Feeding Induces Left Atrial Compression and Impedes Cardiac Filling in Patients With Large Hiatal Hernia

Patients with large hiatal hernias (HH) frequently experience postprandial dyspnea. The aim of this study was to evaluate whether feeding induced cardiac compression in these patients using echocardiography.

Transthoracic echocardiography was performed during fasting and 30 min after feeding (300 g rice pudding) in patients with HHs (n = 32; mean age, 72 ± 9 years). A subset of patients (n = 15; mean age, 76 ± 6 years) were evaluated postoperatively.

Preoperatively, feeding decreased left atrial (LA) volumes (maximal 27.4 ± 11.3 vs 19.2 ± 9.7 mL/m², P < .001; minimal 13.1 ± 7.0 vs 6.9 ± 5.1 mL/m², P < .001), and increased LA inflow velocities (systolic wave 0.62 ± 0.14 vs 0.77 ± 0.17 m/sec, P < .01; diastolic wave 0.46 ± 0.13 vs 0.59 ± 0.13 m/sec, P < .01), mitral inflow velocities (E wave 0.79 ± 0.17 vs 0.94 ± 0.19 m/sec, P < .01; A wave 0.93 ± 0.20 vs 1.05 ± 0.22 m/sec, P < .01), and E/E' ratio (12.1 ± 2.7 vs 13.7 ± 3.9, P < .01). Cardiac output (6.3 ± 1.6 vs 7.24 ± 2.0 L, P < .01) increased postprandially by marked heart rate augmentation (68.8 ± 7.0 vs 84.2 ± 8.4 beats/min, P < .01), with modest stroke volume increase (88.5 ± 16.7 vs 94.3 ± 19.5 mL, P = .03). After HH surgery, feeding did not change LA volumes (maximal 52.9 ± 13.6 vs 53.4 ± 12.5 mL, P = .89; minimal 28.6 ± 12.2 vs 27.4 ± 8.7 mL, P = .59) or E/E' ratio (10.9 ± 2.1 vs 11.3 ± 2.3) and induced more modest alterations in LA inflow (systolic wave 0.58 ± 0.17 vs 0.68 ± 0.16 m/sec, P = .01; diastolic wave 0.41 ± 0.12 vs 0.47 ± 0.13 m/sec, P = .01) and mitral inflow (E wave 0.69 ± 0.15 vs 0.80 ± 0.13 m/sec, P < .01; A wave 0.92 ± 0.13 vs 1.01 ± 0.18 m/sec, P = .02). Postoperatively, feeding increased cardiac output by substantial stroke volume augmentation (81.9 ± 16.5 vs 90.8 ± 16.0 mL, P = .01), with only modest increase in heart rate (69.8 ± 9.1 vs 75.9 ± 10.5 beats/min, P < .01).

Feeding produces marked LA compression in patients with HHs, inducing compensatory exaggerated responses in cardiac inflow and hemodynamic status. These compensatory mechanisms improve postoperatively following resolution of LA compression, likely explaining the debility noted preoperatively.