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Ann Thorac Surg 2009;88:1277-1283. doi:10.1016/j.athoracsur.2009.06.027
© 2009 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

Cardiopulmonary Effects of Continuous Negative Pressure Wound Therapy in Swine

Megan B. Steigelman, MDa,b, Kenneth C. Norbury, PhDc, Deepak V. Kilpadi, PhDc, Jeffrey D. McNeil, MDa,b,*

a Department of Surgery, The University of Texas Health Science Center, San Antonio, Texas
b Department of Surgery, Wilford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas
c Department of Physiology and Models, Global R&D Kinetic Concepts Inc, San Antonio, Texas

Accepted for publication June 9, 2009.

* Address correspondence to Dr McNeil, Division of Cardiothoracic Surgery, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78229 (Email: mcneil{at}uthscsa.edu).


Drs Norbury and Kilpadi disclose that they have financial relationships with Kinetic Concepts Inc.

 

   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: Negative pressure wound therapy (NPWT) has been used for complex sternotomy wounds. Some reports describe foam placement below the posterior sternal table. We compared the hemodynamic and pulmonary effects of foam location during NPWT after median sternotomy.

Methods: Swine were randomized into four groups (n = 6 per group). A polyurethane open cell foam dressing was placed either within or below the sternal table. In one-half, a silicone mesh barrier was placed between the heart and the foam. The NPWT was applied at –125 mm Hg and then released to ambient pressure. This cycle was repeated two more times, and the foam was removed. Heart rate, mean arterial pressure, cardiac output, mixed venous oxygenation, central venous pressure, and pulmonary artery wedge pressure were measured. Peak inspiratory pressure, mean airway pressure, work of breathing, and intrathoracic pressure measurements were recorded.

Results: Intersternal placement of foam did not affect hemodynamic parameters. Substernal placement resulted in depression of hemodynamic variables which improved when negative pressure was applied. Pulmonary mechanics were not affected by foam location.

Conclusions: Initial placement of the foam dressing below the posterior sternal table caused reversible depression of cardiac function which appears to be consistent with direct cardiac compression. NPWT therapy had no clinically significant impact on pulmonary parameters. The use of a protective barrier does not alter hemodynamic or pulmonary parameters but continues to be recommended when NPWT is used for sternotomy wounds.

Continuous negative pressure wound therapy (NPWT) is used to assist in the treatment of poststernotomy mediastinitis (PM). Poststernotomy mediastinitis is a serious complication occurring in 0.4% to 5% of cardiac procedures, with a mortality of 14% to 47% [1]. Pneumonia, respiratory failure, or rarely, ventricular rupture can contribute to this mortality [2]. Morbidity from PM continues to be high despite aggressive surgical debridement, antibiotics, soft tissue flaps, and NPWT. Improved outcomes have led to the use of NPWT on open mediastinal wounds [3, 4] and since introduced in 1996, the use of V.A.C. therapy (KCI, San Antonio, TX) has become fundamental in the treatment of complicated sternal wounds. Recent literature reports favorable outcomes in over 80% of patients treated for sternal wound infections and mediastinitis [4, 5]. Furthermore, NPWT is also thought to immobilize the sternal edges, promote chest wall stability, and facilitate extubation and mobilization of the patient. Because the exposed vital structures are subject to NPWT, an interfacial barrier to separate the mediastinum from the polyurethane foam is often used. Despite the positive clinical results achieved with NPWT, concerns related to the impact of NPWT on cardiac and pulmonary structures remain.

Two animal research studies regarding NPWT have conflicting conclusions. Work by Conquest and colleagues [6] in a swine model found that NPWT (at –50 and –125 mm Hg continuous mode and at –125 mm Hg intermittent mode) significantly reduced cardiac output, stroke volume, left ventricular filling volume, and mean arterial pressure. A subsequent study by Sjögren and colleagues [7] showed no changes in cardiac output at –125 mm Hg. Instead, an increased cardiac output and a decrease in systemic vascular resistance were observed when NPWT was used at –75 mm Hg. No changes were observed in heart rate, mean arterial pressure, or central venous pressure. Sjögren and colleagues attributed these differences in results to differences in placement of the foam. Specifically, Sjögren and colleagues placed the foam dressing at the sternal level (intersternal) while it appears Conquest and colleagues placed the foam dressing below the sternal edges (substernal) without any barrier layer [Wooden, 2006, personal communication].

Gustafsson and colleagues [8] described the effects of NPWT therapy in a porcine model on respiratory mechanics. The application of negative pressures ranging from –50 mm Hg to –175 mm Hg caused no statistically significant changes in tidal volume, peak inspiratory pressure, peak expiratory flow, or static compliance. They hypothesized that negative pressure was not transmitted across the tissues outside the mediastinum, and therefore had no impact on the respiratory mechanics. However, no direct measurements of the pressure within the mediastinum or intrapleural spaces were performed.

With the increasing application of NPWT for complicated sternal wounds and continued concerns about the hemodynamic effects of NPWT in the anterior mediastinum, the aim of this study is to investigate the impact of negative pressure wound therapy at –125 mm Hg on hemodynamic and pulmonary physiology, when the foam is placed either below or between the sternum, with or without an interfacial barrier. In addition, the transmission of NPWT through the thoracic cavity is assessed by direct measurement.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
This study was approved by the Wilford Hall Medical Center Animal Care and Use Committee (Lackland AFB, San Antonio, TX), and all animals used for the study were handled according to the Guide for the Care and Use of Laboratory Animals [9]. Twenty-four juvenile Yorkshire swine (32 to 50 kg) were used. Premedication consisted of ketamine (15 to 30 mg/kg intramusularly [IM]), acepromazine (0.11 to 0.22 mg/kg IM), and atropine (0.04 mg/kg IM). Anesthesia was induced by mask with isoflurane 3.5% to 4.5% in an oxygen-air mixture of 40% to 60%, and animals were orally intubated with a 7-French endotracheal tube. A Narkomed 2C (Drager Medical, Telford, PA) was utilized for ventilation and inhalational anesthesia. The same settings were used for all animals: volume-controlled (10 to 12 mL/kg/breath) ventilation at 10 to 12 breaths/minute. End tidal carbon dioxide was monitored. Positive end expiratory pressure was maintained at 3 cm H2O. Anesthesia was with isoflurane (1.5% to 2.5%) in a 40% to 60% oxygen-air mixture. Isotonic saline was administered at approximately 5 mL/kg/hour throughout the protocol. A 7.5-Fr pulmonary artery catheter (Swan-Ganz, continuous cardiac output; Edwards Lifesciences, Inc, Irvine, CA) was placed and 5-Fr catheters were placed in the femoral artery and vein. A median sternotomy was performed and the pericardium was widely opened. Entry into the pleural spaces was minimized. Pressure catheters with manometers (model HHP-2083; Omega Engineering Inc, Stamford, CT) were placed as follows: directly into the polyurethane foam, at the interface between the heart and foam, and in the right pleural space. Polyurethane foam was placed within the sternotomy, with or without a nonadherent interfacial barrier (Mepitel; Molnlycke Health Care AB, Göteborg, Sweden), according to protocol. Sterile transparent adhesive drape (V.A.C. Drape; Kinetic Concepts Inc, San Antonio, TX) was applied and a continuous vacuum source (V.A.C. ATS therapy unit; Kinetic Concepts Inc) utilized.

Twenty-four animals were equally randomized to four groups (intersternal ± barrier, substernal ± barrier). After foam ± barrier placement, each animal underwent a series of 15 minute intervals of alternating NPWT at –125 mm Hg and 0 mm Hg. Each animal underwent 10 time periods of evaluation. Time interval 1 began after intubation and hemodynamic stability. Time interval 2 began after completion of the sternotomy. Time interval 3 began after placement of the NPWT device and pressure catheters. Time interval 4 began immediately after NPWT was initiated, and continued for 15 minutes. Time interval 5 began immediately after NPWT was terminated, and continued for 15 minutes. These intervals were repeated twice for intervals 6 through 9. Interval 10 began after the NPWT device was completely removed (Fig 1). Data collected at each interval included cardiac output, mixed venous saturation, mean arterial pressure, central venous pressure, pulmonary artery wedge pressure, and heart rate. Stroke volume and cardiac index were calculated. Using the Bicore CP 100 pulmonary monitor (Bicore Monitoring Systems Inc, Irvine, CA), peak inspiratory pressure, work of breathing, and mean airway pressure were also recorded. Baseline measurements were determined with the chest open, prior to the placement of the NPWT system. Data for hemodynamic and pulmonary parameters were collected during the last 5 minutes of each interval. In addition, interfoam, epicardial, and intrapleural pressures were recorded at each interval. The animals were humanely euthanized at the completion of the protocol.


Figure 1
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  		Fig 1. Treatment scheme and position of foam dressing for substernal (A) and intersternal (B) protocols.

 
Initial analysis revealed that the presence or absence of the silicon barrier had no detectable effect on any of the results; therefore, the initial four groups were combined into two groups differentiated only by the location of the foam (intersternal versus substernal). This resulted in two groups, n = 12 each, and simplified the subsequent analysis and increased the power of the study. All results are reported using these two groups. Mean body weight was compared using a two-sample t test (2-tailed test with {alpha} = 0.05) for substernal and intersternal groups. Interval 2 (open chest baseline) was used for all hemodynamic and pulmonary comparisons. A time series cross-section regression was used to perform the primary statistical analyses and the model was estimated using either the Fuller-Battese method (for balanced data) or the RanTwo method (for unbalanced data). In order to evaluate the hypothesis using pooled time series analysis method the model was fitted to include the overall response as a function of NPWT ON/OFF, foam placement, and baseline (interval 2) using the following model: Response = ENPWT EPosition BaselineInterval 2. Probability values less than 0.05 from this model were considered significant. The Wilcoxon signed-rank test was used for post-hoc comparisons of the intra-animal changes in responses at interval 3 versus interval 2, interval 4 versus interval 2, and interval 10 versus interval 2. For all sensitivity tests involving multiple comparisons within a parameter, the Bonferroni method was used to adjust the alpha level. All statistical analyses were carried out using SAS software release 9.1 (SAS Inc, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
Both groups were equivalent regarding body weight with a mean of 42.5 ± 3.9 kg. The baseline values for the measured parameters were consistent with published reports for swine [10–12]. All animals survived the study duration in the intersternal group. Two animals died in the substernal group shortly after the initial application of the foam due to hemodynamic collapse. One of these was found to have pneumonia at necropsy, was excluded from the data, and was replaced with an additional animal. The presence of the pneumonia was presumed to make the animal more susceptible to the detrimental effects of the initial foam placement. In the second animal, no contributing etiology could be identified. Therefore, the animal was not replaced and the limited data available were included. Due to the small sample size, no statistical analysis of mortality was performed.

Intersternal placement of the foam dressing had minimal effect on hemodynamic parameters over the duration of the study. There were no statistically significant effects of NPWT on any hemodynamic parameter evaluated during the intervals when the foam was in place (Fig 2). After foam removal, mean arterial pressure and stroke volume were significantly lower than baseline. There were no significant differences between interval 2 (open chest baseline) and interval 3 (initial placement of foam dressing) or interval 4 (suction on), suggesting there were no adverse effects on hemodynamic parameters simply due to the placement of the foam dressing (Fig 3).


Figure 2
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  		Fig 2. Hemodynamic variables. (A) Cardiac output; (B) Stroke volume; (C) Mean arterial pressure; (D) Mixed venous saturation; (E) Heart rate; (F) Central venous pressure.

 

Figure 3
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  		Fig 3. Comparison of intersternal (A) versus substernal (B), normalized to baseline.

 
In contrast, substernal placement of the foam dressing caused statistically significant changes in cardiac output (p = 0.007), cardiac index (p = 0.022), and stroke volume (p = 0.0002) when tested across all time intervals (Fig 2). The initial placement of substernal foam during interval 3 caused significant changes in cardiac output, cardiac index, central venous pressure, mean arterial pressure, stroke volume, mixed venous saturation, and heart rate, relative to interval 2 (open chest). These parameters generally improved once negative pressure was applied (interval 4) but the differences remained statistically significant for central venous pressure, stroke volume, and mixed venous saturation. After removal of the foam (interval 10), only mean arterial pressure was significantly different than baseline and all other hemodynamic parameters returned to pretreatment levels. These data suggest that there was a notable negative hemodynamic effect of substernal foam placement and a lack of full hemodynamic recovery until the removal of the foam dressing. To more clearly demonstrate these changes, these results are presented as a percentage of baseline at intervals 3, 4, and 10 (Fig 3).

There was a statistically significant treatment effect on mean airway pressure (p = 0.024), peak inspiratory pressure (p = 0.017) and work of breathing (p = 0.037) of NPWT applied after adjusting for the foam placement effect, and baseline value. However, foam location did not have a significant impact on any of the pulmonary values (Fig 4). All variables returned to baseline after the NPWT system was removed with no significant differences between intervals 10 and 2. Although the differences in these variables were highly statistically significant, the changes in the values are not clinically significant and are felt to reflect change in chest wall compliance when suction was applied to the dressing.


Figure 4
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  		Fig 4. Respiratory mechanics. (A) Work of breathing; (B) Peak inspiratory pressure; (C) Mean airway pressure.

 
The amount of negative pressure recorded in the right posterior pleural space (at a location remote from the foam placed in the mediastinum) was recorded when NPWT was applied. There was no significant transmission of mediastinal negative pressure to the pleural spaces when the NPWT was applied (–116 ± 26 mm Hg vs –6 ± 8 mm Hg).


   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
Negative pressure wound therapy has shown numerous benefits in the treatment of postoperative mediastinitis. The NPWT has shown lower rates of recurrent infections, decreased the number of treatment failures, and left smaller defects in patients when compared with standard closed drainage techniques [13]. Animal studies on NPWT in fresh sternotomy wounds have also shown increased sternal stability throughout ranges of negative pressure from –50 mm Hg to –200 mm Hg. This sternal stability can lead to greater comfort and earlier patient mobilization [14, 15]. The most effective setting for chronic wounds has been identified as –125 mm Hg [1, 3, 4, 14, 15] and is the most common negative pressure used in clinical settings today. Lindstedt and colleagues [15] also documented improved microvascular blood flow to areas of ischemic and reperfused myocardium when direct negative pressure was applied. Sternal wound edges and peristernal thoracic cavity tissues also develop increased blood flow and subsequent partial pressure of oxygen increases when negative pressure is utilized [16]. These studies indicate several advantages of NPWT on sternal wounds not seen with conventional dressings and wound management. However, additional studies are needed to establish the hemodynamic and pulmonary consequences of NPWT on the exposed tissues and structures within the mediastinum. The present study contributes to the understanding of the effect of NPWT on these clinically important areas.

Hersh and colleagues [3] published a series of 16 patients treated for sternal wound infections using NPWT as a bridge to closure. They noted improvement in sternal wound stabilization with decreased need for paralysis and mechanical ventilation. Furthermore, they decreased the number of dressing changes and the amount of debridement necessary to prepare the wound for final coverage. They did not separate the foam from the epicardium with an interfacial barrier, but had no hemodynamic complications as a result of the direct negative pressure. One commentary by Abu-Omar and colleagues [17] described two patients who developed ventricular rupture during their treatment with negative pressure therapy, and mobilization of the right ventricle to prevent risk of tearing from adhesions was recommended prior to the use of NPWT. However, subsequent reports with much higher patient numbers have had only positive results, again without documented complications related directly to the effects of NPWT [1, 4, 18–21].

Despite the numerous positive reports to the contrary, the proximity of negative pressure wound therapy to the vital organs unique to sternotomy wounds is a cause for concern and warrants further exploration in animal models. This concern was first addressed by Conquest and colleagues [6] who examined the hemodynamic effects of various negative pressures in swine. They found a significant decrease of the left ventricular volume, stroke volume, cardiac output, and systolic blood pressure when negative pressures of –50 and –125 were applied directly to the sternotomy wound. This variation was mitigated when a muscle flap was placed between NPWT and the epicardium. The conclusions of Conquest and colleagues recommended careful hemodynamic monitoring during NPWT, and that further studies on hemodynamic effects were warranted. However, the location of the foam placement was not described, small swine were used compared to our animals, and it is unclear if the alterations in hemodynamics were clinically significant. In a subsequent paper, Sjögren and colleagues [7] evaluated the hemodynamic effects of negative pressures ranging from –50 to –175 mm Hg on sternotomy wounds. They found that cardiac output remained unimpaired during all of the negative pressures, and even improved in the –75 mm Hg group. They were very specific about the placement of the foam dressing between the sternal edges and no deeper. Furthermore, they did not use an interfacial barrier between the heart and the foam. The conclusion was that the use of NPWT could be applied without compromising the central hemodynamics with correct placement of the foam just between the sternal edges [7].

Our study incorporated features of both prior studies to examine the hemodynamic effects of the most common clinically used negative pressure of –125 mm Hg in conjunction with an interfacial barrier. The use of a nonadherent interfacial barrier had no impact on hemodynamic or pulmonary variables. Substernal foam placement had an immediate significant negative impact on all hemodynamic variables and this trend continued until the foam was removed. These changes seen with placement of the foam into the anterior mediastinum (substernally) are consistent with early cardiac tamponade (approximately a 30% decrease in cardiac output with concomitant decreased mixed venous saturation, decreased mean arterial pressure, increased heart rate, and decreased stroke volume) [22]. These hemodynamic alterations improved after negative pressure was applied (interval 4), and eventually returned to baseline after removal of the foam (interval 10). The improvement noted with application of NPWT may be due to collapse of the foam under negative pressure, thereby somewhat relieving the tamponade effect. No further hemodynamic changes were seen with repeated cycling of the NPWT off and on. Conversely, no change in hemodynamic parameters was seen when the foam was placed just between the sternal edges. Our results confirm the recent study by Petzina and colleagues [23], who showed no statistically significant difference with or without the use of an interfacial dressing when measuring cardiac output and stroke volume at –125 mm Hg when the foam was placed intersternally.

There are several inherent weaknesses to this study. First, the shape of the thoracic cavity of swine differs from humans. Although the pericardium lies directly behind the sternum in both pigs and humans, the pig thorax is more narrow and deep. Therefore, some caution must be used in extrapolating the results to humans. Second, it is important to consider that these hemodynamic changes occurred in healthy animals with normal cardiac function. Clinically, patients with complicated sternal wound problems requiring NPWT are rarely considered healthy with normal cardiac function. More deleterious effects would be expected in patients with impaired ventricular function, shock, or ongoing sepsis. This was seen in our study with the early death of two animals. At necropsy, one animal was found to have pneumonia. This animal had a low mixed venous saturation at baseline and seemed to have no reserve to tolerate the insult of placing the foam into the anterior mediastinum. The second death did not have an identified predisposing factor but the animal had immediate hemodynamic collapse. Another key weakness is the short duration of the study period. Clinically the use of NPWT can be expected to continue for several days to weeks, not merely several hours.

The second set of data collected from this experiment was the pulmonary effects of NPWT in a sternotomy model. Treatment effects that were included in the analysis of the impact of –125 mm Hg NPWT on respiratory parameters in an intubated porcine sternotomy model were foam placement location and NPWT effect. While the position of the foam made no statistically significant impact on the respiratory mechanics, the use of NPWT therapy did have a statistically significant impact on all three. Although statistically significant, the magnitudes of the pulmonary changes are small, did not affect the outcomes of the animals, and are felt to be clinically insignificant. The two deaths in the study were a result of significant hemodynamic compromise during substernal foam placement and not related to pulmonary mechanics. No differences were identified between the baseline open sternotomy condition and the open sternotomy at the completion of the study, suggesting that there was no acute pulmonary parenchymal damage from NPWT during this short period. The applied vacuum was not transmitted across the thorax based on the measurements of intrapleural pressure remote from the anterior mediastinal foam. The lack of pulmonary effects is important as patients with diminished respiratory and cardiac reserve are often treated with NPWT for serious wound complications such as mediastinitis. The use of NPWT in the anterior mediastinum does not alter pulmonary mechanics or intrathoracic pressure in a clinically significant manner in this animal model.

Based on our swine model, caution should be exercised anytime the foam dressing is placed below the posterior sternal table due to potential direct compression of cardiac cavities, resulting in decreased myocardial wall compliance, stroke volume, and ultimately cardiac output. This may be particularly detrimental in patients who have marginal cardiac function or decreased cardiac reserve due to concurrent disease processes. Although this study in healthy swine showed that the barrier layer had no effect on hemodynamic or respiratory profiles, use of a nonadherent barrier when applying NPWT in the anterior mediastinum is still recommended to avoid direct contact of the foam with the epicardial surface and minimize the risk of injury to the underlying structures.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
The authors wish to thank SSgt Tanya Green, Gene Deck, Barbara Collins, and Crissy Jenschke for their technical assistance, Mark Borromeo for preparing the figures, Zhenmei Liu for statistical analysis, and George Hutchinson, Margaret Marsh, Shannon Crenshaw, Nadeem Bridi, Deborah Shanley, and Royce Johnson for reviewing the manuscript. The opinions expressed in this paper are solely those of the authors and do not represent the views of the United States Air Force, United States Department of Defense, or the United States Government. This project was entirely supported by a Cooperative Research and Development Agreement between Wilford Hall Medical Center and Kinetic Concepts Inc.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Agarwal JP, Ogilvie M, Wu LC, et al. Vacuum-assisted closure for sternal wounds: a first-line therapeutic management approach Plast Reconstr Surg 2005;116:1035-1040.[Medline]
  2. Arbulu A, Gursel E, Camero LG, Asfaw I, Stephenson LW. Spontaneous right ventricular rupture after sternal dehiscence: a preventable complication? Eur J Cardiothorac Surg 1996;10:110-115.[Abstract/Free Full Text]
  3. Hersh RE, Jack JM, Dahman MI, Morgan RF, Drake DB. The vacuum-assisted closure device as a bridge to sternal wound closure Ann Plast Surg 2001;46:250-254.[Medline]
  4. Song DH, Wu LC, Lohman RF, Gottlieb LJ, Franczyk M. Vacuum assisted closure for the treatment of sternal wounds: the bridge between debridement and definitive closure Plast Reconst Surg 2003;111:92-97.[Medline]
  5. Domkowski PW, Smith ML, Gonyon Jr DL, et al. Evaluation of vacuum-assisted closure in the treatment of poststernotomy mediastinitis J Thorac Cardiovasc Surg 2003;126:386-390.[Abstract/Free Full Text]
  6. Conquest AM, Garofalo JH, Maziarz DM, et al. Hemodynamic effects of the vacuum-assisted closure device on open mediastinal wounds J Surg Res 2003;115:209-213.[Medline]
  7. Sjögren J, Gustafsson R, Wackenfors A, Malmsjö M, Algotsson L, Ingemansson R. Effects of vacuum-assisted closure on central hemodynamics in a sternotomy wound model Interact Cardiovasc Thorac Surg 2004;3:666-671.[Abstract/Free Full Text]
  8. Gustafsson R, Sjögren J, Malmsjö M, Wackenfors A, Algotsson L, Ingemansson R. Vacuum-assisted closure of the sternotomy wound: Respiratory mechanics and ventilation Plast Reconstr Surg 2006;117:1167-1176.[Medline]
  9. National Research Council Guide for the Care and Use of Laboratory AnimalsWashington, DC: National Academy Press; 1996.
  10. Bajorat J, Hofmockel R, Vagts DA, et al. Comparison of invasive and less-invasive techniques of CO measurement under different haemodynamic conditions in a pig model Eur J Anaesthesiol 2006;23:23-30.[Medline]
  11. Filos K, Vagianos C, Stavropoulos M, et al. Evaluation of the effects of autotransfusion of unprocessed blood on hemodynamic and oxygen transport in anesthetized pigs Crit Care Med 1996;24:855-861.[Medline]
  12. Hannon JP, Bossone CA, Wade CE. Normal physiological values for conscious pigs used in biomedical research Lab Anim Sci 1990;40:293-298.[Medline]
  13. Segers P, de Jong AP, Kloek JJ, de Mol BA. Poststernotomy mediastinitis: comparison of two treatment modalities Interact Cardiovasc Thorac Surg 2005;4:555-560.[Abstract/Free Full Text]
  14. Mokhtari A, Petzina R, Gustafsson L, Sjögren J, Malmsjö M, Ingemansson R. Sternal stability at different negative pressures during vacuum-assisted closure therapy Ann Thorac Surg 2006;82:1063-1067.[Abstract/Free Full Text]
  15. Lindstedt S, Malmsjö M, Ingemansson R. Blood flow changes in normal and ischemic myocardium during topically applied negative pressure Ann Thorac Surg 2007;84:568-573.[Abstract/Free Full Text]
  16. Wackenfors A, Gustafsson R, Sjögren J, Algotsson L, Ingemansson R, Malmsjö M. Blood flow responses in the peristernal thoracic wall during vacuum-assisted closure therapy Ann Thorac Surg 2005;79:1724-1731.[Abstract/Free Full Text]
  17. Abu-Omar Y, Naik MJ, Catarino PA, Ratnatunga C. Right ventricular rupture during use of high-pressure suction drainage in the management of poststernotomy mediastinitis Ann Thorac Surg 2003;76:975author reply 974–5.[Free Full Text]
  18. Petzina R, Gustafsson L, Mokhtari A, Ingemansson R, Malmsjö M. Effect of vacuum-assisted closure on blood flow in the peristernal thoracic wall after internal mammary artery harvesting Eur J Cardiothorac Surg 2006;30:85-89.[Abstract/Free Full Text]
  19. Orgill DP. Utilizing negative pressure wound therapy on open chest/sternotomy wounds Ostomy Wound Manage 2004;50(11A suppl):15S-17S.[Medline]
  20. Cowan KN, Teague L, Sue SC, Mahoney JL. Vacuum-assisted wound closure of deep sternal infections in high-risk patients after cardiac surgery Ann Thorac Surg 2005;80:2205-2212.[Abstract/Free Full Text]
  21. Gustafsson RI, Sjögren J, Ingemansson R. Deep sternal wound infection: A sternal-sparing technique with vacuum-assisted closure therapy Ann Thorac Surg 2003;76:2048-2053.[Abstract/Free Full Text]
  22. Reddy PS, Curtiss EI, O'Toole JD, Shaver JA. Cardiac tamponade: hemodynamic observations in man Circulation 1978;58:265-272.[Abstract/Free Full Text]
  23. Petzina R, Ugander M, Gustafsson L, et al. Hemodynamic effects of vacuum-assisted closure therapy in cardiac surgery: assessment using magnetic resonance imaging J Thorac Cardiovasc Surg 2007;133:1154-1162.[Abstract/Free Full Text]



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