Abstract

Ultrasonic nebulization therapy (U/air) resulted in a decline in PaO<sub>2</sub> of —5 to —22 mm Hg in ten of 15 chronic obstructive lung disease (COLD) patients. A similar decline in PaO<sub>2</sub> occurred in four of ten COLD patients when ultrasonic nebulization was given with intermittent positive pressure breathing (IPPB [IPPB/U/air]). Complaints of discomfort from treatment were elicited in ten of 15 COLD patients treated with U/air and all ten COLD patients treated with IPPB/U/air. No consistent correlation of symptoms with the changes in PaO<sub>2</sub> was noted. The increase in airway resistance with ultrasonic nebulization which occurs only in patients with COLD probably best explains the complaints, since our control patients had a greater incidence and degree of PaO<sub>2</sub> decline and yet remained free of discomfort. Respiratory alkalosis was noted in one of 15 and three of ten COLD patients treated with U/air and IPPB/U/air, respectively. Hypoventilation with a decrease in PaO<sub>2</sub> and pH and a rise in PaCO<sub>2</sub> occurred in two patients receiving U/air. The mechanisms for the reduction in PaO<sub>2</sub> are complex, including hypoventilation, increased workload of breathing, and most commonly, ventilation perfusion abnormalities. Acute blood gas changes are common with ultrasonic therapy and have important clinical implications which must be evaluated along with other known hazards of inhalational therapy.

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