OBJECTIVE: To study the effect of posture on the hypercapnic ventilatory responses (HCVR). DESIGN: Nonrandomized controlled study. SETTING: Rehabilitation hospital and a pulmonary institute. PARTICIPANTS: Patients with neurologically stable C(5-8) tetraplegia (n=12) and healthy control subjects (n=7). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Supine and seated forced vital capacity (FVC) and HCVR, and supine and erect blood pressure. RESULTS: FVC in the sitting position was reduced in patients with tetraplegia (52+/-13% predicted); supine FVC was 21% higher (P=.0005). In the sitting position, HCVR was lower in patients than in controls (0.8+/-0.4 vs 2.46+/-0.3 L/min/mmHg, P<.001). Supine HCVR was not significantly different between the groups. When HCVR was normalized to FVC, there was still a significant difference between patients and controls in the sitting position. Patients with tetraplegia were orthostatic (mean supine blood pressure 91+/-13 mmHg vs mean erect blood pressure 61+/-13 mmHg, respectively, P<.0001). The magnitude of the orthostatism correlated with that of the postural change in HCVR (r=.93, P<.0001). CONCLUSIONS: Respiratory muscle weakness may contribute to the attenuated HCVR in tetraplegia. However, the observation that supine HCVR is still low even when normalized to FVC suggests a central posture-dependent effect on the HCVR, which may be linked to the postural effect on arterial blood pressure.
OBJECTIVE: To study the effect of posture on the hypercapnic ventilatory responses (HCVR). DESIGN: Nonrandomized controlled study. SETTING: Rehabilitation hospital and a pulmonary institute. PARTICIPANTS: Patients with neurologically stable C(5-8) tetraplegia (n=12) and healthy control subjects (n=7). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Supine and seated forced vital capacity (FVC) and HCVR, and supine and erect blood pressure. RESULTS: FVC in the sitting position was reduced in patients with tetraplegia (52+/-13% predicted); supine FVC was 21% higher (P=.0005). In the sitting position, HCVR was lower in patients than in controls (0.8+/-0.4 vs 2.46+/-0.3 L/min/mmHg, P<.001). Supine HCVR was not significantly different between the groups. When HCVR was normalized to FVC, there was still a significant difference between patients and controls in the sitting position. Patients with tetraplegia were orthostatic (mean supine blood pressure 91+/-13 mmHg vs mean erect blood pressure 61+/-13 mmHg, respectively, P<.0001). The magnitude of the orthostatism correlated with that of the postural change in HCVR (r=.93, P<.0001). CONCLUSIONS: Respiratory muscle weakness may contribute to the attenuated HCVR in tetraplegia. However, the observation that supine HCVR is still low even when normalized to FVC suggests a central posture-dependent effect on the HCVR, which may be linked to the postural effect on arterial blood pressure.