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Diaphragm pacing allows certain quadriplegic patients to be weaned from mechanical ventilation. Pacing failure can result from device dysfunction, neurotransmission failure, or degraded lung mechanics (such as atelectasis). We report two cases where progressive pacing failure was attributed to deteriorated chest wall mechanics. The first patient suffered from cervical spinal cord injury at age 45, was implanted with a phrenic stimulator (intrathoracic), successfully weaned from ventilation, and permanently paced for 7 years. Pacing effectiveness then slowly declined, finally attributed to rib cage stiffening due to ankylosing spondylitis. The second patient became quadriplegic after meningitis at age 15, was implanted with a phrenic stimulator (intradiaphragmatic) and weaned. After a year hypoventilation developed without obvious cause. In relationship with complex endocrine disorders, the patient had gained 31 kg. Pacing failure was attributed to excessive mechanical inspiratory load. Rib cage mechanics abnormalities should be listed among causes of diaphragm pacing failure and it should be kept in mind that a “good diaphragm” is not sufficient to produce a “good inspiration”. [ABSTRACT FROM AUTHOR]

Background: Phrenic pacing is an alternative to positive-pressure ventilation in selected patients, mostly in cases of upper spinal cord injury. We evaluated results of phrenic pacing performed by video-assisted thoracic surgery (VATS). Method: Between 1997 and 2007, after complete neuromuscular investigations, 20 patients requiring full-time ventilation were selected for phrenic pacing (19 with posttraumatic tetraplegia and 1 with congenital central hypoventilation syndrome). Quadripolar cuff electrodes were fixed around each intrathoracic phrenic nerve via bilateral VATS. They were connected to a subcutaneous radiofrequency receiver coupled to an external radiofrequency transmitter. All patients participated in a reconditioning program beginning 2 weeks after implantation and continued until ventilatory weaning. Results: Phrenic pacing was successful in all cases. No intraoperative complications or perioperative mortality were observed. Intraoperative testing detected stimulation thresholds in 19 patients (range, 0.05-2.9 mA). Ventilatory weaning was obtained in 18 patients. Median diaphragm reconditioning time was 6 weeks (2 weeks–11 months). Reconditioning was still in process in a young woman and was not achieved in an elderly woman with a 4-year history of tetraplegia. All the patients weaned from mechanical ventilation reported improved quality of life. Failure or delay in recovery of effective diaphragm contraction was due to nonreversible amyotrophy. Conclusions: VATS implantation of 4-pole electrodes around the intrathoracic phrenic nerve is a safe procedure. Ventilatory weaning correlates with the degree of diaphragmatic amyotrophy. Phrenic pacing, performed as soon as neurologic and orthopedic stabilization is achieved, is the most important prognostic factor for successful weaning. [ABSTRACT FROM AUTHOR]

• The human phrenic nerve consistently ends with a free terminal pre-branching segment. • Running from the pericardium to the diaphragm, this segment measures 60–75 mm. • This free terminal pre-branching segment contains the totality of phrenic fibers. • It appears highly suitable for the dissection free implantation of diaphragm pacing electrodes. [Display omitted] Diaphragm pacing allows certain ventilator-dependent patients to achieve weaning from mechanical ventilation. The reference method consists in implanting intrathoracic contact electrodes around the phrenic nerve during video-assisted thoracic surgery, which involves time-consuming phrenic nerve dissection with a risk of nerve damage. Identifying a phrenic segment suitable for dissection-free implantation of electrodes would constitute progress. This study characterizes a free terminal phrenic segment never fully described before. We conducted a cadaver study (n = 14) and a clinical observational study during thoracic procedures (n = 54). A free terminal phrenic segment was observed on both sides in 100% of cases, "jumping" from the pericardium to the diaphragm and measuring 60 mm [95% confidence interval; 48–63] and 72.5 mm [65–82] (right left, respectively; p = 0.0038; cadaver study). This segment rolled up on itself at end-expiration and became unravelled and elongated with diaphragm descent (clinical study). Three categories of fat pads were defined (type 1: pericardiophrenic bundle free of surrounding fat; type 2: single fatty fringe leaving the phrenic nerve visible until diaphragmatic entry; type 3: multiple fatty fringes masking the site of penetration of the phrenic nerve) that depended on body mass index (p = 0.001, clinical study). Hematoxylin-eosin and toluidine blue staining (cadaver study) showed that all of the phrenic fibers in the distal, pre-branching part of the terminal segment were contained within a single epineurium containing a variable number of fascicles (right: 1 [95%CI 0.65–4.01]; left 5 [3.37–7.63]; p = 0.03). Diaphragm pacing through periphrenic electrodes positioned on the terminal phrenic segment should be tested. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Determining the basis for a taxonomy of mechanical ventilation" by R.L Chatburn and colleagues in the April 2012 issue.