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Pharyngoesophageal dysphagia occurred in 51.3 percent of 1,000 consecutive patients with gastroesophageal reflux. Aspiration, secondary to food obstruction, occurred in 30 percent of these patients, and some developed significant secondary respiratory symptoms. The site of obstruction was localized to the cricopharyngeus by timing the interval from swallow to obstruction. Cricopharyngeal incoordination was demonstrated in 20 of 52 patients studied by high speed esophageal manometry. Surgical correction of gastroesophageal reflux in patients with intractable reflux symptoms was shown to be effective in relieving pharyngoesophageal dysphagia in all but a small number of patients with very severe symptoms. In those with persistent dysphagia cricopharyngeal myotomy at a later stage was effective in giving relief.

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Pulmonary function has been assessed in 45 patients with atrial or ventricular septal defect. Moderate and severe dyspnea occurred almost exclusively in patients with high pulmonary artery pressure irrespective of whether this was due to high pulmonary blood flow or high pulmonary vascular resistance. Evidence is presented suggesting that this raised pulmonary artery pressure causes lung damage shown by a low compliance and high nonelastic resistance. These findings suggest an abnormal alveolar-capillary membrane and an abnormality of ventilation-perfusion relationships, which in turn cause a relatively low pulmonary diffusing capacity requiring excessive hyperventilation on exercise to maintain oxygen requriments. In patients with moderate or severe dyspnea, the abnormally high minute volume of ventilation during mild exertion is associated with a high work of breathing, the dual abnormality separating them from patients with only slight dyspnea on exertion.