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.     

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.     

Sigh in acute respiratory distress syndrome

Mechanical ventilation with plateau pressure lower than 35 cm H2O and high positive end-expiratory pressure (PEEP) has been recommended as lung protective strategy. Ten patients with ARDS (five from pulmonary [p] and five from extrapulmonary [exp] origin), underwent 2 h of lung protective strategy, 1 h of lung protective strategy with three consecutive sighs/min at 45 cm H2O plateau pressure, and 1 h of lung protective strategy. Total minute ventilation, PEEP (14.0 +/- 2.2 cm H2O), inspiratory oxygen fraction, and mean airway pressure were kept constant. After 1 h of sigh we found that: (1) PaO2 increased (from 92.8 +/- 18.6 to 137.6 +/- 23.9 mm Hg, p < 0.01), venous admixture and PaCO2 decreased (from 38 +/- 12 to 28 +/- 14%, p < 0.01; and from 52.7 +/- 19.4 to 49.1 +/- 18.4 mm Hg, p < 0.05, respectively); (2) end-expiratory lung volume increased (from 1.49 +/- 0.58 to 1.91 +/- 0.67 L, p < 0.01), and was significantly correlated with the oxygenation (r = 0.82, p < 0.01) and lung elastance (r = 0.76, p < 0.01) improvement. Sigh was more effective in ARDSexp than in ARDSp. After 1 h of sigh interruption, all the physiologic variables returned to baseline. The derecruitment was correlated with PaCO2 (r = 0.86, p < 0.01). We conclude that: (1) lung protective strategy alone at the PEEP level used in this study may not provide full lung recruitment and best oxygenation; (2) application of sigh during lung protective strategy may improve recruitment and oxygenation.     

Treatment effects on carbon dioxide retention in patients with obstructive sleep apnea-hypopnea syndrome

OBJECTIVES: This study was designed to examine respiratory control in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), with or without CO(2) retention. METHODS: We recruited 10 body mass index-matched, apnea-hypopnea index-matched, age-matched, and lung function-matched OSAHS patients, according to their awake PaCO(2). Five patients were hypercapnic (PaCO(2), > or = 45 mm Hg), and five patients were eucapnic. Hypoxic responses (the ratio of the change in minute ventilation [DeltaV(E)] to the change in arterial oxygen saturation [DeltaSaO(2)] and the ratio of the change in mouth occlusion pressure over the first 100 ms of inspiration against an occluded airway [DeltaP(0.1)] to DeltaSaO(2)) and hypercapnic responses (DeltaV(E)/DeltaPCO(2) ratio and DeltaP(0.1)/DeltaPCO(2) ratio) were tested during wakefulness before treatment in all 10 patients, and before and during treatment (at 2, 4, and 6 weeks) with pressure support in the hypercapnic group. RESULTS: Hypercapnic patients had lower mean (+/- SD) DeltaV(E)/DeltaSaO(2) ratio than eucapnic patients (-0.17 +/- 0.04 vs -0.34 +/- 0.04 L /min/%SaO(2), respectively), lower mean DeltaP(0.1)/DeltaSaO(2) ratio (-0.04 +/- 0.02 vs -0.14 +/- 0.03 cm H(2)O/%SaO(2), respectively), and lower DeltaP(0.1)/DeltaPCO(2) ratio (0.23 +/- 0.1 vs 0.49 +/- 0.1 cm H(2)O/mm Hg, respectively) [p < 0.05]. After receiving noninvasive ventilation treatment, the hypercapnic and hypoxic responses of the hypercapnic patients increased. At 4 to 6 weeks, values for both responses had increased to within the normal range and PaCO(2) had fallen to < 45 mm Hg, while weight was unchanged. CONCLUSIONS: Depressed chemoresponsiveness plays a role that is independent of obesity in the development of CO(2) retention in some OSAHS patients, and it may be a response to sleep-disordered breathing.     

Cardiac output effects of high-frequency oscillatory ventilation in normal dogs

We compared the hemodynamic effects of high-frequency oscillatory ventilation (HFOV) with conventional continuous positive pressure ventilation (CPPV). Six mongrel dogs were anesthetized with chloralose and evaluated over a range of mean airway pressures (Pao) during CPPV and HFOV. Pao during HFOV was measured by allowing alveolar pressure to come into equilibrium with airway opening pressure and was set to equal mean Pao during CPPV. Pao during CPPV was set by adding positive end-expiratory pressure (PEEP) of 0, 5, 10, and 15 cm H2O. Transmural pulmonary capillary wedge pressures (Pwp) were maintained at near 11 mm Hg in both groups during all four ventilatory periods. Cardiac output as measured in triplicate by thermal dilution was similar between HFOV and CPPV at each level of mean airway pressure. After matching mean airway pressure and transmural Pwp we were unable to find any sparing effect of HFOV on cardiac output over a wide range of airway pressures. We conclude that there is not an independent effect of HFOV on cardiac output.     

Assisted ventilation in patients with preexisting cardiopulmonary disease. The effect on systemic oxygen consumption, oxygen transport, and tissue perfusion variables

We have evaluated systemic oxygen consumption (VO2), systemic oxygen transport, and tissue perfusion variables in 30 patients with preexisting cardiac and underlying pulmonary disease during continuous positive-pressure ventilation and positive end-expiratory pressure [PEEP], during intermittent mandatory ventilation (IMV and PEEP), and during spontaneous ventilation (continuous positive airway pressure [CPAP]), with end-expiratory pressure held constant during all ventilatory modes. Using radionuclide angiography together with invasive determinations of pressure and flow, we also measured left and right ventricular ejection fractions and calculated the end-systolic (ESVI) and end-diastolic (EDVI) volume indices of both ventricles. We found that oxygen transport was significantly greater during CPAP (583 +/- 172 ml/min/M2)(mean +/- SD) than during either IMV and PEEP (543 +/- 151 ml/min/sq; p less than 0.01) or CPPV and PEEP (526 +/- 159 ml/min/M2; p less than 0.01); however, we found no significant change in systemic VO2 with conversion from CPPV and PEEP to CPAP. The increase in oxygen transport was related to a greater cardiac index and, more specifically, to a higher heart rate during CPAP (CPAP, 106 +/- 16 beats per minute; CPPV and PEEP, 97 +/- 14 beats per minute) (p less than 0.01). Enhanced oxygen transport during CPAP was also associated with an increase in mixed venous oxygenation and a decrease in arterial lactate. Although neither the mean left ventricular EDVI nor ESVI changed from CPPV and PEEP to CPAP, the mean pulmonary capillary wedge pressure increased (CPPV and PEEP, 12 +/- 5 mm Hg; CPAP, 14 +/- 7 mm Hg) (p less than 0.01), suggesting the possibility of a decrease in left ventricular compliance with the spontaneous ventilatory mode. This study suggests that in the absence of ventilatory failure, spontaneous ventilation provides for better systemic oxygen transport and overall tissue perfusion than either controlled ventilation or IMV; however, this benefit of enhanced oxygen delivery with spontaneous ventilation may potentially be offset by a decrease in left ventricular compliance.     

不同通气模式下吸痰对呼吸力学和气体交换的影响

目的比较在压力控制通气（PCV）与容量控制通气（VCV）模式下吸痰对患者气体交换和呼吸力学的影响。方法采取自身交叉对照的方法，在PCV和VCV模式下分别对23例机械通气患者进行开放式吸痰，比较不同时间点气体交换、呼吸力学及血流动力学等指标的变化。结果在PCV模式下，吸痰后30min潮气量、顺应性分别为（6．60±1．95）mL／kg、（18±7）ml／cmH2O（1cmH2O=0．098kPa），与基础水平[（9．05±0．22）mL／kg、（24±6）ml／cmH2O]比较差异有统计学意义（F值分别为8．47、8．01，P均〈0．05）；而30min时动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）分别为[（87±13）mmHg（1mmHg=0．133kPa）、（53±11）mmHg]，与0min[（113±22）mmHg、（41±10）mmHg]比较差异有统计学意义（，值分别为6．18、9．13，P均〈0．05）；在VCV模式下，吸痰后30min顺应性、气道平台压、气道峰压分别为[（18±7）ml／cmH2O、（27±8）cmH2O、（33±8）cmH2O]，与基础水平[（23±7）ml／cmH2O、（22±5）cmH2O、（27±8）cmH2O]比较差异有统计学意义（，值分别为6．83、6．97、7．08，P均〈0．05）；而30min时PaO2、PaCO2分别为（105±26）mmHg、（38±11）mmHg，与0min[（109±21）mmHg、（37±14）mmHg]比较差异无统计学意义（F值分别为1．88、1．32，P均〉0．05）；在PCV模式下，吸痰后5min心率、平均动脉压（MAP）分别为（109±20）次／min、（89±10）mmHg，与基础水平[（97±17）次／min、（83±12）mmHg]比较差异有统计学意义（F值分别为5．86、9．49，P均〈0．05）。在VCV模式下，吸痰后5min心率、MAP分别为（110±17）次／min、（87±11）mmHg，与基础水平[（96±17）次／min、（79±11）mmHg]比较差异有统计学意义（F值分别为7．33、7．96，P均〈0．05）。结论吸痰在PCV和VCV模式下均引起患者气体交换受损和顺应性下降，但对气体交换的影响在PCV模式下比VCV更严重和持久。     

Tidal volume reduction in ARDS. Effect on cardiac output and arterial oxygenation

During continuous positive pressure ventilation (CPPV), mean airway pressure and lung volume will be influenced both by the tidal volume (VT) employed and the amount of positive end-expiratory pressure (PEEP). The effect of varying levels of CPPV on PaO2 and cardiac output (Q) has been previously assessed by adjusting the level of PEEP at constant VT. This study examined the influence of a 200-ml reduction in VT, at a constant PEEP of 15 cm H2O, on the PaO2 and Q of 21 patients with adult respiratory distress syndrome (ARDS). The relationship between change in Q and change in total respiratory system compliance (Cst) after VT reduction was also examined. VT reduction from 14.1 +/- 0.8 ml/kg to 11.2 +/- 0.9 ml/kg yielded an increase in Q (+ 15 +/- 12 percent, p less than 0.01) without a significant change in PaO2 (-6.3 +/- 15.0 mm Hg, p = 0.08). Cst increased with VT reduction (+ 3.1 +/- 1.8 ml/cm H2O). There was only a modest correlation (r = +0.42, p = 0.06) between delta Q percent and delta Cst following VT reduction. VT reduction at high level PEEP may yield a significant improvement in Q and net O2 delivery, but the degree of hemodynamic improvement is variable and is not reliably predicted noninvasively by measurement of Cst.     

Effect of home mechanical ventilation on inspiratory muscle strength in COPD

BACKGROUND: The mechanism responsible for chronic hypercapnic respiratory failure (HRF) in patients with COPD remains unclear. In this study, we tested the hypothesis that chronic HRF in patients with COPD is associated with low-frequency fatigue (LFF) of the diaphragm. METHODS: To test this hypothesis, we measured the twitch transdiaphragmatic pressure (Tw Pdi) elicited by stimulation of the phrenic nerves in 25 patients with chronic HRF (mean [+/- SD] Paco(2), 55.2 +/- 5.2 mm Hg) due to COPD before and 2 months after the initiation of noninvasive mechanical ventilation (NIV) [pressure-cycled ventilation with inspiratory positive airway pressure of 19.0 +/- 2.5 cm H(2)O]. We reasoned that had LFF been present, Tw Pdi should rise after effective NIV. RESULTS: The treatment compliance with NIV was good (median of machine usage was 7.1 h per night). Paco(2) decreased from 55.2 +/- 5.2 to 48.8 +/- 5.9 mm Hg (p < 0.001), and Pao(2) increased from 53.1 +/- 5.9 to 57.7 +/- 7.0 mm Hg (p = 0.007). Mean Tw Pdi at baseline was 11.1 +/- 6.6 cm H(2)O and after treatment was 11.7 +/- 7.2 cm H(2)O (not significant). Also, maximal static inspiratory mouth pressure did not change significantly (44.3 +/- 15.9 cm H(2)O vs 46.5 +/- 19.7 cm H(2)O). CONCLUSION: LFF of the diaphragm does not accompany chronic HRF in patients with COPD.     

Reduction of peak inflation and positive end-expiratory pressure using pressure control with inverse-ratio ventilation: a case report

Pressure control with inverse-ratio ventilation (PcIRV) has been shown to reduce peak inspiratory pressure (PIP) and positive end-expiratory pressure while providing adequate oxygenation and ventilation. This case of a 39-year-old man with a perforated colon who required high PIP after surgery demonstrates the effectiveness of PcIRV in reducing PIP from 72 cm H2O to 44 cm H2O and reducing positive end-expiratory pressure from 24 cm H2O to 6 cm H2O. A maximum inverse ratio of 3:1 was established to achieve a PaO2 of 105 mm Hg and PaCO2 of 37 mm Hg. In this case, the mean airway pressure rose from 32 cm H2O with assist-control ventilation to 39 cm H2O with PcIRV at 3:1. Cardiac output decreased from 9.11 L/min to 8.35 L/min with PcIRV at a 3:1 inspiratory/expiratory ratio.     

Influence of noninvasive positive pressure ventilation on inspiratory muscles

Intermittent positive pressure ventilation reduces inspiratory muscle electromyographic activity among patients with restrictive ventilatory failure. It has therefore been suggested that the reduction of energy expenditure at night could result in improved inspiratory muscle function during the day. Reported successes with nocturnal ventilation have not included measurements of inspiratory muscle endurance. We therefore electively ventilated six (five female, one male) patients (mean +/- SD) aged 36 +/- 13 years in whom respiratory failure (room air PaCO2, 60 +/- 13 mm Hg; PaO2, 44 +/- 11 mm Hg; SaO2, 75 +/- 12 percent) was consequent on restrictive ventilatory disease (vital capacity, 25 +/- 7 percent predicted; FEV1/FVC, 81 +/- 12 percent; total lung capacity, 40 +/- 5 percent predicted; MIPRV -42 +/- 10 cm H2O; MEP, 81 +/- 28 cm H2O). Positive pressure ventilation was administered with a customized closely fitting nasal mask attached to a volume-cycled pressure-limited ventilator. Full respiratory polysomnographic measurements as well as arterial blood gases, pulmonary function, distance walked in six minutes, and inspiratory muscle endurance were measured at baseline and after 3 and 14 months of ventilation. Ventilation improved saturation (baseline on O2; SWS 87 +/- 10, REM 79 +/- 14, ventilator on R/A; SWS 90 +/- 6, REM 89 +/- 5 percent) and transcutaneous Pco2 (baseline on O2; SWS 85 +/- 26, REM 94 +/- 39, ventilator on R/A; SWS 53 +/- 9, REM 58 +/- 9 mm Hg). During ventilation, the quantity and distribution of sleep was similar to that observed prior to ventilation. Daytime gas exchange improved as did the six-minute walking test (initial test = 429 +/- 120 m, three months after ventilation = 567 +/- 121 m), both of these improvements being sustained at 14 months. Inspiratory muscle endurance measured using a pressure threshold load (mean mouth pressure = 45 percent MIPRV) improved from 7.1 +/- 3.4 minutes at baseline to 14.8 +/- 7.6 minutes at 3 months, an improvement sustained at 14 months. There was no change in measured lung volumes or respiratory muscle strength. We conclude that the improvement in nocturnal gas exchange, daytime functioning, and arterial blood gases resulting from nocturnal positive pressure ventilation is associated with an increase in inspiratory muscle endurance sustained at 14 months.     

Facilitation of mechanical ventilation in status asthmaticus with continuous intravenous thiopental

Mechanical ventilation in status asthmaticus is associated with a significant mortality and morbidity. To facilitate intermittent positive pressure ventilation (IPPV), we have used continuous IV thiopental (thiopentone) together with traditional ventilatory techniques. With this policy, we were able to achieve rapid correction of arterial blood gas tensions in a group of 20 severe asthmatics requiring IPPV. By 1 hour, peak airway pressure (PAP) had fallen from 58.6 +/- 15.7 to 30.2 +/- 10.9 cm H2O (p less than 0.001). During the same period, PaCO2 fell from 51.3 +/- 15.3 to 40.17 +/- 8.2 mm Hg (p less than 0.05) and pH rose from 7.25 +/- 0.1 to 7.33 +/- 0.1 (p less than 0.001). Morbidity was low and in particular, no episode of barotrauma was noted. All patients survived the acute attack and were successfully liberated from the ventilator. We conclude that these results are largely attributable to our use of early and continuous IV anesthesia induced by thiopental.     

Physiologic evaluation of 4 weeks of nocturnal nasal positive pressure ventilation in stable hypercapnic patients with chronic obstructive pulmonary disease.

BACKGROUND: The long-term daily use of noninvasive mechanical ventilation (NIMV) to treat chronic respiratory failure in chronic obstructive pulmonary disease (COPD) patients is not widely recommended, partly because of a lack of clear clinical results and partly because the physiological mechanisms by which the daily application of NIMV would be helpful in these patients have not yet been clarified. OBJECTIVES: We designed a physiological study in order to assess the effects of supervised long-term NIMV on gas exchange, respiratory muscle function, pulmonary mechanics and to ascertain the possible effect of the treatment in responders and nonresponders. METHODS: Fourteen consecutive inpatients with stable hypercapnic COPD (pH = 7.37 +/- 0.01; PaCO(2) = 56.73 +/- 6.48 mm Hg) underwent 4 weeks of nocturnal NIMV delivered with a bilevel ventilator 'physiologically' set to reduce tidal transdiaphragmatic pressure (Pdi) by at least 50% and the amount of dynamic intrinsic positive end-expiratory pressure by 70%. Various measurements were compared with those obtained in a control group of consecutive patients with comparable baseline characteristics who refused NIMV and underwent breathing exercises for the same period of time. RESULTS: By the end of the 4 weeks NIMV had induced a slight but significant (p < 0.01) reduction in resting PaCO(2) (53.78 +/- 5.64 mm Hg) associated with a decrease in the pressure time product of the diaphragm per minute (from 172 +/- 60 to 136 +/- 61 cm H(2)O/l/s; p < 0.05). This latter value was primarily due to a significant shortening of the inspiratory duty cycle, while Pdi and lung mechanics were not modified. Eight of the 13 NIMV-treated patients (1 dropped out for nonmedical reasons) had a clear reduction in PaCO(2) (>3 mm Hg or >5% from enrollment) and were classified as responders. The acute reduction in PaCO(2) during the first trial with NIMV resulted to be a strong index of the final response. The subgroup of responders had a significantly increased maximal Pdi (from 41 +/- 19 to 49 +/- 23 cm H(2)O, p < 0.05) and an enhanced ability of the ventilatory pump to clear CO(2) (9.7 +/- 3.4 vs. 7.2 +/- 2.9 cm H(2)O x s/min; p < 0.01). No significant changes were observed in the control group. CONCLUSIONS: These results suggest that in a remarkable and identifyable proportion of patients with stable hypercapnic COPD, nocturnal NIMV may decrease resting PaCO(2), reraising the role of chronically supporting the respiratory pump.     

Long-term follow-up of nocturnal ventilatory assistance in patients with respiratory failure due to Duchenne-type muscular dystrophy

We followed eight patients with Duchenne-type muscular dystrophy for an average of 39 months after initiation of noninvasive intermittent ventilatory assistance using body ventilators. After one to three months of nocturnal use averaging 8 h, mean daytime PaCO2 fell from 63 +/- 2 to 45 +/- 3 mm Hg. At late follow-up, PaCO2 remained stable at 47 +/- 4 mm Hg, but vital capacity fell 33 percent compared with the initial value and the average duration of ventilator use had increased to 18 +/- 2 h daily. Three patients died and five survived; two continued using negative pressure ventilators and three had tracheostomies placed for administration of positive pressure ventilation. We conclude that noninvasive intermittent ventilatory assistance effectively reverses hypoventilation and symptoms in patients with late-stage Duchenne muscular dystrophy, but pulmonary function continues to deteriorate necessitating longer periods of ventilation, and often tracheostomy, within a few years.     

Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury.

Improved gas exchange has been observed during spontaneous breathing with airway pressure release ventilation (APRV) as compared with controlled mechanical ventilation. This study was designed to determine whether use of APRV with spontaneous breathing as a primary ventilatory support modality better prevents deterioration of cardiopulmonary function than does initial controlled mechanical ventilation in patients at risk for acute respiratory distress syndrome (ARDS). Thirty patients with multiple trauma were randomly assigned to either breathe spontaneously with APRV (APRV Group) (n = 15) or to receive pressure-controlled, time-cycled mechanical ventilation (PCV) for 72 h followed by weaning with APRV (PCV Group) (n = 15). Patients maintained spontaneous breathing during APRV with continuous infusion of sufentanil and midazolam (Ramsay sedation score [RSS] of 3). Absence of spontaneous breathing (PCV Group) was induced with sufentanil and midazolam (RSS of 5) and neuromuscular blockade. Primary use of APRV was associated with increases (p < 0.05) in respiratory system compliance (CRS), arterial oxygen tension (PaO2), cardiac index (CI), and oxygen delivery (DO2), and with reductions (p < 0.05) in venous admixture (QVA/QT), and oxygen extraction. In contrast, patients who received 72 h of PCV had lower CRS, PaO2, CI, DO2, and Q VA/Q T values (p < 0.05) and required higher doses of sufentanil (p < 0.05), midazolam (p < 0.05), noradrenalin (p < 0.05), and dobutamine (p < 0.05). CRS, PaO2), CI and DO2 were lowest (p < 0.05) and Q VA/Q T was highest (p < 0.05) during PCV. Primary use of APRV was consistently associated with a shorter duration of ventilatory support (APRV Group: 15 +/- 2 d [mean +/- SEM]; PCV Group: 21 +/- 2 d) (p < 0.05) and length of intensive care unit (ICU) stay (APRV Group: 23 +/- 2 d; PCV Group: 30 +/- 2 d) (p < 0.05). These findings indicate that maintaining spontaneous breathing during APRV requires less sedation and improves cardiopulmonary function, presumably by recruiting nonventilated lung units, requiring a shorter duration of ventilatory support and ICU stay.     

Negative pressure ventilation vs external high-frequency oscillation during rigid bronchoscopy. A controlled randomized trial

STUDY OBJECTIVES: To compare the effectiveness of two modalities of external ventilation during rigid bronchoscopy: intermittent negative pressure ventilation (INPV) and external high-frequency oscillation (EHFO). DESIGN: Prospective, controlled, randomized, nonblinded study. SETTING: University-affiliated hospital. PATIENTS: Seventy patients undergoing interventional rigid bronchoscopy for tracheobronchial lesions were enrolled into the study. INTERVENTIONS: Mechanical ventilation was performed by INPV or EHFO. When pulse oximetry was < 90%, manually assisted ventilation was delivered. Measurements and results: Arterial blood gases were sampled preoperatively and intraoperatively. Most patients in both groups had normal intraoperative PaCO(2) (mean, 43. 6 +/- 11.8 mm Hg under EHFO and 37.4 +/- 8.2 mm Hg under INPV; p = 0.012), and acidemia occurred in 9 of 35 patients of EHFO group and in 2 of 35 patients of INPV group (p = 0.049). Hypercapnia (PaCO(2) > 50 mm Hg) was observed in 10 patients under EHFO and in 2 with INPV (p = 0.026). Intraoperative mean PaO(2) was similar (101.4 +/- 52.9 mm Hg with EHFO and 124.2 +/- 50.3 mm Hg with INPV; p = 0.07), but O(2) supply was different (3.5 +/- 2.3 L/min during INPV and 8.5 +/- 6.2 L/min during EHFO; p < 0.001). Intraoperative hypoxemia (PaO(2) < 60 mm Hg) occurred in five patients with EHFO and two with INPV (p = 0.426). Three EHFO patients required manually assisted ventilation (mean, 0.2 +/- 0.9), but no INPV patient did (p = 0.142). CONCLUSIONS: External negative pressure ventilation appears to be a suitable choice during rigid bronchoscopy: both EHFO and INPV ensure effective ventilation and comfortable operating conditions in the majority of patients. Some patients may receive inadequate ventilation with EHFO, developing respiratory acidosis and requiring manually assisted ventilation. In comparison with INPV, EHFO requires a higher fraction of inspired oxygen.     

Hypoxemic threshold for lung ventilation in the toad

The relationship between the activity of the buccal force pump, expressed as the time integral of positive buccal pressure, and PaO2 was investigated in conscious toads, Bufo marinus, unidirectionally ventilated at a high flow rate (240-260 ml/min). The high ventilatory flow rate meant that PaO2 was largely independent of the animal's ventilatory activity so that the relationship between pulmonary ventilation and PaO2 was effectively open-loop. The hypoxemic threshold (PaO2) for lung ventilation was 54.2 mm Hg in hypocapnia (PaCO2 = 4.7 +/- 0.3 mm Hg), 82.6 mm Hg in normocapnia (PaCO2 = 11.6 +/- 0.2 mm Hg), and 137.9 mm Hg in hypercapnia (PaCO2 = 20.1 +/- 0.1 mm Hg). Unidirectional ventilation with 20% O2 in N2, a condition in which the toads were normoxic but hypocapnic, stopped pulmonary ventilation cycles. Taken with existing evidence that hyperoxia stops pulmonary ventilation even under conditions in which PaCO2 is elevated this suggests that hypoxic and hypercapnic stimuli summate to drive lung ventilation in the toad. Bilateral denervation of the carotid labyrinths decreased pulmonary ventilation in absolute terms, but did not reduce the proportionate increase in pulmonary ventilation in response to normocapnic hypoxia, suggesting that chemoreceptors within the carotid labyrinth may contribute to, but are not solely responsible for, the hypoxemic ventilatory drive.     

Effects of hydralazine on mouth occlusion pressure and ventilatory response to hypercapnia in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Hydralazine has been shown to increase minute ventilation (VE) in patients with chronic obstructive pulmonary disease and pulmonary hypertension. The mechanism by which hydralazine produces this effect has not been defined. We investigated the effects of orally administered hydralazine on hypercapnic ventilatory response (delta VE/delta PaCO2) and central respiratory drive (delta P0.1/delta PaCO2) as well as the effects on hemodynamics, ventilation, and gas exchange in 10 male patients (mean age, 59 +/- 2 yr). The patients had a severe degree of chronic air-flow obstruction (FEV1, 1.07 +/- 0.08 L) and mild pulmonary hypertension (mean pulmonary artery pressure, 25 +/- 4 mm Hg). After hydralazine, the slope of delta VE/delta PaCO2 increased by 177% (p less than 0.005), and the slope of delta P0.1/delta PaCO2 increased by 145% (p less than 0.05). Resting ventilation increased from 14.8 +/- 1.0 to 17.1 +/- 1.4 L/min (p less than 0.02), primarily as a result of increased respiratory frequency. After hydralazine, PaO2 increased from 66 +/- 4 to 70 +/- 3 mm Hg (p less than 0.05) at rest and from 54 +/- 3 to 59 +/- 3 mm Hg (p less than 0.02) during exercise. PaCO2 decreased from 46 +/- 3 to 42 +/- 3 mm Hg (p less than 0.001) at rest and from 50 +/- 3 to 45 +/- 3 mm Hg (p less than 0.001) during exercise. No change was seen in the dead space to tidal volume ratio or the degree of venous admixture. Mean pulmonary artery pressure and total pulmonary resistance both at rest and during exercise were unchanged after hydralazine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of bilevel nasal positive airway pressure ventilation in patients with heart failure

AIMS: Benefits of nasal continuous positive airway pressure (CPAP) in patients presenting with chronic heart failure (CHF) are controversial. The purpose of this study was to compare the hemodynamic effects of CPAP and bilevel positive airway pressure (BiPAP) in patients with or without CHF. METHODS AND RESULTS: Twenty patients with CHF and 7 with normal left ventricular function underwent cardiac catheterization. Measurements were made before and after three 20-min periods of BiPAP: expiratory positive airway pressure (EPAP) = 8 cm H2O and inspiratory positive airway pressure (IPAP) = 12 cm H2O, EPAP = 10 cm H2O and IPAP = 15 cm H2O, and CPAP = EPAP = IPAP = 10 cm H2O administered in random order. Positive pressure ventilation decreased cardiac output (CO) and stroke volume. No change was observed in either pulmonary or systemic arterial pressure. There was no difference in the hemodynamic effects of the three ventilation settings. Only mean pulmonary wedge pressure (MPWP) and heart rate were lower with CPAP than with BiPAP. CO decreased only in patients with low MPWP (相似文献   

肺移植对5例慢性阻塞性肺疾病患者肺功能的影响

目的研究单肺移植手术治疗慢性阻塞性肺疾病(COPD)对呼吸生理及肺功能的影响。方法5例患者均为Ⅳ级COPD男性患者,年龄51～63岁。术前2周测定患者用力肺活量(FVC)、第一秒用力呼气容积(FEV1)、FEV1/FVC、最大通气量(MVV)、残气容积(RV)、肺总量(TLC)、残总比(RV/TLC)、深吸气量(IC)、胸腔气体容积(TGV)、呼气峰流量(PEF)、总气道阻力(Rawtotal)、肺一氧化碳弥散量(DLCO)、每升肺泡容积肺一氧化碳弥散量(DLCO/V·A)、6分钟行走距离(6MWD)、动脉血氧分压(PaO2)、肺泡气动脉血氧分压差[P(Aa)O2]、动脉血氧饱和度(SaO2)、动脉血二氧化碳分压(PaCO2)及平均肺动脉压(mPAP)等参数。术后2个月再行上述测定。结果5例患者术前2周、术后2个月检测的参数为MVV(23.6±5.8)、(71.6±21.8)L,FEV1(0.68±0.21)、(1.85±0.46)L,FEV1/FVC(37.4±8.3)、(75.6±13.9)%,PaO2(60.0±9.1)、(86.2±2.9)mmHg(1mmHg=0.133kPa),SaO2(90.0±4.6)%、(96.8±0.5)%及mPAP(31.2±5.5)、(16.6±1.8)mmHg,均有显著改善(P均<0.05);3例患者IC[(1.16±0.26)、(1.83±0.35)L]、TGV[(6.52±0.27)、(4.52±0.29)L]、RV[(5.12±0.39)、(3.20±0.32)L]、RV/TLC[(71.0±5.6)、(51.3±2.5)%]及Rawtotal[(6.62±0.99)、(2.48±0.87)cmH2O·L-1·s-1]改善显著(P均<0.05);4例患者PEF[(1.65±0.40)、(3.92±1.63)L/s]、DLCO[(8.5±3.0)、(21.0±6.2)ml·min-1·mmHg-1]及6MWD[(46.8±14.7)、(246.8±51.9)m]也显著增加(P均<0.05);FVC[(1.85±0.40)、(2.45±0.49)L]、TLC[(7.19±0.15)、(6.26±0.73)L]、DLCO/V·A[(2.90±1.50)、(5.41±0.87)L·min-1·mmHg-1]、P(Aa)O2[(37.6±16.3)、(17.8±6.3)mmHg]及PaCO2[(44.6±7.7)、(37.4±3.4)mmHg]有所改善,但差异无统计学意义(P均>0.05)。结论COPD患者肺移植术后肺通气、气道阻力、残气、弥散、运动耐力及气体交换功能均明显改善。