P pulmonale in status asthmaticus.
We studied 129 patients during acute, severe asthmatic attacks. Electrocardiograms showed P pulmonale in 49% of patients who had an arterial carbon dioxide tension (PaCo2) greater than or equal to 45 mm Hg and an arterial pH less than or equal to 7.37, whereas P pulmonale was present in only 2.5% of asthmatics who had a PaCO2 less than or equal to 44 mm Hg and a pH greater than or equal to 7.38 (p less than 0.001). P wave and QRS axes were 79 +/- 8 degrees and 80 +/- 20 degrees, respectively, in the presence of P pulmonale. When P pulmonale disappeared, the P wave and QRS axes shifted significantly to the left (p less than 0.001). Electrocardiographic P pulmonale persisted 12 to 60 hr after correction of hypoxemia, hypercapnia, and acidosis. In 7 patients with P pulmonale and respiratory acidosis, cardiac catheterization demonstrated normal artery pressures (PAPs) measured relative to atmospheric pressure. In 12 of these peak inspiratory pulmonary artery transmural pressures (PATPs) were increased. Since increased right heart transumural pressures could result in chamber distention, these data are consistent with the hypothesis that reversible P pulmonale in status asthmaticus is explainable on the basis of markedly negative tidal pleural pressures and increased right heart transmural pressures.
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000150:complications*; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D004562:Electrocardiography; D005260:Female; D005541:Forced Expiratory Volume; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D010100:Oxygen / Q000097:blood; D011651:Pulmonary Artery / Q000503:physiopathology; D014109:Total Lung Capacity; D014797:Vital Capacity
D002245:Carbon Dioxide; D010100:Oxygen