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University of Colorado Health Science Center, President, Snowdrift Pulmonary Conference, Denver, CO
Correspondence to: Thomas L. Petty, MD, Master FCCP, 899 Logan St, Suite 203, Denver, CO 80203-3154; e-mail: tlpdoc{at}aol.com
To the Editor:
The study of the effects of noninvasive positive pressure ventilation to reduce chronic compensated CO2 retention in COPD patients1 ignores the possible adaptive advantage of "resetting" the PCO2 to a higher level than normal. As experts in the mechanics of COPD have argued in the past, chronic compensated CO2 retention will allow for CO2 homeostasis at a lower level of alveolar, and thus minute, ventilation. This may result in decreased dyspnea during exercise.23 Some time ago, we reported on a group of patients with very advanced COPD and quite high PCO2 levels, ranging from 75 to 110 mm Hg (mean, 90 mm Hg) with partial bicarbonate compensation: mean HCO3- of 45 mEq/L and pH 7.32. Of course, these patients also received long-term nasal oxygen. All were functional to a remarkable degree in view of severe airflow obstruction: mean FEV1, 0.41 L (range, 0.31 to 0.67 L). One patient worked daily as a road inspector! Mean survival was 17 months.4 I have also had many patients gain remarkable relief from dyspnea while receiving oxygen and exercise during pulmonary rehabilitation. It is as if their brain adjusts to the work of breathing by "living" at a high but compensated PCO2. Thus, in my view, we should not focus on just one physiologic manifestation of COPD, and we must sometimes be reminded about the wisdom of nature.
References
Department of Pneumology, University Hospital Freiburg. Freiburg, Germany
Correspondence to: Wolfram Windisch, MD, Department of Pneumology, University Hospital Freiburg, Killianstrasse 5, D-79106 Freiburg, Germany; e-mail: windisch{at}med1.ukl.uni-freiburg.de
To the Editor:
We are grateful for the comments of Dr. Petty regarding our article in CHEST (August 2005)1 dealing with noninvasive positive-pressure ventilation (NPPV) treatment in stable patients with hypercapnic COPD. We agree with the statement that chronic compensated CO2 retention reflects an adjustment mechanism that will allow for CO2 homeostasis at a lower level of minute ventilation, thus resulting in decreased dyspnea, particularly if long-term oxygen therapy (LTOT) is applied. We also agree that this compensatory mechanism reflects the wisdom of nature. Nevertheless, chronic hypercapnia indicates long-term failing of the respiratory pump. Accordingly, COPD patients with higher PaCO2 levels have a lower ventilatory reserve,2 and this has been suggested to be a limiting factor both during daily living and particularly during exacerbation.
Recently, we have shown3 that controlled nocturnal NPPV therapy is capable of increasing tidal and minute ventilation during the 3 subsequent hours of daytime spontaneous breathing and of sustaining increased tidal and minute ventilation until reconnection to the ventilator in the evening. Here, augmented alveolar ventilation caused a decrease of PaCO2 followed by respiratory alkalosis that allowed renal elimination of elevated bicarbonate levels. This indicates reversion of the adjustment mechanism of chronic hypercapnia and may provide beneficial clinical effects in the addition to the positive effects gained by LTOT. Accordingly, health-related quality of life (HRQL) was reported to be higher in stable patients with hypercapnic COPD to whom NPPV leading to a decrease of PaCO2 was administered in the addition to LTOT when compared to LTOT alone.4 Further, improvements of HRQL have been shown to be dependent on the ability of NPPV to lower bicarbonate levels following PaCO2 reduction.3
In stable patients with COPD, survival has yet not been shown to be improved when NPPV is applied in addition to LTOT compared to LTOT alone.5 However, studies5 that formed these results have used low ventilator settings that were not sufficient enough to increase alveolar ventilation and consecutively to decrease PaCO2 values. As discussed in our article, NPPV using higher inspiratory pressures in a controlled mode is well-tolerated and capable of markedly improving hypercapnia in these patients.1 Survival rates were higher than previously reported. Since COPD is known to be one of the most important causes of chronic morbidity and mortality worldwide, we strongly think that the existing data regarding the potential benefits of NPPV that is aimed at more aggressively reducing PaCO2 levels justify further controlled outcome studies.
In summary, COPD patients with chronic ventilatory failure metabolically and clinically adapt to chronic hypercapnia. LTOT further decreases dyspnea, increases PaO2, and may thereby rest the exhausted respiratory pump, which could in part explain the improved prognosis. Moreover, NPPV aimed at a maximal reduction of PaCO2 has been suggested to reverse this adjustment mechanism of chronically tolerated hypercapnia by augmentation of alveolar ventilation, thus decreasing PaCO2 and bicarbonate levels. This has been suggested to provide additional clinical benefits regarding improvements of HRQL and prolongation of life, which need to be estimated in a more quantitative fashion following controlled trials.
References
, S, Dreher, M, et al Outcome of patients with stable COPD receiving controlled NPPV aimed at maximal reduction of PaCO2. Chest 2005;128,657-662
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