No abstract

Inspiratory positive airway pressure delivered by a face mask can obviate the need for conventional mechanical ventilation in patients with acute exacerbations of chronic obstructive pulmonary disease.

Polymorphonuclear neutrophil (PMN) migration across basement membrane is thought to be dependent on the degradation of membrane constituents. PMN gelatinase B, a metalloproteinase able to degrade type IV collagen, may be involved in this phenomenon. PMN gelatinase B is released in the extracellular medium as a latent proform and then activated, mainly by PMN elastase. We investigated the role of gelatinase B in PMN migration across a Matrigel basement membrane matrix coated onto a filter, in a Boyden chamber. The effects of gelatinase and elastase inhibitors on PMN migration in this system were tested. Chemokinesis of PMN was tested in the same Boyden chamber across a filter free of basement membrane. The agarose method was used to test the same inhibitors for effects on PMN chemotaxis. In both systems, FMLP 10(-7)M was used as a chemoattractant. Addition of 10(-8)M TIMP-1 (the preferential gelatinase B inhibitor) inhibited trans-basement membrane PMN migration by 52 +/- 6% (P<0.05), without affecting PMN chemokinesis, chemotaxis, or degranulation. Also, (Ala)(2) Pro Val chloromethyl ketone (AAPVCK) 100 micron, a specific elastase inhibitor, inhibited trans-basement membrane PMN migration by 51 +/- 8% (P<0.05), without affecting PMN chemokinesis, chemotaxis, or degranulation. The AAPVCK-TIMP combination led to a decrease in migration across Matrigel basement membrane (46 +/- 2%, P,0.05)similar to that seen with TIMP alone. AAPVCK was responsible for inhibition of gelatinase B activation, leading to a decrease in activated gelatinase from 14% to 2% of total gelatinase release (P<0.05). All these results strongly suggest that gelatinase B is a major factor of PMN migration across basement membrane and that elastase may contribute to this process by activating pro-gelatinase B.

Persistent inability to tolerate discontinuation from mechanical ventilation is frequently encountered in patients recovering from acute respiratory failure. We studied the ability of inspiratory pressure support, a new mode of ventilatory assistance, to promote a nonfatiguing respiratory muscle activity in eight patients unsuccessful at weaning from mechanical ventilation. During spontaneous breathing, seven of the eight patients demonstrated electromyographic signs of incipient diaphragmatic fatigue. During ventilation with pressure support at increasing levels, the work of breathing gradually decreased (p less than 0.02) as well as the oxygen consumption of the respiratory muscles (p less than 0.01), and electrical signs suggestive of diaphragmatic fatigue were no longer present. In addition, intrinsic positive end-expiratory pressure was progressively reduced. For each patient an optimal level of pressure support was found (as much as 20 cm H2O), identified as the lowest level maintaining diaphragmatic activity without fatigue. Above this level, diaphragmatic activity was further reduced and untoward effects such as hyperinflation and apnea occurred. When electrical diaphragmatic fatigue occurred, the activity of the sternocleidomastoid muscle was markedly increased, whereas it was minimal when the optimal level was reached. We conclude that in patients demonstrating difficulties in weaning from the ventilator: (1) pressure support ventilation can assist spontaneous breathing and avoid diaphragmatic fatigue (pressure support allows adjustment of the work of each breath to provide an optimal muscle load); (2) clinical monitoring of sternocleidomastoid muscle activity allows the required level of pressure support to be determined to prevent fatigue.

No abstract

Nasal obstruction has frequently been mentioned as a possible risk factor in obstructive sleep apnoea syndrome (OSAS). Over a 2‐yr period, 541 unselected consecutive snorers referred for suspected breathing disorders during sleep were included to undergo posterior rhinomanometry. In addition cephalometric landmarks and body mass index (BMI) were obtained. Polysomnography was used to determine the number of abnormal respiratory events that occurred during sleep. OSAS was defined as 15 episodes, or more, of apnoea or hypopnoea per hour of sleep (AHI). Of the 541 consecutive snorers 528 underwent nasal resistance measurement by posterior rhinomanometry (failure rate: 2.4%). Patients with OSAS (259 patients) had higher nasal resistance than patients without OSAS (2.6±1.6 hPa·L·s‐1versus 2.2±1.0 hPa·L·s‐1, respectively, p<0.005). A stepwise multiple regression analysis showed that BMI, male sex, nasal resistance, and cephalometric parameters were contributing factors to the AHI. The r2‐value of the multiple regression analysis was 0.183. Nasal resistance contributed 2.3% of the variance (p<0.0001), whereas mandibular plane‐hyoid distance, BMI, male sex and age contributed 6.2%, 4.6%, 3% and 1.3% of the variance, respectively. To conclude, daytime nasal obstruction is an independent risk factor for OSAS.

No abstract

The ventilatory and hemodynamic effects of continuous positive airway pressure (CPAP) delivered via a face mask (at 0, 5, and 10 cm H2O, and after a return to 0 cm H2O) were studied in nine patients with acute left heart failure (pulmonary artery occlusion pressure [PAOP] > or = 18 mm Hg, and cardiac index [CI] < or = 2.8 L/min/m2). CPAP at 10 cm H2O induced an improvement in lung compliance (60 +/- 10 ml/cm H2O to 87 +/- 20 ml/cm H2O, p < 0.05) and in lung and airway resistance (5.7 +/- 1.0 cm H2O/L/s to 3.4 +/- 1.0 cm H2O/L/s, p < 0.05), a reduction in work of breathing (18 +/- 3 J/min to 12 +/- 2 J/min, p < 0.05), and in the pressure-time index of the respiratory muscles (279 +/- 22 cm H2O/s/min to 174 +/- 25 cm H2O/s/min, p < 0.05), without significant changes in breathing pattern. Despite a significant reduction in the negative swings in intrathoracic pressure (15.2 +/- 1.9 cm H2O to 10.8 +/- 1.8 cm H2O, p < 0.001), no significant change was observed in CI or stroke volume during CPAP. However, mean transmural filling pressures decreased significantly with CPAP, suggesting a better cardiac performance. Neither the level of stroke volume nor of PAOP, was predictive of changes in CI or in stroke volume. In patients with respiratory insufficiency caused by congestive heart failure (CHF), CPAP reduces respiratory muscle effort without altering cardiac output. The slight decrease in mean transmural left and right atrial pressures suggests an improvement in cardiac performance.