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):
Hideaki Kado
Yosuke Nishimura
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 Nakano, T.
Right arrow Articles by Fusazaki, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakano, T.
Right arrow Articles by Fusazaki, N.
Related Collections
Right arrow Cardiac - other

Ann Thorac Surg 2004;77:908-912
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

The low resistance strategy for the perioperative management of the Norwood procedure

Toshihide Nakano, MDa, Hideaki Kado, MDa*, Yuichi Shiokawa, MDa, Koji Fukae, MDa, Yosuke Nishimura, MDa, Kazuyuki Miyamoto, MDa, Yoshihisa Tanoue, MDa, Hideki Tatewaki, MDa, Naoki Fusazaki, MDb

a Department of Cardiovascular Surgery, Fukuoka, Japan
b Department of Neonatal Cardiology, Fukuoka Children's Hospital, Fukuoka, Japan

Accepted for publication September 5, 2003.

* Address reprint requests to Dr Kado, Department of Cardiovascular Surgery, Fukuoka Children's Hospital, 2-5-1 Tojin-machi, Chuo-ku, Fukuoka 810-0063, Japan
e-mail: kado{at}pluto.dti.ne.jp


   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Comment
 References
 
BACKGROUND: Postoperative course of the Norwood procedure is fragile because of an unstable pulmonary to systemic blood flow ratio caused by fluctuation of systemic and pulmonary vascular resistance.

METHODS: Twenty-seven patients with hypoplastic left heart syndrome who underwent the Norwood procedure from June 1998 to February 2002 were managed with the following low-resistance strategy. Intraoperative high-flow and low-resistance cardiopulmonary bypass was achieved with total avoidance of circulatory arrest and a large dose of chlorpromazine. In weaning from the bypass, pulmonary vascular resistance was maximally decreased by inspired oxygen fraction (100%), inhaled nitric oxide (20 ppm), and nitroglycerin (2 to 4 µg/kg/min). Then pulmonary blood flow was determined by adjusting the systemic to pulmonary shunt. Postoperatively, with continuous infusion of chlorpromazine and nitroglycerin as a systemic and pulmonary vasodilator, the inspired oxygen fraction and inhaled nitric oxide were tapered as the arterial oxygen saturation improved.

RESULTS: In most patients, inhaled nitrous oxide and inspired oxygen fraction were weaned within 3 days. The postoperative course was stable with minimum changes in circulatory and respiratory status for the survivors. Patients were extubated on a median of 6 postoperative days. Early mortality was 11.1% (3 of 27), and none of the patients died of hemodynamic deterioration.

CONCLUSIONS: The low resistance strategy is a simple and useful method for perioperative management of the Norwood procedure, minimizing fluctuation in both pulmonary and systemic vascular resistance and maintaining stable circulatory and respiratory status.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 References
 
Most of the mortality occurs in the early postoperative period in patients with hypoplastic left heart syndrome (HLHS) palliated with the Norwood procedure. The lethal hemodynamic deterioration is mainly attributable to the sudden change in pulmonary to systemic flow ratio (Qp/Qs) [1–3]. Thus, the success of the Norwood procedure largely depends on how appropriately patients are managed in this hazardous period. We herein report our treatment strategy as the intraoperative and early postoperative management of patients who underwent the Norwood procedure.


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 References
 
Twenty-seven patients with HLHS who underwent the Norwood procedure from June 1998 to February 2002 were enrolled in this study. HLHS was defined as normal segmental anatomy, aortic and mitral atresia, or stenosis with hypoplasia of the left ventricle, ascending aorta, and aortic arch. The patient's characteristics are shown in Table 1. Three patients who underwent the Norwood procedure in the same period, but who were not managed with the postoperative strategy previously described were excluded from this study. Of these, 2 patients had severe pulmonary obstructive disease with 1 of these patients requiring postoperative extracorporeal membrane oxygenator insertion. The other patient had preoperative ductal shock and disseminated intravascular coagulopathy and died immediately after admission to the intensive care unit.


View this table:
[in this window]
[in a new window]
  		Table 1. Patient's Characteristics

 
Operative technique
After a median sternotomy and mobilizing of the arch vessels, a 3 mm or 3.5 mm polytetrafluoroethylene graft was anastomosed to the innominate artery for selective cerebral perfusion. Two venous cannulas were inserted into superior and inferior vena cavae. A 2.1 mm metal-tipped arterial cannula (Japan Medical Supply Co, Hiroshima, Japan) was inserted into the thoracic descending aorta immediately superior to the diaphragm for the lower body perfusion as previously described [4, 5]. Thus, cardiopulmonary bypass was established with bi-caval venous cannulas and double arterial lines, which enabled us to achieve complete avoidance of circulatory arrest throughout the procedure. First the ductus arteriosus was ligated and divided, and then the descending aorta was extensively mobilized. Vascular clamps were placed on the proximal transverse arch and descending aorta. All ductal tissue was removed. The undersurface of the aortic arch was cut back. The distal end of the aortic arch was anastomosed to the back wall of the descending aorta. Then the heart was arrested by crystalloid cardioplegic solution and the atrial septal defect was enlarged through a right atriotomy. The main pulmonary trunk and ascending aorta were transected and the facing surfaces were incised longitudinally, and then they were anastomosed using a side to side fashion. The neo-aorta reconstruction was performed by direct anastomosis of the pulmonary trunk to the combination of transverse arch and descending aorta except in 1 patient who had a glutaraldehyde-treated autologous pericardial roll that was interposed between the pulmonary trunk and the transverse arch. Pulmonary blood flow was supplied through the right modified Blalock-Taussig shunt with a polytetrafluoroethylene graft in 3 patients (3 mm in 1 patient and 3.5 mm in 2 patients), or right ventricle-pulmonary artery conduit (RV-PA conduit) [5] with polytetrafluoroethylene graft in 24 patients (5 mm in 11 patients with body weights of 2.5 ± 0.5 kg, and 6 mm in 13 patients with body weights of 3.1 ± 0.3 kg). Tricuspid annuloplasty was performed in 4 neonates who had moderate regurgitation preoperatively. Anteroseptal commissural plication was performed in 2 neonates, and De Vega annuloplasty was performed in the other 2 neonates. Two neonates with mitral stenosis associated with moderate mitral regurgitation underwent bilateral commissural plication. One patient with anomalous pulmonary venous return and multiple pulmonary venous stenosis required pulmonary venous reconstruction.

The low resistance strategy
Intraoperative management
A large dose of chlorpromazine (4.6 ± 1.8 mg/kg) was used as an {alpha}-blocker during the cardiopulmonary bypass [6, 7]. Pump flow rate was 168.9 ± 12.8 mL/kg/min, and the lowest rectal temperature was 29.5 ± 1.1C°. Thus, high-flow, low-resistance and moderate hypothermia cardiopulmonary bypass was achieved with complete avoidance of deep hypothermic circulatory arrest that contributes to keep systemic vascular resistance low. In addition, dilution ultrafiltration was routinely used during the bypass. In weaning from the cardiopulmonary bypass after peripheral temperature was completely rewarmed, pulmonary vascular resistance was maximally decreased with oxygen (100%), nitric oxide gas inhalation (20 ppm), and nitroglycerin (2 to 4 µg/kg/min). Under these conditions, pulmonary artery flow was adjusted at the target systolic blood pressure of 60 to 65 mm Hg and arterial oxygen saturation (SaO2) of 75% to 80%. In patients with a RV-PA conduit, the conduit was banded or partially clipped (n = 14) to reduce the blood flow or another modified Blalock-Taussig shunt was added (n = 2) to increase the blood flow. In 1 patient with modified Blalock-Taussig shunt, a stitch was placed on the inferior surface of the innominate artery just proximal to the graft anastomosis to reduce the shunt flow. Hematocrit was kept in 45% to 50%. The sternum was left open in all but 1 patients.

Postoperative management
In the intensive care unit, heart rate, systemic blood pressure, right atrial pressure, and pulse oximetry saturation (Spo2) were monitored continuously. Arterial blood gas analysis including pH, Po2, Pco2, SaO2, HCO3-, base excess, hematocrit, electrolytes, blood glucose, and more recently, lactate level were repeated every 30 to 60 minutes for the first 24 hours, and as needed afterwards. Patients were sedated and paralyzed with fentanyl and vecuronium for 2.3 ± 1.9 days. Commonly used inotropic agents were dopamine (3 to 10 µg/kg/min), dobutamine (3 to 10 µg/kg/min), and epinephrine (0.05 to 0.2 µg/kg/min). Chlorpromazine was continuously used as a systemic vasodilator [6]. Inspired oxygen fraction and inhaled nitrous oxide were tapered as SaO2 increased constantly since admission to the intensive care unit. Nitroglycerin was continuously used as a pulmonary vasodilator [8]. In closing the sternum on the median of postoperative day 3, pulmonary artery flow was readjusted by loosening the band or removing the clip from the conduit (n = 6) or tightening the band of the conduit (n = 1). Peritoneal dialysis was applied in 24 patients (88.9%) to correct water balance and electrolytes.


   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 References
 
Inhaled nitrous oxide gas and inspired oxygen fraction could be smoothly tapered without notable changes in pO2, pCO2, and SaO2 thereafter (Fig 1) (Table 2). Ventilator manipulation for respiratory rate and airway pressure to control pulmonary vascular resistance was rarely required. Inotropic agents were safely tapered as well, with a minimum change in blood pressure and atrial pressure (Fig 2 ) (Table 2). Chlorpromazine and nitroglycerin were continuously administrated as systemic and pulmonary vasodilator until extubation. Patients were extubated on the median of postoperative day 6 (range, 3 to 28 days). Three patients died within 30 days after the operation. The first patient died of massive bleeding from the intrathoracic artery 2 days after the operation. The second patient had preoperative ductal shock, renal failure, and disseminated intravascular coagulopathy, and died on postoperative day 6 due to low cardiac output and sepsis. The third patient with chromosomal abnormality had preoperative ductal shock and died of sepsis on postoperative day 28. No patient died from hypoxia, pulmonary overcirculation, or other circulatory deterioration. Operative mortality (< 30 days) was 11.1% in this group of patients.



View larger version (32K):
[in this window]
[in a new window]
  		Fig 1. Postoperative course changes in (A) inspired oxygen fraction, (B) inhaled nitric oxide, and (C) nitroglycerin. X-axis shows time after admission to the intensive care unit (ICU). The error bars indicate a standard deviation. (Hrs = hours.)

 

View this table:
[in this window]
[in a new window]
  		Table 2. Hemodynamic and Respiratory Variables in the Intensive Care Unit

 


View larger version (38K):
[in this window]
[in a new window]
  		Fig 2. Postoperative course changes in the doses of (A) dopamine (solid bars) and dobutamine (shaded bars), (B) epinephrine, and (C) chlorpromazine. X-axis shows time after admission to the intensive care unit (ICU). The error bars indicate standard deviation. (Hrs = hours.)

 

   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
References
 
Surgical results of the stage 1 palliation for HLHS, or Norwood procedure, have been evolving with improvements in operative technique and perioperative managements [2, 9, 10]; however, the early mortality still remains high compared with other neonatal open heart surgery. Early after the Norwood procedure, systemic and pulmonary vascular resistances change easily and cause fluctuation in Qp/Qs. Most mortality after the Norwood procedure occurs in this early postoperative time mainly from myocardial ischemia or abrupt changes in Qp/Qs, which result in lethal circulatory deterioration [2, 3]. The concept of low resistance strategy described here is to aggressively decrease both the pulmonary and systemic vascular resistances to reduce the range for these vascular resistances to fluctuate and thereby obtain invariable postoperative Qp/Qs. To achieve this purpose, perioperative factors that may raise vascular resistance have to be removed; then large dose of vasodilators should be used with adequate inotropic support.

Deep hypothermic circulatory arrest is widely used in the Norwood procedure, but this procedure has been reported to cause an increase in pulmonary vascular resistance [11–13] postoperatively. In addition, Tweddell and coworkers [14] found that systemic vascular resistance was also elevated after the Norwood procedure using deep hypothermic circulatory arrest. Moreover, Tokunaga and coworkers [15] demonstrated that sympathetic nerve activity and systemic vascular resistance significantly increased immediately after deep hypothermic circulatory arrest in an animal model. We have developed a new cardiopulmonary bypass technique that enables us to completely avoid deep hypothermic circulatory arrest, and we have been using this technique with the Norwood procedure [4, 5]. In this perfusion technique, high-flow, low-resistance, and moderate hypothermic perfusion can be achieved with a high dose of chlorpromazine as a systemic vasodilator [6]. We also adopt routine use of dilution ultrafiltration during the bypass and peritoneal dialysis after the operation expecting their beneficial effects on removing inflammatory substances from the blood, which may increase vascular resistance [16, 17].

Several reports have acknowledged the beneficial effects of systemic vasodilator on postoperative management of the Norwood procedure [10, 18, 19]. Phenoxybenzamine was reported to be useful in reducing and stabilizing systemic vascular resistance as well as improving systemic oxygen delivery [14, 18]. We have been using chlorpromazine as a systemic vasodilator for its {alpha}-blocking effect as well as a sedative in neonatal open-heart surgery. Administration of chlorpromazine during the operation effectively decreases systemic vascular resistance in an arterial switch operation [6]. After the Norwood procedure, we also recognized the beneficial effects of continuous infusion of chlorpromazine on keeping low and less variable systemic vascular resistance and reducing afterload of the volume-overloaded right ventricle. Tweddell and coworkers [18] reported that phenoxybenzamine effectively decreased systemic vascular resistance to achieve stable Qp/Qs after the Norwood operation. However, we aim to achieve more invariable Qp/Qs by stabilizing pulmonary vascular resistance in addition to systemic vascular resistance in our low resistance strategy.

In patients with HLHS, pulmonary vascular resistance is elevated due to high pulmonary blood flow and high pulmonary artery pressure preoperatively, and long-lasting cardiopulmonary bypass can contribute the further elevation of pulmonary vascular resistance [20–22]. The recovery from this elevated pulmonary vascular resistance alters the balance between Qp and Qs very easily in a single ventricle physiology early after the operation. In order to reduce the range for pulmonary vascular resistance to fluctuate, pulmonary vasculature was dilated maximally at weaning from cardiopulmonary bypass with inhaled nitrous oxide and a high concentration of inspired oxygen as potent pulmonary vasodilators [23]. Under this condition, pulmonary blood flow was determined by adjusting systemic to pulmonary shunt. This is a totally opposite conception to the conventional management, in which pulmonary vascular resistance has to be kept high in order to prevent pulmonary overcirculation. After all, postoperative management in the intensive care unit was simply to taper inhaled nitrous oxide and inspired oxygen fraction as SaO2 improved, with continuous drip of chlorpromazine to keep systemic vascular resistance low. This one-directional treatment facilitated postoperative management of the Norwood procedure. Frequent ventilator manipulation was rarely required.

We tapered inhaled nitrous oxide and inspired oxygen fraction as SaO2 steadily improved after the operation. However, in a parallel circulation, SaO2 does not reflect Qp/Qs [24]. The rise in SaO2 may indicate two situations: one is when the value of Qp/Qs is high because of decreasing pulmonary vascular resistance or increasing systemic vascular resistance that results in pulmonary overcirculation and systemic hypoperfusion. In this situation, weaning of pulmonary vasodilators is the right way to keep Qp/Qs balanced. The other is when total cardiac output increases with Qp/Qs well-balanced. In this situation, tapering of pulmonary vasodilators does not make sense, but we did not observe significant hemodynamic changes or progress in metabolic acidosis during the postoperative course, suggesting that there was no negative influence of tapering pulmonary dilators on the Norwood circulation in our series.

Currently, some institutions adopt continuous mixed venous saturation monitoring in post-Norwood management [18, 24]. With a value of mixed venous saturation, Qp/Qs, cardiac output, and vascular resistances can be assumed, and they seem to make post-Norwood management easier.

In conclusion, the low resistance strategy is a simple and useful method for perioperative management of the Norwood procedure, minimizing fluctuation in both pulmonary and systemic vascular resistance and maintaining stable circulatory and respiratory status.


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

  1. Malec E., Januszewska K., Kolz J., Pajak J. Factors influencing early outcome of Norwood procedure for hypoplastic left heart syndrome. Eur J Cardiothorac Surg 2000;18:202-206.[Abstract/Free Full Text]
  2. Daebritz S.H., Nollert G.D., Zurakowski D., et al. Results of Norwood stage I operation: comparison of hypoplastic left heart syndrome with other malformations. J Thorac Cardiovasc Surg 2000;119:358-367.[Abstract/Free Full Text]
  3. Bartram U., Grunenfelder J., Van Praagh R. Causes of death after the modified Norwood procedure: a study of 122 postmortem cases. Ann Thorac Surg 1997;64:1795-1802.[Abstract/Free Full Text]
  4. Imoto Y., Kado H., Shiokawa Y., Fukae K., Yasui H. Norwood procedure without circulatory arrest. Ann Thorac Surg 1999;68:559-561.[Abstract/Free Full Text]
  5. Imoto Y., Kado H., Shiokawa Y., Minami K., Yasui H. Experience with the Norwood procedure without circulatory arrest. J Thorac Cardiovasc Surg 2001;122:879-882.[Abstract/Free Full Text]
  6. Imoto Y., Kado H., Masuda M., Yasui H. Effects of chlorpromazine as a systemic vasodilator during cardiopulmonary bypass in neonates. Jpn J Thorac Cardiovasc Surg 2002;50:241-245.[Medline]
  7. Sakihara C., Nishimura J., Kobayashi S., Takahashi S., Kanaide H. Direct inhibitory effect of chlorpromazine on smooth muscle of the porcine pulmonary artery. Anesthesiology 1996;85(3):616-625.[Medline]
  8. Matot I., Neely C.F. Pulmonary vasodilator responses to nicardipine: comparison with other vasodilators. Critic Care Med 1995;23(11):1851-1857.
  9. Azakie T., Merklinger S.L., McCrindle B.W., et al. Evolving strategies and improving outcomes of the modified Norwood procedure: a 10-year single-institution experience. Ann Thorac Surg 2001;72:1349-1353.[Abstract/Free Full Text]
  10. Pearl J.M., Nelson D.P., Schwartz S.M., Manning P.B. First-stage palliation for hypoplastic left heart syndrome in the twenty-first century. Ann Thorac Surg 2002;73:331-339.[Abstract/Free Full Text]
  11. Kirshbom P.M., Jacobs M.T., Tsui S.S., et al. Effects of cardiopulmonary bypass and circulatory arrest on endothelium-dependent vasodilation in the lung. J Thorac Cardiovasc Surg 1996;111:1248-1256.[Abstract/Free Full Text]
  12. Kirshbom P.M., Page S.O., Jacobs M.T., et al. Cardiopulmonary bypass and circulatory arrest increase endothelin-1 production and receptor expression in the lung. J Thorac Cardiovasc Surg 1997;113:777-783.[Abstract/Free Full Text]
  13. Nagashima M., Stock U., Nollert G., et al. Effects of cyanosis and hypothermic circulatory arrest on lung function in neonatal lambs. Ann Thorac Surg 1999;68:499-504.[Abstract/Free Full Text]
  14. Tweddell J.S., Hoffman G.M., Mussatto K.A., et al. Improved survival of patients undergoing palliation of hypoplastic left heart syndrome: lessons learned from 115 consecutive patients. Circulation 2002;106(Suppl 1):I82-89.
  15. Tokunaga S., Imaizumi T., Fukae K., et al. Effects of hypothermia during cardiopulmonary bypass and circulatory arrest on sympathetic nerve activity in rabbits. Cardiovasc Res 1996;31(5):769-776.[Medline]
  16. Nagashima M., Shin'oka T., Nollert G., Shum-Tim D., Rader C.M., Mayer J.E., Jr High-volume continuous hemofiltration during cardiopulmonary bypass attenuates pulmonary dysfunction in neonatal lambs after deep hypothermic circulatory arrest. Circulation 1998;98(Suppl 19):II378-384.
  17. Bokesch P.M., Kapural M.B., Mossad E.B., et al. Do peritoneal catheters remove pro-inflammatory cytokines after cardiopulmonary bypass in neonates?. Ann Thorac Surg 2000;70:639-643.[Abstract/Free Full Text]
  18. Tweddell J.S., Hoffman G.M., Fedderly R.T., et al. Phenoxybenzamine improves systemic oxygen delivery after the Norwood procedure. Ann Thorac Surg 1999;67:161-167.[Abstract/Free Full Text]
  19. Reinoso-Barbero F., Garcia-Fernandez F.J., Diez-Labajo A., del Cerro M.J., Cordovilla G. Postoperative use of milrinone for Norwood procedure. Paediatr Anaesthesia 1996;6(4):342-343.
  20. Schulze-Neick I., Li J., Reader J.A., Shekerdemian L., Redington A.N., Penny D.J. The endothelin antagonist BQ123 reduces pulmonary vascular resistance after surgical intervention for congenital heart disease. J Thorac Cardiovasc Surg 2002;124:435-441.[Abstract/Free Full Text]
  21. Schulze-Neick I., Li J., Penny D.J., Redington A.N. Pulmonary vascular resistance after cardiopulmonary bypass in infants: effect on postoperative recovery. J Thorac Cardiovasc Surg 2001;121:1033-1039.[Abstract/Free Full Text]
  22. Asimakopoulos G., Smith P.L., Ratnatunga C.P., Taylor K.M. Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass. Ann Thorac Surg 1999;68:1107-1115.[Abstract/Free Full Text]
  23. Reddy V.M., Liddicoat J.R., Fineman J.R., McElhinney D.B., Klein J.R., Hanley F.L. Fetal model of single ventricle physiology: hemodynamic effects of oxygen, nitric oxide, carbon dioxide, and hypoxia in the early postnatal period. J Thorac Cardiovasc Surg 1996;112:437-449.[Abstract/Free Full Text]
  24. Taeed R., Schwartz S.M., Pearl J.M., et al. Unrecognized pulmonary venous desaturation early after Norwood palliation confounds Qp: Qs assessment and compromises oxygen delivery. Circulation 2001;103(22):2699-2704.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
Y. Naito, M. Aoki, M. Watanabe, N. Ishibashi, K. Agematsu, K. Sughimoto, and T. Fujiwara
Factors Affecting Systemic Oxygen Delivery After Norwood Procedure With Sano Modification.
Ann. Thorac. Surg., January 1, 2010; 89(1): 168 - 173.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
T. Sakurai, H. Kado, T. Nakano, K. Hinokiyama, A. Shiose, M. Kajimoto, K. Joo, and Y. Ueda
Early results of bilateral pulmonary artery banding for hypoplastic left heart syndrome
Eur. J. Cardiothorac. Surg., December 1, 2009; 36(6): 973 - 979.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
T. Shinkawa, M. Yamagishi, K. Shuntoh, T. Miyazaki, T. Hisaoka, and H. Yaku
Pulmonary Arterial Reconstruction for Pulmonary Coarctation in Early Infancy
Ann. Thorac. Surg., January 1, 2007; 83(1): 188 - 192.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
K. S. Sundareswaran, K. R. Kanter, H. D. Kitajima, R. Krishnankutty, J. F. Sabatier, W. J. Parks, S. Sharma, A. P. Yoganathan, and M. Fogel
Impaired power output and cardiac index with hypoplastic left heart syndrome: a magnetic resonance imaging study.
Ann. Thorac. Surg., October 1, 2006; 82(4): 1267 - 1277.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
D. B. McElhinney and D. F. Teitel
From Theory to Practice: Optimizing the Efficiency of an Inefficient Circulation
Circulation, September 19, 2006; 114(12): 1226 - 1228.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
P. Oishi, A. Azakie, C. Harmon, R. K. Fitzgerald, A. Grobe, J. Xu, K. Hendricks-Munoz, S. M. Black, and J. R. Fineman
Nitric oxide-endothelin-1 interactions after surgically induced acute increases in pulmonary blood flow in intact lambs
Am J Physiol Heart Circ Physiol, May 1, 2006; 290(5): H1922 - H1932.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
S. Takabayashi, H. Kado, Y. Shiokawa, K. Fukae, and T. Nakano
Comparison of hemodynamics between Norwood procedure and systemic-to-pulmonary artery shunt for single right ventricle patients
Eur. J. Cardiothorac. Surg., June 1, 2005; 27(6): 968 - 974.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
Y. Tanoue, H. Kado, Y. Shiokawa, N. Fusazaki, and S. Ishikawa
Midterm Ventricular Performance After Norwood Procedure With Right Ventricular-Pulmonary Artery Conduit
Ann. Thorac. Surg., December 1, 2004; 78(6): 1965 - 1971.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
Y. Tanoue, H. Kado, T. Maeda, Y. Shiokawa, N. Fusazaki, and S. Ishikawa
Left ventricular performance of pulmonary atresia with intact ventricular septum after right heart bypass surgery
J. Thorac. Cardiovasc. Surg., November 1, 2004; 128(5): 710 - 717.
[Abstract] [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):
Hideaki Kado
Yosuke Nishimura
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 Nakano, T.
Right arrow Articles by Fusazaki, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakano, T.
Right arrow Articles by Fusazaki, N.
Related Collections
Right arrow Cardiac - other

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