Pathophysiological mechanisms of cardiogenic dyspnoea in patients with large hiatal hernia

Abstract

The pathophysiological mechanisms of cardiogenic dyspnoea in patients with large hiatal hernia (HH) are poorly understood. Data obtained from 163 HH patients (Doppler-echocardiography, cardiac CT, MRI, respiratory function and exercise testing) were analysed. Cardiac compression in HH patients involves the left atrium (LA), coronary sinus, inferior pulmonary veins and posterobasal left ventricle; and is associated with significant exercise impairment that improves following corrective surgery. LA compression appears to modulate atrial function at rest to preserve left ventricular (LV) filling by increasing passive LA emptying function to compensate for decreased active emptying volume. LA filling is impaired further after a standardised meal and during preload reduction induced by Valsalva manouevre. Baseline exercise capacity is independently predicted by LA compression and right ventricular outflow tract diameter and, moreover, the improvement in exercise capacity post-operatively is independently predicted by the magnitude of increase in LA diameter. While improvements in lung volumes and reduced gas-trapping are also seen following HH surgery, these are relatively modest compared to the significant resolution of cardiac compression and improvement in exercise capacity. This thesis has systematically defined the cardiac pathophysiology associated with cardiac compression in HH patients and the relationship between these abnormalities and exercise impairment.