Well, it boils down to figuring out what you're trying to fix, then getting a plan together how to fix it. Getting PSG results will, of course, be helpful. Then you can see if there's an OSA component than can be addressed, as well as seeing what nocturnal oxygen levels do. BTW, what's his pCO2 level? That is probably the best gauge of determining improvement with nocturnal BiPAP.
In 20 words or less, BiPAP is simply pressure therapy that starts out with a baseline pressure (like your CPAP, only now it is termed EPAP), but then applies bursts of pressure to support inspiration. The peak of this pressure burst is termed IPAP. These pressures can be adjusted independently, and here's where treatment philosophies diverge in the treatment of OSA vs some sort of respiratory failure.
If you're addressing OSA, then EPAP is increased to take care of apneas (total closure, or near total closure of the airway), and IPAP is increased to take care of hypopneas (partial closure of the airway), flow limitations and snoring.
If you're addressing respiratory failure, then EPAP is set at a minimum level, and IPAP is increased until a desired
volume is supplied to the lungs. So an IPAP pressure could be considerably higher in this case, and it's the pressure differential between EPAP and IPAP that supplies the
volume. The bigger the differential the higher the resulting
volume.
OK, how this relates to COPD. In acute exacerbations of COPD, respirations become shallow and rapid, so BiPAP is the first-line attack in the ED because it will increase the individual breath
volume. It's much tougher to gain benefit in stable COPD because the
volume of each breath may be normal, or near-normal, but much of the breath goes to areas of lung that don't do anything, CO2 is not exchanged, and this becomes "wasted ventilation." Or technically, increased dead space ventilation or Vd/Vt. A normal Vd/Vt is about 30% (only 30% of each breath is dead space) but Vd/Vt in COPD can be about 60%. You can jack up the amount of each breath (
tidal volume) with BiPAP, and thus temporarily reduce pCO2, but the disease state remains unchanged.
Which brings us to what good is nocturnal BiPAP. In severe COPD, with pCO2 in the neighborhood of pCO2 >55 mmHg, nocturnal BiPAP may afford the respiratory muscles some rest, and permit a little more energy during the day. In addition, there could be a residual drop in daytime pCO2. Studies, or summaries of studies, will typically say something like:
COPD
In contrast to the consistently favorable results of studies on the use of NIV in patients with restrictive pulmonary disease, those on patients with severe obstructive lung disease yield conflicting results. A review of these studies is beyond the scope of the present study. However, the long-term follow-up study by Leger et al found not only a sustained reduction in PaCO2 in patients with severe COPD but also a significant drop in hospital days for 2 years after starting NPPV. A similar finding was recently reported by Janssens et al who found that NPPV decreased the number of hospitalizations for cardiac or respiratory failure in patients with hypercapnic COPD for up to 2 years and thus may improve QoL. These latter studies suggest that the effect of NPPV on health resource utilization in severe COPD deserves examination. The conflicting results of studies on the use of NIV for severe stable COPD make it virtually impossible to assemble guidelines based on solid evidence. Nevertheless, a number of inferences can be drawn. First, NPPV appears to be well tolerated in this patient population. Ease of administration, potentially favorable effects of EPAP on intrinsic PEEP and work of breathing, as well as the ability to eliminate obstructive sleep apneas (overlap syndrome, present in 15% of COPD) makes NPPV the noninvasive mode of first choice. Patients with little or no CO2 retention, regardless of the severity of airway obstruction, appear to gain little or no benefit from NIV. This may be because these patients tend to have less nocturnal hypoventilation and fewer episodes of sleep-disordered breathing in the first place, and have less to gain from nocturnal ventilatory assistance. Also, respiratory muscle fatigue is probably not an important contributing factor at rest during periods of clinical stability. Rather, the studies suggest that if any patient subpopulation is likely to benefit, it is those with substantial daytime CO retention. This contention is supported by the fact that average initial PaCO2 values were 10 mm Hg higher (57 vs 47 mm Hg) among studies using negative pressure ventilation that showed a clinical benefit compared to those showing none. In conclusion, although the evidence is conflicting and far from definitive, COPD patients with severe CO2 retention appear most apt to respond favorably to nocturnal NPPV.
From Contribution of polygraphy and polysomnography to nocturnal monitoring of patients with obesity-hypoventilation syndrome (OHS) and non-invasive ventilation (NIV) by Dr Yan Fei Guo at University of Geneva 2004
If there does turn out to be an OSA component, and there is an Overlap Syndrome, then that will have to be factored in as well. And obviously, it will up to your physicians to determine the risk/benefit of pressure therapy vs additional barotrauma.
But a good example of how
not to go about it was posted here by Slinky (and thank you Slinky, because that information will be critically important to a lot of people):
The Slinky Experience
So anyway, you may have a ways to go before you decide on the treatment approach.
SAG