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J Thorac Cardiovasc Surg 2003;125:430-432
© 2003 The American Association for Thoracic Surgery
Brief Communications |
From the Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St Louis, Mo.
Received for publication April 18, 2002. Accepted for publication July 15, 2002. Address for reprints: Bryan Meyers, MD, Suite 3108, Queeny Tower, One Barnes-Jewish Hospital Plaza, St Louis, MO 63110-1013 (E-mail: meyersb{at}msnotes.wustl.edu).
In our program, postoperative lung recipients are temporarily maintained on positive-pressure ventilation, with suction routinely applied to the thoracostomy tubes. We have occasionally seen negative pleural pressure applied to a large pleural space alter the respiratory mechanics of lung allografts and contribute to primary graft failure. We hypothesize that the combination of undersized lung grafts and negative pleural pressure may inhibit the lung's elastic recoil and lead to detrimental hyperinflation. If alveoli decompress incompletely during exhalation, functional residual capacity increases, and subsequent mechanical ventilations are delivered to partially distended lungs. After several stacked breaths, lungs hyperinflate and operate on a flatter portion of the volume-pressure curve. During volume-cycled ventilation, this manifests as increased airway pressure, with an increased potential for barotrauma. We prospectively studied this phenomenon after bilateral lung transplantation.
Methods
Consent was obtained from the patients, and the study was approved by the human studies committee. Twenty-four bilateral lung transplant recipients were studied between July 17, 2001, and April 9, 2002. Transplant indications included emphysema (n = 16), cystic fibrosis (n = 6), idiopathic pulmonary fibrosis (n = 1), and lymphangioleiomyomatosis (n = 1). Patients were evaluated within 6 hours of reperfusion while they were receiving mechanical ventilation at a tidal volume of 10 mL/kg (volume-cycled ventilation). Thoracostomy tubes were placed to atmospheric pressure for at least 2 minutes to allow system stabilization before the following parameters were measured: tidal volume, peak and plateau airway pressures, compliance, heart rate, and pulmonary arterial and systemic blood pressures. Thoracostomy tubes were then connected to suction (-20 cm H2O) for 2 minutes before repetition of the measurements.
We evaluated the collective effects on these parameters measured in the setting of negative versus atmospheric pleural pressure. Statistical analysis was performed with the Student t test with a Dunn-Sidak adjustment for multiple t tests. The transplant recipient total lung capacity was obtained from the last set of pulmonary function tests obtained before transplantation. The donor total lung capacity was estimated from the donor height and age with a standard nomogram.
1
Results
When the 24 patients were evaluated collectively, negative pleural pressure significantly (P 
.05) increased airway pressures and reduced compliance relative to atmospheric pleural pressure (Table 1). Three patients who received transplants for emphysema demonstrated dramatic adverse responses to negative pleural pressure. Negative pleural pressure increased their peak airway pressures by 135%, 108%, and 93%, whereas their compliances decreased by 66%, 71%, and 53%, respectively (Table 2).
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Thoracostomy tubes are frequently placed to suction after lung transplantation to facilitate the removal of intrapleural air and fluid. However, negative pleural pressure may have a detrimental effect on patients who receive relatively undersized lungs. A total of 1035 lung transplants were performed in North America in 2000, with the most common indication being emphysema or chronic obstructive pulmonary disease (40.6%). 2 Patients with emphysema, along with recipients of living related lobar transplants, are at greatest increased risk for receiving undersized allografts. If this occurs, chest wall compliance offers less restriction on lung volume. Negative pleural pressure may counteract the lung's elastic recoil, promoting alveolar hyperinflation within the enlarged pleural space.
Lung hyperinflation during mechanical ventilation can produce stress fractures in alveoli and pulmonary capillaries, resulting in pulmonary edema. 3 Similarly, hyperinflation of lung grafts during cold storage also increases endothelial permeability. 4 This phenomenon may have significance for aspects of pulmonary pathophysiology other than transplantation. In cases of postpneumonectomy edema, increased blood flow and catecholamine release may increase endothelial permeability in the remaining lung, creating a microvascular environment analogous to that seen in reperfused allograft lungs. 5 Furthermore, suction applied to the postpneumonectomy space may induce hyperinflation of the remaining lung and reduce perivascular hydrostatic pressure and further promote pulmonary edema. 6
This study was designed to prospectively evaluate a phenomenon that we have observed intermittently during the past few years. Negative pleural pressure dramatically increased airway pressures and reduced lung compliance in 3 patients who underwent transplantation for emphysema. In this small series, the incidence of this phenomenon among patients with emphysema was 3 of 16 (19%, 70% confidence interval 6%-39%). Theoretically, patients with cystic fibrosis receiving living related lobar transplants are at even greater risk for this phenomenon. Lobar grafts are usually undersized, and patients with cystic fibrosis usually have a hyperexpanded thoracic cavity. The calculation of donor total lung capacity in this study was imprecise and based only on the donor age and height. We do not make such a calculation in clinical practice, and this part of the analysis was performed only for the purposes of better understanding these observations.
In conclusion, negative pleural pressure in an enlarged pleural space may induce hyperinflation of the transplanted lung and contribute to primary graft failure. A potential solution is to normalize pleural pressure during mechanical ventilation with an empty water seal chamber in the chest bottles or in standard devices such as the Pleur-Evac (Deknatel, Inc, Fall River, Mass). Any chest drainage device that is disabled by not filling the water seal will behave like an open pneumothorax during the exhalation phase of mechanical ventilation. This will prevent the stacking of breaths and should make the described phenomenon impossible. It is obviously important that the water seal chamber be filled at the precise moment of extubation to avoid a true open pneumothorax in an extubated patient. We currently test all recipients of undersized lungs and avoid the combination of pleural suction and positive-pressure ventilation if patients demonstrate any evidence of breath stacking.
References
This article has been cited by other articles:
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  S. Haddy and V. A. Starnes Lobar transplantation J. Thorac. Cardiovasc. Surg., December 1, 2003; 126(6): 2106 - 2106. [Full Text] [PDF]
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B. Kozower and B. Meyers Reply to the editor J. Thorac. Cardiovasc. Surg., December 1, 2003; 126(6): 2106 - 2106. [Full Text] [PDF]
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