STUDY OBJECTIVE: Dyspnea is a common symptom in patients with diaphragm weakness or paralysis. In particular, dyspnea may be aggravated by immersion. We hypothesized that immersion to the neck in water would decrease vital capacity and consequently increase the demand/capacity ratio of the respiratory muscles. DESIGN: Case series study. SUBJECTS: Seven patients with profound diaphragm weakness or paralysis proven by phrenic nerve stimulation, and seven normal control subjects. INTERVENTION AND MEASUREMENTS: We measured land-based and water-based spirometry, breathing pattern, and mouth occlusion pressures. RESULTS: We found that the patients could preserve minute ventilation despite a fall in vital capacity from a mean of 2.3 to 1.3 L, but this required an increased respiratory rate (RR) [21.4 to 26.7 breaths/min, p = 0.018]. We used mouth occlusion pressure 100 ms after the start of inspiration (P(0.1)) as an estimation of the drive to breath; P(0.1) increased from 1.4 to 3.9 cm H(2)O (p = 0.018) without significant change in tidal volume. CONCLUSIONS: Relative to control subjects, patients with diaphragm weakness have augmented drive to breathe in order to attempt to defend gas exchange. This conclusion is implied by the presevered minute ventilation with immersion, the augmented RR, and elevated P(0.1) relative to maximum static inspiratory pressure.
STUDY OBJECTIVE:Dyspnea is a common symptom in patients with diaphragm weakness or paralysis. In particular, dyspnea may be aggravated by immersion. We hypothesized that immersion to the neck in water would decrease vital capacity and consequently increase the demand/capacity ratio of the respiratory muscles. DESIGN: Case series study. SUBJECTS: Seven patients with profound diaphragm weakness or paralysis proven by phrenic nerve stimulation, and seven normal control subjects. INTERVENTION AND MEASUREMENTS: We measured land-based and water-based spirometry, breathing pattern, and mouth occlusion pressures. RESULTS: We found that the patients could preserve minute ventilation despite a fall in vital capacity from a mean of 2.3 to 1.3 L, but this required an increased respiratory rate (RR) [21.4 to 26.7 breaths/min, p = 0.018]. We used mouth occlusion pressure 100 ms after the start of inspiration (P(0.1)) as an estimation of the drive to breath; P(0.1) increased from 1.4 to 3.9 cm H(2)O (p = 0.018) without significant change in tidal volume. CONCLUSIONS: Relative to control subjects, patients with diaphragm weakness have augmented drive to breathe in order to attempt to defend gas exchange. This conclusion is implied by the presevered minute ventilation with immersion, the augmented RR, and elevated P(0.1) relative to maximum static inspiratory pressure.