same time, the ST segment on lead II of the ECG was noted to be acutely increased to 5 mm. Inhaled NO at 40 ppm was administered to reverse the pulmonary hypertension, and simultaneously a rapid resolution of the ECG changes was noted. The rest of the procedure was uneventful, and the NO was weaned off with a mild elevation in PAP to a mean pressure of 32 mmHg.Posttransplantation in the intensive care unit, the PAPs remained increased at a mean pressure of 35 mmHg; therefore, the epoprostenol infusion was continued. The patient went home on the tenth postoperative day, still receiving an epoprostenol infusion at 9 ng [middle dot] kg-1[middle dot] min-1. At 3 months postoperatively, the patient was reevaluated by echocardiography and noted to have near-normal PAPs (mean 25 mmHg). A slow weaning of the epoprostenol infusion was commenced.It is intriguing as to why this patient responded to inhaled NO when previous patients with end-stage liver disease have not shown a response. [9,10]However, a single case report showed an intraoperative response to inhaled NO in a patient undergoing liver transplantation who had severe pulmonary hypertension. [11]Inhaled NO may have caused the reversal of an acute pulmonary vasoconstrictive episode after the perfusion of the lung by cold blood from the donor organ. The severe ischemia noted on the ECG may have been the result of acute right-side heart strain caused by a sudden increase in afterload to the right ventricle, although the PVR did not reach previously increased levels. The ischemia may have been induced by coronary vasospasm caused by the placement of the cold donor organ directly beneath the heart. [12]The rapid resolution of this episode may not be related to the NO therapy, or it may have been the result of the reduction in right ventricular afterload by NO. The transport of NO by red corpuscles combined with hemoglobin as S-nitrosohemoglobin and its release of NO on deoxygenation in the coronary artery, causing direct vasodilatation, has been suggested. [13]The concept, that inhaled NO can be delivered to the distant microvasculature, recently has been confirmed in the feline model. [14]The positive preoperative response to inhaled NO in this patient may have been the result of a lack of increased levels of endogenous NO because the typical hyperdynamic circulation of severe liver cirrhosis did not exist in this patient. The measured cardiac outputs were in the normal range and there was mild systemic hypertension. The pulmonary hypertension may have been coincidental to the portal hypertension as opposed to being the result of it, or the patient may have had increased levels of systemic NO but decreased pulmonary microvasculature NO levels. Pulmonary hypertension may represent a collection of disease processes with diverse phenotypic expression and, therefore, differing responses to therapy.An infusion of epoprostenol has been shown as a successful therapy in reducing pulmonary hypertension before liver transplantation. [15]For how long after transplantation should the epoprostenol infusion be maintained is unknown. More severe hypertension continues to develop postoperatively in the majority of patients with severe pulmonary hypertension at the time of transplantation, and the patients die of right ventricular failure over the next 18 months. [7]Whether remodeling of pulmonary arteriolar wall hypertrophy can occur with chronic vasodilator therapy, and over what time period, is an intriguing thought. [16,17]Whether the chronic exposure of the patient to inhaled NO via nasal cannulae would be equally as effective as an infusion of epoprostenol is being explored. [18]The advantage of this technique would be the avoidance of an indwelling intravenous cannula and its associated morbidity.The role of inhaled NO and endogenous NO in endstage liver disease deserves further evaluation. Perhaps, the presence, or absence, of an elevated exhaled NO level may indicate which patients with portopulmonary hypertension will respond to exogenous inhaled NO.

S122 INTRODUCTION: The concentration of nitric oxide (NO) in exhaled breath has been demonstrated to be at increased levels in patients with severe liver cirrhosis [1]. This prospective study investigates the variation in levels of exhaled NO in patients undergoing orthotopic liver transplantation. METHOD: After IRB approval and informed consent, 8 patients with severe liver cirrhosis undergoing orthotopic liver transplantation had intraoperative levels of exhaled NO monitored. A chemiluminecence analyzer (Sievers Inc. Boulder, Co) was utilized and samples were measured from the elbow connector attaching the breathing circuit to the endotracheal tube. Nasopharyngeal produced NO was excluded from the sample by the endotracheal tube. Peak concentrations of NO were recorded during exhalation. RESULTS: See Table 1.Table 1: Peak concentrations for exhaled nitric oxide in patients during three stages of orthotopic liver transplantation.DISCUSSION: The NO measured in the exhaled breath of patients with severe liver cirrhosis may be the result of an increased production of NO by hepatocytes and Kuppfer cells in the liver, where it is then transported to the lungs as s-nitrosyl hemoglobin and released, or it may have originated from the local production of NO in the lungs [2-4]. Both of these pathways may exist together. If the liver is a significant source of this NO production, then the anhepatic phase of the transplant procedure should result in a reduction of exhaled NO levels. In this preliminary study, the trend seen in some patients corroborates this hypothesis. If this finding is confirmed by further investigation then exhaled NO analysis may provide an early indication of liver graft function.

S227 Introduction: The assessment of ventilation in the spontaneously breathing, extubated patient in the postanesthesia care unit (PACU) can be easily misinterpreted. Common observations are, respiratory rate and pattern, level of consciousness, and pulse oximetry. Despite severe hypoventilation, pulse oximetry may continue to record high oxygen saturation in patients who are receiving added O2. Respiratory rate may also correlate poorly with ventilatory depression. End-tidal carbon dioxide (ETCO (2)), which is already routinely monitored in the operating room, may be a more reliable measure of ventilatory status in extubated patients in the PACU. This prospective study evaluates the monitoring of ETCO2 in the PACU in extubated patients. Method: After IRB approval and informed consent, 17 patients who had undergone either carotid artery surgery or major orthopedic surgery were studied. These patients are routinely monitored with an intra-arterial catheter. On arrival in the PACU, ETCO2 was monitored continuously via a nasal cannula. This nasal cannula combined a sampling tube connected to an infra-red ETCO2 analyzer and an oxygen delivery tube (Salter Labs, Arvin, CA). Arterial blood gas samples were taken within 15 minutes once the patient was in the PACU and again 45 min to 1 hour later. Continuous pulse oximetry and vital signs including respiratory rate, pattern, and level of consciousness were recorded. Comparative data was analyzed using a Pearson's Correlation and a Student's t-test. Results: (Table 1)Table 1The poor correlation between ETCO2 and PaCO2 in early recovery was due to the display of multiple zero readings from the ETCO2 monitor. The corresponding pulse oximeter readings were within normal limits (> 95%); an assessment of breathing character revealed a paradoxical pattern with only intermittent nasal flow of expired air. This may be the result of residual anesthetic effects. As recovery continued, the correlation between ETCO2 and PaCO2 showed marked improvement. Conclusion: The lack of correlation between ETCO2 and PaCO2 in early recovery from general anesthesia indicates that careful observation of other clinical signs, such as respiratory pattern and level of consciousness are necessary.

S93 Introduction: Nitric oxide (NO) is used as a selective pulmonary vasodilator in adult cardiac surgery patients with acute pulmonary hypertension and right heart dysfunction. In this study we report on a two-year experience with inhaled NO in patients undergoing cardiac bypass surgery and heart transplantation. This group of patients may encounter acute increases in pulmonary artery pressures (PAP), pulmonary vascular resistance (PVR), right heart dysfunction, and alveolar-arterial gradients, especially on separating from cardiopulmonary bypass. A review of the time taken to wean off the NO was also made. Method: After FDA and IRB approval and informed consent, 24 patients met criteria to receive NO (systolic PAP >or=to 45 mm Hg, PVR > 180 dynes/s/cm5, transpulmonary gradient > 10 mm Hg, and/or right heart dysfunction). Nitric oxide was blended into the ventilatory circuit and monitored at the inspiratory limb of the Y-junction close to the endotracheal tube. Arterial blood gases were analyzed, NO and NO2 concentrations were closely monitored, and hemodynamic parameters were monitored continuously. The time taken to wean off NO was also analyzed and correlated with the duration of NO therapy. Data were analyzed using Student's t-tests and Pearson's correlations. Results: (Table 1 and Table 2)Table 1: HemodynamicsTable 2: Duration of Nitric Oxide TherapyConclusion: Nitric oxide is effective at reversing acute increases in PAP and PVR as well as improving right ventricular performance in select cardiac surgery patients. The amount of time spent on NO therapy correlated significantly with the time required to successfully wean off NO. It is of interest that over 25% of the weaning period is spent on reducing NO from 5ppm to 0ppm.