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Radiographic lung disease and response of persistent pulmonary hypertension to mean airway pressure and alkalosis
Author(s) -
Deluga Karl S.,
Schlesinger Alan E.
Publication year - 1994
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950170407
Subject(s) - medicine , hyperventilation , respiratory alkalosis , mean airway pressure , metabolic alkalosis , respiratory disease , cardiology , airway , alkalosis , blood pressure , pulmonary hypertension , anesthesia , mechanical ventilation , lung , acidosis , metabolic acidosis
Persistent pulmonary hypertension of the newborn (PPHN) is associated with multiple cardiopulmonary diseases. Therapy often includes hyperventilation/alkalosis despite little evidence as to its efficacy in diverse conditions. To determine (1) if part of the improvement of arterial oxygen tension (P ao 2) attributed to alkalosis is actually related to increased mean airway pressure (P aw ) and (2) if the presence of radiographic pulmonary disease predicts the response to alkalosis or mean airway pressure, we reviewed records of 19 newborns with well‐documented PPHN. Arterial blood gases and corresponding ventilator settings were recorded during the first day of life. To adjust for lower F io 2corrected P ao 2(cP ao 2) was calculated when the F io 2< 1.0, such that cP ao 2= calculated arterial/alveolar oxygen ratio x (71 3 ‐ P aco 2/0.8). Regression equations were obtained and mean slopes of these were compared for P aw vs. cP ao 2, and pH vs. cP ao 2by one group t‐tests (with assumed population slope of zero). There was no correlation between P aw and cP ao 2(mean slope ± SD = −8.4 ± 30.8, P = 0.25), but there was a moderate correlation between p d and cP ao 2(mean slope = 333.1 ± 480.5, P = 0.007). Patients were then classified by chest radiographs as having severe or minima/no lung disease. Relationships of P aw and pH to cP ao 2were then re‐examined. No correlation was present between P aw and cP ao 2, in 11 patients with PPHN and severe radiographic disease (mean slope = −7.4 ± 26.97 P = 0.38) or in eight patients with PPHN and minima/no lung disease (mean slope = −9.8 2 37.5, P = 0.48). There was no correlation between pH and CP in patients with severe radiographic lung disease and PPHN (mean slope = 92.1 t 399.5, P 7 0.46), but patients with PPHN and minimal/no lung disease showed a strong correlation (mean slope = 664.5 ± 385.8, P = 0.002). We conclude that Paw (≤18 cm H 2 ,O) with conventional mechanical ventilation has no apparent effect on oxygenation in patients with PPHN regardless of lung disease; however, severe radiographic lung disease may be a predominant variable predicting a poor response to alkalosis. We speculate that different diseases cause pulmonary hypertension by different mechanisms. Pediatr Pulmonol. 1994; 17:239–245. © 1994 Wiley‐Liss, Inc.