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

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.

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.

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).

These results support the view that hypocapnia is essential for CSA, and demonstrated that increased EVLW causes tachypnoea but not CSA.