Pulmonary artery pressure response to hypoxia in sleep apnea.

The pulmonary artery pressure (Ppa) responses to short runs of acute hypoxia at two different levels of end-tidal CO2 were measured in nine normal subjects and in 20 patients with moderate to severe obstructive sleep apnea (OSA). In normal subjects the mean increase in Ppa in response to eucapnic hypoxia was 8 +/- 2 mm Hg (SEM) and was not different from the response to hypercapnic hypoxia (9 +/- 2 mm Hg, p > 0.2). In patients with OSA, the mean increase of Ppa was 8 +/- 1 mm Hg to eucapnic hypoxia, and the response to hypercapnic hypoxia was higher at 10 +/- 1 mm Hg (p = 0.01). Pulmonary pressor response to hypoxia was augmented (> 10 mm Hg) by hypercapnia in four of 20 patients with OSA but in none of the normal subjects. Normoxic hypercapnia alone was a weak stimulus, increasing Ppa by > 5 mm Hg in only two of nine patients with OSA studied. In conclusion, Ppa increases in both normal subjects and patients with OSA exposed to a ramp of acute isocapnic hypoxia. There were clear interindividual differences in pulmonary artery response. Hypercapnia did not produce clinical significant changes in Ppa in either group.

Pulmonary hypertension in obstructive sleep apnoea.

To determine the frequency and correlates of pulmonary hypertension in sleep-disordered breathing, pulmonary artery pressure, lung function and arterial blood gases were measured in 100 consecutive patients with obstructive sleep apnoea (OSA) (respiratory disturbance index (RDI) of > 20 episodes.h-1). Twenty six of the patients had significant chronic airflow limitation (CAL). Overall, 42% of patients had awake pulmonary artery pressure > 20 mmHg. Patients with pulmonary hypertension were older, had higher arterial carbon dioxide tension (PaCO2), lower arterial oxygen tension (PaO2) and lower forced expiratory volume in one second (FEV1) values compared with normotensive patients. Pao2, PaCO2 and FEV1 were correlated with the levels of pulmonary artery pressure (correlation coefficient (r2) 0.50, 0.46 and 0.49, respectively). These three factors combined could explain 33% of the variability in pulmonary artery pressure. Six patients had pulmonary hypertension despite a PaO2 in excess of 10.7 kPa (80 mmHg). We conclude that pulmonary hypertension is common in patients with moderate and severe sleep apnoea, especially those with coexisting chronic airflow limitation. The presence of daytime hypoxaemia is not a prerequisite in the development of pulmonary hypertension in these patients.

Improvement in gas exchange with nasal continuous positive airway pressure in pulmonary alveolar microlithiasis.

A 37-yr-old man with pulmonary alveolar microlithiasis (PAM) presented with respiratory failure and cor pulmonale. The FEV1/FVC was 1.4/1.8 L with total lung capacity of 3.2 L using the helium dilution method (54% predicted) and 6.1 L using body plethysmography (102% predicted), indicating large noncommunicating regions. The KCO (transfer factor per liter lung volume) was 3.05 ml/min/mm Hg/L (47% predicted). Despite home oxygen (3 L/min) and diuretic therapy, the patient remained hypoxic (PaO2, 55 mm Hg) and incapacitated with dyspnea. Nasal continuous positive airway pressure (nCPAP) at 12 cm H2O and oxygen at 1 L/min improved his oxygenation (PaO2, 93 mm Hg), and introduction of this regimen at night resulted in subjective improvement in daytime function. A Grandjean right heart catheter was introduced at the bedside, and the multiple inert gas elimination technique (MIGET) was used to measure ventilation and blood flow distributions at ambient pressure and with the addition of 10 cm H2O nCPAP. The patient had severe pulmonary hypertension (mean Ppa, 57 mm Hg) and severe hypoxemia (PaO2 37 mm Hg), which was mainly due to shunt (16% of cardiac output) and a broadening of the main mode of the ventilation-perfusion (VA/Q) distribution (log SD Q, 0.94). There was a significant reduction in shunt during nCPAP to 6% of cardiac output without increasing Ppa, and this effect appeared to extend past the period of application. We conclude that nCPAP reduces intrapulmonary shunt in this rare condition and allows for correction of hypoxemia with a smaller oxygen flow rate.