Airway secretions influence upper airway patency in the rabbit

The hypothesis tested in these experiments was that the properties of the upper airway mucosal surface may be important in reopening of the closed airway, and that mucosal surface properties may depend on airway secretions. The intraluminal pressures required to close and reopen the upper airways were measured in the isolated upper airways of anesthetized rabbits. Atropine (0.1 mg/kg i.v.), given to reduce the volume of upper airway secretions, had no effect on closing or on reopening pressures. Stimulation of upper airway secretions in 6 animals with methacholine (0.2 mg/kg subcutaneously) changed closing pressures from -10.63 +/- 0.57 to -16.91 +/- 0.60 cm H2O (p less than 0.05) but made the airway less likely to reopen, changing reopening pressures from -3.45 +/- 0.48 to -2.12 +/- 0.39 cm H2O (p less than 0.04), and caused frequent failure of the airway to reopen spontaneously. Filling the upper airways with saline to mimic the hydrostatic forces present in the mucus-filled airway caused both closing and reopening pressures to become more negative. We conclude that reopening pressure is influenced by the secretions lining the airway surface, and, therefore, that airway closure and airway reopening may be substantially independent.     

The role of vascular tone in the control of upper airway collapsibility

Upper airway collapsibility may be influenced by both muscular and nonmuscular factors. Because mucosal blood volume (and therefore vascular tone) is an important determinant of nasal airway patency, vascular tone may be an important nonmuscular determinant of pharyngeal collapsibility. This hypothesis was tested in two experimental models. First, upper airway closing (CP) and opening (OP) pressures and static compliance were measured in nine anesthetized, sinoaortic-denervated, paralyzed cats with isolated upper airways. Vascular tone was decreased with either papaverine or sodium nitroprusside (NTP), and increased with phenylephrine (PE), whereas blood pressure and end-tidal CO2 were maintained constant. Vasodilation increased CP (control = -10.4 +/- 1.3, NTP = -7.3 +/- 1.2 cm H2O; p less than 0.05) and OP (control = -7.9 +/- 1.5, NTP = -3.3 +/- 1.8 cm H2O; p less than 0.05). In contrast, vasoconstriction tended to decrease CP (control = -10.7 +/- 1.5, PE = -11.7 +/- 1.4 cm H2O; p less than 0.09) and OP (control = -8.1 +/- 1.2, PE = -9.9 +/- 1.9 cm H2O; p less than 0.1). Thus, vasodilation increased and vasoconstriction tended to decrease upper airway collapsibility. Upper airway static compliance was unchanged during either drug infusion. In order to assess changes in pharyngeal cross-sectional area (CSA) that occurred during vasodilation, magnetic resonance imaging was utilized in seven cats. During vasodilation with NTP, pharyngeal CSA was reduced from 0.44 +/- 0.10 to 0.30 +/- 0.09 cm2 (p less than 0.05), and pharyngeal volume was reduced from 15.3 +/- 2.4 to 13.9 +/- 2.7 cm3 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

High-frequency oscillatory ventilation compared with conventional mechanical ventilation in newborn lambs: effects of increasing airway pressure on intracranial pressures.

We tested the hypothesis that intracranial pressures and cerebral perfusion pressure in the newborn are more seriously affected by increasing airway pressure during high-frequency oscillatory ventilation (HFOV) than during conventional mechanical ventilation (CMV). Mean airway pressure was acutely elevated in stepwise fashion to 25 cm H2O in six anesthetized, paralyzed newborn lambs. Pressure (mean +/- SE) increased similarly during HFOV and CMV in the jugular vein (7 +/- 1 and 8 +/- 1 cm H2O, respectively), the sagittal sinus (6 +/- 1 and 7 +/- 1 cm H2O), and the cerebrospinal fluid of the lateral ventricle (4 +/- 1 and 6 +/- 1 cm H2O). Decreases in arterial blood pressure (-13 +/- 2 and -10 +/- 2 cm H2O) and cerebral perfusion pressure (-17 +/- 2 and -16 +/- 2 cm H2O) were also similar during HFOV and CMV. Intracranial pressure-volume curves were generated by incrementing cerebrospinal fluid volume in eight lambs. Curves generated during HFOV and CMV were similar, reflecting a similar intracranial compliance during the two ventilatory modes. These data indicate that intracranial compliance and the effects of increasing airway pressure upon intracranial pressures are not significantly different between HFOV and CMV.     

Effect of oral appliance therapy on upper airway collapsibility in obstructive sleep apnea

Oral appliance therapy is emerging as an alternative to continuous positive airway pressure for the treatment of obstructive sleep apnea (OSA). However, its precise mechanisms of action are yet to be defined. We examined the effect of a mandibular advancement splint (MAS) on upper airway collapsibility during sleep in OSA. Ten patients with proven OSA had a custom-made MAS incrementally adjusted during an acclimatization period until the maximum comfortable limit of mandibular advancement was reached. Polysomnography with the splint was then performed. After a 1-week washout period, upper airway closing pressures during sleep (with and without MAS) were determined. Significant improvements with MAS therapy were seen in the apnea/hypopnea index (25.0 +/- 3.1 vs. 13.2 +/- 4.5/hour, p < 0.03) and upper airway closing pressure in Stage 2 sleep (-1.6 +/- 0.4 vs. -3.9 +/- 0.6 cm H2O, p < 0.01) and in slow wave sleep (-2.5 +/- 0.7 vs. -4.7 +/- 0.6 cm H2O, p < 0.02) compared with no therapy. These preliminary data indicate that MAS therapy is associated with improved upper airway collapsibility during sleep. The mediators of this effect remain to be determined.     

Pressure controlled inverse ratio ventilation in severe adult respiratory failure

Thirty-one patients with severe respiratory failure who were failing volume controlled conventional ratio ventilation were placed on pressure controlled inverse ratio ventilation (PC-IRV) for a total of 4,426 patient-hours. The PC-IRV resulted in a reduction of minute ventilation from 22 +/- 1.0 L/min (mean +/- SEM) to 15 +/- 0.7 L/min. Peak inspiratory pressure (PIP) was reduced from 66 +/- 2.3 cm H2O to 46 +/- 1.6 cm H2O and positive end expiratory pressures (PEEP) from 15 +/- 1.0 cm H2O to 2.5 +/- 0.5 cm H2O. Mean airway pressure increased from 30 +/- 1.7 cm H2O to 35 +/- 1.7 cm H2O. Oxygenation (PaO2) improved from 69 +/- 4.0 mm Hg to 80 +/- 4.5 mm Hg. The PaCO2 and arterial pH were not significantly changed. There were no significant changes in mean hemodynamic pressures. A lung compromise index (FIO2.PIP.10/PaO2) retrospectively distinguished between successful and unsuccessful PC-IRV episodes. These data suggest that PC-IRV can be successfully and safely implemented in critically ill patients with severe respiratory failure over prolonged periods of time resulting in significant improvement in oxygenation at lower minute volume, peak airway pressure and PEEP requirements.     

Effects of upper airway carbon dioxide on upper airway resistance and muscle activity in young guinea-pigs.

The upper airway (UA) of adult animals is known to contain carbon dioxide-sensitive receptors and UA CO2 reflexly affects breathing, UA dilator muscle activity and UA resistance. These effects may function in the control of UA patency. There is evidence that some UA reflexes are stronger in young than in adult animals, but it is not known whether CO2-sensitive receptors are present in the UA of young animals, and the effects of UA CO2 on UA resistance and on UA dilator muscle activity have not been investigated in young animals. The responses of ventilation, UA resistance and geniohyoid muscle electromyographic activity to warm air containing 10% CO2 applied to the isolated UA were measured in anaesthetized, vagotomized young guinea-pigs breathing spontaneously through a low-cervical tracheostomy. Upper airway carbon dioxide caused an increase in ventilation (46.7+/-16.3 to 49.9+/-16.8 mL x min(-1) x 100 g body weight(-1)) and upper airway resistance (56.8+/-14.8 to 63.7+/-17.7 cmH2O x L(-1) x s(-1) x kg body weight(-1)). Similar effects were obtained following vagotomy. Geniohyoid activity became apparent following vagotomy and this activity was reduced by upper airway carbon dioxide. These responses were abolished by topical anaesthesia of the upper airway. This suggests that the reflexes seen are due to carbon dioxide-sensitive receptors in the upper airway.     

Comparison of conventional and high-frequency ventilation in piglets after lung lavage

A piglet model of respiratory failure was used to compare airway pressures required for adequate gas exchange by a conventional positive pressure ventilator (CMV) and a high-frequency pneumatic flow interrupter (HFFI). Twelve newborn piglets (age means = 3.8 days and weight means = 1.4 kg) were given saline lung lavages after receiving intravenous Ketamine and Pavulon. Femoral and jugular vessels were catheterized for measurements of aortic and pulmonary blood pressures and gases, cardiac output, hematocrit, glucose and for the infusion of fluids. Airway pressures were measured 5 mm above the distal tip of the endothracheal tube. Lung lavage resulted in decreased static compliance and a twofold increase in pulmonary shunting. Following lavage the animals were kept on 100% oxygen and randomly assigned to either CMV (30/min) or HFFI (600/min) ventilation and thereafter were switched every 30 minutes to the alternate mode. Inspiratory duration was 33% of the total respiratory cycle during CMV and 30-50% for HFFI. Sixteen pairs of data comparing both ventilator modes were used. Blood gases, cardiovascular variables, alveolar-arterial oxygen gradient, and pulmonary shunting were not different with either ventilator. Positive end-expiratory pressure (5.3 and 5.6 cm H2O) and mean airway pressure (12.5 and 11.9 cm H2O) were equal for CMV and HFFI, respectively. Peak inspiratory pressure was significantly lower for HFFI (23.1 +/- 3.7 SD cm H2O) than for CMV (30.4 +/- 5.5 SD cm H2O). The lower peak inflation pressure required during HFFI ventilation may reduce the potential for lung rupture.     

Expiratory washout versus optimization of mechanical ventilation during permissive hypercapnia in patients with severe acute respiratory distress syndrome.

The aim of this study was to compare three ventilatory techniques for reducing PaCO2 in patients with severe acute respiratory distress syndrome treated with permissive hypercapnia: (1) expiratory washout alone at a flow of 15 L/min, (2) optimized mechanical ventilation defined as an increase in the respiratory frequency to the maximal rate possible without development of intrinsic positive end- expiratory pressure (PEEP) combined with a reduction of the instrumental dead space, and (3) the combination of both methods. Tidal volume was set according to the pressure-volume curve in order to obtain an inspiratory plateau airway pressure equal to the upper inflection point minus 2 cm H2O after setting the PEEP at 2 cm H2O above the lower inflection point and was kept constant throughout the study. The three modalities were compared at the same inspiratory plateau airway pressure through an adjustment of the extrinsic PEEP. During conventional mechanical ventilation using a respiratory frequency of 18 breaths/min, respiratory acidosis (PaCO2 = 84 +/- 24 mm Hg and pH = 7.21 +/- 0.12) was observed. Expiratory washout and optimized mechanical ventilation (respiratory frequency of 30 +/- 4 breaths/min) had similar effects on CO2 elimination (DeltaPaCO2 = -28 +/- 11% versus -27 +/- 12%). A further decrease in PaCO2 was observed when both methods were combined (DeltaPaCO2 = -46 +/- 7%). Extrinsic PEEP had to be reduced by 5.3 +/- 2.1 cm H2O during expiratory washout and by 7.3 +/- 1.3 cm H2O during the combination of the two modes, whereas it remained unchanged during optimized mechanical ventilation alone. In conclusion, increasing respiratory rate and reducing instrumental dead space during conventional mechanical ventilation is as efficient as expiratory washout to reduce PaCO2 in patients with severe ARDS and permissive hypercapnia. When used in combination, both techniques have additive effects and result in PaCO2 levels close to normal values.     

Effects of intrapulmonary CO2 and airway pressure on pulmonary vagal afferent activity in the alligator

The effects of airway CO2 and pressure on pulmonary vagal afferent fibers were studied in seven anesthetized alligators Alligator mississippiensis, at room temperature (24 degrees C). Of 49 receptors which fired in phase with ventilation, 13 behaved like mammalian rapidly adapting pulmonary stretch receptors, 19 like mammalian slowly adapting pulmonary stretch receptors (PSR), and 17 like avian intrapulmonary CO2-sensitive chemoreceptors (IPC). PSR and IPC were positively localized to the lung by punctate stimulation or response to airway CO2 changes during pulmonary artery occlusion. PSR discharge frequency (fPSR) was measured at airway pressures (Paw) from 0 to 15 cm H2O at FICO2 = 0.01 in 14 receptors. fPSR increased in all receptors throughout the range of Paw studied. In 13 PSR, increasing FICO2 from 0.01 to 0.07 decreased fPSR 23 +/- 13% (+/- SEM) at Paw = 2 cm H2O and 14 +/- 7% at 15 cm H2O. IPC discharge frequency (fIPC) decreased as FICO2 increased and most discharged less than 1 sec-1 at FICO2 = 0.03. In 7 IPC at FICO2 = 0.01, increasing Paw from 2 to 15 cm H2O increased fIPC 17 +/- 5% after pulmonary artery occlusion demonstrating some mechanosensitivity in alligator IPC. Although both IPC and PSR showed mechanosensitivity and CO2-sensitivity, the two receptor types were distinct. PSR were 13 times more sensitive to Paw changes than IPC and IPC were 14 times more sensitive to FICO2 changes than PSR. We did not find any receptors with intermediate CO2- or mechanosensitivities that could represent a transitional form of receptor. These results predict that IPC and PSR may have different roles in reflex ventilatory control.     

Ventilatory control and airway anatomy in obstructive sleep apnea

Ventilatory instability may play an important role in the pathogenesis of obstructive sleep apnea. We hypothesized that the influence of ventilatory instability in this disorder would vary depending on the underlying collapsibility of the upper airway. To test this hypothesis, we correlated loop gain with apnea-hypopnea index during supine, nonrapid eye movement sleep in three groups of patients with obstructive sleep apnea based on pharyngeal closing pressure: negative pressure group (pharyngeal closing pressure less than -1 cm H(2)O), atmospheric pressure group (between -1 and +1 cm H(2)O), and positive pressure group (greater than +1 cm H(2)O). Loop gain was measured by sequentially increasing proportional assist ventilation until periodic breathing developed, which occurred in 24 of 25 subjects. Mean loop gain for all three groups was 0.37 +/- 0.11. A significant correlation was found between loop gain and apnea-hypopnea index in the atmospheric group only (r = 0.88, p = 0.0016). We conclude that loop gain has a substantial impact on apnea severity in certain patients with sleep apnea, particularly those with a pharyngeal closing pressure near atmospheric.     

Airway pressure release ventilation in severe acute respiratory failure

Airway pressure release ventilation (APRV), a new ventilatory support technique, was compared with conventional intermittent positive-pressure ventilation plus PEEP (CPPV) in 18 patients with severe acute respiratory failure. Patients were initially stabilized on CPPV and then switched to APRV. The APRV provided effective ventilatory support in 17 of 18 patients; APRV achieved similar levels of alveolar ventilation as CPPV (for APRV, mean PaCO2 = 45.0 +/- 6.2 mm Hg; vs for CPPV, mean PaCO2 = 43.3 +/- 5.7 mm Hg), with significantly lower mean maximum airway pressures (38.9 +/- 10.1 cm H2O vs 64.6 +/- 15.4 cm H2O; p = 0.0001) and mean VT (0.79 +/- 0.11 L vs 1.05 +/- 0.15 L; p = 0.0002). No significant differences in mean airway pressure, end-expiratory pressure, FIO2, ventilator rate, arterial blood gas levels, and hemodynamic function were noted between APRV and CPPV.     

Respiratory distress syndrome in immature lambs. Prevention through antenatal accelerated conditioning of the lung

We tested the effectiveness of constant distending pressure applied to immature lungs in preventing respiratory distress syndrome. Fetal lambs of 131 to 134 days gestation were delivered by cesarean section, but the umbilical circulation was kept intact for CO2 removal through the natural in situ placenta. The lungs were inflated to a pressure of 35 cm H2O (Group I, 11 animals) or 25 cm H2O (Group II, 14 animals), after which the airway pressure was maintained at 15 cm H2O through apneic oxygenation until total static compliance exceeded 0.5 ml (cm H2O)- 1kg -1. After a mean of 1.1 and 5.7 h, respectively, the animals were delivered and were given mechanical ventilation for 24 h. Twenty-four animals reached this aimed-for compliance and survived the period of mechanical ventilation in excellent health. A control group of fetal lambs was delivered immediately and treated with mechanical ventilation. Three of 10 control animals developed severe respiratory distress syndrome and died; 1 additional animal survived but with central nervous system involvement from severe hypoxia. We conclude that pulmonary inflation to 35 cm H2O pressure, followed by a constant distending pressure of 15 cm H2O, held until compliance reaches 0.5 ml (cm H2O)- 1kg -1, is an important element in the prevention of respiratory distress syndrome.     

Effects of lung volume and positive airway pressure on collateral resistance

Nine mongrel dogs were anesthetized, paralysed, ventilated, and placed in an iron lung. Each animal was transiently connected to a spirometer and the respiratory system compliance measured by applying negative or positive extrathoracic pressures (from -20 cm H2O to +20 cm H2O in 5 cm H2O steps). A sub-lobar bronchus was wedged with a 5.5 mm bronchoscope, and a 5f Swan-Ganz catheter was inserted into the lumen of the bronchoscope; one port served to introduce a 200 ml.min-1 flow of 5% CO2 in air, the other to measure the pressure in the wedged segment. Rcoll was measured with extrathoracic pressures in the iron lung ranging from 0 to -20 cm H2O (NEP) and 0 to +20 cm H2O (PEP) in 5 cm H2O steps, and under expiratory positive airway pressure (EPAP) of 5, 10, 15, and 20 cm H2O. The maximal changes in FRC were an increase of 1009 +/- 49 ml (mean +/- SEM) with NEP and a decrease of 397 +/- 33 ml with PEP. Increasing FRC decreased Rcoll while decreasing FRC markedly increased it. EPAP induced similar decreases in Rcoll as NEP of equal pressure. This effect of EPAP was inhibited by simultaneously applying PEP of equal pressure. We conclude that resistance to collateral flow is highly dependent on lung volume, and that positive airway pressure decreases Rcoll by its effects on lung volume.     

Effect of hypercapnia on upper airway resistance and collapsibility in anesthetized dogs

The upper airway (UAW) is intrinsically unstable and susceptible to collapse when the negative inspiratory intraluminal pressure exceeds the stabilizing forces which prevent obstruction. In the present study we evaluated mechanisms by which UAW patency is maintained in the presence of increased inspiratory flows when respiration is stimulated. In seven anesthetized dogs breathing spontaneously through a low tracheostomy, the UAW was isolated by a second tracheostomy directed rostrally. UAW pressure-flow relationship and stability against collapse were evaluated during steady flow in the inspiratory direction while the animals were breathing 100% O2 or a hypercapnic gas mixture. The pressure-flow curves of the isolated UAW demonstrated the characteristic pattern of collapsible tubes. Steady state hypercapnia resulted in lower UAW resistance during both inspiration and expiration. UAW resistance decreased linearly as PCO2 and ventilation increased over the course of CO2 rebreathing. In addition, during hypercapnia the critical negative intraluminal pressure required to induce UAW collapse and obstruction increased from -4.3 +/- 0.9 to -8.5 +/- 1.5 SE cm H2O (p less than 0.01), indicating increased stability of the UAW. Since hypercapnia is known to stimulate UAW muscles, our findings suggest that increased UAW muscle activity improves UAW patency both by decreasing their resistance to airflow, and by increasing UAW walls rigidity and stability against collapse.     

The effects of breath-holds and Muller manoeuvres on upper airway carbon dioxide concentration in humans

BACKGROUND: Obstructive sleep apnoea is caused by collapse of the upper airway. The presence of CO(2) in the upper airway lumen evokes a number of reflexes which favour upper airway re-opening, and we have proposed previously that CO(2) would build up in the upper airway following airway collapse and that this would contribute to reflex airway re-opening. However, it is not known if CO(2) can transfer from the alveoli to the anatomical dead space of the upper airway during apnoea. OBJECTIVES: To determine if alveolar CO(2) can enter the upper airway during breath-holds and Muller manoeuvres. MATERIAL AND METHODS: With local ethics committee approval, 6 male volunteers (aged 22-48 years), following a quiet inspiration, carried out breath-holds and Muller manoeuvres until breaking point. CO(2) was measured continuously in samples obtained from the hypopharynx using an infrared analyser with a sample rate of 50 ml/min. Muller manoeuvres (forced inspirations against a closed upper airway) mimic the respiratory efforts which occur during obstructive apnoeas. RESULTS: In all cases, CO(2) increased progressively during apnoeas. There was a much larger increase in Muller manoeuvres (3.78 +/- 0.51%, mean +/- SEM at breaking point) compared to breath-holds. DISCUSSION: These results show that upper airway CO(2) concentration rises substantially during apnoeas and suggest that transfer of CO(2) from the lungs to the upper airway may evoke a number of reflex effects which could affect breathing and upper airway re-opening during obstructive apnoeas.     

Spinal cord stimulation: a new method to produce an effective cough in patients with spinal cord injury

Patients with spinal cord injury have an increased risk of developing respiratory tract infections as the result of expiratory muscle paralysis and consequent inability to cough. We have developed a method by which the expiratory muscles can be activated via lower thoracic and upper lumbar spinal cord stimulation to produce an effective cough mechanism. In a tetraplegic patient who required frequent (8.57+/-2.3 times per week [mean+/-SEM]) caregiver assistance to facilitate airway clearance and expectoration of secretions, three epidural electrodes were applied in the T9, T11, and L1 spinal cord regions. During stimulation at the T9 and L1 levels, airway pressures were 90 and 82 cm H2O, respectively. Peak expiratory flow rates were 6.4 L/s and 5.0 L/s; respectively. During combined (T9+L1) stimulation, airway pressure and expiratory flow rate increased to 132 cm H2O and 7.4 L/s, respectively. Addition of the third lead did not result in further increases in pressure generation. These values are characteristic of those observed with a normal subject. Because the patient is able to trigger the device independently, he no longer requires caregiver support for airway management. If confirmed in additional patients, spinal cord stimulation may be a useful method to restore an effective cough mechanism in patients with spinal cord injury.     

Physiologic effects of noninvasive ventilation during acute lung injury

A prospective, crossover, physiologic study was performed in 10 patients with acute lung injury to assess the respective short-term effects of noninvasive pressure-support ventilation and continuous positive airway pressure. We measured breathing pattern, neuromuscular drive, inspiratory muscle effort, arterial blood gases, and dyspnea while breathing with minimal support and the equipment for measurements, with two combinations of pressure-support ventilation above positive end-expiratory pressure (10-10 and 15-5 cm H2O), and with continuous positive airway pressure (10 cm H2O). Tidal volume was increased with pressure support, and not with continuous positive airway pressure. Neuromuscular drive and inspiratory muscle effort were lower with the two pressure-support ventilation levels than with other situations (p < 0.05). Dyspnea relief was significantly better with high-level pressure-support ventilation (15-5 cm H2O; p < 0.001). Oxygenation improved when 10 cm H2O positive end-expiratory pressure was applied, alone or in combination. We conclude that, in patients with acute lung injury (1) noninvasive pressure-support ventilation combined with positive end-expiratory pressure is needed to reduce inspiratory muscle effort; (2) continuous positive airway pressure, in this setting, improves oxygenation but fails to unload the respiratory muscles; and (3) pressure-support levels of 10 and 15 cm H2O provide similar unloading but differ in their effects on dyspnea.     

Prone position increases collapsibility of the passive pharynx in infants and small children

On the basis of two observations that avoiding prone sleeping decreased incidence of sudden infant death syndrome and that obstructive sleep apnea is closely linked with the syndrome, we hypothesized that the prone position may increase upper airway collapsibility in infants and small children. Passive pharyngeal collapsibility of 19 infants and small children (10-101 weeks old) was examined in three postures: supine with face straight up, supine with neck rotated, and prone with neck rotated. The collapsibility was evaluated with the maximal distension of the most collapsible region, pharyngeal stiffness, and pharyngeal closing pressure, estimated from static pressure-area relationship of the passive pharynx. No significant changes in pharyngeal stiffness were detected; however, maximal distension was reduced in the prone position (mean +/- SD, 0.56 +/- 0.26 versus 0.44 +/- 0.20 cm(2); supine with face straight up versus prone position, p < 0.05). Pharyngeal closing pressure increased at neck rotation in the supine position (-4.5 +/- 2.4 versus -2.8 +/- 2.3 cm H(2)O; supine with face straight up versus supine with neck rotated, p < 0.05), and a further increase was observed in the prone position (-0.3 +/- 2.9 cm H(2)O, p < 0.05 versus supine with neck rotation). Pharyngeal closing pressure in the prone position was above atmospheric pressure in half of our subjects, whereas all subjects had negative pharyngeal pressure in the supine position. We conclude that the prone position increases upper airway collapsibility, although the mechanism is yet unclear.     

Lung edema caused by high peak inspiratory pressures in dogs. Role of increased microvascular filtration pressure and permeability

Mechanical ventilation with high peak airway pressures (Paw) has been shown to induce pulmonary edema in animal experiments, but the relative contributions of transvascular filtration pressure and microvascular permeability are unclear. Therefore, we examined the effects of positive-pressure ventilation on two groups of open-chest dogs ventilated for 30 min with a peak Paw of 21.8 +/- 2.3 cm H2O (Low Paw) or 64.3 +/- 3.5 cm H2O (High Paw). No hemodynamic changes were observed in the Low Paw group during ventilation, but mean pulmonary artery pressure (Ppa) increased by 9.9 cm H2O, peak inspiratory Ppa by 24.6 cm H2O, and estimated mean microvascular pressure by 12.5 cm H2O during High Paw ventilation. During the same period, lung lymph flow increased by 435% in the High Paw and 35% in the Low Paw groups, and the terminal extravascular lung water/blood-free dry weight ratios were 5.65 +/- 0.27 and 4.43 +/- 0.13 g/g, respectively, for the two groups. Lung lymph protein clearances and minimal lymph/plasma ratios of total protein were significantly higher (p less than 0.05) after 2 h of increased left atrial pressure (PLA) in the High Paw group versus the Low Paw group, which indicates a significant increase in microvascular permeability. Lymph prostacyclin concentration in pulmonary lymph, measured as the stable metabolite 6-0-PGF1 alpha, was increased significantly by 70 to 150% from baseline (p less than 0.05) in both groups during the periods of increased Paw and increased PLA, but it was not significantly different between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pharyngeal compliance in snoring subjects with and without obstructive sleep apnea

Recent studies have demonstrated a reduction in pharyngeal cross-sectional area and in upper airway muscle tone in patients with obstructive sleep apnea. These findings suggest that the pharynx in such patients may be more compliant than normal even in the awake state. We have tested this hypothesis by examining the pressure-area relationship of the pharynx in 13 patients and in 7 control subjects. Measurements were performed during wakefulness, with the subject seated, and at a constant lung volume near functional residual capacity. Pharyngeal area was measured by an acoustic reflection technique. Pharyngeal pressure was varied by having the subject perform gradual inspiratory and expiratory isovolume maneuvers against a distally occluded airway while mouth pressure was recorded. Specific compliance of the pharynx was calculated as the fractional change in pharyngeal area between a pressure of 0 and -10 cm H2O and and between 0 and 10 cm H2O. Specific pharyngeal compliance was 0.036 +/- 0.004 cm H2O-1 (mean +/- SE) in the control group and 0.094 +/- 0.012 cm H2O-1 in patients with OSA (p less than 0.01). These findings indicate that patients with obstructive sleep apnea have increased pharyngeal compliance. This abnormality predisposes to pharyngeal occlusion during sleep when negative transmural pressures are generated in the pharynx.