Increased lung water without hypocapnia does not cause central sleep apnoea in a lamb model.

Abstract

OBJECTIVE: Central sleep apnoea (CSA) in patients with heart failure is associated with an extremely poor prognosis. It is unclear as to whether pulmonary congestion contributes to CSA. METHODOLOGY: We developed a sheep model of congestive cardiac failure (CCF) to address the question of whether pulmonary congestion without hypocapnia could cause CSA. Fourteen lambs were given CCF by overdrive pacing for 3 weeks. CCF was defined by a pulmonary artery occlusion pressure (PAOP) > or = 15 mmHg. There were 11 controls. Extravascular lung water (EVLW) was measured by the double indicator dilution method. RESULTS: The CCF lambs had a PAOP = 18 +/- 3 mmHg and controls had a PAOP = 10 +/- 2 mmHg (P < 0.01). EVLW was 12.6 +/- 1.8 (CCF) compared to 8.9 +/- 2 mL/kg (controls) (P < 0.01). The respiratory rate was 74 +/- 21 b.p.m. (CCF) compared to 47 +/- 6 b.p.m. (controls) (P < 0.05). Acute volume loading with saline raised PAOP without changing respiration. pH and PaCO(2) were the same in both groups (PaCO(2)-37 mmHg). CONCLUSIONS: These results support the view that hypocapnia is essential for CSA, and demonstrated that increased EVLW causes tachypnoea but not CSA.