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Case Reports  |   November 2002
Hyperinflation Resulting in Hemodynamic Collapse following Living Donor Lobar Transplantation
Author Affiliations & Notes
  • Steven M. Haddy, M.D.
    *
  • Ross M. Bremner, M.D., Ph.D.
  • Earl W. Moore-Jefferies, M.D.
    *
  • Durai Thangathurai, M.D.
  • Felicia A. Schenkel, R.N.
    §
  • Mark L. Barr, M.D.
  • Vaughn A. Starnes, M.D.
    #
  • *Assistant Professor, ‡Professor, Department of Anesthesiology. †Assistant Professor, ∥Associate Professor, #Professor and Chair, Department of Cardiac Surgery. §Senior Coordinator, Cardiothoracic Transplantation.
  • Received from the Departments of Anesthesiology and Cardiac Surgery, University of Southern California University Hospital and the Keck School of Medicine, Los Angeles, California.
Article Information
Case Reports
Case Reports   |   November 2002
Hyperinflation Resulting in Hemodynamic Collapse following Living Donor Lobar Transplantation
Anesthesiology 11 2002, Vol.97, 1315-1317. doi:
Anesthesiology 11 2002, Vol.97, 1315-1317. doi:
BILATERAL living lobar transplantation has become an established strategy to deal with the long-term shortage of suitable donor tissue for patients with end-stage lung disease; this technique has been in use at the Keck School of Medicine at the University of Southern California since 1993. We present a case in which the disparity in size between the donated lobes and the recipient's thorax led to life-threatening ventilatory and hemodynamic compromise in the immediate postoperative period.
Case Report
A 30-yr-old woman was admitted with end-stage cystic fibrosis for scheduled bilateral living lobar transplant. She was oxygen dependent at home and had been hospitalized several times in the preceding weeks for decompensation of her disease.
At the time of admission, arterial blood gas measurements on 2 l/min oxygen were as follows: pH, 7.43; Paco2, 55 mmHg; Pao2, 44 mmHg. Forced vital capacity was 47% of the predicted value. The patient's weight was 46 kg and her height was 153 cm. Physical examination was remarkable for an increased S2, and examination of the bony thorax showed increased anterior-posterior diameter typical of patients with cystic fibrosis.
Because of the patient's progressive deterioration, the decision was made to proceed with lobar lung transplantation using living donors. The indications for and technique of performing this procedure have been previously described. 1–3 In brief, the lower right lobe is harvested from a healthy donor at the same time that the lower left lobe is harvested from a second donor, and the donated lobes are then implanted into the recipient patient.
The patient was taken to the operating room without premedication. Following venous access and radial artery catheter placement, anesthesia was induced with etomidate and maintained with isoflurane, vecuronium, and fentanyl. A pulmonary artery catheter was placed following induction of anesthesia; the initial blood pressures were 60/30 mmHg with a pulmonary artery occlusion pressure of 20 mmHg. Cardiopulmonary bypass is instituted because the severe pleural adhesions in these patients increase the duration and technical difficulty of performing the native pneumonectomies.
The chest was opened using a bilateral thoracosternotomy or “clam shell” incision. Dynamic hyperinflation was observed and treated by decreasing the inspiratory to expiratory ratio, with use of bronchodilators and vigorous tracheal toilet, and by initiating brief periods of apnea. Permissive hypercapnia (Paco2, 80–90 mmHg) allowed unhurried dissection of the lungs and hilar structures without significant arterial desaturation. Cardiopulmonary bypass was instituted and bilateral pneumonectomies were performed. The lobes were subsequently transplanted as described elsewhere. 1 
Following implantation of the lobes, the patient was weaned from bypass using 5 μg · kg−1· min−1of dopamine. The pulmonary artery catheter which had been advanced into the newly implanted lobes showed pressures of 40/20–45/25 mmHg. Protamine, methylprednisolone, and furosemide were also administered. Hemostasis was induced, and the chest was closed. Arterial blood gases on Fio2of 0.5 and 5 cm H20 positive end expiratory pressure (PEEP) using tidal volumes of 500 ml at 12 breaths/min volume-controlled mechanical ventilation were pH: 7.32; Paco2: 45; and PaO2: 375.
Prior to transport to the cardiac intensive care unit, the thoracostomy tubes were set on −20 cm H20 suction. Almost immediately the patient's hemodynamic status deteriorated, with the blood pressure dropping from 100 mmHg systolic to 50–60 mmHg systolic with corresponding decreases in the pulmonary artery pressures. This responded minimally to increased fluid administration and inotropic support, including dopamine, phenylephrine, and epinephrine. Although the chest tubes did not show significant drainage of blood, the surgical team decided to reopen the incision. During the preparation for reexploration of the chest, the thoracostomy tubes were disconnected from the water-seal drainage devices. Almost immediately, the patient's blood pressure returned to its prior value.
After a period of observation, the decision was made not to reopen the chest and the tubes were again connected to suction. Hemodynamic deterioration recurred, and this time the peak inspiratory pressure increased from the mid 30s to 50–60 cm H2O. Suspecting some interaction between the negative pleural pressure and the change in hemodynamics, we elected to discontinue suction on the thoracostomy tubes. The nurse disconnected the water-seal pleural drainage canisters from suction, but there was no improvement in the hemodynamic profile. On realizing that the water seal was maintaining a negative intrapleural pressure, we disconnected the chest tubes from the canister to allow pleural pressure to return to atmospheric level. Improvement was immediate, with restoration of blood pressure and a decrease in peak inspiratory pressure. After a period of observation, the patient was transported uneventfully to the intensive care unit, with the chest tubes to water seal at atmospheric pressure.
Discussion
Physicians caring for patients with severe obstructive pulmonary disease are familiar with the phenomenon of dynamic hyperinflation also known as “auto-PEEP,”“intrinsic-PEEP,” or “occult-PEEP.” This is usually defined as an increase of the end-expiratory lung volume greater than the elastic equilibrium volume (volume of relaxation). 4,5 The management of this condition in patients with chronic obstructive pulmonary disease has been well described. Dynamic hyperinflation can have profound effects on the hemodynamic status of patients experiencing ventilatory failure. 6 The etiologies of these hemodynamic difficulties include mechanical pressure on the right heart from the hyperinflated lungs, causing decreased venous return, and impedance to right-sided heart ejection caused by distended alveoli compressing the pulmonary microvasculature, leading to right-sided heart failure. The interaction becomes even more complicated when spontaneous (or assisted), rather than controlled, ventilation is used. 7,8 
This patient did not meet the criteria for dynamic hyperinflation. The donor lungs showed no signs of flow limitation and no bronchospasm was evident. The patient's skeletal muscles were well relaxed after administration of vecuronium, and her lungs underwent mechanical ventilation using conventional rates. In spite of this, hemodynamic changes were similar to those seen in dynamic hyperinflation. We believe that the negative intrapleural pressure, resulting from the suction placed on the chest tubes, created a situation in which the lungs were kept hyperinflated and thus on the flat portion of the compliance curve. Negative intrathoracic pressure, combined with positive intrapulmonary pressure, leads to hyperinflation with decreased venous return and impedance to right-sided heart outflow. This was caused by the size discrepancy between the single pulmonary lobes and the larger hemithoraces into which they were implanted. In subsequent cases, we have observed that these hemodynamic changes are more severe as size discrepancy increases. 9 The size discrepancy may be even greater than predicted on the basis of donor and recipient height, since an increased anterior-posterior diameter develops in cystic fibrosis patients as an adaptive change resulting from long-term lung hyperinflation during the period of rib cage development. 10 
While the hemodynamic and pulmonary mechanical effects of dynamic hyperinflation are similar to those found in our case, the cause is quite different. Return of the lobes to their end expiratory volume was probably limited because the chest tube suction mechanically produced continuous negative end-expiratory pleural pressure. Since the bony thorax is not collapsible, the negative intrapleural pressure is transmitted directly to the transplanted lobe. Physiologically, the negative end-expiratory pleural pressure places the healthy lobes near the maximum flat portion of their pressure-volume relation, even though normal intrinsic elastic recoil may be present. With the lungs held in this inflated configuration, successive breaths rapidly “stack” to produce dangerous levels of inspiratory pressure. Hyperinflation from either excessive positive intrapulmonary pressures (as might be seen with high levels of PEEP) or constant negative intrapleural pressures (as in our patient) has similar hemodynamic effects.
At the University of Southern California, we have chosen to deal with the shortage of donors for our cystic fibrosis patients, in part, by using living donors. Since the first living-donor lobar transplant in 1993, we have performed more than 120 of these procedures. The small stature of these patients makes the use of a single lobe adequate for implantation into a hemithorax; however, there is still usually a residual space as the lobe does not conform completely to the shape of the chest. Figure 1shows a computerized tomographic scan from one of our recipient lobar transplant patients, several weeks after transplantation, demonstrating the space remaining in the chest after lobe insertion. This ultimately fills with fluid in a similar fashion to that seen after lobectomy or pneumonectomy. The complication described previously, while not unique to lobar transplantation, may be expected to occur more frequently when a significant donor-to-recipient size discrepancy exists. A large size discrepancy would result in a larger potential space into which the lobes may expand to the point of severe hyperinflation when suction is applied to the chest tubes. Figure 2shows a diagram illustrating the pathophysiology we believe to be operating in these patients. As noted previously, our clinical impression is that the degree of physiologic influence is directly related to the degree of discrepancy between the size of the implanted lobes and that of the recipient's thorax.
Fig. 1. Computerized tomogram from a lobar recipient several weeks following transplantation. The outlined areas have filled with fluid. In the immediate postoperative setting these spaces are empty and may allow hyperinflation of the implanted lobes, causing the hemodynamic changes described.
Fig. 1. Computerized tomogram from a lobar recipient several weeks following transplantation. The outlined areas have filled with fluid. In the immediate postoperative setting these spaces are empty and may allow hyperinflation of the implanted lobes, causing the hemodynamic changes described.
Fig. 1. Computerized tomogram from a lobar recipient several weeks following transplantation. The outlined areas have filled with fluid. In the immediate postoperative setting these spaces are empty and may allow hyperinflation of the implanted lobes, causing the hemodynamic changes described.
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Fig. 2. Comparison of the pulmonary mechanics in a hemithorax at atmospheric pressure, with one under negative intrathoracic pressure, following lobar transplantation. Failure of the lungs to empty due to the negative intrathoracic pressure causes hyperinflation and subsequent hemodynamic deterioration.
Fig. 2. Comparison of the pulmonary mechanics in a hemithorax at atmospheric pressure, with one under negative intrathoracic pressure, following lobar transplantation. Failure of the lungs to empty due to the negative intrathoracic pressure causes hyperinflation and subsequent hemodynamic deterioration.
Fig. 2. Comparison of the pulmonary mechanics in a hemithorax at atmospheric pressure, with one under negative intrathoracic pressure, following lobar transplantation. Failure of the lungs to empty due to the negative intrathoracic pressure causes hyperinflation and subsequent hemodynamic deterioration.
×
This and subsequent cases have provided us with a better understanding of the physiology involved in lobar transplantation and has led us to modify the postoperative treatment of these patients in the following ways:
  1. Chest tubes are placed next to water-seal drain, but no negative pressure is applied for the first several hours postoperatively.

  2. PEEP (5–10 cm H20) is applied progressively in the cardiac surgery intensive unit, as tolerated.

  3. Negative pressure is applied to the chest tubes (two in each hemithorax) in sequence: 5–10 cm H20 to each tube, for 1 h intervals, rotating for the first 24 h. Later, continuous suction is applied to each tube and gradually increased to −20 cm H2O over the next 48 h.

Using this procedure on all patients, we have minimized the hemodynamic consequences of the donor-to-recipient size discrepancies inherent in lobar transplantation and have not seen similar acute deterioration in the last 90–100 patients examined.
In summary, we describe a case of hemodynamic deterioration following bilateral living-donor lobar transplantation. The hemodynamic changes are similar to those seen in dynamic hyperinflation. 5 However, the etiology is negative intrapleural pressure rather than positive intrapulmonary pressure. As a result of this experience, we have modified our treatment of these patients to include small but gradually increasing application of negative pressure to the chest tubes.
References
Starnes VA, Barr ML, Cohen RG: Lobar transplantation. Indications, technique, and outcome. J Thorac Cardiovasc Surg 1994; 108: 403–10; discussion 410–1Starnes, VA Barr, ML Cohen, RG
Starnes VA, Barr ML, Schenkel FA, Horn MV, Cohen RG, Hagen JA, Wells WJ: Experience with living-donor lobar transplantation for indications other than cystic fibrosis. J Thorac Cardiovasc Surg 1997; 114: 917–21; discussion 921–2Starnes, VA Barr, ML Schenkel, FA Horn, MV Cohen, RG Hagen, JA Wells, WJ
Barr ML, Schenkel FA, Cohen RG, Chan KM, Marboe CC, Hagen JA, Barbers RG, Starnes VA: Bilateral lobar transplantation utilizing living related donors. Artif Organs 1996; 20: 1110–1Barr, ML Schenkel, FA Cohen, RG Chan, KM Marboe, CC Hagen, JA Barbers, RG Starnes, VA
Gibson GJ: Pulmonary hyperinflation a clinical overview. Eur Respir J 1996; 9: 2640–9Gibson, GJ
Leith DE, Brown R: Human lung volumes and the mechanisms that set them. Eur Respir J 1999; 13: 468–72Leith, DE Brown, R
Ranieri VM, Dambrosio M, Brienza N: Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure. Eur Respir J 1996; 9: 1283–92Ranieri, VM Dambrosio, M Brienza, N
Dambrosio M, Fiore G, Brienza N, Cinnella G, Marucci M, Ranieri VM, Greco M, Brienza A: Right ventricular myocardial function in ARF patients. PEEP as a challenge for the right heart. Intensive Care Med 1996; 22: 772–80Dambrosio, M Fiore, G Brienza, N Cinnella, G Marucci, M Ranieri, VM Greco, M Brienza, A
Dambrosio M, Cinnella G, Brienza N, Ranieri VM, Giuliani R, Bruno F, Fiore T, Brienza A: Effects of positive end-expiratory pressure on right ventricular function in COPD patients during acute ventilatory failure. Intensive Care Med 1996; 22: 923–32Dambrosio, M Cinnella, G Brienza, N Ranieri, VM Giuliani, R Bruno, F Fiore, T Brienza, A
Starnes VA, Barr ML, Cohen RG, Hagen JA, Wells WJ, Horn MV, Schenkel FA: Living-donor lobar lung transplantation experience: Intermediate results. J Thorac Cardiovasc Surg 1996; 112: 1284–90; discussion 1290–1Starnes, VA Barr, ML Cohen, RG Hagen, JA Wells, WJ Horn, MV Schenkel, FA
Guignon I, Cassart M, Gevenois PA, Knoop C, Antoine M, Yernault JC, Estenne M: Persistent hyperinflation after heart-lung transplantation for cystic fibrosis. Am J Respir Crit Care Med 1995; 151: 534–40Guignon, I Cassart, M Gevenois, PA Knoop, C Antoine, M Yernault, JC Estenne, M
Fig. 1. Computerized tomogram from a lobar recipient several weeks following transplantation. The outlined areas have filled with fluid. In the immediate postoperative setting these spaces are empty and may allow hyperinflation of the implanted lobes, causing the hemodynamic changes described.
Fig. 1. Computerized tomogram from a lobar recipient several weeks following transplantation. The outlined areas have filled with fluid. In the immediate postoperative setting these spaces are empty and may allow hyperinflation of the implanted lobes, causing the hemodynamic changes described.
Fig. 1. Computerized tomogram from a lobar recipient several weeks following transplantation. The outlined areas have filled with fluid. In the immediate postoperative setting these spaces are empty and may allow hyperinflation of the implanted lobes, causing the hemodynamic changes described.
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Fig. 2. Comparison of the pulmonary mechanics in a hemithorax at atmospheric pressure, with one under negative intrathoracic pressure, following lobar transplantation. Failure of the lungs to empty due to the negative intrathoracic pressure causes hyperinflation and subsequent hemodynamic deterioration.
Fig. 2. Comparison of the pulmonary mechanics in a hemithorax at atmospheric pressure, with one under negative intrathoracic pressure, following lobar transplantation. Failure of the lungs to empty due to the negative intrathoracic pressure causes hyperinflation and subsequent hemodynamic deterioration.
Fig. 2. Comparison of the pulmonary mechanics in a hemithorax at atmospheric pressure, with one under negative intrathoracic pressure, following lobar transplantation. Failure of the lungs to empty due to the negative intrathoracic pressure causes hyperinflation and subsequent hemodynamic deterioration.
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