Efficacy and Compliance With Noninvasive Positive Pressure Ventilation in Patients With Chronic Respiratory Failure: COPD patients

In: Respiratory Failure

14 Sep 2014

Efficacy and Compliance With Noninvasive Positive Pressure Ventilation in Patients With Chronic Respiratory Failure: COPD patientsWhy different investigators have found varying results in using NPPV in COPD patients, in contrast to patients with restrictive disorders, is not known, but several theories exist. First, patients with restrictive ventilatory disorders and hypercapnia suffer primarily from hypoventilation resulting from either respiratory muscle weakness or chronic resetting of the CO2 threshold. Application of noninvasive ventilation in this patient group improves nocturnal ventilation and acts to reset the CNS CO2 threshold. Some have suggested that the use of noninvasive ventilation provides intermittent chronic respiratory muscle resting and/or improves lung and chest wall compliance, thereby resulting in an improvement in respiratory mechanics that improves respiratory function, gas exchange, and functional status. The latter mechanisms appear less tenable because the presence of respiratory muscle fatigue has never been shown to exist in a chronic state in any patient group; also, several studies have failed to document an improvement in spirometric values or respiratory muscle strength, suggesting that NPPV does not improve respiratory mechanics. natural asthma treatment

COPD patients develop hypercapnia by very different mechanisms than patients who become hyper-capnic because of restrictive ventilatory disorders. Most commonly, hypercapnia exists in this patient group because of an increase in physiologic dead space secondary to a ventilation/perfusion imbalance induced by bronchospasm or by the effect of emphysema altering CO2 elimination across a significantly reduced alveolar capillary bed. In COPD patients, therefore, hypercapnia does not always signify hypoventilation, but may signify high physiologic dead space as a result of either reactive airways disease or structural changes in the lung. The application of NPPV in this scenario would be much less likely to uniformly improve gas exchange or functional tolerance. Moreover, the application of NPPV in patients with COPD whose lungs are severely hyperinflated and obstructed may further worsen the development of hyperinflation, thereby contributing to poorer tolerance of NPPV in contrast to patients with restrictive ventilatory disorders.

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