Purpose: Apnea divers hyperinflate the lung by taking a deep breath followed by glossopharyngeal insufflation. The maneuver can lead to symptomatic arterial hypotension. We tested the hypotheses that glossopharyngeal insufflation interferes with cardiac function further reducing cardiac output (CO) using cardiac magnetic resonance imaging (MRI) to fully sample both cardiac chambers.
Methods: Eleven dive athletes (10 men, 1 woman; age = 26 ± 5 yr, body mass index = 23.5 ± 1.7 kg·m(-2)) underwent cardiac MRI during breath holding at functional residual capacity (baseline), at total lung capacity (apnea), and with submaximal glossopharyngeal insufflation. Lung volumes were estimated from anatomic images. Short-axis cine MR images were acquired to study biventricular function. Dynamic changes were followed by long-axis cine MRI.
Results: Left and right ventricular end-diastolic volumes (LVEDV, RVEDV) decreased during apnea with and without glossopharyngeal insufflation (baseline: LVEDV = 198 ± 19 mL, RVEDV = 225 ± 30 mL; apnea: LVEDV = 125 ± 38 mL, RVEDV = 148 ± 37 mL, P < 0.001; glossopharyngeal insufflation: LVEDV = 108 ± 26 mL, RVEDV = 136 ± 29 mL, P < 0.001 vs baseline). CO decreased during apnea (left = -29 ± 4 %, right = -29 ± 4 %) decreasing further with glossopharyngeal insufflation (left = -38% ± 4%, right = -39% ± 4%, P < 0.05). HR increased 16 ± 4 bpm with apnea and 17 ± 5 bpm with glossopharyngeal insufflation (P < 0.01). Ejection fraction moderately decreased (apnea: left = -5% ± 2%, right = -7% ± 2%, glossopharyngeal insufflation: left = -6% ± 2%, right = -10% ± 2%, P < 0.01). With continued apnea with and without glossopharyngeal insufflation, LVEDV and CO increased over time by a similar but small amount (P < 0.01).
Conclusions: The major finding of our study was that submaximal glossopharyngeal insufflation decreased CO further albeit by a small amount compared to maximal inspiratory apnea. The response was not associated with severe biventricular dysfunction.