Search

The aim of this randomised study was to compare the effects of iron lung ventilation (ILV) with invasive mechanical ventilation (IMV) in patients with acute respiratory failure (ARF) due to exacerbation of chronic obstructive pulmonary disease. Forty-four patients with ARF were assigned either to ILV (22 patients) or IMV (22 patients). Primary end-points were the improvement in gas exchange and complications related to mechanical ventilation. On admission ILV and IMV groups did not differ in age, simplified acute physiology score II, arterial oxygen tension (Pa,O2)/inspiratory oxygen fraction (FI,O2), arterial carbon dioxide tension (Pa,CO2) and pH. Compared with baseline, ILV and IMV induced a similar and significant improvement in Pa,O2/FI,O2, Pa,CO2 and pH after 1 h of treatment and at discontinuation of mechanical ventilation. Major complications tended to be more frequent in patients treated with IMV than in those treated with ILV (27.3% versus 4.5%), whereas mortality rate was similar (27.3% versus 18.2%). The ventilator-free days and the length of hospital stay were significantly lower in the ILV than in the IMV group. This study suggests that iron lung ventilation is as effective as invasive mechanical ventilation in improving gas exchange in chronic obstructive pulmonary disease patients with acute respiratory failure, and is associated with a tendency towards a lower rate of major complications.

This case-control study was aimed to evaluate the effectiveness of negative pressure ventilation (NPV) versus conventional mechanical ventilation (CMV) for the treatment of acute respiratory failure (ARF) in patients with chronic obstructive pulmonary disease (COPD) admitted to a respiratory intermediate intensive care unit (RIICU) and four general intensive care units (ICU). Twenty-six COPD patients in ARF admitted in 1994-95 to RIICU and treated with NPV (cases) were matched according to age (+/-5 yrs), sex, causes triggering ARF, Acute Physiology and Chronic Health Evaluation (APACHE) II score (+/- 5 points), pH (+/-0.05) and arterial carbon dioxide tension (Pa,CO2) on admission with 26 patients admitted to ICU and treated with CMV (controls). The primary end points of the study were inhospital death for both groups and the need for endotracheal intubation for cases. The secondary endpoints were length and complications of mechanical ventilation and length of hospital stay. The effectiveness of matching was 91%. Mortality rate was 23% for cases and 27% for controls (NS), five cases needed endotracheal intubation, four of whom subsequently died. The duration of ventilation in survivors was significantly lower in cases than in controls, with a median of 16 h (range 2-111) versus 96 h (range 12-336) (P<0.02), whereas the length of hospital stay was similar in the two groups, with a median of 12 days (range 2-47) for cases vs 12 days (range 3-43) (NS) for controls. No complications were observed in cases, whereas three controls developed infective complications. These results suggest that negative pressure ventilation is as efficacious as conventional mechanical ventilation for the treatment of acute respiratory failure in patients with chronic obstructive pulmonary disease and that it is associated with a shorter duration of ventilation and a similar length of hospital stay compared with conventional mechanical ventilation.

Ultrasonography has recently been proposed for assessing changes in thickness and motion of the diaphragm during contraction in humans. Data on ultrasound assessment of abdominal muscles in humans are scarce. We therefore investigated the changes in thickness and the relevant mechanical effects of abdominal muscles using this technique during respiratory manoeuvres in normal subjects. We evaluated the thickness of the abdominal muscle layers in six normal male subjects (aged 26-36 yrs) using a 7.5 MHz B-mode ultrasound transducer. Gastric (Pg) and mouth pressures, muscle thickness of external oblique (EO), internal oblique (IO), transversus abdominis (TA) and rectus abdominis (RA) were assessed at functional residual capacity (FRC), residual volume (RV), total lung capacity (TLC), during progressive (PEEs) and maximal expiratory efforts (MEEs) against a closed airway and during homolateral (HTR) and contralateral (CTR) trunk rotation. Abdominal muscle thickness was found to be reproducible (coefficient of variation and two-way analysis of variance). Compared to FRC, the thickness of IO, TA and RA significantly increased at RV and during MEEs, whereas EO remained unchanged; at TLC, the thickness of IO and TA significantly decreased. During PEEs, a significant relationship between increase in Pg and TA thickness was observed in all subjects, the thickness of the other abdominal muscles being inconsistently related to Pg. Finally, a significant increase in the thickness of IO and EO was found during HTR and CTR, respectively. We conclude that during maximal expiratory manoeuvres, transversus abdominis, internal oblique and rectus abdominis thickened similarly. Transversus abdominis seems to be the major contributor in generating abdominal expiratory pressure during progressive expiratory efforts. External oblique seems to be preferentially involved during trunk rotation. These results suggest the possible value of studying the abdominal muscles by ultrasonography in various respiratory disorders.

Lung volumes are decreased by tense ascites and increase after large volume paracentesis (LVP). The overall effect of ascites and LVP on the respiratory function is poorly understood. We studied eight cirrhotic patients with tense ascites before and after LVP. Inspiratory muscle force (maximal transdiaphragmatic pressure (Pdi,max), and the lowest pleural pressure (Pp1,min)) was assessed while the patients were seated. Rib cage and abdominal volume displacements, as well as pleural and gastric pressures were measured during quiet breathing while the patients were supine. Pdi,max and Ppl,min were normal and did not change after LVP (from 84.2+/-19.7 to 85.2+/-17.0 cmH2O and from 68.3+/-19.7 to 74+/-15.9 cmH2O, respectively). The abdominal contribution to the generation of tidal volume was greater than that of the rib cage (79 vs 21%), a pattern which did not change after LVP (73 and 27%). Before LVP, tidal swings both of pleural pressure (Ppl,sw) and transdiaphragmatic pressure (Pdi,sw) were large (15.3+/-4.3 and 18.5+/-3.9 cmH2O, respectively) and the load on inspiratory muscles was increased as a consequence of elevated dynamic elastance of the lung (El,dyn) (11.4+/-2.6 cmH2O x L(-1)) and ("intrinsic") positive end-expiratory pressure (PEEPi) (4.3+/-3.5 cmH2O). LVP reduced the load on the inspiratory muscles, as shown by the significant decrease in Ppl,sw (10.6+/-2.0 cmH2O), Pdi,sw (12.8+/-3.0 cmH2O), El,dyn (10.0+/-2.0 cmH2O x L(-1)) and PEEPi (1.1+/-1.3 cmH2O). The amount of fluid removed was closely related to changes in Ppl,sw and PEEPi. We conclude that the strength of the inspiratory muscles is normal or reduced in seated cirrhotic patients. In the supine position, tense ascites results in an increase in lung elastic load and development of positive end-expiratory pressure, with a consequent overload and increased activation of inspiratory muscles. Large volume paracentesis decreases overloading and activation, but does not change the strength of the inspiratory muscles.

Increase in lung size has been described in acromegalic patients, but data on respiratory muscle function and control of breathing are relatively scarce. Lung volumes, arterial blood gas tensions, and respiratory muscle strength and activation during chemical stimulation were investigated in a group of 10 patients with acromegaly, and compared with age- and sex-matched normal controls. Inspiratory muscle force was evaluated by measuring pleural (Ppl,sn) and transdiaphragmatic (Pdi,sn) pressures during maximal sniffs. Dynamic pleural pressure swing (Ppl,sw) was expressed both as absolute value and as percentage of Ppl,sn. Expiratory muscle force was assessed in terms of maximal expiratory pressure (MEP). In 8 of the 10 patients, ventilatory and respiratory muscle responses to hyperoxic progressive hypercapnia and to isocapnic progressive hypoxia were also evaluated. Large lungs, defined as total lung capacity (TLC) greater than predicted (above 95% confidence limits), were found in five patients. Inspiratory or expiratory muscle force was below normal limits in all but three patients. During unstimulated tidal breathing, respiratory frequency (fR) and mean inspiratory flow (tidal volume/inspiratory time (VT/tI)) were greater, while inspiratory time (tI) was shorter than in controls. Minute ventilation (V'E) and mean inspiratory flow response slopes to hypercapnia were normal In contrast, four patients had reduced delta(VT/tI)/arterial oxygen saturation (Sa,O2) and three had reduced deltaV'E/Sa,O2. Ppl,sw(%Ppl,sn) response slopes to increasing end-tidal carbon dioxide tension (PET,CO2) and decreasing Sa,O2 did not differ from the responses of the normal subjects, suggesting normal central chemoresponsiveness. At a PET,CO2 of 8 kPa or an Sa,O2 of 80%, patients had greater fR and lower tI compared with controls. Pdi,sn and Ppl,sn related both to deltaV'E/deltaSa,O2 (r=0.729 and r=0.776, respectively) and delta(VT/tI)/deltaSa,O2 (r=0.860 and r=0.90, respectively). Pdi,sn also related both to deltaV'E/deltaPET,CO2 (r=0.8) and delta(VT/tI)/deltaPET,CO2 (r=0.76). In conclusion, the data suggest the relative independence of pneumomegaly and respiratory muscle strength. Peripheral (muscular) factors appear to modulate a normal central motor output to give a more rapid pattern of breathing.

Noninvasive mechanical ventilatory techniques include the use of negative and positive pressure ventilators. Negative pressure ventilators, such as the "iron lung", support ventilation by exposing the surface of the chest wall to subatmospheric pressure during inspiration; whereas, expiration occurs when the pressure around the chest wall increases and becomes atmospheric or greater than atmospheric. In this review, after a description of the more advanced models of tank ventilators and the physiological effects of negative pressure ventilation (NPV), we summarize the recent application of this old technique in the treatment of acute respiratory failure (ARF). Several uncontrolled studies suggest that NPV may have a potential therapeutic role in the treatment of acute on chronic respiratory failure in patients with chronic obstructive pulmonary disease and restrictive thoracic disorders, reducing the need for endotracheal intubation. In the paediatric field, after substantial technical improvement, NPV has been successfully reintroduced for the treatment of ARF due to neonatal distress syndrome and bronchopulmonary dysplasia, and for the weaning from positive pressure ventilation in intubated patients. The positive results of these reports need to be formally confirmed by further prospective and controlled studies before recommending the generalized use of negative pressure ventilation in acute respiratory failure as a standard of care.

To ascertain whether and to what extent the reduced ventilatory response to a hypercapnic stimulus in chronic obstructive pulmonary disease (COPD) patients depends on a blunted chemoresponsiveness of central origin or to mechanical impairment, we studied two groups of COPD patients without (group A) and with (group B) chronic hypercapnia, but with similar degrees of airway obstruction and hyperinflation. The study was performed on 17 patients (9 normocapnic and 8 hypercapnic). Six age-matched normal subjects (group C) were also studied as a control. During a CO2 rebreathing test, ventilation (VE), mouth occlusion pressure (P0.1), and the electromyographic activity of diaphragm (Edi) were recorded and then plotted against end-tidal carbon dioxide tension (PCO2). Inspiratory muscle strength was significantly lower in the hypercapnic group (group B) compared to normocapnic group (A), and in these groups compared to the control group (C). Both patient groups exhibited significantly lower delta VE/delta PCO2 than the control group. In hypercapnics, delta P0.1/delta PCO2 was significantly lower than in normocapnics and control group, whilst mouth occlusion pressure as % of maximal inspiratory pressure delta P0.1 (% MIP)/delta PCO2 did not differ significantly among the three groups. delta Edi/delta PCO2 increased from C to A. At a PCO2 of 8.65 kPa, VE was similar in the normocapnic and control group, but lower in hypercapnics; Edi was similar in hypercapnic and control group; but greater in normocapnics. P0.1(% MIP) did not differ significantly among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Broxaterol, a new selective beta 2-agonist, has been shown to exert inotropic effects on both fresh and fatigued canine diaphragm. We evaluated the effect of broxaterol on the activation and force output of the respiratory muscles in patients with chronic obstructive pulmonary disease (COPD). We studied 9 patients with moderate to severe COPD. Each patient was infused with saline and Broxaterol (200 micrograms) in saline alternately. We measured lung volumes, maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), breathing pattern, P0.1, respiratory muscle EMG (diaphragm, EMGd, and parasternal, EMGp) and P0.1/EMGd ratio. Measurements were made under control conditions and at 15, 30, 60, and 120 min after each infusion. Broxaterol, but not saline, resulted in a slight but significant increase in vital capacity (VC), forced expiratory volume in one second (FEV1) and MIP, and a decrease in functional residual capacity (FRC). Breathing pattern did not change, while EMG significantly decreased, and P0.1/EMGd significantly increased in 5 of the 9 patients after broxaterol. These data seem to indicate that by partially unloading the respiratory muscles, broxaterol results in decreased muscle activation (EMG). Increase in chest wall neuromuscular coupling (P0.1/EMGd) may also be observed.

This study was undertaken in order to assess the neural drive to the respiratory muscles and the inspiratory neuromuscular coupling in patients with bronchial asthma during histamine-induced bronchoconstriction. Bronchoconstriction was produced in a graded fashion, with histamine phosphate aerosol of increasing dose, in twelve asymptomatic asthmatic patients and was measured by FEV1. Inspiratory drive was measured by electromyographic activity of the diaphragm (EMGd) and the coupling of the neural drive to the respiratory muscles was assessed by the relationship of mouth occlusion pressure (P0.1) to EMGd. During the test we also measured electromyographic activity of the inspiratory intercostal (EMGint), sternomastoid (EMGsm) and expiratory abdominal (EMGab) muscles. Histamine caused a significant decrease in FEV1, a significant increase in P0.1, EMGd, EMGint, and a relevant increase in EMGsm, with no substantial increase in EMGab. An inverse significant relationship between the change in FEV1 and changes in P0.1, EMGd and EMGint and a significant correlation between the change in FEV1 and in the P0.1/EMGd ratio were observed. We conclude that a progressive increase in bronchospasm is accompanied by a progressive increase in respiratory neural drive and decrease in neuromuscular coupling. This could be caused both by an increase in lung volume and a lack of abdominal expiratory muscle recruitment.