Reversal of Nocturnal Periodic Breathing: Discussion

In September 2000, the patient received a double-lung transplant (at the University Hospital of Homburg/Saar; Dr. Schafers). The postoperative clinical course was complicated by acute renal failure requiring intermittent hemodialysis and cytomegalovirus infection of the transplanted lungs, but finally the patient recovered. Four months later, polysomnography was again performed with the patient breathing room air and without any cardiac medications. At this time, blood gases were normal and echocardiography was without evidence for any persistent pulmonary hypertension (Table 1). The patient reported a better sleep quality and a reduction in her daytime sleepiness (Epworth sleepiness scale score of 9). The sleep study now showed completely normal breathing with well-preserved nocturnal Sao2 (Table 2; Fig 1, bottom).

In our opinion, this case illustrates the complex interaction of blood gas alterations and hemodynamic impairment in the emergence of PB in patients with PPH. In the patient under discussion, multiple factors were present predisposing to PB: a reduced CI, a pronounced decrease of Paco2 to a point that was presumably below the apneic threshold, and marked hypoxemia that increases chemore-flex gain. Following lung transplantation, hemodynamic parameters, circulation time, and blood gases were normalized, and the SDB was no longer observed. The same is true for CSR in CHF, which disappears after successful cardiac transplantation.
In our original series of 20 patients with PPH, a beneficial effect of nasal oxygen administration on nocturnal PB was observed in the majority of the affected patients. In the present case, the PB was unresponsive to oxygen therapy. Similar observations have been made in CSR-CHF patients in whom the SDB persists despite optimal medical therapy and oxygen supplementation. In these patients, noninvasive positive pressure ventilation may be initiated and has been shown to result in better overall survival. In contrast, as suggested by a case study, treatment with continuous positive airway pressure or bilevel ventilation might be harmful to patients with PPH and PB, and therefore we did not start this form of therapy in our patient.
A possible limitation of the polysomnographic recordings employed in the present study is that they were carried out without esophageal probes. We decided not to insert such a device in this severely ill, anticoagulated patient, and to rely on the characteristics of the thoracoabdominal breathing movements when differentiating between obstructive and central apneas.
The fact that we did not obtain invasive hemodynamic data after lung transplantation might be regarded as a further drawback. However, we think that the echocardio-graphic examination performed after lung transplantation sufficiently excluded any persistent pulmonary hypertension.
In summary, we herein describe for the first time the reversal of nocturnal PB in patients with PPH by successful lung transplantation. In our opinion, this case report underlines the importance of blood gas alterations and hemodynamic impairment for the development of PB in patients with PPH. In addition, as there was no evidence for CHF or a neurologic disease process, a genuine association between severe right-heart failure and the development of SDB might be inferred from the present study.

This entry was posted in Lung Transplantation and tagged lung transplantation, periodic breathing, primary pulmonary hypertension.