Biomedical subjects

G Misuri

Publications and source records attributed to G Misuri.

At least 19 recordsLinked to original sources

PubMed2001

Respiratory dynamics during laughter.

Lung and chest wall mechanics were studied during fits of laughter in 11 normal subjects. Laughing was naturally induced by showing clips of the funniest scenes from a movie by Roberto Benigni. Chest wall volume was measured by using a three-dimensional optoelectronic plethysmography and was partitioned into upper thorax, lower thorax, and abdominal compartments. Esophageal (Pes) and gastric (Pga) pressures were measured in seven subjects. All fits of laughter were characterized by a sudden occurrence of repetitive expiratory efforts at an average frequency of 4.6 +/- 1.1 Hz, which led to a final drop in functional residual capacity (FRC) by 1.55 +/- 0.40 liter (P < 0.001). All compartments similarly contributed to the decrease of lung volumes. The average duration of the fits of laughter was 3.7 +/- 2.2 s. Most of the events were associated with sudden increase in Pes well beyond the critical pressure necessary to generate maximum expiratory flow at a given lung volume. Pga increased more than Pes at the end of the expiratory efforts by an average of 27 +/- 7 cmH2O. Transdiaphragmatic pressure (Pdi) at FRC and at 10% and 20% control forced vital capacity below FRC was significantly higher than Pdi at the same absolute lung volumes during a relaxed maneuver at rest (P < 0.001). We conclude that fits of laughter consistently lead to sudden and substantial decrease in lung volume in all respiratory compartments and remarkable dynamic compression of the airways. Further mechanical stress would have applied to all the organs located in the thoracic cavity if the diaphragm had not actively prevented part of the increase in abdominal pressure from being transmitted to the chest wall cavity.

Adult↗

PubMed2001

Assessing inspiratory muscle strength in patients with neurologic and neuromuscular diseases : comparative evaluation of two noninvasive techniques.

STUDY OBJECTIVES: Static mouth pressure during maximal inspiratory efforts is commonly used to evaluate inspiratory muscle strength. However, maximal inspiratory pressure (MIP) presents some potential limitations likely to be overcome by the measure of mouth pressure during a maximal sniff maneuver in patients with respiratory muscle weakness. The aim of the present study was to assess whether mouth pressure during sniff maneuver (Pmosn) is a better index of inspiratory muscle strength than MIP in patients with neurologic and neuromuscular diseases (NNMD) with and without inspiratory muscle weakness. SUBJECTS AND MEASUREMENTS: Both MIP and Pmosn were measured in 30 patients affected by various types of NNMD and in 41 control subjects. Pmosn was measured with a 5-cm latex balloon-catheter system, the balloon being held in the oral cavity with the lips closed. RESULTS: In control subjects, MIP was either similar (in female subjects) or higher (in male subjects) than Pmosn, the variation coefficients for the two tests being similar both in male subjects (19.3% vs 19.1% for MIP and Pmosn, respectively) and in female subjects (27.5% vs 26.2%, respectively). There was no difference in the Pmosn/MIP ratios observed in the different diseases (one-way analysis of variance, F = 0.29, p = 0.91). In control subjects, a significant inverse relationship between Pmosn/MIP ratio and MIP (r = - 0.66, p < 0.00001) was found, ie, the lower the MIP, the higher the Pmosn/MIP ratio, suggesting an increasing difficulty in performing MIP as MIP values decreased. The majority of patients were between the prediction limits of the regression calculated for control subjects. At variance, patients with Duchenne dystrophy and low MIP were under the prediction limits of the regression calculated for control subjects, indicating a lower-than-expected PMOSN. CONCLUSIONS: In patients with NNMD, irrespective of the etiology, we found the following: (1) Pmosn does not overcome the limitations of MIP measurement; (2) the two maneuvers are not interchangeable, but rather complement one another in the assessment of inspiratory muscle strength; (3) Pmosn may underestimate muscle strength as assessed by MIP in patients with NNMD with inspiratory muscle weakness; and (4) in patients with low MIP, the lower-than-expected Pmosn/MIP ratio confirms inspiratory muscle weakness.

Adult↗

PubMed2001

Perception of dyspnea in patients with neuromuscular disease.

BACKGROUND: The perception of dyspnea is not a prominent complaint of resting patients with neuromuscular disease (NMD). To our knowledge, no study has been addressed at evaluating the interrelationships among lung mechanics, respiratory motor output, and the perception of dyspnea in patients with NMD receiving ventilatory stimulation. MATERIAL: Eleven patients with NMD (mean +/- SD age, 44 +/- 11.8 years; 5 men) of different etiology and a group of normal subjects matched for age and sex (control subjects). METHODS: While patients were breathing room air, lung volumes, arterial blood gases, the pattern of breathing (minute ventilation [E], tidal volume [VT], respiratory frequency, inspiratory time), and maximal (less negative) esophageal pressure during a sniff maneuver (Pessn), as an index of inspiratory muscle strength, were measured. Then we evaluated the response to hypercapnic-hyperoxic stimulation (hypercapnic-hyperoxic rebreathing test [RT]) in terms of breathing pattern, inspiratory swing of pleural pressure (Pessw), and inspiratory effort (Pessw[%Pessn]). During the RT, dyspnea was assessed every 30 s using a modified Borg scale (0 to 10). RESULTS: Pulmonary volumes were reduced in seven patients, and PCO(2) was out of proportion to E in four patients. Group Pessn was 42.8 +/- 23.6 cm H(2)O in patients and 107 +/- 20.4 cm H(2)O in control subjects (p < 0.001). Dynamic elastance (Eldyn) [p = 0.0016] and Pessw(%Pessn) [p < 0.0005] were higher in patients. During the RT, Borg/CO(2), Pessw(%Pessn)/CO(2), and Borg/Pessw(%Pessn) were similar in the two groups, while E/CO(2) and VT/CO(2) were lower in patients (p < 0.0002 for both). As a consequence, for unit change in VT (percentage of predicted vital capacity [%VC]), greater changes in Pessw(%Pessn) were associated with greater Borg scores in patients. Baseline Eldyn related to Pessw(%Pessn)/VT(%VC) during hypercapnia (r(2) = 0.85), an index of neuroventilatory coupling of the ventilatory pump (NVC). NVC predicted a good amount of the variability in Borg/E (r(2) = 0.46, p < 0.02). CONCLUSIONS: In this subset of NMD patients during hypercapnic stimulation, a normal inspiratory motor output per unit change in PCO(2) results in a shallow breathing pattern. The consequent impairment of NVC underlies the higher scoring of dyspnea in these patients.

Adult↗

PubMed2000

Mechanism of CO(2) retention in patients with neuromuscular disease.

BACKGROUND: In many studies of patients with muscle weakness, chronic hypercapnia has appeared to be out of proportion to the severity of muscle disease, indicating that factors other than muscle weakness are involved in CO(2) retention. In patients with COPD, the unbalanced inspiratory muscle loading-to-strength ratio is thought to trigger the signal for the integrated response that leads to rapid and shallow breathing and eventually to chronic hypercapnia. This mechanism, although postulated, has not yet been assessed in patients with muscular dystrophy. SUBJECTS: Twenty consecutive patients (mean age, 47.6 years; range, 23 to 67 years) were studied: 11 patients with limb-girdle dystrophy, 3 with Duchenne muscular dystrophy, 1 with Charcot-Marie-Tooth syndrome, 1 with Becker muscular dystrophy, 1 with myotonic dystrophy, 1 with facioscapulohumeral dystrophy, and 2 with amyotrophic lateral sclerosis, without any respiratory complaints. Seventeen normal subjects matched for age and sex were studied as a control group. METHODS: Routine spirometry and arterial blood gases, maximal inspiratory and expiratory muscle pressures (MIP and MEP, respectively), and pleural pressure during maximal sniff test (Pplsn), were measured. Mechanical characteristics of the lung were assessed by evaluating lung resistance (RL) and dynamic elastance (Eldyn). Eldyn was assessed as absolute value and as percent of Pplsn; Eldyn (%Pplsn) indicates the elastic load per unit of inspiratory muscle force. Breathing pattern was assessed in terms of time (inspiratory time [TI]; respiratory frequency [Rf]) and volume (tidal volume [VT]) components of the respiratory cycle. RESULTS: A rapid shallow breathing pattern, as indicated by a greater Rf/VT ratio and a lower TI, was found in study patients compared to control subjects. Eldyn was greater in study patients, while MIP, MEP, and Pplsn were lower. PaCO(2) inversely related to VT, TI, and Pplsn (p = 0.012, p = 0.019, and p = 0.002, respectively), whereas it was directly related to Rf, Rf/VT, Eldyn, and Eldyn (%Pplsn) (p < 0.004 to p < 0.0001). Also Eldyn (%Pplsn) inversely related to TI, and the latter positively related to VT. In other words, increase in Eldyn (%Pplsn) was associated with decrease in TI, and the latter was associated with lower VT and greater PaCO(2). Mechanical and breathing pattern variables were introduced in a stepwise multiple regression that selected Eldyn (%Pplsn) (p < 0.0001; r(2) = 0.62) as a unique independent predictor of PaCO(2). CONCLUSIONS: The present study shows that in patients with neuromuscular disease, elastic load and respiratory muscle weakness are responsible for a rapid and shallow breathing pattern leading to chronic CO(2) retention.

Adult↗

PubMed2000

Hypoxic and hypercapnic breathlessness in patients with type I diabetes mellitus.

STUDY OBJECTIVES: The putative role of the performance of inspiratory muscles and breathing pattern in inducing dyspnea has been recently assessed during hypoxic stimulation in patients with type I diabetes (IDDM). Compared to a hypoxic stimulus, a hypercapnic stimulus, which may differently affect the pattern of breathing, could therefore modulate the coupling between respiratory effort and ventilatory output, which is involved in dyspnea sensation. SUBJECTS: Eight stable patients aged 19 to 48 years old, with IDDM (duration of disease, 36 to 240 months) and no smoking history, cardiopulmonary involvement, or autonomic neuropathy; and an age- and sex-matched control group. MEASUREMENTS: Pulmonary volumes, diffusing capacity of the lung for carbon monoxide, time and volume components (tidal volume [VT] and respiratory frequency), dynamic elastance (Eldyn), and swings in pleural pressure (Pessw) were measured. Maximal inspiratory pleural pressure (Pes) during a maximal sniff maneuver (Pessn), respiratory muscle effort or output (Pessw%Pessn), tension time index (TTI) = TI/total breathing cycle time x Pessw(%Pessn), and swing in Pes during VT as a percentage of Pessn were also evaluated. Dyspnea sensation was assessed by a modified Borg scale. Subjects were studied at baseline and during hypoxic and hypercapnic rebreathing tests. RESULTS: Compared to control subjects, patients exhibited normal routine spirometric function and Pessn, but a higher Eldyn, indicating peripheral airway involvement. In patients, but not in control subjects, Eldyn increased during both chemical stimuli and increased more during hypoxia than during hypercapnia. Also, changes in both VT and Pessw(%Pessn) on changes in PCO(2) were lower, while changes in Pessw(%Pessn)/VT, an index of neuroventilatory dissociation (NVD) of the ventilatory pump, on changes in PCO(2) were greater. Changes in VT and NVD for unit change in arterial oxygen saturation were lower and higher, respectively. Changes in Borg scale per changes in NVD were greater during both stimuli. Furthermore, compared to hypoxic conditions, a greater VT for any level of both minute volume and Pessw(%Pessn), and lower changes in Borg scale on changes in Pessw(%Pessn) and Pessw(%Pessn)/VT were found in hypercapnia. Changes in NVD and Borg scale related to changes in Eldyn with both chemical stimuli. CONCLUSIONS: In IDDM, the greater perception of dyspnea is associated with changes in inspiratory effort being out of proportion to changes in VT. The greater increase in Eldyn and the lower increase in VT may, in part, account for the greater perception of breathlessness during hypoxia.

Adult↗

PubMed1999

Chest wall kinematics and respiratory muscle action in walking healthy humans.

We studied chest wall kinematics and respiratory muscle action in five untrained healthy men walking on a motor-driven treadmill at 2 and 4 miles/h with constant grade (0%). The chest wall volume (Vcw), assessed by using the ELITE system, was modeled as the sum of the volumes of the lung-apposed rib cage (Vrc,p), diaphragm-apposed rib cage (Vrc,a), and abdomen (Vab). Esophageal and gastric pressures were measured simultaneously. Velocity of shortening (V(di)) and power [Wdi = diaphragm pressure (Pdi) x V(di)] of the diaphragm were also calculated. During walking, the progressive increase in end-inspiratory Vcw (P < 0.05) resulted from an increase in end-inspiratory Vrc,p and Vrc,a (P < 0.01). The progressive decrease (P < 0.05) in end-expiratory Vcw was entirely due to the decrease in end-expiratory Vab (P < 0.01). The increase in Vrc,a was proportionally slightly greater than the increase in Vrc,p, consistent with minimal rib cage distortion (2.5 +/- 0.2% at 4 miles/h). The Vcw end-inspiratory increase and end-expiratory decrease were accounted for by inspiratory rib cage (RCM,i) and abdominal (ABM) muscle action, respectively. The pressure developed by RCM,i and ABM and Pdi progressively increased (P < 0.05) from rest to the highest workload. The increase in V(di), more than the increase in the change in Pdi, accounted for the increase in Wdi. In conclusion, we found that, in walking healthy humans, the increase in ventilatory demand was met by the recruitment of the inspiratory and expiratory reserve volume. ABM action accounted for the expiratory reserve volume recruitment. We have also shown that the diaphragm acts mainly as a flow generator. The rib cage distortion, although measurable, is minimized by the coordinated action of respiratory muscles.

Abdominal Muscles↗

PubMed1999

Chest wall hyperinflation during acute bronchoconstriction in asthma.

The mechanics of the chest wall was studied in seven asthmatic patients before and during histamine-induced bronchoconstriction (B). The volume of the chest wall (VCW) was calculated by three-dimensional tracking of 89 chest wall markers. Pleural (Ppl) and gastric (Pga) pressures were simultaneously recorded. VCW was modeled as the sum of the volumes of the pulmonary-apposed rib cage (VRC,p), diaphragm-apposed rib cage (VRC,a), and abdomen (VAB). During B, hyperinflation was due to the increase in end-expiratory volume of the rib cage (0.63 +/- 0.09 L, p < 0.01), whereas change in VAB was inconsistent (0.09 +/- 0.07 L, NS) because of phasic recruitment of abdominal muscles during expiration. Changes in end-expiratory VRC,p and VRC,a were along the rib cage relaxation configuration, indicating that both compartments shared proportionally the hyperinflation. VRC,p-Ppl plot during B was displaced leftward of the relaxation curve, suggesting persistent activity of rib cage inspiratory muscles throughout expiration. Changes in end-expiratory VCW during B did not relate to changes in FEV(1) or time and volume components of the breathing cycle. We concluded that during B in asthmatic patients: (1) rib cage accounts largely for the volume of hyperinflation, whereas abdominal muscle recruitment during expiration limits the increase in VAB; (2) hyperinflation is influenced by sustained postinspiratory activity of the inspiratory muscles; (3) this pattern of respiratory muscle recruitment seems to minimize volume distortion of the rib cage at end-expiration and to preserve diaphragm length despite hyperinflation.

Abdominal Muscles↗

PubMed1999

Reduction in bronchodilation following a deep inhalation is poorly related to airway inflammation in asthma.

In patients with bronchial asthma, forced expiratory flows are differently sensitive to a previous volume history. A reduced ability of a deep inhalation (DI) to dilate obstructed airways has been hypothesized to be a physiological marker for the degree of airway responsiveness and to relate to the presence and magnitude of inflammation in the lung, even in mild stable asthma. However, there are at present doubts as to whether functional changes could be used as a substitute for airway inflammation studies. In order to investigate the interrelations among airway inflammation, bronchial hyperresponsiveness and effects of volume history, 58 consecutive asthmatics with mild to moderate asthma were studied. The effects of DI were assessed as the isovolumic ratio of flows from forced expiratory manoeuvres started from maximal (M) or partial (P) lung inflation. Airway inflammation was assessed by using induced sputum. Sputum was analysed for total and differential cell counts, and levels of eosinophil cationic protein (ECP) which reflects eosinophil activation. Airway responsiveness was assessed as the provocative concentration of histamine which caused a 20% fall in forced expiratory volume in one second (FEV1) from control (PC20). The M/P ratio was significantly related to ECP (r=-0.31, p<0.03) and eosinophils (r=-0.29, p<0.03), FEV1/vital capacity (VC) (r=0.32; p<0.01), clinical score (r=-0.33; p<0.03) and age (r=-0.41; p<0.0001). In a stepwise multiple regression analysis including age, score, baseline lung function, ECP, number of eosinophils and the response to beta2-agonist, age (p<0.037) predicted a small amount of the variance in M/P ratio (r2=0.12). It is concluded that volume history response is substantially independent of both sputum outcomes (inflammatory cell number and eosinophil cationic protein) and bronchial hyperresponsiveness; rather it seems to be associated with anthropometric characteristics. Functional aspects do not provide information on eosinophilic, probably central, airway inflammation.

Adult↗

PubMed1999

Dyspnoea, peripheral airway involvement and respiratory muscle effort in patients with type I diabetes mellitus under good metabolic control.

Dyspnoea and pulmonary dysfunction have recently been associated with Type I (insulin-dependent) diabetes mellitus. The putative role of altered pulmonary mechanics and of performance of inspiratory muscles in inducing dyspnoea has not been yet assessed in Type I diabetes. To better focus on this topic we evaluated nine patients with Type I diabetes mellitus, aged 19 to 48 years with good and stable metabolic control, without a history of smoking and microvascular complications, alongside a group of 14 healthy control subjects. In each subject, pulmonary volumes, static and dynamic compliance, pleural pressure swings (Pplsw), maximal inspiratory pressures (Pplsn), Pplsw(%Pplsn), a measure of respiratory muscle effort, and tension-time index [TTI=TI/TTOTxPplsw(%Pplsn)] were measured (TI=inspiratory time;TTOT=total time of the respiratory cycle). All subjects were studied at baseline and during hypoxic rebreathing. Patients had normal pulmonary volumes. During hypoxic rebreathing, a normal change in respiratory muscle effort [DeltaPplsw(%Pplsn)/DeltaSaO2] and DeltaTTI/DeltaSaO2, and a lower change in tidal volume versus change in oxygen saturation [DeltaVT(% vital capacity)/DeltaSaO2], resulted in a higher ratio of respiratory effort to tidal volume [Pplsw(%Pplsn)/VT(% vital capacity)], a measure of neuroventilatory dissociation of the respiratory pump. Hypoxic dyspnoea, assessed by a modified Borg scale, showed a greater rate of rise (DeltaBorg/DeltaSaO2) and a greater increase for a given level of respiratory effort in patients. Moreover, neuroventilatory dissociation related to the expression of peripheral airway involvement, as assessed in terms of low dynamic compliance, and to concurrent change in dyspnoea sensation. Patients with Type I diabetes mellitus under good metabolic control and with normal lung volumes may have abnormal peripheral airway function. The latter is thought to be responsible for the association between dyspnoea sensation and neuroventilatory dissociation.

Adult↗

PubMed1999

Respiratory muscles in internal medicine.

This review provides evidence that respiratory muscle abnormalities are present in many illnesses of internal medicine and emphasizes that clinicians should look for respiratory muscle weakness in many circumstances, particularly immunological disorders. Controversial results in hormonal diseases, metabolic diseases and abdominal disorders indicate areas for further research.

Humans↗

PubMed1999

Physiological changes during severe airflow obstruction in chronic obstructive pulmonary disease.

Chronic expiratory flow limitation and hyperinflation are the mechanical hallmarks of chronic obstructive pulmonary disease (COPD). Although carbon dioxide retention is dependent on the severity of airflow limitation, there is considerable variability in the relationships between arterial carbon dioxide tension (Pa,CO2) and forced expiratory volume in one second (FEV1) or total lung resistance (RL). In stable COPD patients with severe airflow obstruction, shallow breathing and inspiratory muscle weakness are the main factors associated with CO2 retention. In stable COPD patients, the diaphragm is less effective than in normal subjects and, with increasing airflow obstruction and hyperinflation, the contribution to the generation of ventilatory pressure of the ribcage inspiratory muscles increased. Abdominal muscles are recruited during expiration in severe COPD patients and the expiratory rise in gastric pressure is directly related to intrinsic positive end-expiratory (alveolar) pressure (PEEPi). During acute bronchoconstriction, COPD patients with severe airflow obstruction recruited the rib cage inspiratory muscles proportionally more than the diaphragm. The associated recruitment of abdominal muscles results in a reduction in abdominal volume at end-expiration and contributes to a significant extent to PEEPi. Dynamic hyperinflation can be overestimated during chronic and acute airway obstruction if abdominal muscle function is not evaluated.

Acute Disease↗

PubMed1997

Short-term effects of bracing on exercise performance in mild idiopathic thoracic scoliosis.

In adolescent idiopathic thoracic scoliosis (ITS) working capacity may be reduced during exercise. Despite concern about its usefulness, bracing is still being used in ITS. Thus the effects of bracing on exercise performance need to be examined. We studied six females, ages 12-15 years who had mild ITS (Cobb angle range 20-35 degrees). Pulmonary volumes, maximal voluntary ventilation (MVV), breathing pattern, the lowest (most negative in sign) pleural pressure during sniff maneuver (Pplsn), and pleural pressure swings (Pplsw) were measured first. Then, Pplsw, O2 uptake (VO2), CO2 output (VCO2), heart rate (HR) at rest and during progressive incremental exercise on a cycling ergometer (10 watts/min) were recorded. The exercise test was performed under control conditions without bracing (C) and after 7 days of bracing with the braced on (B). Dyspnea was measured by a modified Borg scale. At rest, bracing mildly affected total lung capacity and forced vital capacity (p < 0.03 for both) but not breathing pattern, Pplsn, or Pplsw (%Pplsn), a measure of respiratory effort. Furthermore, bracing did not consistently affect maximum work rate (WRmax). In both B and C VO2 was below (< 70%) the predicted value, VE was below (< 45%) MVV, and HR reserve was < 15 beats/min, indicating some cardiovascular deconditioning. On the other hand, respiratory frequency (Rf) increased more in B than in C (p < 0.03). In addition, Pplsw, Pplsw (%Pplsn), and Pplsw (%Pplsn)/VT, an index of neuroventilatory dissociation (NVD) of the respiratory pump, were greater in B (p < 0.03 for all). At a similar work rate, the Borg rating score was greater with bracing on than off, and the difference (delta Borg) tended to relate to concurrent changes in Pplsw (%Pplsn)/VT (r2 = 0.71; p < 0.07). We conclude that bracing affects respiratory effort, NVD, and dyspnea score during progressive exercise. These effects are consistent with increased lung elastance. Diminished exercise tolerance in patients with mild ITS probably reflects impaired physical fitness but is not affected by bracing. Training programs proposed for this subset of patients to increase peripheral muscle performance might also consider NVD of the respiratory pump.

Adolescent↗

PubMed1997

Chronic exertional dyspnea and respiratory muscle function in patients with chronic obstructive pulmonary disease.

The symptom of breathlessness is an important outcome measure in the management of patients with chronic obstructive pulmonary disease (COPD). Clinical ratings of dyspnea and routine lung function are weakly related to each other. However, in the clinical setting breathlessness in COPD is encountered under conditions of increased respiratory effort, impeded respiratory muscle action, or functional weakness. Thus, the present study was carried out to determine whether and to what extent clinical ratings of dyspnea and respiratory muscle dysfunction relate to each other. In 21 patients with COPD two methods were used to rate dyspnea: a modified Medical Research Council Scale (MRC) and the Baseline Dyspnea Index (BDI), which is a multidimensional instrument for measuring dyspnea based on three components: magnitude of task, magnitude of effort, and functional impairment. A baseline focal score was obtained as the sum of the three components. Measures were: pulmonary volumes; arterial blood gases; maximal voluntary ventilation (MVV); maximal inspiratory and expiratory pressures (MIP and MEP, respectively); and breathing patterns ventilation (VE), tidal volume (VT), and respiratory frequency (Rf). In 15 patients pleural pressure was also measured during both quiet breathing (Pplsw) and maximal inspiratory sniff maneuver at FRC (Pplsn). BDI and MRC ratings related to each other and showed comparable weak associations with standard parameters (FEV1, PaCO2, VT), MIP, and MEP. In contrast, MVV closely and similarly related to both ratings. Pplsw (%Pplsn), a measure of respiratory effort, and Pplsw (%Pplsn)/VT(%VC), an index of neuroventilatory dissociation, related significantly to both the BDI (r2 = -0.77 and r2 = -0.75, respectively) and the MRC (r2 = 0.81 and r2 = 0.74, respectively). Using MVV, Pplsw (%Pplsn), and Pplsw (%Pplsn)/VT(%VC) in a stepwise multiple regression as independent variables with BDI rating as dependent variable, MVV explained an additional 14.5% of the variance of the BDI over the 67.8% predicted by Pplsw (%Pplsn). Our results demonstrate that the level of chronic exertional dyspnea in COPD increases as the ventilatory muscle derangement increases. The level of the relationships among dyspnea ratings and MVV and respiratory effort helps to explain some of the mechanisms of chronic dyspnea of COPD. These measures should be considered for therapeutic intervention to reduce dyspnea.

Dyspnea↗

PubMed1997

Abdominal muscle recruitment and PEEPi during bronchoconstriction in chronic obstructive pulmonary disease.

BACKGROUND: It has been recently shown that, when breathing at rest, many patients with severe chronic obstructive pulmonary disease (COPD) contract abdominal muscles during expiration, and that this contraction is an important determinant of positive end expiratory alveolar pressure (PEEPi). In this study the effects of acute bronchoconstriction on abdominal muscle recruitment in patients with severe COPD were studied, together with the consequence of abdominal muscle action on chest wall mechanics. METHODS: Breathing pattern, pleural (PPL) and gastric (PGA) pressures, and changes in abdomen anteroposterior (AP) diameter were studied in 14 patients with COPD (mean forced expiratory volume in one second (FEV1) 1.06 (0.08) 1) under control conditions and during histamine-induced bronchoconstriction. RESULTS: The analysis of plots of PGA versus the AP diameter of the abdomen revealed that during maximal broncho-constriction (decrease in FEV1 of 34.8% (95% confidence intervals (CI) 29.9 to 39.7)) the expiratory rise in PGA increased significantly whereas end expiratory abdomen AP diameter decreased, indicating marked abdominal muscle recruitment. As a consequence, the rib cage compartment accounted for all of the volume of hyperinflation during bronchoconstriction (mean value 0.66 I, 95% CI 0.49 to 0.83). Positive end expiratory alveolar pressure during progressive bronchoconstriction was related directly to the expiratory rise in PGA and inversely to the expiratory time. CONCLUSIONS: The results indicate that, in patients with severe COPD, the abdominal muscles are recruited during acute bronchoconstriction. This recruitment probably preserves diaphragm length at the beginning of inspiratory muscle contraction despite the hyperinflation, and contributes significantly to positive end expiratory alveolar pressure. The degree of dynamic pulmonary hyperinflation during bronchoconstriction can be overestimated if abdominal muscle contraction is not assessed.

Abdominal Muscles↗

PubMed1997

Respiratory muscle function and control of breathing in patients with acromegaly.

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.

Acromegaly↗

PubMed1997

Respiratory mechanics in patients with tense cirrhotic ascites.

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.

Ascites↗

PubMed1997

In vivo ultrasound assessment of respiratory function of abdominal muscles in normal subjects.

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.

Abdominal Muscles↗

PubMed1997

Breathlessness and control of breathing in patients with COPD.

We tried to verify, in a clinical setting, the hypothesis that enhanced perception of dyspnoea (PD) and increased respiratory drive (RD): 1) relate to each other; and 2) elicit an integrated response that leads to a decrease in RD and tidal volume (VT) aimed at minimizing PD. In 34 patients with chronic obstructive pulmonary disease (COPD), dyspnoea was graded on a four-point scale after a Medical Research Council (MRC) questionnaire concerning respiratory symptoms. Patients were divided into four groups according to the dyspnoea score. Pulmonary volumes, arterial blood gases, VT, respiratory frequency (fR), inspiratory time (tI), expiratory time (tE), maximal inspiratory pressure (MIP), and maximal expiratory pressure (MEP) were measured. RD was also assessed in terms both of mouth occlusion pressure (P0.1) and electromyographic (EMG) activity of the respiratory muscles. Increase in dyspnoea rating was associated with decrease in vital capacity (VC), forced expiratory volume in one second (FEV1), MIP, VT and tI; and increase in arterial carbon dioxide tension (Pa,CO2), P0.1, and EMG (analysis of variance (ANOVA) and Bonferroni's test). A rapid and shallow pattern of breathing (RSB) characterized the group with the highest dyspnoea rating. Stepwise multiple regression analysis showed that: 1) tI and FEV1 accounted for a substantial proportion of the variability in VT and tI, respectively; 2) VT and MIP, together, predicted a substantial proportion of the variability in Pa,CO2 (r2 = 0.50). We conclude that, in patients with chronic obstructive pulmonary disease clinical rating of dyspnoea appears to be associated with muscle weakness and increase in respiratory drive. The increased respiratory drive is modulated into a rapid and shallow pattern of breathing, which leads to hypercapnia.

Aged↗